Cuccurullo

Question 1

Gait cycle

Answer 1

Single sequence of functions of one limb

One gait cycle = 1 stride

1 stride = 2 steps

Question 2

Stride

Answer 2

Linear distance between successive points of contact of same foot (heel strike to heel strike of same foot)

Question 3

Step

Answer 3

Linear distance between successive contact points of opposite feet (heel strike of one foot to heel strike of other foot)

Question 4

Normal step length

Answer 4

15-20 inches (~40 cm)

Question 5

Gait cycle phases

Answer 5

Stance phase & swing phase

Question 6

Gait cycle at normal walking speed

Answer 6

60% stance
40% swing

Walking faster decreases the time spent in stance phase (increasing time in swing phase)

Question 7

Double limb support

Answer 7

Occurs at beginning & end of stance phase

20% of normal gait cycle (vs 80% of single limb support)

Question 8

When is a person considered to be running?

Answer 8

When there is no longer a double support period

Question 9

Cadence

Answer 9

Number of steps per unit time

Question 10

Center of Gravity (CoG)

Answer 10

5-cm anterior to the S2 vertebra

CoG is displaced 5-cm (<2 inches) horizontally & 5-cm vertically during an average step

Question 11

Stance Phase sub-divisions

Answer 11

I Like My Tea Pre-sweetened:

I: Initial contact

L: Loading response (body has lowest CoG during this)

M: Mid-stance (time period from lift of the contralateral extremity from the ground to the point where ankles of both extremities are aligned in frontal (or coronal plane) (body has the highest CoG during this)

T: Terminal stance

P: time period from initial contact of contralateral extremity to just prior to lift of the ipsilateral extremity from the ground (unloading weight)

Question 12

Base of support

Answer 12

Space outlined by the feet & any assistive device in contact with the ground

Falling is avoided if the CoG remains positioned over the base of support

Normal base of support (distance between heels): 6-10 cm

Question 13

Swing Phase

Answer 13

In My Teapot:

I: Initial swing (lift of the extremity from the ground to position of maximum knee flexion)

M: Midswing (knee flexion to vertical tibia position)

T: terminal Swing (vertical tibia position to just prior to initial contact)

Question 14

Determinants of gait

Answer 14

1. Pelvic rotation: rotates anteriorly on swinging leg side, lengthening limb as it prepares to accept weight
2. Pelvic tilt: pelvis on side of swinging leg lowered 4-5 degrees, which lowers CoG at mid-stance
3. Knee flexion in stance: early knee flexion at foot strike (15 degrees). Bending of the knee reduces the vertical elevation of the body at mid-stance. This lowers the CoG (by minimizing its vertical displacement), decreasing energy expenditure. Also tends to absorb shock of impact at heel strike by lengthening contraction of quadriceps
4. Foot mechanisms (ankle flexion/extension): at heel strike, ankle PF smoothens the curve of the falling pelvis. A/w controlled PF during the first part of the stance. 3 pivot points (rockers) at the heel, ankle, & forefoot help to functionally lengthen the stance limb at initial contact & pre-swing, & shorten the limb at mid-stance
5. Knee mechanisms: after mid-stance, the knee extends as the ankle PF & the foot supinates to restore the length to the length & diminish the fall of the pelvis at the opposite heel strike
6. Lateral displacement of the pelvis: displacement toward the stance limb

1-5 reduce displacement on the vertical plane. 6 reduces displacement on the horizontal plane

Question 15

Why does foot slap occur at initial contact?

Answer 15

Moderately weak dorsiflexors (grade 3/5)

Question 16

Why does genu recurvatum occur from initial contact through mid-stance??

Answer 16

1. Weak, short, or spastic quadriceps
2. Compensated hamstring weakness
3. Achilles tendon contracture
4. PF spasticity

Question 17

Why does excessive foot supination occur from initial contact through mid-stance?

Answer 17

1. Compensated forefoot valgus deformity
2. Pes cavus
3. Short limb

Question 18

Why does excessive trunk extension occur from initial contact through mid-stance?

Answer 18

1. Weak hip extensor or flexor
2. Hip pain
3. Decreased knee ROM

Question 19

Why does excessive trunk flexion occur from initial contact through mid-stance?

Answer 19

1. Weak glut max & quadriceps
2. Hip flexion contracture

Question 20

Why does excessive knee flexion occur from initial contact through pre-swing?

Answer 20

1. Hamstring contracture
2. Increased ankle DF
3. Weak PF
4. Long limb
5. Hip flexion contracture

Question 21

Why does excessive medial femur rotation occur from initial contact through pre-swing?

Answer 21

1. Tight medial hamstrings
2. Anteverted femoral shaft
3. Weakness of opposite muscle group

Question 22

Why does excessive lateral femur rotation occur from initial contact through pre-swing?

Answer 22

1. Tight lateral hamstrings
2. Retroverted femoral shaft
3. Weakness of opposite muscle group

Question 23

Why does wide base of support occur from initial contact through pre-swing?

Answer 23

1. Hip abductor muscle contracture
2. Instability
3. Genu valgum
4. Leg length discrepancy

Question 24

Why does narrow base of support occur from initial contact through pre-swing?

Answer 24

1. Hip adductor muscle contracture
2. Genu varum

Question 25

Why does excessive trunk lateral flexion (compensated Trendelenburg gait) occur from loading response through pre-swing?

Answer 25

1. Ipsilateral glut med weakness 2. Hip pain

Question 26

Why does pelvic drop (uncompensated Trendelenburg gait) occur from loading response through pre-swing?

Answer 26

Ipsilateral glut med weakness

Question 27

Why does waddling gait occur from loading response through pre-swing?

Answer 27

Bilateral glut med weakness

Question 28

Why does excessive foot pronation occur from mid-stance through pre-swing?

Answer 28

1. Compensated forefoot or hindfoot varus deformity 2. Uncompensated forefoot valgus deformity 3. Pes planus 4. Decreased ankle DF 5. Increased tibial varum 6. Long limb 7. Uncompensated internal rotation of tibia or femur 8. Weak tibialis posterior

Question 29

Why does bouncing or exaggerated motion occur from mid-stance through pre-swing?

Answer 29

1. Achilles tendon contracture 2. Gastroc-soleus spasticity in PF

Question 30

Why does inadequate hip extension occur from mid-stance through pre-swing?

Answer 30

1. Hip flexor contracture 2. Weak hip extensor

Question 31

Why does steppage gait/foot drop occur in swing phase?

Answer 31

1. Severely weak dorsiflexors 2. Equinus deformity 3. PF spasticity

Question 32

Why does circumduction occur in swing phase?

Answer 32

1. Long limb 2. Abductor muscle shortening or overuse 3. Stiff knee

Question 33

Why does hip hiking occur in swing phase?

Answer 33

1. Long limb 2. Weak hamstring 3. QL shortening 4. Stiff knee

Question 34

Gait impairment in Parkinson disease

Answer 34

Stooped posture, festinating gait, shuffling, decreased arm swing, reduced trunk rotation, "start hesitation," freezing while walking/turning (when severe) Primary disturbance: reduced step length

Question 35

Gait impairment with hip flexion contracture

Answer 35

Decreased hip extension ROM results in compensation with anterior pelvic tilt, decreased contralateral step length, & increased knee flexion Increases energy consumption. A 35-degree contracture due to iliopsoas tightness results in a 60% increase in energy consumption

Question 36

Energy expenditure during wheelchair propulsion

Answer 36

Only 9% increased compared to ambulation in normal subjects

Question 37

Energy expenditure during crutch walking

Answer 37

Requires more energy than walking with a prosthesis

Question 38

Muscles that need strengthening in preparation for crutch walking

Answer 38

Latissimus dorsi, triceps, pec major, quads, hip extensors, hip abductors

Question 39

What type of amputation has higher energy expenditure?

Answer 39

Vascular > traumatic (usually sicker)

Question 40

What is a major risk factor for LE amputation?

Answer 40

DM- contributes to 67% of all LE amputations 55% of those will require amputation of contralateral LE within 2-3 years Since 1996, rate of LE amputation from DM is actually declining- prevention is key

Question 41

What is the leading cause of UE amputations?

Answer 41

Trauma- 80% of UE amputations Majority are limited to digital amputations Mostly male between ages 15-30 MVC is most common cause UE amputations account for 67% of all trauma-related amputations

Question 42

What is a mangled hand?

Answer 42

An amputation causing irreparable damage when 4 of the following 6 basic parts are not salvageable: skin, vessels, skeleton, nerves, extensor tendons, flexor tendons Initial goal: save all feasible length

Question 43

What is the most common terminal device for a body-powered device (hook or hand)

Answer 43

Voluntary opening

Question 44

Prosthetic wrist units

Answer 44

Wrist units are used for attaching terminal devices to prostheses & providing pronation/supination to place the terminal device in its proper position

Question 45

What does a wrist flexion unit allow for terminal device?

Answer 45

For TD to be in the flexed position, facilitating ability to perform activities close to the body, which is important for bilateral UE amputees

Question 46

What are the two types of wrist units?

Answer 46

Friction control or locking

Question 47

What is a friction control wrist unit?

Answer 47

Permits pronation & supination of the TD & hold it in a selected position by means of friction derived from a compressed rubber washer or from forces applied to the stud of the TD

Question 48

What is a locking wrist unit?

Answer 48

Prevents inadvertent rotation of the TD in the wrist unit when a heavy object is grasped

Question 49

What are the two types of wrist flexion units?

Answer 49

Add-on & combination

Question 50

What is an add-on wrist flexion unit?

Answer 50

Worn between wrist & TD, allowing manual positioning of the TD in either the straight or the flexed position

Question 51

What is the combination type wrist flexion unit?

Answer 51

Combines a friction wrist & a wrist flexion component in one & provides for setting & locking in one position

Question 52

What is a Muenster socket (self-suspended socket)?

Answer 52

Alternative to the split socket (for short trans-radial amputees) Socket & forearm are set in a position of initial flexion & the socket encloses the olecranon & epicondyle of the humerus The intimate residual limb encapsulation, flexion attitude, & high trim lines provide suspension Although there is some limitation in flexion-extension ROM, this is compensated by pre-flexing the socket When this type of suspension is used, a figure-9 harness can be used for control purposes only With these prostheses, the patient can operate the TD in common positions & still apply full torque about the elbow. Although these techniques yield less EF than the split socket, the reduction in force requirements & ease of use more than compensate for this limitation

Question 53

What is a Figure-8 (O-ring) harness?

Answer 53

Most commonly used harness The axilla loop, worn on the sound side, acts as a reaction point for the transmission of body force to the TD The anterior suspension strap on the involved side gives additional support for pulling or lifting, & acts as the attachment point for the elbow loading strap on a body-powered above-elbow prosthesis

Question 54

What is an elbow disarticulation prosthesis?

Answer 54

Variation of a trans-humeral prosthesis Socket is flat & broad distally to conform to epicondyles of distal humerus, which provides self-suspension & allows for IR & ER of humerus Length of residual limb requires use of external elbow joint with cable-operated locking mechanism Harness and control system are the same as for trans-humeral prostheses

Question 55

What harness designs are used most frequently for trans-humeral prostheses?

Answer 55

Modifications of the basic figure-8 & chest strap patterns used with trans-radial prostheses

Question 56

Dual-control cable mechanism operation in the trans-humeral amputee

Answer 56

Elbow flexion: humeral flexion & bi-scapular abduction --> dual-control cable Lock elbow (in desired degree of flexion): shoulder depression, extension, & abduction (down, back, & out) --> single-control cable (elbow-lock cable) TD operation (open & close): further humeral flexion & bi-scapular abduction --> dual-control cable Unlock elbow: shoulder depression, extension, & abduction (down, back, & out) --> single-control cable (elbow-lock cable). After desired TD function is accomplished, the elbow is unlocked & the elbow extends by gravity

Question 57

Body-powered vs myo-electric control systems

Answer 57

Body-powered devices: less expensive, lighter, more durable, easier to repair, higher sensory feedback. Disadvantages: mechanical appearance, difficult to use for some people, dependent on motor strength Myo-electric devices: better cosmesis, less harnessing, stronger grasp force. Disadvantages: more expensive, heavier, decreased durability due to electronic components & the need for daily recharging of batteries

Question 58

Trans-radial amputee training (myo-electric)

Answer 58

Myo-electric trans-radial prostheses use muscle contractions to activate the prosthesis (such as activation of wrist flexors closing TD & activation of wrist extensors opening TD)

Question 59

Diagnostic testing for PAD

Answer 59

ABI, Doppler velocity waveform analysis, intra-arterial contrast angiography

Question 60

ABI

Answer 60

Ratio of brachial systolic pressure to ankle systolic pressure Accuracy is limited for large vessels & for calcified vessels, which can occur in diabetic, elderly, or renal failure patients Not a reliable tool for determining level of amputation 0.91 - 1.30 --> normal 0.71 - 0.90 --> mild PAD 0.41 - 0.70 --> moderate PAD 0.00 - 0.40 --> severe PAD >1.30 --> calcified, non-compressible vessels (false negative)

Question 61

Doppler velocity waveform analysis

Answer 61

Performed when screening ABI is abnormal, done to localize lesion Obtained at multiple sites. Change in waveform from one level to next is indicative of PAD

Question 62

Intra-arterial contrast angiography

Answer 62

Gold standard testing for PAD Invasive test & should not be used for screening purposes

Question 63

Myodesis

Answer 63

Muscles & fascia are sutured directly to bone through drill holes Residual limb is more structurally stable Contra-indicated in severe dysvascularity- blood supply to the bone may be compromised

Question 64

Myoplasty

Answer 64

Opposing muscles are sutured to each other & to the periosteum at the end of the cut bone with minimal tension Less operating time, procedure of choice in severely dysvascular residual limbs

Question 65

Where does Lisfranc amputation occur?

Answer 65

Tarsometatarsal junction

Question 66

What is a Chopart amputation?

Answer 66

Removes all tarsals & metatarsals. Only talus & calcaneus remain

Question 67

What occurs after both the Lisfranc & Chopart amputation?

Answer 67

Remaining foot often develops a significant equinovarus deformity resulting in excessive anterior WB with breakdown Adequate dorsiflexor tendon re-attachment with Achilles tendon lengthening can be used to prevent this deformity

Question 68

Syme's amputation

Answer 68

Essentially an ankle disarticulation with attachment of the distal heel pad to the end of the tibia; may include removal of the malleoli and/or distal tibial/fibular flares Indications: trauma of the foot, congenital anomalies, tumors, & deformities that necessitate amputation Disadvantages: healthy plantar heel skin is necessary for WB in this area. Patient also must have good perfusion in this area, so difficult procedure for the dysvascular patient Pros: functionally, this procedure represents an excellent level of amputation because: - maintains length of limb - preservation of heel pad, excellent WB residual limb - early fitting of prosthesis is possible with excellent results - partial WB of residual limb is possible almost immediately after the procedure with a proper rigid casting (within 24 hours) Cons: - decreased cosmesis (bulky, bulbous residual limb) - fitting for a prosthesis may be more difficult than for other amputation levels

Question 69

Functional ability after BKA in the elderly

Answer 69

50% of patients have worse functional ability

Question 70

Ideal shape for trans-tibial residual limb

Answer 70

Cylindrical

Question 71

Ideal shape for trans-femoral residual limb

Answer 71

Conical

Question 72

Medicare's functional levels of ambulation for amputees (K levels)

Answer 72

K0: non-ambulatory (bed-bound), no prosthesis allowed K1: limited to transfers or limited household ambulator --> manual lock or stance-control knee, SACH, or single-axis foot K2: unlimited household but limited community ambulator --> pneumatic or polycentric knee, multi-axis foot K3: unlimited community ambulator, VARIABLE CADENCE --> hydraulic knee, micro-processor knee, energy-storing foot K4: high-energy activities (sports work) --> same as K3

Question 73

Prosthetics for Syme's amputation

Answer 73

Patient can stand easily & walk on the end of the residual limb without wearing a prosthesis for short household distances Prosthesis either has a posterior or medial opening. Both require removal of a portion of the socket wall to get the bulbous residual limb in. Major disadvantage is poor cosmesis. Newer socket designs that incorporate an expandable air suspension chamber inside the socket or a thin removable expandable inner socket liner provide a more cosmetically acceptable prosthetic design. Pros: thinner, tighter, stronger prosthetic socket, maintain structural integrity of prosthesis Prosthetic feet available for a Syme's amputation: - SACH - SAFE (syme stationary ankle flexible endoskeleton) - Energy-storing carbon fiber foot (low profile)

Question 74

Patellar tendon bearing socket

Answer 74

Standard socket used for the average BKA --> total contact PTB socket PTB socket is a custom-molded thermoplastic or laminated socket that distributes weight through convex build-ups (bulges) over pressure-tolerant areas & provides concavities (relief areas) on pressure-sensitive areas Bar in anterior wall designed to apply pressure on the patellar tendon Trim line extends anteriorly to the mid-patellar level, may extend medially & laterally to the femoral condyles, & extends posteriorly to level of the PTB bar Pressure should be equally distributed over pressure-tolerant areas

Question 75

Pressure-tolerant areas

Answer 75

1. Patella tendon 2. Pre-tibial muscles 3. Popliteal fossa (gastroc-soleus muscles via gastroc depression) 4. Lateral shafter of fibula 5. Medial tibial flare

Question 76

Pressure-sensitive areas (relief areas)

Answer 76

1. Tibial crest, tubercle, & condyles 2. Fibular head 3. Distal tibia & fibula 4. Hamstring tendons 5. Patella

Question 77

How is PTB socket aligned to relieve pressure on pressure-sensitive areas?

Answer 77

Socket is aligned on the shank on slight flexion (5-8 degrees) to enhance loading of the patellar ligament, prevent genu recurvatum, resist the tendency of the residual limb to slide down the socket, & to place quadricep in a more efficient & mechanically advantageous position, facilitating its contraction A maximum of 25 degrees of flexion is possible to accommodate knee flexion contracture Alignment of socket also includes a slight lateral tilt to reduce pressure on fibular head Liner added to socket to protect fragile or insensate skin, reduce shear forces, provide a more comfortable socket for tender residual limbs, or accommodate for growth Custom gel liners without the suspension pin are helpful in managing shear problems that can occur with residual limbs covered with split-thickness skin grafts, or boney prominences

Question 78

Suction suspension for BKA

Answer 78

Silicone or other gel insert with use of a one-way expulsion valve in the distal aspect of the socket. Valve allows air to escape from the socket but not enter Advantages: does not create pressure distributions that are likely to disturb normal circulation & soft tissue fluid balance as much as pin suspension. Provides excellent suspension for amputees with greater suspension demands (like athletes), & for those with short residual limbs, as well as excellent skin protection for the scarred residual limb Elevated vacuum socket systems use a mechanical or electric pump to generate negative pressure between the limb & socket for enhanced suspension & contact Disadvantage: expensive because gel liners are typically replaced annually

Question 79

What are different types of prosthetic feet?

Answer 79

Rigid keel, single-axis foot, multi-axis foot, flexible keel, Seattle foot (energy-storing/dynamic response), Flexfoot (carbon fiber or fiberglass foot; energy-storing/dynamic response)

Question 80

What are examples of a rigid keel?

Answer 80

1. SACH (solid ankle cushion heel) 2. Wooden keel 3. Compressible heel

Question 81

What are main uses of rigid keel?

Answer 81

For general use, kids-durable, limited ambulation needs, & K1 users Advantages: inexpensive, light (lightest foot available), durable, reliable Disadvantages: energy-consuming, rigid, best on flat surface

Question 82

What is a single-axis foot?

Answer 82

Movement in one plane (DF/PF). Heel-height adjustable versions available

Question 83

What is the main use of a single-axis foot?

Answer 83

To enhance knee stability AKA who needs greater knee stability (goes to flat foot quick before knee buckles); knee goes back into extension (gives stability in early stance) K1 users Advantages: adds stability to prosthetic knees Disadvantages: increased weight (70% heavier than SACH), increased cost, increased maintenance

Question 84

What is function of a multi-axis foot?

Answer 84

Allows PF, DF, inversion, eversion, & rotation

Question 85

What is the main use of a multi-axis foot?

Answer 85

Used for ambulation on uneven surfaces, absorbs some of the torsional forces created in ambulation, K2 users Advantages: multi-directional motion, permits some rotation, accommodates uneven surfaces, relieves stress on skin & prosthesis Disadvantages: relatively bulky, heavy, expensive, increased maintenance, greater latitude of movement may create instability in patients with decreased coordination

Question 86

What are examples of a flexible keel?

Answer 86

1. SAFE (stationary ankle flexible endoskeleton) - used in Syme's amputation 2. STEN (stored energy)

Question 87

What are main uses for a flexible keel?

Answer 87

Used for ambulation on uneven surfaces, K2 users Advantages: multi-directional motion, moisture & grit resistance, accommodates uneven surfaces, absorbs rotary torques, smooth rollover Disadvantages: heavy, increased cost, not cosmetic, does NOT offer inversion/eversion

Question 88

Why would you specifically use a STEN for flexible keel?

Answer 88

Used when smooth rollover needed. Has an elastic keel & accommodates numerous shoe styles. The ML stability is similar to SACH Major disadvantage: cannot be used with Syme amputation

Question 89

Seattle foot (energy-storing foot/dynamic response)

Answer 89

Consists of a canti-levered plastic C- or U-shaped keel, which acts as a compressed spring Used for jogging, general sports, conserves energy. Used for K3 & K4 users Advantages: energy storing, smooth rollover Disadvantages: high cost, no SACH heel makes it difficult to change compressibility of heel

Question 90

Flexfoot (carbon fiber or fiberglass foot) (energy-storing foot/dynamic response)

Answer 90

Pylon & foot incorporated into one unit. The dynamic keel extends to the bottom of the trans-tibial socket (& in AKA, to the level of the knee unit). Flex-walk is a shorter version of the Flexfoot, attaching to the shank at the ankle level Used for running, jumping, vigorous sports, conserves energy. K3 & K4 users Advantages: very light, most energy-storing most stable ML, lowest inertia Disadvantages: very high cost, alignment can be cumbersome

Question 91

Why is polycentric knee different than single-axis knee?

Answer 91

Polycentric knee has an instantaneous center of rotation that changes & is proximal & posterior to the knee unit itself. This allows greater knee stability, more symmetrical gait, & equal knee length when sitting

Question 92

Ischial containment socket

Answer 92

Also known as a narrow ML socket or contoured adducted trochanteric-controlled alignment method (CAT-CAM) socket ML dimension is narrower than the AP measurement ML design provides a more normal anatomic (adducted) alignment of the femur inside the socket Ischial tuberosity is contained inside the socket, providing a bony lock between the ischium & greater trochanters WB is concentrated in the medial aspect of the ischium & ischial ramus Socket is pre-flexed 5-7 degrees to maximize hip extensor muscle control. Maximum 20 degree flexion is allowed to accommodate flexion contracture Fabricated with a flexible inner thermoplastic liner & a rigid outer frame. Cutouts can be made in the outer frame to accommodate bony or sensitive areas

Question 93

What are advantages of an ischial containment socket?

Answer 93

1. Stabilizes relationship between pelvis & proximal femur since the ischial tuberosity is controlled inside socket rather than on top of posterior brim like in quad socket 2. Narrow ML design keeps femur in adduction during stance phase, permitting hip abductors to be in a more stretched & efficient position 3. More energy-efficient ambulation at high speed 4. Increased comfort in groin area compared to quad socket (in which WB is done primarily on the ischial tuberosity) 5. Less lateral thrust of prosthesis at midstance 6. Higher trim line results in better control of the residual limb especially for short AKA amputation 7. Able to accommodate smaller residual limb 8. Greater ML control of pelvis with this design

Question 94

What are disadvantages of ischial containment socket?

Answer 94

1. More expensive & difficult to fabricate than quad socket 2. Wider AP dimension at level of ischial ramus leads to increased movement in AP plane

Question 95

What are the different types of knee units available for AKA?

Answer 95

1. Constant friction knee (single axis with constant friction unit) 2. Stance control knee/Safety knee/Weight-activated friction brake 3. Polycentric/Four-bar knee 4. Manual locking knee 5. Fluid-controlled knee units- hydraulic (oil), pneumatic (air) 6. Microprocessor-control hydraulic knee

Question 96

Constant Friction Knee (Single axis with constant friction unit)

Answer 96

Friction mechanisms are devices used in swing control knee to dampen the pendular action of the prosthetic knee during the swing phase, to decrease the incidence of high heel rise in early swing & decrease terminal impact in late swing Single walking speed when used, may be used in kids Does NOT give stance control; a screw is used to adjust the friction to determine how fast or slow the knee swings Good for a K1 ambulator Inexpensive, durable, & reliable Disadvantages: low stability (in early stance the single axis has the lowest zone of stability), fixed single cadence, too much friction prevents knee from flexing, too little friction causes the knee to swing too easily so patient needs to vault, no stance control

Question 97

Stance-Control Knee/Safety Knee/Weight-Activated Friction Brake

Answer 97

Single axis knee with stance control. Stance control acts as a brake system Indications: geriatrics, short residual limb, general disability, uneven surfaces, amputees with weak hip extensors Good for K1 ambulator & for preparatory prosthesis. Provides improved knee stability. Braking mechanism if weight applied with knee flexed 0-20 degrees Disadvantages: slightly increased weight, increased cost, increased maintenance, must unload fully to flex, cannot use in b/l AKA since knees would not bend with loading & cannot bend both knees at same time (patient cannot sit down), activities that require knee motion under WB (such as step over step stair descent) are incompatible with this knee

Question 98

Polycentric/Four-Bar Knee

Answer 98

No stance control, but inherently stable. Short knee unit, so can be used in knee disarticulation & long residual limb Good for K1 ambulator. Excellent knee stability & improved cosmesis in knee disarticulation & long residual limb patients Disadvantages: greater weight, bulk, cost, & maintenance. Although durable, needs maintenance every 3-6 months

Question 99

Manual Locking Knee

Answer 99

Knee of last resort used in the blind or CVA patient with amputation Uses a spring-loaded pin that automatically locks the knee when the amputee stands or extends the knee Knee is kept extended throughout the entire gait cycle to increase stability Good for K1 ambulator. Ultimate knee stability in stance phase Disadvantages: abnormal gait, awkward sitting, cannot use in b/l AKA because (like in stance-control knee), patient cannot sit. Knees lock on loading; therefore, person cannot bend both knees at same time to sit down

Question 100

Fluid-Controlled Knee Units

Answer 100

Hydraulic (oil) & Pneumatic (air) Pneumatic (air): cadence-responsive knee units through cadence-dependent resistance. Allows for either swing phase, or swing & stance phase control. Indications: For patients who vary cadence frequency, active walkers, ambulation in uneven terrain, K3 & K4 ambulators Advantages: variable cadence, smoothest gait, stable (will not lock unless at full extension). Pneumatic units are lighter but hydraulic units tolerate more weight (can support the heavier & more athletic amputee), can unlock for some activities (biking0 Disadvantages: greatest weight, increased cost, increased maintenance

Question 101

Microprocessor-Control Hydraulic Knee

Answer 101

Function similar to other hydraulic swing & stance phase knees. Has additional features of computer-programmed custom settings for each individual. Microprocessor re-calibrates stability of the knee 50x/second to adapt to changing conditions & ultimately prevent falls Advantages: computer-adjusting knee for variable gait cycles, energy-saving Disadvantages: highest cost, heavy, increased maintenance, inconvenience of daily charging, unproven track record for dependability

Question 102

Swim prostheses

Answer 102

Waterproof prosthesis or special swim leg Peg leg with or without fin attached for BKA or AKA Rubber suspension sleeve used for BKA that prevents water from entering the socket Hollow-chambered leg for BKA or AKA Exoskeletal leg with knee lock for AKA Waterproof suspension belt for AKA Flatfoot for barefoot walking for BKA or AKA

Question 103

What is choke syndrome?

Answer 103

Caused by proximal prosthetic socket being too tight & lack of total contact between residual limb & socket leads to impairment of venous return. Occurs most commonly at the distal trans-tibial residual limb due to atrophy over time & use of additional socks or when the residual limb becomes larger (excessive weight gain)

Question 104

Exam findings a/w choke syndrome

Answer 104

Initially with wearing a prosthesis, patient develops a well-circumscribed indurated area; if acute, edema can have weeping/blistering of skin Area is TTP & prone to cellulitis When chronic, skin becomes thickened & hyper-pigmented due to hemosiderin accumulation

Question 105

What is the treatment for choke syndrome?

Answer 105

Relieving proximal constriction & restoring total contact between the socket & residual limb by reducing number of socks & modification of the distal end pad. Often a new total contact socket is needed

Question 106

What is verrucous hyperplasia?

Answer 106

Wart-like skin overgrowth, usually of the residual distal limb resulting from inadequate socket wall contact with subsequent edema formation Chronic choke syndrome can lead to this Reversible by re-establishing total contact with the socket

Question 107

Trans-tibial amputee gait deviations: excessive knee flexion (increased knee flexion at moment of initial contact)

Answer 107

Increased ankle dorsiflexion Excessive anterior displacement of the socket over the foot Excessive posterior displacement of the foot in relation to the socket Too hard heel cushion (or plantar flexion bumper) Knee flexion contracture

Question 108

Trans-tibial amputee gait deviations: excessive knee extension (recurvatum; increased knee extension at moment of initial contact)

Answer 108

Increased ankle plantarflexion Moving socket too posteriorly in relation to the foot Moving foot anteriorly in relation to the socket Too soft heel cushion (or plantarflexion bumper) Quad weakness (excessive knee extension used as a stabilizing technique) Distal anterior tibial discomfort Habit

Question 109

Trans-femoral amputee gait deviations

Answer 109

1. Lateral trunk bending 2. Abducted gait 3. Circumduction 4. Vaulting 5. Medial & lateral whips (swing pase) 6. Foot rotation at heel strike 7. Foot slap 8. Uneven heel rise 9. Terminal impact 10. Uneven step length 11. Exaggerated lordosis 12. Instability of prosthetic knee during stance 13. Drop-off at end of stance phase

Question 110

Trans-femoral gait deviation: lateral bending of trunk

Answer 110

Excessive bending occurs laterally from midline, generally to prosthetic side Prosthetic causes: - Prosthesis may be too short - Improperly shaped lateral wall may fail to provide adequate support for femur - High medial wall may cause amputee to lean away to minimize discomfort - Prosthesis aligned in abduction may cause wide-based gait, resulting in this defect Amputee causes: - May not have adequate balance - May have hip abduction contracture - Residual limb may be over-sensitive & painful - Very short residual limb may fail to provide a sufficient lever arm for pelvis - Habit pattern

Question 111

Trans-femoral gait deviation: abducted gait

Answer 111

Very wide-based gait with prosthesis held away from midline at all times Prosthetic causes: - Prosthesis may be too long - Too much abduction may have been built into prosthesis - High medial wall may cause amputee to hold prosthesis away to avoid ramus pressure - Improperly shaped lateral wall can fail to provide adequate support for femur - Pelvic band may be positioned too far away from patient's body Amputee causes: - Hip abduction contracture - Habit

Question 112

Trans-femoral gait deviation: circumducted gait

Answer 112

Prosthesis swings laterally in wide area during swing phase Prosthetic causes: - May be too long - May have too much alignment stability or friction in knee, making it difficult to bend knee in swing-through Amputee causes: - Inadequate suspension - Abduction contracture of residual limb

Question 113

Trans-femoral gait deviation: vaulting

Answer 113

Rising on toe of sound foot permits amputee to swing prosthesis through with little knee flexion Prosthetic causes: - Prosthesis may be too long - Socket suspension may be inadequate - Excessive stability in alignment or some limitation of knee flexion, such as knee lock or strong extension aid, may cause this deficit Amputee causes: - Vaulting is a fairly frequent habit pattern - Fear of stubbing toe may cause this defect - Residual limb discomfort may be a factor

Question 114

Trans-femoral gait deviation: medial or lateral whips

Answer 114

Best observed when patient walks away from observer. Medial whip is present when heel travels medially on initial flexion at beginning of swing phase. Lateral whip exists when heel moves laterally Prosthetic causes: - Lateral whips may result from excessive IR of prosthetic knee - Medial whips may result from excessive ER of knee - Socket may fit too tightly, thus reflecting residual limb rotation - Excessive valgus in prosthetic knee may contribute to this defect - Badly aligned toe break in a conventional foot may cause twisting on toe-off Amputee causes: - Improper donning of socket or socket rotated on limb

Question 115

Trans-femoral gait deviation: foot rotation at heel strike

Answer 115

As heel contacts ground, the foot rotates laterally, sometimes with vibrating motion Prosthetic causes: - Too hard heel cushion or plantar flexion bumper Amputee causes: - Weakness at hip muscles

Question 116

Trans-femoral gait deviation: foot slap

Answer 116

Foot PF too rapidly & strikes the floor with a slap Prosthetic causes: - PF bumper is too soft, offering insufficient resistance to foot motion as weight is transferred to the prosthesis Amputee causes: - None

Question 117

Trans-femoral gait deviation: uneven heel rise

Answer 117

Prosthetic heel rises markedly & rapidly when knee is flexed at beginning of swing phase Prosthetic causes: - Knee joint may have insufficient friction - Extension aid may be inadequate Amputee causes: - May be using more power than necessary to force knee into flexion

Question 118

Trans-femoral gait deviation: terminal swing impact

Answer 118

Rapid forward movement of shin piece allows knee to reach maximum force before heel strike Prosthetic causes: - Knee friction is insufficient - Knee extension aid may be too strong Amputee causes: - Amputee may try to assure that knee is in full extension by deliberately & forcibly extending the residual limb

Question 119

Trans-femoral gait deviation: uneven step length

Answer 119

Length of the step taken with the prosthesis differs from that of the sound leg Prosthesis causes: - Insufficient socket flexion - Insufficient friction at the prosthetic knee or too loose an extension aid Amputee causes: - Pain or insecurity causing amputee to transfer weight quickly from the prosthesis to the sound leg - Hip flexion contracture

Question 120

Trans-femoral gait deviation: exaggerated lordosis

Answer 120

Exaggerated when the prosthesis is in stance phase, & the trunk may lean posteriorly Prosthetic causes: - Knee joint may be too far ahead of trochanter-knee-ankle line - Socket is mounted with excess flexion - PF resistance may be too great, causing knee to buckle at heel strike - Failure to limit DF can lead to incomplete knee control Amputee causes: - May have hip extensor weakness - Severe hip flexion contracture may cause instability

Question 121

Trans-femoral gait deviation: drop-off at end of stance phase

Answer 121

Downward movement of trunk as body moves forward over prosthesis Prosthetic causes: - Limitation of DF of prosthetic foot is inadequate - Heel of a SACH-type foot may be too short, or toe break of a conventional foot may be too far posterior - Socket may have been placed too far anterior in relation to foot Amputee causes: - None

Question 122

Bony overgrowth in amputation

Answer 122

Much more common in acquired amputations in children than in adults Bone usually grows faster than overlying skin & soft tissue in the distal end of amputated long bones (residual limb) Formation of bursa may occur over the sharp end & at times the bone may actually protrude through the skin Seen most frequently in: humerus --> fibula --> tibia --> femur Has been reported in congenital limb deficiencies, but very rarely May require surgical revision several times before skeletal maturity. Capping the end of the involved long bone with a cartilage epiphysis to eliminate overgrowth is an option Avoided in through-joint disarticulation; epiphyseal growth is preserved in through-joint disarticulation

Question 123

Cane measurement for ambulation

Answer 123

20-30 degree EF or height of the greater trochanter of the hip for cane height Cane typically goes on opposite side of weak extremity for bigger base of support

Question 124

Indications for a walker

Answer 124

1. Bilateral weakness and/or incoordination of the lower limbs or whole body 2. Whenever a firm, free-standing aid is appropriate to increase balance (like MS or Parkinsonism) 3. Relieve WB either fully or partially on a LE (allow the UE to transfer body weight to the floor) 4. Unilateral weakness or amputation of the lower limb where general weakness makes the greater support offered by the frame necessary (OA or fractured femur) 5. General support to aid mobility & confidence (after prolonged bedrest & sickness in the elderly)

Question 125

Advantages of a walker

Answer 125

- Provide wider base of support - More stable base of support - Sense of security for patients fearful of ambulation

Question 126

Disadvantages of a walker

Answer 126

- More conspicuous in appearance - Interferes with development of a smooth reciprocal gait pattern (decreased step length with step-to gait pattern) - Interferes with stair negotiation/difficult to maneuver through doorways or bathrooms

Question 127

UCBL orthosis (internal modification)

Answer 127

University of California Biomechanics Lab orthosis Custom-molded orthosis used to control flexible calcaneal deformities (rear-foot valgus or varus) & transverse plane deformities of the mid-tarsal joints (forefoot abduction or adduction) Encompasses the heel & hindfoot & holds the mid-foot with high medial & lateral trim lines Provides effective longitudinal arch support & realigns a flexible flat foot Allows for sub-talar supination, holds the calcaneus in place, & prevents sub-talar pronation

Question 128

What is a rocker bar (external sole modification?)

Answer 128

Convex strip placed across the sole just posterior to the metatarsal heads. Longer than the metatarsal bar Can be used to relieve metatarsal pain (by relieving pressure), quicken the gait cycle (by assisting rollover during stance), or assist DF or decrease demand on weak PF (push-off) Rigid rocker-bottom shoes are recommended for use in cases of plantar fasciitis, neuropathic ulceration, & trauma to mid-foot or metatarsal region Can include entire heel & sole to become a rocker-bottom sole Rocker bottom is good for a Charcot foot --> minimize forces the foot sees during standing/ambulatory activity; minimizes plantar area in contact with ground at any one time

Question 129

Line of gravity (weight line)

Answer 129

Line passing through the COG to the ground Behind the cervical vertebrae, in front of the thoracic vertebrae, & behind the lumbar vertebrae Slightly posterior to hip joint & tends to passively extend the hip joint Anterior to knee joint & tends to passively extend the knee Passes 1-2 inches anterior to ankle joint & tends to DF the ankle. Resisted by the soleus & gastroc While standing, the COG is midline & just anterior to S2 vertebra

Question 130

Line of gravity (weight line) during quiet standing passes through:

Answer 130

Posterior to hip joint --> extension Anterior to knee joint --> extension Anterior to ankle joint --> ankle DF

Question 131

What are thermoplastics?

Answer 131

Soften & become moldable when heated & harden when cooled so they can be molded & re-molded by heating Low-temperature thermoplastics: - Molded at temperatures just above body temperature (<80C or < 180F) - Can be shaped directly to the body without the need for a cast - Cannot be used effectively when high stress is anticipated, as in spasticity or in many LE applications - Main use is UE limb orthotics High-temperature thermoplastics: - Used to manufacture permanent orthotic devices using vacuum-forming techniques - Major types: acryclic, polyethylene, polypropylene, polycarbonate, ABS, vinyl polymers, & co-polymers Thermosetting plastics: develop a permanent shape when heat & pressure are applied & maintain a memory. More difficult to use than thermoplastics & cause more body irritation & allergic reactions Carbon fiber- advantages: lightweight, high strength. Disadvantages- very expensive, difficult to shape or modify

Question 132

Single channel ankle joint

Answer 132

Three options: 1. Inserting spring in the channel for dorsiflexion assist 2. Inserting a steel pin for plantarflexion stop 3. Inserting both a pin & a spring for dorsiflexion assist & plantarflexion stop

Question 133

Dual channel ankle joints

Answer 133

Have both anterior & posterior channels Posterior channel functions exactly the same as single channel ankle joint Anterior channel has additional option of an adjustable steel pin to block the forward progression of the tibia at mid-stance (dorsiflexion stop), or to lock the joint in a fixed position. Can be useful when quad muscle is weak or when there is a Charcot joint deformity at the ankle

Question 134

What is the best type of knee joint for an obese patient with quadriceps weakness?

Answer 134

KAFO with double metal uprights & a posterior offset knee joint (single axis knee joint)

Question 135

Offset knee joint

Answer 135

Places the hinge posterior to the knee joint so patient's weight line falls anterior to the offset joint, stabilizing the knee early during stance phase Allows sitting without needing to manipulate the lock Should not be used in patients with knee or hip flexion contractures, or with a PF stop at the ankle Must be careful when walking on a ramp as the knee may flex inadvertently

Question 136

Scott Craig orthosis

Answer 136

Bilateral KAFOs designed for standing & ambulation in adults with paraplegia Provides patient with a complete neurological level at L1 or lower with a more functional & comfortable gait Eliminates unnecessary hardware to reduce weight & facilitate donning/doffing (eliminates lower thigh & calf band) Components: - Sole plate extending to the met heads w/a crossbar added to the met heads for ML stabilization - Ankle joint set at 10 degrees of DF - Anterior rigid tibial band (patellar tendon strap) - Offset knee joint with bail lock - Proximal posterior thigh bind

Question 137

Is unsupported standing possible with a Scott Craig orthosis?

Answer 137

Yes! With the ankles & knees locked, hip stabilization can be achieved by leaning the trunk backward so that the CoG of the trunk rests posterior to the hip joint, resulting in tightening of the anterior hip capsule & the Y ligament

Question 138

Can paraplegic patients ambulate with Scott Craig orthosis?

Answer 138

Yes! If they also use crutches or walker using a swing-to or swing-through gait pattern

Question 139

Reciprocal Gait Orthosis (RGO)

Answer 139

A special design of the HKAFO used for upper lumbar paralysis in which active hip flexion is preserved Consists of bilateral HKAFO's with offset knee joints with drop locks, posterior plastic AFO's, thigh pieces, custom-molded pelvic girdle, hip joints, & a thoracic extension with Velcro straps in addition to the control mechanism Several designs are available, such as cord & pulley design, single cable, dual cable, & isocentric (IRGO, latest design) In all RGO's, the hip joints are coupled together with cables (or to the pivoting band in the IRGO), which provides mechanical assistance to hip extension while preventing simultaneous bilateral hip flexion As a step is initiated & hip flexion takes place on one side, the cable coupling induces hip extension on the opposite side, producing a reciprocal walking pattern Forward stepping is achieved by active hip flexion, lower abdominal muscles, and/or trunk extension Using two crutches & an RGO, paraplegics can ambulate with a four-point gait. A walker may also be used

Question 140

Isocentric RGO (IRGO)

Answer 140

Cord is substituted by a pelvic band attached to the posterior surface of the molded thoracic section Advantages: less bulky appearance (no protruding cables in the back), may be more cost-efficient than cable RGO (no energy loss due to cable friction)

Question 141

What does adding a footplate to a knee immobilizer do?

Answer 141

Decreases rotational instability of the knee

Question 142

Opponens orthosis

Answer 142

Immobilizes the thumb & first MCP joint to promote tissue healing and/or protection, or for positioning of the weak thumb in opposition to other fingers to facilitate three-jaw chuck pinch

Question 143

Long opponens orthosis with wrist-control attachments

Answer 143

Similar to short opponens orthosis but crosses the wrist Stabilizes 1st MCP while forearm bar maintains wrist in extension & prevents radial & ulnar deviation deformities Examples: long opponens splint, thumb spica splint

Question 144

Wrist-driven prehension orthosis (tenodesis orthosis, flexor hinge splint)

Answer 144

Used in C6 complete tetraplegia (no muscles to flex or extend; fingers remain innervated, but wrist extension, through the ECR, is intact) to provide prehension through tenodesis action & maintain flexibility of the hand, wrist, & elbow Wrist extensors should be 3+ or better to use body-powered tenodesis PIP & DIP joints of fingers 2 & 3 and the CMC & MCP joints of the thumb are immobilized May interfere with manual wheelchair propulsion Rarely accepted by C7 & C8 tetraplegics who prefer to use their residual motor power or utensil holders

Question 145

RIC Tenodesis Splint (Rehabilitation Institute of Chicago)

Answer 145

Made of low-temperature thermoplastics in 3 separate pieces (wristlet, short opponens, & dorsal plate over index & middle finger) Easily & quickly fabricated; made as a training & evaluation splint for patients; lightweight Uses a cord/string running from the wrist piece, across the palm, & up between the index & ring fingers. String is lax when wrist is flexed & tightens with wrist extension, bringing the fingers close to the immobilized thumb, accomplishing three-jaw chuck prehension

Question 146

Balanced forearm orthosis

Answer 146

Shoulder-elbow-wrist-hand orthosis that consists of a forearm trough (attached by a hinge joint to a ball-bearing swivel mechanism) & a mount (which can be mounted on the WC, on a table or working surface, or onto the body jacket) Helps support the forearm & arm against gravity & allows patients with weak shoulder & elbow muscles to move the arm horizontally & flex the elbow to bring hand to the mouth

Question 147

What are the requirements of the balanced forearm orthosis?

Answer 147

- Some residual muscle strength of biceps & pec (at least grade 2 or better) & coordination of elbow flexion (can be used for C5 tetraplegia) - Adequate trunk stability & balance - Adequate endurance in sitting position - Preserved ROM of the shoulder & elbow joints - Other uses: may be used in spastic patients to allow self-feeding by dampening muscle tone through a friction device

Question 148

Soft cervical collar

Answer 148

Made of polyethylene foam or sponge rubber Provides no significant control of motion of the C-spine, but does provide a kinesthetic reminder (through sensory feedback) to limit motion Retains body heat, which may help reduce muscle spasm & aid in healing of soft-tissue injuries Indications: symptomatic tx of soft tissue injuries of the neck (like whiplash injury) Maximum amount of time should be worn: 10 days Risks with prolonged use: muscle atrophy, psychological dependency

Question 149

Sterno-Occipital Mandibular Immobilizer (SOMI)

Answer 149

Cervico-thoracic orthosis with chest piece connected by uprights (going from anterior to posterior) to occipital plate Can easily be applied to a supine patient Has removable mandibular piece so patient can eat, wash, or shave while lying supine Indications: cervical arthritis, post-surgical fusions, stable cervical fractures

Question 150

Minerva CTO/Thermoplastic Minerva Body Jacket

Answer 150

Encloses the entire posterior skull, includes a band around the forehead, & extends downward to the inferior costal margin Forehead band provides good control of all cervical motions Advantages: lighter weight than the halo vest; no pins (no invasive supports that carry risks of infection & slippage) Disadvantages: less restriction of motion compared to a halo vest Indications: management of unstable cervical spine (although halo vest is usually preferred for maximum motion control) May be the preferred orthosis (over halo) in management of cervical spine instability in preschool age children due to increased comfort, decreased weight, & allows for early mobilization of the patient for rehabilitation, in addition to providing the necessary stability

Question 151

Halo vest CTO

Answer 151

Provides the best control of motion (in all planes) in the C-spine of all the cervical CTO Permits early mobilization without risk of compromising spinal alignment Non-removable Consists of a rigid halo ring secured to the skull with 4 external fixation pins (anterolateral above the orbital rim & posterolateral below the largest diameter of the skull). Pins are placed where they are to prevent cephalad pin migration, piercing the temporalis muscle, frontal & temporal fossae, or injury to CN's) Halo supports 4 posts attached to the anterior & posterior part of the vest (thoracic component) Indications: management of unstable fractures of the C-spine (especially high cervical fractures); non-surgical alternative in cases where surgery is contraindicated or refused Complications: risk of pressure ulcers with bedrest- especially scapula & sternum

Question 152

TLSO

Answer 152

Extend from sacrum to above the inferior angle of the scapulae & are used to support & stabilize the trunk & to prevent progression of moderate scoliosis (20-45 degrees) until patient reaches skeletal maturity, & used for thoracic kyphosis Except for thoracolumbosacral flexion-control orthoses, TLSO's can increase intra-abdominal pressure (which in turn decreases load on spine/IVD by transmission of the load to the surrounding soft tissues) Cause an increase in O2 consumption & EE During ambulation, with axial rotation between the pelvis & shoulders, there may be increased motion at the unrestrained segments cephalad & caudal to the orthosis

Question 153

Jewett Brace (flexion-control TLSO)

Answer 153

Consists of a sternal pad, suprapubic pad, & anterolateral pads connected by oblique lateral uprights counteracted by a dorsolumbar pad Suprapubic band may be substituted by a boomerang band, which applies force on the iliac crests (used in females to avoid direct pressure on the bladder) Indications: - Used to permit the upright position while preventing flexion after compression fracture of the TL spine (use in tx of compression fractures in osteoporotic elderly patients is controversial because it can place excessive hyper-extension forces on the lower lumbar vertebrae, which can induce posterior element fractures or exacerbate a degenerative arthritis condition) - TL Scheurmann's disease - Thoracic osteoporotic kyphosis (limited efficacy)

Question 154

Milwaukee brace

Answer 154

CTLSO used for scoliosis Consists of a rigid plastic pelvic girdle connected to a neck ring over the upper thorax by one anterior, broad aluminum bar & 2 paraspinal bars The cervical ring has mandibular & occipital bars, which rest 20-30 mm inferior to occiput & mandible Pads strapped to the bars apply a transverse load to the ribs & spine to correct scoliotic curvatures Indications: - Idiopathic or flexible congenital scoliosis with curves 25-40 degrees if curve apex is located superior to T8, the scoliosis shows signs of progression, & puberty has not finished - Thoracic Scheuermann's disease kyphosis

Question 155

Definition of CVA

Answer 155

Rapidly developing clinical signs of focal or global disturbances of cerebral function lasting 24 hours or longer OR leading to death with no apparent cause other than of vascular origin If <24 hours --> TIA

Question 156

What are the 2 categories of CVA risk factors?

Answer 156

Non-modifiable & modifiable

Question 157

Non-modifiable risk factors for CVA

Answer 157

- Age (most important; after age 55, incidence increases (risk more than doubles each decade after 55)) - Sex (male > female) - Race (AA >> white > asian) - Family h/o CVA

Question 158

Modifiable risk factors for CVA

Answer 158

- HTN (most important for both ischemic & hemorrhagic; 7-fold increased risk)); lower rates of recurrent CVA with lower BP's. Target SBP <130 - H/o prior TIA/CVA - Heart disease (CHF, CAD) - Valvular heart disease, arrhythmias (increased risk of embolic stroke for these) - AF - DM - Cigarette smoking (for ischemic CVA & SAH) - Carotid stenosis (& carotid bruit) - EtOH/cocaine abuse - High-dose estrogens (birth control pills) (considerable increased risk when combined with cig smoking) - Systemic diseases a/w hyper-coagulable states (elevated RBC, hematocrit, fibrinogen; Protein C & S deficiencies; sickle cell anemia; CA) - HLD (LDL-C a/w increased risk of CVA & has stronger association for large artery atherosclerotic subtype) - Migraine HA - OSA - PFO - Sedentary physical activity - Nutrition (Mediterranean diet reduces incidence of CVA)

Question 159

Where is CSF produced?

Answer 159

In the brain mostly by modified ependymal cells in the choroid plexus in the lateral, 3rd, & 4th ventricles, with the remainder formed around blood vessels & along ventricular walls

Question 160

CSF circulation

Answer 160

From the lateral ventricles to the foramina of Monro (IVF), 3rd ventricle, aqueduct of Sylvius (cerebral aqueduct), 4th ventricle, foramen of Magendie (Median aperture) & foramina of Luschka (lateral apetures), & sub-arachnoid space over brain & spinal cord

Question 161

Types of CVA

Answer 161

Ischemic (87%) Hemorrhagic Subtypes of ischemic: - Thrombotic - Embolic - Lacunar Subtypes of hemorrhagic: - ICH- hypertensive - SAH- ruptured aneurysm

Question 162

Thrombotic CVA's (large artery thrombosis)

Answer 162

- 48% of all CVA's - Usually occurs during sleep (patient awakens unaware of deficits) - May have stuttering, intermittent progression of neuro deficits, or be slowly progressive (over 24-48 hours) - Profound LOC is rare except when area of infarction is large or when brainstem is involved - Perfusion failure distal to site of severe stenosis or occlusion of major vessels - Emboli from incompletely thrombosed artery may precipitate an abrupt deficit. May have embolism from extra-cranial arteries affected by stenosis or ulcer

Question 163

Embolic CVA's

Answer 163

- 26% of all CVA's - Immediate onset of neuro deficits, usually occurs during waking hours - Seizures may occur at onset of CVA - Most commonly due to cardiac source: mural thrombi & platelet aggregates - Emboli most commonly originate from cardiac thrombus caused by AF. Also occur in rheumatic heart disease (like MS), post-MI, & vegetations on heart valves in bacterial/marantic endocarditis) or prosthetic heart valves - Emboli may dislodge spontaneously or after invasive CV procedures (like cath) - 75% of cardiogenic emboli go to the brain - Embolus can consist of fat (from fractured long bones, air (decompression sickness), or venous clot that passes through a PFO with shunt (paradoxical embolus) - Rarely, a subclavian artery thrombosis may embolize to the VA or its branches

Question 164

Lacunar CVA's

Answer 164

- 13% of all CVA's - Onset may be abrupt or gradual; up to 30% develop slowly over 36 hours - Lacunes are small infarcts (<15 mm) seen in the putamen, pons, thalamus, caudate, & internal capsule - Due to occlusive arteriolar or small artery disease (occlusion of deep penetrating branches of large vessels) - Occlusion occurs in small arteries of 50-200 mm in diameter - Strong correlation with HTN; also a/w microatheroma, micro-embolism, or rarely arteritis - CT shows lesion is about 2/3 of cases (MRI more sens) - Often relatively pure syndromes (motor or sensory) - Absence of higher cortical function involvement (language, praxis, non-dominant hemisphere syndrome, vision)

Question 165

What is the most common cause of occlusion of the superior division of the MCA?

Answer 165

Embolus *Superior division of the MCA supplies Rolandic & pre-rolandic areas (AKA horizontal M1)

Question 166

What happens with occlusion of one ACA DISTAL to an anterior communicating artery?

Answer 166

- Contralateral weakness & sensory loss, affecting mainly the distal contralateral leg (foot/leg more affected than thigh) - Mild/no UE involvement - Head & eyes may be deviated toward side of lesion acutely - Urinary incontinence with contralateral grasp reflex & paratonic rigidity (Gegenhalten) may be present - May produce transcortical motor aphasia if left side is affected - Gait apraxia: disturbances in gait & stance

Question 167

What occurs if both ACA's arise from one stem & there is a CVA distal to anterior communicating arteries?

Answer 167

Major disturbances occur with infarction occurring at the medial aspects of both cerebral hemispheres --> aphasia, paraplegia, incontinence, & frontal lobe/personality dysfunction (emotional instability, disinhibition, apathy)

Question 168

Clinical presentation in PCA CVA

Answer 168

- Occlusion can produce a variety of clinical effects because PCA supplies the upper brainstem & inferior parts of the temporal lobe, as well as medial parts of the occipital lobe - 70% of time, both PCA's arise from the basilar artery & are connected to the ICA's through the posterior communicating artery - 20-25% of the time, one PCA comes from basilar & other comes from ICA - 5-10% of time, both PCA's come from carotids - Visual field cuts --> when bilateral, may have denial of cortical blindness (Anton syndrome) - May have prosopagnosia (cannot read faces) - Palinopsia (abnormal recurring visual imagery) - Alexia (cannot read) - Alexia without agraphia (patient able to write but not read or recognize written words) - Transcortical sensory aphasia (loss of power to comprehend written or spoken words; patient can repeat)

Question 169

What structures are supplied by the inter-peduncular branches of the PCA?

Answer 169

CN 3 (oculomotor nerve) & CN 4 (trochlear) nuclei & nerves

Question 170

What is Weber syndrome?

Answer 170

Clinical syndrome caused by occlusion of the inter-peduncular branches of the PCA: oculomotor palsy with contralateral hemiplegia

Question 171

What else can happen with occlusion of the inter-peduncular branches of the PCA?

Answer 171

Trochlear nerve palsy (vertical gaze palsy)

Question 172

What are symptoms in CVA with vetebro-basilar system involvement?

Answer 172

- Nystagmus - Vertigo, Abnormalities of motor function, often b/l - Ipsilateral CN dysfunction - Crossed signs: motor or sensory deficit on ipsilateral side of face & contralateral side of body; ataxia, dysphagia, dysarthria

Question 173

What is the main difference between symptoms in CVA comparing vetebro-basilar system involvement to anterior circulation involvement?

Answer 173

There is absence of cortical signs when there is involvement of the vertebro-basilar system (such as aphasia or cognitive deficits)

Question 174

Vertigo in vertebro-basilar insufficiency

Answer 174

Isolated attacks can be the initial & only symptom, however attacks of vertigo in vertebro-basilar insufficiency usually lasts <30 minutes & have NO associated hearing loss

Question 175

Wallenberg (lateral medullary syndrome)

Answer 175

- AKA PICA syndrome or vertebral artery syndrome - Occurs due to occlusion of the one of the following: vertebral arteries (involved in 8 of 10 cases), PICA, superior lateral/middle lateral/inferior lateral medullary artery) - Signs & symptoms: Ipsilateral: Horner syndrome (ptosis, anhidrosis, miosis); decrease in pain & temp sensation on face; cerebellar signs such as ataxia on ipsilateral extremities (patient falls to side of lesion) Contralateral: decreased pain & temp on body, dysphagia/dysarthria/hoarseness/vocal cord paralysis, vertigo/n/v, hiccups, nystagmus, diplopia There is NO facial or extremity muscle weakness in this syndrome

Question 176

Symptoms & site of lesion of Wallenberg syndrome

Answer 176

- Ipsilateral Horner's syndrome: Pupillodilator (sympathetic) fibers) - Ipsilateral face pain & temp loss: Spinal trigeminal tract - Ipsilateral ataxia (UE > LE): Spinocerebellar tract - Contralateral arm/leg pain & temp loss: Spinothalamic tract - Dysphagia, hiccups, hoarseness: nucleus ambiguus, CN 9, CN 10 nerves - Vertigo, n/v: Vestibular nuclei

Question 177

Gross locations of CN brainstem nuclei

Answer 177

Midbrain: 1-4 (CN1 & 2 nuclei are located in forebrain) Pons: 5-8 Medulla: 9-12 (CN 11 has 2 divisions- the cranial & spinal division; the spinal division arises from the ventral horns of CN1-6 levels)

Question 178

Weber syndrome

Answer 178

- Clinical syndrome caused by occlusion of the inter-peduncular branches of the PCA: oculomotor palsy with contralateral hemiplegia - Paramedian (medial) brainstem syndrome

Question 179

Millard-Gubler syndrome

Answer 179

- Paramedian (medial) brainstem syndrome - Obstruction of circumferential branches of basilar artery - Ipsilateral CN (abducens; LR) 6 paralysis (often 7 involved- facial) - Contralateral hemiplegia (if extends into medial lemniscus --> Raymond-Foville syndrome with gaze palsy to side of lesion) - Contralateral lemniscus (tactile sensation) sensory loss 2/2 damage to medial lemniscus with analgesia, hypoesthesia

Question 180

Medial medullary syndrome AKA "another lesion"

Answer 180

- Paramedian (medial) brainstem syndrome - Caused by infarction of the medial medulla due to occlusion (usually athero-thrombotic) of penetrating branches of the VA's (upper medulla) or anterior spinal artery (lower medulla & medullocervical junction) - Rare; much less common than lateral medullary syndrome Ipsilateral hypoglossal (CN 12) palsy with deviation toward side of lesion - Contralateral hemiparesis - Contralateral lemniscal sensory loss (proprioception & position sense)

Question 181

Region of brainstem syndromes

Answer 181

Midbrain: - Main artery: PCA - Paramedian: Weber - Lateral: N/a Pons: - Main artery: Basilar artery - Paramedian: Millard-Gubler syndrome - Lateral: N/a Medulla: - Main artery: VA (or ASA) - Paramedian: medial medullary synrome - Lateral: Wallenberg syndrome

Question 182

Locked-in syndrome

Answer 182

- Quadriparesis with patients who are only able to move eyes vertically or blink - Patient remains fully conscious due to sparing of RAS (which is located primarily in midbrain) - Caused by b/l lesions of the ventral pons (basilar artery occlusion)

Question 183

What is dysarthria/clumsy hand syndrome?

Answer 183

Lacunar CVA at location of basis pontis & anterior limb of internal capsule

Question 184

Where is the most common location for a hypertensive ICH?

Answer 184

Putamen Hemiplegia occurs 2/2 compression of adjacent internal capsule Vomiting occurs in half of cases HA is frequent but not constant With smaller hemorrhages --> HA leading to aphasia, hemiplegia, eyes deviate away from paretic limbs

Question 185

Where do most saccular aneurysms occur?

Answer 185

Anterior part of circle of Willis

Question 186

What makes saccular arterial aneurysms more likely to rupture?

Answer 186

If 10 mm or larger

Question 187

What is peak age for rupture of saccular arterial aneurysm?

Answer 187

40's-50's

Question 188

Hunt & Hess Scale for Atraumatic SAH

Answer 188

Grade 1: asx, mild HA, slight nuchal rigidity Grade 2: moderate to severe HA, nuchal rigidity, no neuro deficit other than CN palsy Grade 3: drowsiness/confusion, mild focal neuro deficit Grade 4: stupor, moderate-severe hemiparesis Grade 5: coma, decerebrate posturing

Question 189

Clinical presentation of saccular aneurysm/SAH

Answer 189

Compression of adjacent structures such as CN3 with a posterior communicating-internal carotid junction aneurysm or posterior communicating-PCA aneurysm Signs of CN3 involvement: - Deviation of ipsilateral eye to lateral side (lateral or divergent strabismus) - Ptosis - Mydriasis & paralysis of accommodation due to interruption of parasympathetic fibers in CN3

Question 190

What is a sentinel HA?

Answer 190

Sudden, intense, & persistent HA, preceding SAH by days or weeks in half of patients

Question 191

What is mortality in rupture of aneurysm producing SAH with or without ICH?

Answer 191

25% during first 24 hours

Question 192

What is the risk of re-bleeding in rupture of aneurysm producing SAH with or without ICH?

Answer 192

Within 1 month: 30% 2.2% per year during first decade

Question 193

What are AVM's?

Answer 193

Low-pressure systems; larger the shunt, the lower the interior pressure. With these large dilated vessels, there needs to be an occlusion distally to raise luminal pressures to cause hemorrhage

Question 194

Clinical presentation of AVM rupture

Answer 194

- Hemorrhage is the initial presentation in half of cases - May be parenchymal (41%), subarachnoid (23%), or intra-ventricular (17%) hemorrhage - Seizures occur in 30% of cases - HA occurs in 20% of cases, 10% overall with migraine-like HA - Neurologic deficit varies according to area affected

Question 195

Ischemic CVA BP Management

Answer 195

IV Labetalol, Nicardipine, & Clevidipine Can also consider Hydralazine & Enalapril If BP remains uncontrolled or DBP >140, consider IV sodium nitroprusside

Question 196

Hemorrhagic CVA BP Management

Answer 196

IV Labetalol (does not cause cerebral vasodilation, which could worsen increased ICP)

Question 197

What is the best indication for AC in CVA?

Answer 197

Cardiac emboli - Primarily from non-valvular AF & mural thrombus from MI - There is a probable risk of inducing cerebral hemorrhage or hemorrhagic infarction within large infarcts if AC in the first 24-36 hours - If neuro deficit is mild (& CT shows no hemorrhage), may begin AC immediately - If deficit is severe (clinically and/or with CT), wait 3-5 days before starting AC - Most common cause is chronic AF

Question 198

Who should get CEA?

Answer 198

Symptomatic lesions with 70-90% stenosis is effective in reducing the incidence of ipsilateral hemisphere CVA (moderate, symptomatic carotid stenosis)

Question 199

What decreases cerebral vasospasm after SAH & has been shown to improve outcome after SAH?

Answer 199

PO Nimodipine 60 mg q4h for 21 days; should initiate therapy within 4 days of onset of hemorrhage

Question 200

Rehabilitation methods for motor deficits

Answer 200

1. PNF (Proprioceptive NM facilitation) 2. Bobath/Neurodevelopmental Technique (NDT) 3. Brunnstrom/Movement Therapy 4. Sensorimotor/Rood 5. Motor Relearning Program/Carr & Shepherd

Question 201

PNF (Proprioceptive NM Facilitation)

Answer 201

Uses spiral & diagonal components of movement rather than the traditional movement in cardinal planes of motion with the goal of facilitating movement patterns that will have more functional relevance than the traditional technique of strengthening individual group muscles

Question 202

Bobath approach/NDT

Answer 202

Goal is to normalize tone, inhibit primitive patterns of movement, & facilitate automatic, voluntary reactions & subsequent movement patterns Abnormal patterns are modified at the proximal key points of control (shoulder & pelvic girdle)

Question 203

Brunnstrom approach/Movement therapy

Answer 203

Uses primitive synergistic patterns in training in an attempt to improve motor control through central facilitation

Question 204

Sensorimotor/Rood

Answer 204

Modification of muscle tone & voluntary motor activity using cutaneous sensorimotor stimulation

Question 205

Motor Relearning program/Carr & Shepherd Approach

Answer 205

Goal is for patient to relearn how to move functionally & how to problem-solve during attempts at new tasks

Question 206

Constraint-induced movement therapy (CIMT)

Answer 206

Restrain the less affected arm (like Brunnstrom) In the EXCITE Trial, participants were required to have at least 10 degrees active wrist extension, 10 degrees thumb abduction/extension, & 10 degrees extension in at least two additional digits

Question 207

Post-CVA shoulder pain

Answer 207

70-84% of CVA patients with hemiplegia have shoulder pain with varying degrees of severity Majority (85%) will develop it during the spastic phase of recovery Most common causes of hemiplegic shoulder pain are CRPS Type 1 & soft-tissue lesions (including plexus lesions)

Question 208

CRPS (Complex Regional Pain Syndrome)

Answer 208

Neuropathic pain c/b exaggerated response to a traumatic lesion or peripheral nerve that results in severe neuropathic pain & sensory, autonomic, motor, & trophic impairments Includes sympathetic-maintained pain & related sensory abnormalities, abnormal blood flow, abnormalities in motor system, & changes in both superficial & deep structures with trophic changes CRPS Type 1: RSD, shoulder-hand syndrome, Sudeck's atrophy. Follows an injury without nerve injury in affected limb CRPS Type 2: develops following peripheral nerve injury to affected limb

Question 209

Stages of CRPS

Answer 209

Stage 1 (acute): burning pain, diffuse swelling/edema, exquisite tenderness, hyperpathia &/or allodynia, vasomotor changes in hand/fingers (increased nail & hair growth, hyperthermia or hypothermia, sweating). Lasts 3-6 months Stage 2 (dystrophic): pain becomes more intense & spreads proximally, skin/muscle atrophy, brawny edema, cold insensitivity, brittle nails/nail atrophy, decreased ROM, mottled skin, early atrophy, & osteopenia (late). Lasts 3-6 months Stage 3 (atrophic): pain decreases, trophic changes occur, hand/skin appear pale & cyanotic with a smooth, shiny appearance, feeling cool & dry; bone demineralization progresses with muscular weakness/atrophy, contractures/flexion deformities of shoulder/hand, tapering digits. No vasomotor changes in this stage

Question 210

Diagnostic approaches to CRPS

Answer 210

XR: normal in initial stages; periarticular osteopenia may be seen in later stages. Need 30-50% demineralization for detection Triple phase bone scan: high sens, only 56% spec. High NPV. Main thing to look for is juxta-articular tracer activity on delayed images (most sensitive for Type 1) EMG: association between spontaneous activity & eventual development of CRPS Clinical exam: shoulder pain with ROM (flexion/abduction/ER), absence of pain in elbow & with forearm pronation/supination; wrist DF pain with dorsal edema; pain in MCP/PIP flexion with fusiform PIP edema. Shoulder/hand pain preceded by rapid ROM loss. Most valuable is MCP tenderness to compression Skeletal scintigraphy (bone scan): delayed image showing increased uptake in wrist, MCP, & IP joints Stellate ganglion block: successful when patient develops an ipsilateral Horner syndrome. Alleviation of pain following sympathetic blockage of the stellate ganglion using local anesthetic is the gold standard for diagnosis of sympathetically-mediated CRPS Type 1

Question 211

Treatment for CRPS

Answer 211

ROM exercises of involved joint, passive stretch Systemic corticosteroids (high doses tapered over 2 weeks). More effective in CRPS Type 1 confirmed by bone scan than in clinical CRPS Type 1 with a negative bone scan Other meds: - NSAIDs - TCA's - Bisphosphonates - Calcitonin - Anti-convulsants (gabapentin, carbamazepine) - Alpha-adrenergic blockers (clonidine, prazosin) - BB - CCB - Topical capsaicin Modalities: - Edema control measures - TENS - Desensitization techniques - Contrast baths - Ultrasound Injections: - IA CSI - Local injections - Sympathetic stellate ganglion blocks may be diagnostic & therapeutic Other: - RFA, surgical sympathectomy

Question 212

Treatment for shoulder subluxation in CVA

Answer 212

Friedland (1975): slings do not prevent/correct subluxation & are not necessary to support pain-free shoulder Hurd er al (1974): no difference in shoulder ROM, subluxation, or shoulder pain in patients with or without slings

Question 213

Brachial plexus/peripheral nerve injury in CVA

Answer 213

Etiology: traction injury to plexus/nerve Diagnosis: atypical functional return, segmental muscle atrophy, finger extensor contracture, delayed onset of spasticity EMG will show LMN findings of a brachial plexopathy Treatment: - Proper bed positioning to prevent patient from rolling onto paretic arm, trapping it behind the back or through bed rails & causing traction stress - ROM to prevent contracture while traction avoided - 45 degree shoulder abduction sling for nighttime positioning - Sling for ambulation to prevent traction by gravity - Armrest in wheelchair as needed Prognosis: may require 8-12 months for re-innervation

Question 214

Other ddx for post-CVA shoulder pain

Answer 214

Inferior subluxation, RTC tear, adhesive capsulitis, RTC impingement, biceps tendinopathy

Question 215

Shoulder subluxation in CVA diagnostic test & treatment

Answer 215

Testing: XR in standing position, scapular plane view Treatment: sling when upright, FES

Question 216

Adhesive capsulitis in CVA exam, diagnostic test, & treatment

Answer 216

Exam: ER < 15 degrees, early decrease in scapular motion, spastic Diagnostic test: arthrogram Treatment: PT/ROM, debridement manipulation, SAS/GH CSI (large distention), oral steroids, reduction of internal rotator cuff tone

Question 217

Diagnosis of dysphagia in CVA

Answer 217

Bedside swallow to evaluate gag reflex or pharyngeal sensation, observing for overt signs of cough or other difficulty during swallowing trials VFSS (videofluorographic swallowing evaluation) AKA MBS (modified barium swallow): gold standard for evaluation & treatment of dysphagia FEES (fiberoptic endoscopic evaluation of swallowing): used as a comprehensive functional evaluation of the pharyngeal stage of swallowing; visualizes anatomic structures that might cause potential bolus obstruction & natural bolus flow & containment

Question 218

Aspiration

Answer 218

Entry of a substance through the vocal folds (true vocal cords) into the trachea Missed on bedside swallowing evaluations in 40-60% of patients (silent aspiration) Can be reliable diagnosed on VFSS, showing penetration of contrast material below true vocal cords

Question 219

Predictors of aspiration on bedside swallowing exam

Answer 219

- Abnormal cough - Cough after swallow - Dysphonia - Dysarthria - Abnormal gag reflex - Voice change after swallow (wet voice)

Question 220

Aspiration PNA

Answer 220

Risk factors include: - Decreased level of consciousness - Trach - Emesis - GERD - NGT feeds - Dysphagia - Prolonged pharyngeal transit time

Question 221

Four phases of swallowing

Answer 221

1. Oral prep 2. Oral 3. Pharyngeal 4. Esophageal

Question 222

Oral preparatory phase of swallowing

Answer 222

Voluntary Variable duration, influenced by consistency of material ingested, number of chews, etc Hallmark of phase: preparation of bolus Requires: - Tension in labial & buccal musculature to close the anterior & lateral sulci - Rotatory jaw motion for mastication/grinding - Lateral tongue movement to position food on the teeth during mastication (tongue moves food back to teeth) - Depression & forward movement of the soft palate to seal the oral cavity posteriorly & widen the nasal airway - Saliva Problems seen in this phase: drooling, pocketing

Question 223

Oral phase of swallowing

Answer 223

Voluntary Lasts usually <1 second Hallmarks of this phase: - Tongue that elevates & occludes the anterior oral cavity & compresses the bolus toward the oropharynx - Contraction of the palato-pharyngeal folds - Elevation of the soft palate Phase requires: - Tension in the labial & buccal musculature to close the anterior & lateral sulci - Anterior-posterior tongue movement to transport the bolus to the pharynx - Soft palate elevation & velo-pharyngeal port closure (also seen in pharyngeal phase) to close off the nasal cavity & prevent regurgitation into the nasopharynx Problems seen in this phase: drooling, pocketing, head tilt

Question 224

Pharyngeal phase of swallowing

Answer 224

Reflex Lasts 0.6-1 second Hallmarks of this phase: - Bolus propelled from mouth to esophagus - Aspiration is most likely to occur during this phase - With initiation of pharyngeal phase, inhibition of breathing occurs to prevent aspiration Phase requires: - Soft palate elevation & velo-pharyngeal port closure to close off the nasal cavity & prevent regurgitation into naso-pharynx - Laryngeal elevation, with forward movement of the hyoid bone & folding of epiglottis to protect airway - Adduction of ventricular & true vocal cords to protect airway - Coordinated pharyngeal constriction & cricopharyngeal (UES) relaxation to facilitate bolus transport into esophagus

Question 225

Esophageal phase of swallowing

Answer 225

Reflex Longest phase- lasts 6-10 seconds Hallmarks of this phase: - Bolus pass from pharynx --> esophagus --> stomach - Esophageal clearance is assisted by gravity but requires relaxation of the GES Phase requires: - Cricopharyngeal muscle contraction - Coordinated peristalsis & LES relaxation Problems seen in this phase: heartburn, food sticking

Question 226

Compensatory strategies for treatment of dysphagia/prevention of aspiration

Answer 226

Chin tuck: provides airway protection by preventing entry of liquid into larynx by facilitating forward motion of the larynx; also decreases the space between the base of the tongue & the posterior pharyngeal wall, creating increased pharyngeal pressure to move the bolus through the pharyngeal region Head rotation: closes ipsilateral pharynx, forces bolus into contralateral pharynx, & decreases cricopharyngeal pressures. Turn the head TO the paretic side

Question 227

Recovery of dysphagia in CVA

Answer 227

Ickenstein et al (2012): subjects 72 hours post-CVA rated at a level 1-3 on the Functional Communication Measure (FCM) of Swallowing & level 5-8 on the Penetration-Aspiration Scale (PAS) were 11.8x less likely to be orally fed 90 days post-stroke

Question 228

Nasal speech

Answer 228

Hyper-nasality caused by partial or complete failure of soft palate to close off the nasal cavity from the oral cavity or by incomplete closure of the hard palate Uplifting the soft palate prevents nasal speech

Question 229

Anatomic location of major speech areas: Wernicke's aphasia

Answer 229

Posterior part of superior (first) temporal gyrus of the dominant (usually left) hemisphere

Question 230

Anatomic location of major speech areas: Broca's aphasia

Answer 230

Posterior-inferior frontal lobe (3rd frontal convolution) of dominant (usually left) hemisphere --> anterior to motor cortex areas that supply the tongue, lips, & larynx

Question 231

Anatomic location of major speech areas: Global aphasia

Answer 231

Vary in size & location but usually involve the distribution of the left MCA (entire peri-sylvian region)

Question 232

Anatomic location of major speech areas: Anomic aphasia

Answer 232

Temoro-parietal injury, angular gyrus. At the lateral Sylvian fissure

Question 233

Anatomic location of major speech areas: Conduction aphasia

Answer 233

Lesion of the parietal operculum (arcuate fasciculus) or insula or deep to the supra-marginal gyrus (usually left side)

Question 234

Anatomic location of major speech areas: Transcortical motor aphasia

Answer 234

Frontal lobe, anterior or superior to Broca's area or in the sub-cortical region deep to Broca's area

Question 235

Anatomic location of major speech areas: Transcortical sensory aphasia

Answer 235

Watershed lesion isolating perisylvian speech structures (Broca & Wernicke areas) from the posterior brain; angular gyrus or posterior-inferior temporal lobe

Question 236

Errors in speech: paraphasia

Answer 236

Incorrect substitution of words or parts of words Literal or phonemic: similar sounds (sound for found) Verbal or semantic: words substituted for another from same class (fork for spoon)

Question 237

Errors in speech: anomia (aka nominal aphasia)

Answer 237

Difficulty recalling words; word-finding difficulty Unimpaired comprehension & repetition

Question 238

Errors in speech: echolalia

Answer 238

Repetition of words or vocalizations made by another person

Question 239

Errors in speech: circumlocution

Answer 239

Roundabout way of describing a word that cannot be recalled Often seen with anomia

Question 240

Errors in speech: neologism

Answer 240

A "new word" that is well-articulated but has meaning only to the speaker

Question 241

Errors in speech: jargon

Answer 241

Well-articulated but mostly incomprehensible, unintelligible speech A/w Wernicke's aphasia

Question 242

Errors in speech: stereotype

Answer 242

Repetition of non-sensical syllables (no, no no) during attempts at conversation

Question 243

Melodic intonation therapy

Answer 243

Recruits the right hemisphere for communication by incorporating melodies or rhythms with simple statements May be useful in patients with non-fluent (Broca's) aphasia

Question 244

Post-CVA aphasia recovery

Answer 244

Greatest improvement occurs in first 2-3 months After 6 months, there is a big drop in rate of recovery Usually, spontaneous recovery does not occur after 1 year (but can get better many years later with therapy)

Question 245

Negative risk factors for return to work post-CVA

Answer 245

Low score on Barthel index at time of rehab discharge Prolonged rehab length of stay Aphasia Prior alcohol abuse

Question 246

Barthel index

Answer 246

Functional assessment tool that measures independence in ADLs on 0-100 scale

Question 247

What is the single most common cause of death & injury in MVAs

Answer 247

Ejection of occupant from vehicle

Question 248

TBI based on marital status

Answer 248

Single (46%) > married (33%) > divorced (16%) > widowed/separated (5%)

Question 249

What substance is attributed to 50% of all TBI?

Answer 249

Alcohol, likely under-estimated/reported

Question 250

Examples of primary brain injury

Answer 250

- Contusion (bruising of cortical tissue) +/- DAI - Impact depolarization: massive surge in extracellular K & glutamate release (excitatory) occurring after severe head injury leading to excitotoxicity (secondary injury)

Question 251

Diffuse axonal injury definition

Answer 251

Immediate disruption of the axons due to acceleration-deceleration & rotational forces that cause shearing upon impact Evidence of a secondary axotomy due to increased axolemmal permeability, calcium influx, & cytoskeletal abnormalities that propagate after the injury Leads to white matter punctate petechial hemorrhages characteristic of DAI

Question 252

Focal brain hemorrhages

Answer 252

Epidural hematoma, SDH, SAH

Question 253

Epidural hematoma

Answer 253

90% occur with skull fracture in the temporal bone crossing MMA (60-90%) or veins (MMV, diploic veins, or venous sinus; 10-40%) Hematoma expansion is slowed by the tight adherence of the dura to the skull Lucid interval presentation happens 50% of the time. Biconvex acute hemorrhagic mass seen on CTH

Question 254

Subdural hematoma

Answer 254

Occurs in 30% of severe head trauma Result from shearing of the bridging veins between the pia-arachnoid & the dura Usually larger in the elderly due to generalized loss of brain parenchyma High density, crescentic, extra-cerebral masses seen on CTH Acute: immediately symptomatic lesions Subacute: 3 days-3 weeks Chronic: >3 weeks

Question 255

Subarchnoid hemorrhage

Answer 255

Closely a/w ruptured cerebral aneurysms & AVMs creating blood around the cisterns, although they could also result from leakage from an IPH & trauma CT shows blood within the cisterns around the brainstem & the sub-arachnoid space within 24 hours CT sensitivity decreases to 30% 2 weeks after the initial bleed

Question 256

What is the most common cause of unconsciousness during & following the first 24 hours of injury after TBI

Answer 256

Axonal injury (DAI)

Question 257

Brain plasticity (PUN)

Answer 257

Plasticity = Unmasking + Neuronal Sprouting

Question 258

What is brain plasticity?

Answer 258

Represents the capability of the damaged brain to "repair" itself by means of morphologic & physiologic responses Influenced by the environment, complexity of stimulation, repetition of tasks, & motivation

Question 259

Brain plasticity: collateral (neuronal) sprouting

Answer 259

Intact axons establish synaptic connections through dendritic & axonal sprouting in areas where damage has occurred May enhance recovery of function, may contribute to unwanted symptoms, or may be be neutral (with no increase or decrease of function) Occurs weeks to months post-injury

Question 260

Brain plasticity: unmasking neural re-organization (functional re-organization)

Answer 260

Healthy neural structures not formerly used for a given purpose are developed (or reassigned) to do functions formerly subserved by the lesioned area (vicariation)

Question 261

What are synaptic alterations that occur after TBI?

Answer 261

Diaschisis & increased sensitivity to neurotransmitter levels

Question 262

Diaschisis

Answer 262

Mechanism to explain spontaneous return of function Lesions/damage to one region of the CNS can produce altered function in other areas of the brain (at a distance from the original site of injury) that were not severed if there is a connection between the 2 sites (through fiber tracts) Function is lost in both injured & in morphologically intact brain tissue There is some initial loss of function 2/2 depression of areas of the brain connected to the primary injury site, & resolution of this functional de-afferentation parallels recovery of the focal lesion

Question 263

What is consciousness?

Answer 263

Function of the ascending RAS & cerebral cortex RAS is composed of cell bodies in the central reticular core of the upper brainstem (mainly midbrain) & their projections to widespread areas of the cerebral cortex via both the thalamic & extra-thalamic pathways Lesions that interrupt the metabolic or structural integrity of the RAS or enough of the cortical neurons receiving RAS input can cause DOC

Question 264

Vegetative state (unresponsive wakefulness syndrome)

Answer 264

C/b the resumption of the sleep-wake cycle on EEG No awareness of self/environment, no purposeful behavior There is presence of verbal or auditory startle but no localization or tracking Patient opens eyes (either spontaneously or with noxious stim) Related to diffuse cortical injury Bilateral thalamic lesions are prominent findings Persistent: Present for 1 months or more after TBI or non-traumatic BI Permanent: Present for >3 months after non-traumatic & 12 months for TBI

Question 265

When is decerebrate posturing seen?

Answer 265

With midbrain lesions/compression. Also with cerebellar & posterior fossa lesions

Question 266

When is decorticate posturing seen?

Answer 266

Seen in cerebral hemisphere/white matter, internal capsule, & thalamic lesions

Question 267

What is a simple scale for assessing depth of coma?

Answer 267

GCS

Question 268

Severity of TBI based on GCS score

Answer 268

Severe: 3-8 Moderate: 9-12 Mild: 13-15

Question 269

What is the best predictor of outcome in GCS?

Answer 269

Best motor response 2 weeks post-injury

Question 270

What is the second-best acute predictor of outcome in GCS?

Answer 270

Verbal response

Question 271

Glasgow Outcome Scale (GOS)

Answer 271

1. Death: self-evident criteria 2. VS (UWS) 3. Severe disability (conscious but dependent): patient unable to be independent for any 24-hour period by reason of residual mental and/or physical disability 4. Moderate disability (independent but disabled): patient with residual deficits that do not prevent independent daily life; patient can travel by public transport & work in a sheltered environment 5. Good recovery (mild to no residual effects): return to normal life; may be minor or no residual deficits

Question 272

What does resolution of PTA correspond with?

Answer 272

Period when incorporation of ongoing daily events occurs in the working memory

Question 273

Galveston Orientation & Amnesia Test (GOAT)

Answer 273

Developed by Harvey Levin & colleagues, it is a standard technique for assessing PTA Brief, structured interview that quantifies the patient's orientation & recall of recent events Assesses orientation to person, place, time; recall of circumstances of hospitalization; & last pre-injury & first post-injury memories

Question 274

When is the end of PTA using GOAT?

Answer 274

When patient scores 75 or higher for 2 consecutive days Period of PTA is defined as the number of days beginning at the end of the coma to the time the patient attains the first of two successive GOAT scores 75 or higher Attempts at more involved neuropsych assessment are usually unproductive until patient consistently obtains 70 or greater

Question 275

Post-traumatic amnesia & severity of TBI based on time

Answer 275

0-1 days: mild 1-7 days: moderate >7 days: severe

Question 276

Functional Independence Measure (FIM)

Answer 276

Ordinal scale with 18 items & 7 levels to assess physical & cognitive function with documented validity & reliability Motor items: self-care, sphincter control, mobility Cognition items: communication, psychosocial adjustment, cognitive function Level of function scoring: - Independent: 7 for complete independence (timely, safe), 6 for mod-I (extra time, devices) - Modified dependence: 5 for supervision (cueing, coaxing, prompting), 4 for min-A (patient performs 75% of task), 3 for mod-A (patient performs 50-75% of task) - Complete dependence: 2 for max-A (patient performs 25-50%), 1 for total assist (patient performs <25%)

Question 277

Neuropsychosocial testing

Answer 277

Halstead-Reitan Neuropsychological Battery (HRNB): diagnostic test for all kinds of brain damage. Original battery was used to assess frontal lobe disorders by Halstead (1947) & then used by Reitan (1970-1974) who added tests & expanded to all brain damage Most examiners use HRNB in conjunction with the Weschler Adult Intelligence Scale (revised WAIS-R) & Weschler Memory Scale (WMS) or the Minnesota Multiphasic Personality Inventory (MMPI)

Question 278

What is the WAIS-R?

Answer 278

Weschler Adult Intelligence Scale-Revised Sub-tests (6 determine verbal IQ & 5 determine performance IQ) Most frequently used measure of general IQ The revised version of WAIS-R is called WAIS-III: - Verbal IQ: vocab, similarities, arithmetic, digit span, information, comprehension, letter-number sequencing - Performance IQ: picture completion, digit-symbol coding, block design, matrix reasoning, picture arrangement, object assembly

Question 279

What is the MMPI?

Answer 279

Minnesota Multiphasic Personality Inventory 550 T/F questions that yield info about aspects of personality

Question 280

What is the Token test?

Answer 280

Correlates with scores on tests of auditory comprehension & language production Comprised of 20 tokens (circles/squares, big/little, five colors), laid out horizontally Increasingly complex oral commands (touch the white circle --> before touching the yellow circle, pick up the red square) 90% sens discriminating people with aphasias from people without

Question 281

Evaluation of ICP

Answer 281

In a normal adult, reclining with the head & trunk elevated to 45 degrees, normal ICP is 2-5 mmHg ICP levels up to 15 mmHg are considered harmless

Question 282

Elevated ICP

Answer 282

ICP >20 mmHg for >5 minutes Common after severe TBI A unilateral mass lesion causes distortion of the brain, a reduction of CSF volume, increased ICP in the closed skull --> formation of internal hernias (including tentorial/uncal herniation) If unchecked, increased ICP leads to death because of deformation of tissue, brain herniation, & cerebral ischemia ICP > 40 mmHg --> neuro dysfunction & impairment of brain's electrical activity ICP > 60 mmHg --> fatal Fever, hyperglycemia, hyponatremia, & seizures can worsen cerebral edema by increasing ICP It is more important to maintain an adequate CPP then controlling only ICP

Question 283

Indications for continuous monitoring of ICP & for MV

Answer 283

1. Patient in coma (GCS <8) & with CTH showing elevated ICP (absence of 3rd ventricle & CSF cisterns) 2. Deep coma (GCS <6) without hematoma 3. Severe chest & facial injuries AND mod/severe head injury (GCS <12) 4. After evacuation of intracranial hemorrhage if patient in coma (GCS <8) beforehand

Question 284

Factors that may increase ICP

Answer 284

- Turning head, especially to left side if completely horizontal or head down - Loud noise - Vigorous PT - Chest physiotherapy - Suctioning - Elevated BP

Question 285

What type of seizures are majority of post-traumatic seizures?

Answer 285

Simple, partial

Question 286

Risk factors a/w late post-traumatic seizures

Answer 286

- Penetrating head injury (biggest risk factor) - ICH - Early PTS (>24 hours-7 days) - Depressed skull fracture - Prolonged coma or PTA (>24 hours) - Other: dural tearing, presence of foreign bodies, focal signs (aphasia, hemiplegia), age, EtOH abuse, use of TCA's

Question 287

When are therapeutic anti-convulsant medications started?

Answer 287

Once late seizures occur

Question 288

What AED's are preferred in TBI population?

Answer 288

Carbamazepine (partial) & valproic acid (generalized) are preferred over meds that are more sedating or a/w cognitive impairment (such as phenobarb & phenytoin) (although carbamazepine may be as sedating as phenytoin)

Question 289

AED's: Carbamazepine

Answer 289

Uses: Partial seizures, tonic-clonic (generalized) seizures, stabilization of agitation & psychotic behavior, bipolar affective disorder, neuralgia ADRs: - Acute: stupor/coma, hyper-irritability, convulsions, respiratory depression, SJS - Chronic: drowsiness, vertigo, ataxia, diplopia, blurred vision, n/v, aplastic anemia, agranulocytosis, hypersensitivity reactions (dermatitis, eosinophilia, splenomegaly, lymphadenopathy), transient mild leukopenia, transient thrombocytopenia, water retention with decreased serum osmolality & Na, transient elevation of LFTs

Question 290

AED's: Gabapentin

Answer 290

Use: partial seizures ADRs: somnolence, dizziness, ataxia, fatigue

Question 291

AED's: Levetiracetam (Keppra)

Answer 291

Uses: partial seizures, myoclonic seizures ADRs: - Acute: hyperirritability, depression - Chronic: drowsiness, vertigo, ataxia, hallucinations, flu-like symptoms, poor coordination, rash, BPD, suicidality

Question 292

AED's: Phenobarbital

Answer 292

Uses: partial seizures, tonic-clonic; generalized seizures ADRs: sedation, irritability, & hyperactivity in children; rash; exfoliative dermatitis; hypothrombinemia with hemorrhage in newborns whose mothers took phenobarbital; megaloblastic anemia; osteomalacia; nystagmus & ataxia at toxic doses

Question 293

AED's: Phenytoin (Dilantin)

Answer 293

Uses: partial seizures, tonic-clonic (generalized) seizures, neuralgia ADRs: - IV: cardiac arrhythmias, hypotension, CNS depression - PO: disorders of cerebellar & vestibular systems, cerebellar atrophy, blurred vision, mydriasis, diplopia, ophthalmoplegia, behavioral changes (hyperactivity, confusion, dullness, drowsiness, hallucination), increased seizure frequency, GI sx, gingival hyperplasia, osteomalacia, megaloblastic anemia, hirsutism, transient elevation in LFT's, decreased ADH secretion, hyperglycemia, glycosuria, hypocalcemia, SJS, SLE, neutropenia, leukopenia, red cell aplasia, agranulocytosis, thrombocytopenia, lymphadenopathy, hypothrombinemia in newborns whose mothers received phenytoin, drug allergy (skin, BM, liver function involvement)

Question 294

AED's: Valproic Acid (Depakote)

Answer 294

Uses: partial seizures, tonic-clonic (generalized) seizures, myoclonic seizures, absence seizures, stabilization of agitation & psychotic behavior ADRs: transient GI sx (anorexia, n/v), increased appetite, sedation, ataxia, tremor, rash, alopecia, LFT elevation, fulminant hepatitis (rare but fatal), acute pancreatitis, hyperammonemia

Question 295

AED's drug interactions: Carbamazepine

Answer 295

- Increased metabolism (decreased levels) with co-use of phenobarb, phenytoin, & valproic acid - Enhances metabolism of phenobarb - Enhances metabolism of primidone into phenobarb - Reduces concentration & effectiveness of Haldol - Metabolism inhibited by propoxyphene & erythromycin

Question 296

AED's drug interactions: Lamotrigine

Answer 296

- When used with carbamazepine, may increase levels of 10,11-epoxide (an active metabolite of carbamazepine) - Half-life is reduced to 15 hours when used with carbamazepine, phenobarb, or primidone - Reduces valproic acid concentration

Question 297

AED's drug interactions: Levetiracetem (Keppra)

Answer 297

When used with anti-histamines, or meds that potentiate GABA, may cause AMS and/or respiratory depression

Question 298

AED's drug interactions: Phenobarbital

Answer 298

- Increased levels when valproic acid or phenytoin given concurrently - Variable reaction with phenytoin levels

Question 299

AED's drug interactions: Phenytoin (Dilantin)

Answer 299

- Levels may increase with concurrent use of chloramphenicol, cimetidine, dicumarol, disulfiram, isoniazid, & sulfonamides - Free phenytoin levels may increase with concurrent use of valproic acid & phenobarb - Decreased total levels may occur with sulfisoxazole, salicylates, & tolbutamide - Decreased levels with concurrent use of carbamazepine (& vice versa) - When concurrently used with theophylline, levels may be lowered & theophylline metabolized more rapidly - May decrease effectiveness of OCP's - Enhances metabolism of corticosteroids

Question 300

AED's drug interactions: valproic acid (Depakote)

Answer 300

- Increases level of phenobarb - Inhibits metabolism of phenytoin - Rare development of absence status epilepticus a/w concurrent use of clonazepam

Question 301

When is it reasonable to consider withdrawal of AED's in post-traumatic epilepsy?

Answer 301

2-year, seizure-free interval

Question 302

CN 1 (olfactory nerve) injury in TBI

Answer 302

Most often CN damaged by blunt head trauma due to tearing of the olfactory nerve filaments in or near the cribiform plate through which they traverse Sx: anosmia, apparent loss of taste Overall incidence: 7% & increases with severity of TBI Injury to this nerve is the only CN neuropathy present in mild TBI Often a/w: CSF rhinorrhea, anosmia, dysnosmia, hyposmia, parosmia (sensation of smell in absence of stimulus), cacosmia (awareness of foul odor that does not exist; may be aura) In higher level patients --> decrease in appetite, weight loss, and/or altered feeding pattern Recovery occurs in more than one-third of cases, usually during the first 3 months

Question 303

Agitated Behavioral Scale

Answer 303

Designed for serial assessment of agitated patients after TBI Ratings are based on behavioral observations made after an 8-hour nursing shift or therapy treatment session Consists of 14 items or behaviors rated from 1 (absent) to 4 (present to an extreme) Scoring: - Below 21: normal - 22-28: mild agitation - 29-35: moderate agitation - 35-54: severe agitation

Question 304

Enteral feeding after TBI

Answer 304

Preferred when oral feeding is compromised because it directly uses the GI tract (distal to the site of tube placement), provides the most physiologic approach in nutritional administration & absorption, low in cost, & lower risk of metabolic complications

Question 305

What is the primary risk in tube feeding?

Answer 305

Aspiration (increased if patient has GERD, or with more proximal tube placement) Risks with distal tube placement include decreased absorptive capacity & tolerance of the remaining gut

Question 306

What are enteral feeding products composed of?

Answer 306

Pureed foods, liquid nutritional supplements, elemental nutritional supplements, or a combination of products

Question 307

Options for enteral routes of feeding

Answer 307

NG, naso-enteric, esophago-gastric, PEG, PEJ, & more surgically invasive tubes (Janeway gastrotomy, esophago-gastrotomy

Question 308

When should feeding tube be placed after TBI?

Answer 308

No current guidelines (also no guidelines as to where it should be placed)

Question 309

Factors to consider for enteral tube placement

Answer 309

- Direct gastrostomy or jejunostomy has decreased risk of aspiration or GERD-related problems; preferred when there is a potentially prolonged length of time of non-oral nutrition - Direct routes should be in place at least 30 days to avoid complications on removal - Perc placement has added advantages of decreased surgical risks & ability to start tube feeds within 24 hours of placement, whereas more surgically placed tubes have mechanical parts that can more easily be inserted (during mealtimes only) & removed (especially when in therapy) - Enteral routes that allow for bolus feeding are advantageous because they more closely approximate natural feeding, making daily routines & therapies more manageable, especially in patients more likely to go home

Question 310

Associated problems with enteral feeding

Answer 310

- In patients with GERD, recurrent PNA, or possible aspiration, distal tube placement is preferred Patients suspicious for aspiration or aspiration PNA should have a gastric source of aspirate confirmed to rule out aspiration of oral secretions - GERD has a high prevalence in TBI patients & can also lead to aspiration & esophagitis - Head elevation may reduce the risk of aspiration, & antacids may improve esophagitis - High level of gastric residue was the most common feeding intolerance found in TBI patients & the delivery of erythromycin by NGT may control GI disorders - Although Metoclopramide (Reglan) increases gastroesophageal sphincter tone & can aid in GERD, it should be avoided due to its ability to cause sedation & EPS

Question 311

Parenteral feed in TBI

Answer 311

IV-delivered nutrition, usually through a central venous line, or in limited circumstances, a peripheral line Can be either supplemental or primary (TPN) Utilized when there is a temporary interruption of GI function or in any condition with an increased metabolic demand TPN is preferred when a segment of GI tract is non-functional or must be free of food for a prolonged period of time Because parenteral feeding products bypass essential GI metabolism, they are made of nutrients that must be in elemental form. Optimal portions vary widely & should be frequently re-assessed Risks of parenteral feeding: central/peripheral line complications (infection, clot formation, edema); electrolyte & metabolic abnormalities are common with parenteral feeding & should be closely monitored

Question 312

What drug is a common cause of SIADH?

Answer 312

Carbamazepine

Question 313

Treatment for SIADH

Answer 313

Fluid restriction to about 1.0 L/day, either alone or with a loop diuretic Careful daily monitoring of weight changes & serum Na until Na level > 135 mmol/L Hypertonic saline: 200-300 mL should be infused over 3-4 hours in patients with severe symptoms as confusion, convulsions, or coma Na may not be corrected more than 10 mEq/L over 24 hours until Na reaches 125. NaCl repletion with salt tablets Chronic SIADH maybe treated with demeclocycline, which normalizes serum Na by inhibiting ADH action in the kidney Lithium carbonate acts similar to demeclocycline, but is rarely used because it is more toxic

Question 314

Why does DI occur?

Answer 314

Severe injuries; often a/w fractures of the skull A fracture in or near the sella turcica may tear the stalk of the pituitary gland, with resulting DI (due to disruption of ADH secretion from posterior pituitary) in addition to other clinical syndromes, depending on extent of lesion

Question 315

What is cognitive remediation in TBI?

Answer 315

Includes visuospatial rehabilitation, executive control, self-monitoring, pragmatic interventions, memory retraining, & strategies to improve attention

Question 316

Post-concussive syndrome

Answer 316

Reduced alcohol intolerance was included in old criteria DSM-5: neuro-cognitive disorder within spectrum of mild or major TBI (ICD refers to this as a syndrome, DSM-5 refers to it as a state, not syndrome). Noted to resolve within days to weeks after the injury, with complete resolution by 3 months Loss of consciousness is NOT included in DSM-5 A/w social & vocational difficulties that appear out of proportion to severity of neurologic insult Persistent PCS has been used to describe sx lasting over 3-6 months

Question 317

What is pannus formation in RA?

Answer 317

Most important destructive element in RA Pannus is a membrane of granulation tissue that covers the articular cartilage at joint margins. It is a synovial membrane-derived tissue that overgrows cartilage Fibroblast-like & macrophage-like cells invade & destroy the peri-articular bone & cartilage at joint margins Osteoclasts invade bone, leading to marginal erosions at the pannus-bone interface

Question 318

What is vascular granulation tissue composed of in pannus in RA?

Answer 318

- Proliferating fibroblasts - Numerous small BV - Various inflammatory cells, but mainly CD-4 T-lymphocytes - PMN's predominate in the synovial fluid - Occasionally, collagen fibers are seen within phagolysosomes of cells at the leading edge of pannus Pannus is vascular - CD4 & T-cells predominate in pannus (but PMNs are in synovial fluid) - Cytokines mediate inflammation (IL-1, TNF-a, IL-6, IL-17, GM-CSF, & TGF-beta)

Question 319

Clinical Diagnosis of RA

Answer 319

Based on 2010 ACR/EULAR classification criteria Patient must have at least one joint with definite clinical synovitis (swelling) that is not best explained by another disease process A score of 6/10 or greater is needed for classification of a patient having definite RA

Question 320

2010 ACR/EULAR Classification Criteria for RA

Answer 320

A. Joint Involvement - 1 large joint: 0 - 2-10 large joints: 1 - 1-3 small joints: 2 - 4-10 small joints: 3 - >10 joints (with at least one small joint): 5 B. Serology (at least one test result is needed for classification) - Negative RF & negative Anti-CCP: 0 - Low positive RF or low-positive Anti-CCP: 2 - High positive RF or high-positive Anti-CCP: 3 C. Acute-phase reactants (at least one test result is needed for classification) - Normal CRP & normal ESR: 0 - Abnormal CRP or abnormal ESR: 1 D. Duration of sx - <6 weeks: 0 - > 6 weeks: 1

Question 321

Insidious onset in RA

Answer 321

Occurs in 50-70% of patients. Initial symptoms can be systemic or articular Slow onset from weeks to months Constitutional symptoms: fatigue, malaise Diffuse MSK pain may be the first non-specific complaint with joint involvement later. Most commonly symmetric involvement although asymmetric involvement may be seen early Morning stiffness in involved joints lasting 1 or more hours Joint swelling, erythema. Muscle atrophy around affected joints Low-grade fever without chills

Question 322

Morning stiffness of major arthritides: duration & location

Answer 322

RA: MCP, PIP, MTP joints. >1 hour OA: DIP, knees, hips. <30 mins AS: LS spine. ~3 hours

Question 323

Synovial fluid analysis in RA

Answer 323

Low viscosity WBC: 1K-75K >70% PMN's Transparent-cloudy

Question 324

RF in RA

Answer 324

70-80% of patients with RA are RF+ RF+ is a/w increased severity of disease with increased systemic manifestation Serial titers are of no value RF+ can be seen in other disease: rheumatic (SLE, scleroderma, Sjogren's), viral, parasitic, bacterial infections, neoplasms, hyperglobulinemic, cryoglobulinemia, Hep C

Question 325

Radiographic findings in RA

Answer 325

Early findings: soft tissue swelling, joint space narrowing Late findings: uniform joint space narrowing due to loss of articular cartilage, axial migration of the hip (protrusio acetabuli), malalignment & fusion of joints Marginal bone erosions near attachment of joint capsule Juxta-articular osteopenia (bone washout) Predilection of swelling of joints in wrists (MCPs, PIPs, MTPs, but not DIPs) Erosion of ulnar styloid & met head of MTP joint C-spine involvement may lead to cervical A-A subluxation (>2.5-3 mm) Radial deviation of the radiocarpal joint Hallux valgus

Question 326

Hand & Wrist Deformities in RA

Answer 326

- Boutonniere - Swan neck - Ulnar deviation of fingers - Flexor tenosynovitis - Instability of carpal bones - Floating ulnar head (piano key sign) - Resorptive arthropathy - Pseudobenediction sign

Question 327

Hand & Wrist Deformities in RA: Boutonniere

Answer 327

Weakness or rupture of the terminal portion of the extensor hood (tendon or central slip) at the PIP joint, which holds the lateral bands in place Initially caused by PIP synovitis Lateral bands of the extensor hood slip downward (sublux) from above the axis of the PIP joint to below axis, turning them into flexors at the PIP joint The PIP then protrudes through the split tendon as if it were a buttonhole, hyper-extending the distal phalanx

Question 328

Hand & Wrist Deformities in RA: Swan neck

Answer 328

May be due to synovitis at the MCP, PIP, or DIP (rare) joint Flexor tenosynovitis --> MCP flexion contracture Contracture of the intrinsic (lumbricals, interosseous) --> PIP hyperextension Contracture of deep finger flexor muscles & tendons --> DIP flexion

Question 329

Hand & Wrist Deformities in RA: ulnar deviation of the fingers

Answer 329

Synovitis & weakening of the ECU, UCL, RCL results in radial wrist deviation, increasing the torque of the stronger ulnar finger flexors Flexor/extensor mismatch causes ulnar deviation of the fingers as the patient tries to extend the joint

Question 330

Hand & Wrist Deformities in RA: flexor tenosynovitis

Answer 330

Early RA may be confused with deQuervain's disease Diffuse swelling of the extensor & flexor tendon sheaths One of the most common manifestations of the hands in RA, can be a major cause of hand pain & weakness

Question 331

Hand & Wrist Deformities in RA: instability of the carpal bones

Answer 331

Ligament laxity, carpal bone erosions, radial deviation of the wrist, ulnar styloid deviates dorsally, & carpal bones rotate (proximal row: volar, distal row: dorsal, rotating in a zig-zag pattern)

Question 332

Hand & Wrist Deformities in RA: floating ulnar head (piano key sign)

Answer 332

Synovitis at the ulnar styloid leads to rupture/destruction of the UCL, which results in laxity of the radioulnar joint Ulnar head floats up dorsally in the wrist Easily compressible elevated ulnar styloid

Question 333

Hand & Wrist Deformities in RA: resorptive arthropathy

Answer 333

Digits are shortened & phalanges appear retracted with skin folds Possible mechanism via osteoclastogenesis & osteoclastic bone resorption Telescoping appearance of digits Most serious arthritic involvement

Question 334

Hand & Wrist Deformities in RA: pseudobenediction sign

Answer 334

stretched radioulnar ligaments allow the ulna to drift upward Extensor tendons of the 4th & 5th digits are subject to abrasion from rubbing on the sharp, elevated ulnar styloid & can rupture Result: extensor tendon rupture, inability to fully extend the 4th & 5th digit

Question 335

C-Spine instability in RA

Answer 335

A-A joint subluxations --> most common are anterior subluxations With cervical flexion, the A-A space normally should not increase significantly. Any space >2.5-3 mm is considered abnormal

Question 336

What diseases are subcutaneous nodules found in?

Answer 336

RA & gout

Question 337

Cardiac findings in RA

Answer 337

Pericarditis, may lead to constrictive pericarditis with right-sided HF May be found in about half of RA patients, but rarely symptomatic Can also see valvular heart disease

Question 338

Felty syndrome

Answer 338

Triad: RA, splenomegaly, leukopenia, often a/w leg ulcers

Question 339

Exercise in treatment of RA

Answer 339

Mild disease (moderate synovitis) requires an ISOMETRIC program Isometric exerise: - Least amount of peri-articular bone destruction & joint inflammation/pain, especially during an acute flare - Restores & maintains strength - Generates maximal muscle tension with minimal work, fatigue, & stress - Isotonic & isokinetic exercise may exacerbate the flare & should be avoided

Question 340

What is therapeutic range for ASA in RA?

Answer 340

15-25 mg/dL. Toxic >30 mg/dL

Question 341

Non-biological DMARDs in RA

Answer 341

Hydroxychloroquine, Sulfasalazine, Methotrexate, Leflunomide, Cyclosporine, Gold, Azathioprine

Question 342

Non-biological DMARDs in RA: Hydroxychloroquine

Answer 342

Retinopathy, hyperpigmentation

Question 343

Non-biological DMARDs in RA: Sulfasalazine

Answer 343

Myelosuppression, GI disturbances

Question 344

Non-biological DMARDs in RA: Methotrexate

Answer 344

Stomatitis, myelosuppression, hepatic fibrosis, cirrhosis, pulmonary involvement, worsens rheumatoid nodules, teratogenicity

Question 345

Non-biological DMARDs in RA: Leflunomide

Answer 345

Hepatotoxicity, nausea, diarrhea, HTN, teratogenicity

Question 346

Non-biological DMARDs in RA Cyclosporine

Answer 346

Renal dysfunction, tremor, hirsutism, HTN, gum dysplasia

Question 347

Non-biological DMARDs in RA: Gold IM, oral

Answer 347

Myelosuppression, renal --> proteinuria Diarrhea (#1 oral), rash (#1 IM)

Question 348

Non-biological DMARDs in RA: Azathioprine

Answer 348

Myelosuppression, hepatotoxicity, lymphoproliferative disorders

Question 349

Pathology in OA

Answer 349

Early: hypercellularity of chondrocytes - Cartilage breakdown: swelling & loosening of collagen framework - Increased proteoglycan synthesis - Minimal inflammation Late: cartilage fissuring, pitting, & destruction - Hypocellularity of chondrocytes - Inflammation secondary to synovitis - Osteophyte spur formation seen at joint margins - Subchondral bone sclerosis (eburnation) - Cyst formation in the juxta-articular bone Increased water content of OA cartilage leads to damage of the collagen network --> increased chondrocytes, collagen, & enzymes

Question 350

Hallmark of DISH

Answer 350

Ossification spanning 4 contiguous vertebral bodies (3 or more IVD's) Can see dysphagia with cervical involvement NOT a/w sacroiliitis, apophyseal joint ankylosis, or HLA-B27 positivity (distinguishes from ankylosing spondylitis)

Question 351

Oligoarticular JIA

Answer 351

Knee is the most common joint involved, followed by ankle, wrist, & then elbows ANA+, RF- HLA B27+ Iridocyclitis No erosions When diagnosing Oligoarticular JIA, must refer to ophtho as they need slit lamp exam 4x/year for 4-5 years

Question 352

Key points of juvenile arthritides

Answer 352

JIA: A. Multi-systemic involvement: RF- in 98%, Stills disease, high fever, rheum rash, lymphadenopathy, HSM, anemia B. Polyarticular (5+ joints involved): no extra-articular manifestations of systemic onset disease, gradual onset of swelling, stiffness affecting c-spine & hip, growth retardation with early closure of epiphyseal plates. This group has worst prognosis when disease is unremitting C. Oligoarticular (1-4 joints involved): RF- 98%, chronic iridocyclitis (<6 y old occurs in 20-40%; more frequently in females ANA+, must have ophtho referral, HLA B27+, no bony erosions on XR Juvenile spondyloarthropathies (all present like adult): - AS - Reiter syndrome - Psoriatic arthritis - IBD-associated Juvenile spondyloarthropathy unique to kids: - SEA syndrome (seronegative enthesopathy & arthropathy) with RF-, ANA-, enthesitis/arthritis/arthralgia, may have uveitis (painful & acute)

Question 353

Inflammatory vs non-inflammatory arthritis

Answer 353

Inflammatory: - Increase in WBC & ESR, acute painful onset, erythema, warmth, & tenderness - CTD- SLE, polymyositis/dermatomyositis, PSS, RA - Crystal: gout & pseudogout - Infectious - Seronegative spondyloarthoprathies Non-inflammatory: - DJD- OA, AVN - Traumatic - Joint tumors - Hemophilia - Metabolic- hemochromatosis, alkaptonuria, rheumatic fever, Wilson's disease

Question 354

Crystal-induced synovitis

Answer 354

Gout & pseudogout Gout: monosodium urate crystals, acute synovitis in synovial membrane & joint cavity Pseudogout: articular chondrocalcinosis, CPPD crystals, hyaline cartilage & fibrocartilage joints Gout: negative birefringence (moderate-severe inflammation WBC 15-20K- neutrophils) Pseudogout: positive birefringence

Question 355

What is a/w pseudogout?

Answer 355

Hypothyroid, hyperparathyroid, hemochromatosis, amyloidosis, hypomag, hypophos

Question 356

Most common site for pseudogout

Answer 356

Knee

Question 357

Drugs that may precipitate gout flare

Answer 357

Thiazides, ASA, loop diuretics, niacin

Question 358

Lab finding in gout vs pseudogout

Answer 358

Gout: hyperuricemia Pseudogout: uric acid normal

Question 359

Seronegative spondyloarthropathies

Answer 359

HLA B27+, but no RF positivity AS Reactive arthritis Psoriatic arthritis (HLA Cw6) Enteropathic arthropathy Pauci/oligoarticular JIA

Question 360

Ankylosing spondylitis

Answer 360

Chronic, inflammatory rheumatic disorder of the axial skeleton affecting the SIJ & spine Most common sx are back pain & significant stiffness, notably in AM & night Symptoms worsen with rest & improve with activity Hallmark: bilateral sacroiliitis Onset as late adolescent & early adulthood, males >> females, more common in whites Synovitis & inflammation with intimal cell hyperplasia- lymphocyte & plasma cell infiltrate Will see pre-spinous calcifications

Question 361

Clinical manifestations of AS: skeletal involvement

Answer 361

Insidious onset of back/gluteal pain: first site of involvement is SIJ. Initially asymmetric but eventually b/l Persistent sx of pain for at least 3 months Decreased lumbar lordosis & increased thoracic kyphosis Cervical ankylosis develops in 75% of patients who have AS for 16 years or longer L- or C-spine is the most common site of fracture Enthesitis: tenderness over ischial tuberosity, greater trochanter, ASIS, & iliac crests Hip & shoulder involvement is more common in juvenile onset, <16 years old Respiratory restriction with limited chest expansion: - Normal is 7-8 cm; if less, risk of restrictive lung disease - Once restrictive lung disease ensues, chest expansion decreases, patient develops diaphragmatic breathing, & T-spine involvement (costovertebral, costosternal, manubriosternal, sternoclavicular)

Question 362

Clinical manifestations of AS: extra-skeletal involvement

Answer 362

Fatigue, weight loss, low grade fever Acute iritis/iridocyclitis (anterior uveitis that involves the iris & ciliary body) --> most common extra-skeletal manifestation. More progressive in Reiter syndrome (Reiter has unilateral, recurrent & pain/photophobia/blurred vision) Cardiac: aortitis leading to fibrosis, conduction defects Apical pulmonary fibrosis: dyspnea, cough Amyloidosis Neuro: CES, C1-C2 subluxation

Question 363

Clinical manifestations of AS: radiographic findings

Answer 363

SI joint narrowing: symmetric, erosions & sclerosis may lead to ankylosis of the SIJ Pseudo-widening of the joint space: - Sub-chondral bone resorption, blurring of joint line - Erosion sclerosis - Calcification leading to ankylosis Bamboo spine: - Ossification of the annulus fibrosis, resulting in bridging syndesmophytes that completely bridge adjacent VB's Interspinous ligament ossification can give dagger sign appearance on XR Along with above, ankylosis of facet joints leads to complete spinal fusion: - Squaring of lumbar vertebrae's anterior concavity - Reactive bone sclerosis - Squaring & fusion of the VB's secondary to ossification of the outer annulus fibrosis at the dorsolumbar & lumbosacral area Associated osteoenia/osteoporosis (bone washout) Loss of cervical lordosis Hip & shoulder involved to lesser extent

Question 364

Treatment for AS (bed)

Answer 364

Firm mattress, sleep in position to keep spine straight/prevent spine flexion deformity- lie prone

Question 365

Triad of reactive arthritis

Answer 365

Conjunctivitis, arthritis, non-gonococcal urethritis

Question 366

How many patients with reactive arthritis progress to AS?

Answer 366

3-10%

Question 367

Clinical manifestation in reactive arthritis

Answer 367

Asymmetric May be confused with plantar fasciitis

Question 368

Radiographic findings in reactive arthritis

Answer 368

Lover's heel: erosion & periosteal changes at the insertion of the plantar fascia & Achilles tendons Ischial tuberosities & greater trochanter with similar findings Asymmetric SIJ involvement Syndesmophytes Pencil-in-cup deformities of hands & feet (more common in psoriatic arthritis)

Question 369

Psoriatic arthritis

Answer 369

Male:female equal Age of onset 30-55 More common in whites, a/w HIV: - Foot & ankle involvement is most common & severe - Treatment is same as psoriatic: first line NSAIDs, no oral corticosteroids, no MTX Unknown pathogenesis, may be environmental like infectious or trauma, or immunologic Stiffness of spine lasting about 30 mins Asymmetric mono or oligoarticular involvement: - Large joints --> knee - DIP involvement --> arthritis mutilans: osteolysis of phalanges & metacarpals of the hand resulting in "telescoping of the finger" Enthesopathy, spondylitis, sacroiliitis 1/3 experience conjunctivitis Aortic insufficiency Radiographic findings: - Pencil in cup appearance of the DIP - Asymmetric sacroiliitis --> fusion - Fluffy periostitis --> hands, feet, spine, & SIJ

Question 370

Clinical manifestations of enteropathic arthropathy

Answer 370

Large joints: knees, ankles, feet. 2 types can occur: enteropathic arthritis or AS A/w ANCA+ (antimyeloperoxidase)

Question 371

What do all the seronegative spondyloarthopathies have in common?

Answer 371

Mucocutaneous lesions, frequent inflammation of the enthesitis, spondylitis with SIJ involvement

Question 372

Causes of Raynaud's

Answer 372

Collagen vascular disease- PSS, SLE, RA, dermato/polymyositis Arterial occlusive disease Pulmonary HTN Neurologic- SCI, CVA Blood dyscrasia Trauma Drugs: ergots, BB, cisplatin

Question 373

Eosinophilic fasciitis

Answer 373

Precipitated by strenuous exercise Exercise should be done in a non-inflammatory state Pain & swelling Treatment: steroids

Question 374

What area of upper GI system is involved with poly/dermatomyositis

Answer 374

Pharynx --> dysphagia

Question 375

Type III poly/dermatomyositis

Answer 375

Can be either poly or dermatomyositis 5-8% a/w malignancy Male >40 years old Poor prognosis

Question 376

Type IV poly/dermatomyositis

Answer 376

Childhood Severe joint contractures, more disabling in a child. Rapid, progressive weakness, respiratory weakness

Question 377

Muscle biopsy in poly/dermatomyositis

Answer 377

- Perifascicular atrophy - Evidence of necrosis of Type 1 & 2 fibers - Variation in fiber size - Large nuclei

Question 378

Clinical features/ACR Criteria for poly/dermatomyositis

Answer 378

Hips involved first then shoulders, +/- respiratory muscle involvement, dysphagia Must have minimum 5.5 for diagnosis: Age at onset: 18-40- 1.3 Age at onset: >40- 2.1 Symmetric weakness of proximal UE: 0.7 Symmetric weakness of proximal LE: 0.8 Neck flexors weaker than extensors: 1.9 Proximal legs weaker than distal legs: 0.9 Heliotrope rash: 3.1 Gottron's papules: 2.1 Gottron's sign: 3.3 Dysphagia/esophageal dysmotility: 0.7 Anti-Jo-1+: 3.9 Elevated CPK or LDH or AST/ALT: 1.3 Muscle bx w/ endomysial infiltration of mononuclear cells surrounding but not invading myofibers: 1.7 Muscle bx with perimysial and/or perivascular infiltration of mononuclear cells: 1.2 Muscle bx with peri-fascicular atrophy: 1.9 Muscle bx with rimmed vacuoles: 3.1

Question 379

EMG in poly/dermatomyositis

Answer 379

Myopathic changes, PSW, fibs, CRDs

Question 380

Juvenile dermatomyositis

Answer 380

Seen more commonly than polymyositis in children A/w generalized vasculitis (unlike adult form) Slight female preponderance heliotrope is predominant feature Presence of clumsiness often unrecognized Transient arthritis, elevated rsh 80-90% respond well to steroids No a/w malignancy in children

Question 381

Arthridites: ANA & RF status

Answer 381

MCTD: Both + RA: Both + SLE: ANA+, RF - PSS: ANA+, RF - Polymyositis: ANA+, RF - Sjogren's: Both +

Question 382

Treatment for temporal arteritis

Answer 382

High-dose steroids ASAP imperative to preventing permanent vision loss ASA 325 mg qD improves prognosis

Question 383

PMR

Answer 383

Some feel it is an expression of temporal arteritis (a vasculitidy) Symptoms: - Fever, weight loss, malaise - Morning stiffness, muscle tenderness - Hallmark: difficulty abducting shoulders above 90 - Affects proximal muscles- neck, pelvic - Diagnosis: ESR >50 - Treatment: steroids

Question 384

What can polyarteritis nodosa be seen in?

Answer 384

RA, SLE, Sjogren's

Question 385

Sjogren's clinical presentation (sicca symptoms)

Answer 385

Dry eyes, dry mouth, skin lesions, parotid involvement Primary: no other rheum diseases Secondary: commonly a/w RA & SLE

Question 386

Most common organisms in septic arthritis

Answer 386

Neonates: Staph, GBS 6 months-2 years: H flu Children >2: Staph, GBS Adults: Neisseiria gonorrhea RA: Staph

Question 387

Other causes of septic arthritis: TB

Answer 387

TB arthritis affecting hips & knees Monoarticular Radiologic findings: Phemister's triad 1. Juxta-articular osteoporosis 2. Marginal erosions 3. Joint space narrowing

Question 388

Other causes of septic arthritis: Lyme

Answer 388

Intermittent migratory episodes of polyarthritis

Question 389

Arthritis in hemophilic arthropathy

Answer 389

Arthritis caused by remaining blood in the joint depositing hemosiderin into the synovial lining --> synovial proliferation & pannus formation

Question 390

Treatment for hemophilic arthropathy

Answer 390

Joint aspiration as a last resort. Blood in joint acts as a tamponade to prevent further bleeding

Question 391

Causes of Charcot joint (STD --> SKA)

Answer 391

Syringomyelia --> Shoulder Tabes dorsalis (syphilis) --> Knee Diabetic neuropathy --> Ankle

Question 392

Charcot joint vs OA

Answer 392

Both have soft tissue swelling, osteophytes, joint effusion Charcot joints have: - Bony fragments - Subluxation - Peri-articular debris

Question 393

What is a/w SCFE?

Answer 393

Endocrinopathies: - Hypothyroidism (most common) - GH abnormalities - Down syndrome

Question 394

ACR criteria for fibromyalgia

Answer 394

1990: widespread pain in all 4 quadrants of body, axial involvement: cervical, anterior chest, thoracic, & low back, pain in 11-18 tender points (occipital, lower cervical, trap, supraspinatus, 2nd rib, lateral epicondyle, gluteal, greater troch, knee) 2010: non-tender point diagnostic criteria based on: - Widespread pain index score - Symptom severity score (includes fatigue, cognitive & somatic symptoms) - Sx must be present consistently for 3 or more months - Must rule out other disorders that could cause pain syndrome

Question 395

Clinical stages of CRPS

Answer 395

Acute: few weeks- 6 months - Allodynia, hyperpathia, hypersensitivity, swelling, vasomotor changes - Increased blood flow creating temperature & skin color changes - Hyperhidrosis Dystrophic: 3-6 months - Persistent pain, disability, atrophic skin changes - Decreased blood flow, decreased temp - Hyperhidrosis Atrophic - Atrophy & contractures - Skin glossy, cool, dry

Question 396

Radiographic findings in CRPS

Answer 396

Plain XR: Sudeck's atrophy: patchy osteopenia, ground-glass appearance Triple phase bone scan: first 2 phases are non-specific, third phase is abnormal with enhanced uptake in peri-articular structures

Question 397

Treatment in CRPS

Answer 397

Advise patients to continue activities as tolerated to avoid disuse atrophy

Question 398

CRPS in children vs adults

Answer 398

Children/adolescents: - Common in LE - 4:1 female > male - Three phase bone scan has mixed results & mostly used to rule out other pathology; will see decreased uptake of the extremity & decreased atrophic changes; occasionally normal; will have increased uptake normally secondary to bone growth - Tx: PT alone, non-invasive TENS, biofeedback, TCA's, blocks in UE are more common - Good prognosis Adults: - UE more common - Gender ratio equal - Sympathetic blocks more common - Poor prognosis

Question 399

Sympathetically-mediated CRPS

Answer 399

4 tests used: 1. Sympathetic block with local (proper response to stellate ganglion block is ipsilateral Horner's, anhidrosis, conjunctival injection, nasal congestion, vasodilation, increased skin temp 2. Guanethidine test: injection of this into extremity distal to a suprasystolic cuff. Test is + if pain is reproduced after injection & immediately relieved after cuff released 3. Phentolamine test: IV of this will reproduce pain 4. Ischemia test: inflation of suprasystolic cuff decreases pain

Question 400

Dupuytren's contracture

Answer 400

Abnormal fibrous hyperplasia & contracture of the palmar fascia, causing a flexion contracture at the MCP & PIP joints More common in white men 50-70 years old A/w epilepsy, pulmonary TB, alcoholism, & DM Mechanism: palmar fascia is a continuation of the palmaris longus tendon attaching to the sides of the PIP & middle phalanges as well as to the skin. Fibromatosis of the palmar fascia & contracture of the fibrous bands that develop into nodules can lead to development of a finger flexion contracture & skin dimpling Most commonly 4th & 5th digits Treatment: trpsin, chymotrypsin, lidocaine injection followed by forceful extension, rupturing the contracture & improving ROM

Question 401

Mallet finger

Answer 401

Most common extensor tendon injury Rupture of the extensor tendon into the distal phalanx 2/2 forceful flexion DIP joint remains in a flexed position & cannot be actively extended Treatment: DIP splint immobilizes the distal phalanx in hyperextension - Acute: 6 weeks - Chronic: 12 weeks Surgical indications: poor healing, volar subluxation, avulsion >1/3 of bone

Question 402

How is arm abduction achieved?

Answer 402

GH & scapulothoracic motion. You get 2 degrees of GH for every 1 of scapulothoracic (120 GH to 60 degrees scapulothoracic) The scapulothoracic motion allows the glenoid to rotate & permits GH abduction without acromial impingement

Question 403

Rockwood classification for AC separations

Answer 403

Type 3: clavicle elevated above superior border of acromion Type 4: clavicle displaced posteriorly through the trapezius, can see skin tenting Type 5: CC distance >100% of contralateral side, severe shoulder droop that does not improve with shrug Type 6 (rare): distal clavicle inferior to coracoid

Question 404

Direction of GH instability

Answer 404

Anterior: most common direction, common direction in younger population with high recurrence rate; mechanism is arm abduction & ER; complication: axillary nerve injury Posterior: less common, may occur as result of seizure; patient may p/w arm in adducted & IR position; landing on a forward flexed adducted arm Multidirectional: rare; patient may display laxity in other joints

Question 405

Bankart lesion

Answer 405

Labral tear off the anterior glenoid allows the humeral head to slip anteriorly Most commonly a/w anterior instability May be a/w avulsion fracture off glenoid rim

Question 406

Hill-Sachs lesion

Answer 406

Compression fracture of the posterolateral humeral head caused by abutment against the anterior rim of the glenoid fossal A/w anterior dislocations A lesion that accounts for >30% of the articular surface may cause instability A notch occurs on the posterior lateral aspect of the humeral head

Question 407

O'Brien's test

Answer 407

Used to detect SLAP lesions 2 parts: typical part, then apply a downward force to patient's supinated arm Positive test: deep shoulder pain that improves when downward force is applied with hand in supination

Question 408

Where is the critical zone of hypovascularity in supraspinatus?

Answer 408

About 1 cm from insertion site

Question 409

Pain in shoulder (RTC) from swimming

Answer 409

Occurs at the "catch" phase of the overhead swimming stroke via flexion abduction, IR More commonly: freestyle, backstroke, butterfly Less common: breast stroke

Question 410

How many degrees of abduction can be achieved with thumb pointing down?

Answer 410

120

Question 411

Shoulder arthrogram

Answer 411

Beneficial in assessing full thickness tears of RTC but unable to delineate the size of the tear or partial tears

Question 412

Functional phase of RTC rehab

Answer 412

Happens after acute phase (up to 4 weeks) & recovery phase (months) Continue strengthening, increasing power & endurance (plyometrics), activity-specific training, rehab in swimmers focuses on strengthening RTC muscles & scap stabilizers (including serratus anterior & lower trap) CSI can be considered (although too much may weaken the collagen tissue, leading to more microtrauma)

Question 413

Shoulder arthrodesis fusion position

Answer 413

50 degrees abduction 30 degrees flexion 50 degrees IR

Question 414

Biceps tendon rupture

Answer 414

Most common site of rupture is at proximal end of long head of biceps tendon

Question 415

Medial scapular winging

Answer 415

Serratus anterior weakness, long thoracic nerve palsy Bench pressing very heavy weights or wearing heavy pack straps can also impinge the nerve Scapula is elevated & retracted Winging of the medial border of the scapula away from the ribs, more evident when patient flexes arms or does a wall push-up

Question 416

Lateral scapular winging

Answer 416

Trap weakness, due to spinal accessory nerve lesions Nerve injury occurs in the posteiror triangle of the neck Scapula is depressed & protracted Rotary lateral winging of scapula around thorax Upper trap muscles can be tested by resisted shrug; mid & lower trap fibers can be tested by prone rowing exercise

Question 417

Most common location for proximal humerus fracture

Answer 417

Surgical neck When fractures at surgical neck occur, the supraspinatus is the principal abductor, which causes abduction of proximal fragment of humerus

Question 418

Complications from proximal humerus fracture

Answer 418

Brachial plexus injury Axillary nerve injury with surgical neck fractures

Question 419

Fusion position for elbow arthrodesis

Answer 419

Unilateral: flexion to 90 degrees Bilateral: flexion to 110 in one arm & 65 for the other

Question 420

Cozen's test

Answer 420

Examiner stabilizes the elbow with a thumb over the extensor tendon origin just distal to lateral epicondyle Pain in the lateral epicondyle is seen with patient making a fist, pronating the forearm, & radially deviating & extending the wrist against resistance by the examiner Test may be more sensitive when done in full extension at the elbow

Question 421

Racket adjustments for lateral epicondylalgia

Answer 421

Decrease string tension, increase grip size

Question 422

Valgus extension overload (VEO) test

Answer 422

Provocative maneuver Flex elbow to 30 degrees & repeatedly extend the elbow fully while applying a valgus stress Pain may be elicited, particularly at the last 5 degrees to 10 degrees of extension Valgus stress should also be performed at >90 degrees to rule out UCL injury

Question 423

What are potential sites for median nerve compression at the elbow?

Answer 423

Ligament of Struthers, lacterus fibrosis, pronator teres, between the 2 heads of the FDS

Question 424

Radial nerve injury with fracture at humeral shaft

Answer 424

Patients may exhibit weakness of radial nerve innervated muscles with sparing of triceps

Question 425

Testing CMC for OA of wrist

Answer 425

Axial compression of the metacarpal on the trapezium giving a painful grinding sensation

Question 426

Osteonecrosis of the lunate

Answer 426

Kienbock's disease (AVN)

Question 427

Where is majority of blood supply to scaphoid?

Answer 427

Distal one-third of the bone Therefore, the middle & proximal portion of the bone have a large non-union rate, with 1/3 developing ostenecrosis Most fractures occur at the scaphoid waist

Question 428

Hamate fractures

Answer 428

Body fractures often from direct trauma; can occur involving axial loading through 4th or 5th metacarpal Fractures of hook of hamate can occur as result of direct trauma on the palmar surface of wrist/hand or due to avulsion from shear forces from adjacent/attached tendons during forceful twisting motion of wrist (Mike Trout swing) Hamate is located slightly distal & radial to the pisiform & forms radial border of the tunnel of Guyon, through which ulnar nerve traverses Vascular supply at radial base & ulnar tip Pain may occur over the hook of hamate or over dorsal ulnar hamate

Question 429

Imaging for hamate fractures

Answer 429

PA, lateral, carpal tunnel, & 45 degrees supinated oblique CT may be needed for fractures at the base of the hook

Question 430

Treatment for hamate fractures

Answer 430

Non-displaced body fractures:4-6 weeks short arm cast Displaced body fractures: surgical referral Acute hook fractures: 50% heal after prolonged casting (6 weeks-4 months) Most acute hook fractures should have adequate vascular supply to heal if immobilized within first week Cast should maintain slight wrist flexion & slight MCP flexion to reduce shear forces from 4th & 5th digit flexor tendons Injuries older than 2 weeks may require excision

Question 431

Stenosing tenosynovitis (trigger finger)

Answer 431

Repetitive trauma that causes an inflammatory process to the flexor tendon sheath of the digits Forms a nodule in the tendon, resulting in abnormal gliding through the A1 pulley system. As the digit flexes, the nodule passes under the pulley system & gets caught on the narrow annular sheath; as a result, the finger is locked in a flexed position

Question 432

Skier's/Gamekeeper's thumb

Answer 432

May occur with chronic lateral laxity or acute disruption of the UCL UCL attaches dorsally at the metacarpal head & runs distally to insert on the volar side of the proximal phalanx base Most acute tears occur at the distal insertion point Complete tears can lead to entrapment of the adductor aponeurosis between the ruptured portions of the ligament --> Stener's lesion & will impair healing. Avulsion or avulsion fracture can also occur; both are surgical indications Will see instability of the MCP joint To examine, stabilize the radial portion of the MCP & position joint in about 30 degrees of flexion --> radial deviation force to stress the UCL Fullness at MCP may indicate a Stener's lesion: - Grade I: pain, no increased motion - Grade 2: increased opening with pain on stressing - Grade 3: no pain, continued motion while stressing Stress radiographs should be done comparing both hands. Instability is indicated by radial deviation >40 degrees in extension & >20 degrees in flexion on XR Treatment: - Short arm cast with thumb spica splint for 4-6 weeks. RTP when thumbs is painless, with firm end point on radial deviation stress & at least 80% recovery or ROM & pinch strength

Question 433

Jersey Finger

Answer 433

Unable to flex the DIP joint due to complete or incomplete injury to the FDP tendon, most commonly at 4th digit

Question 434

Internal rotators of the hip (TAGGGSS)

Answer 434

T: TFL A: Adductor magnus/longus/brevis G: Glut med G: Glut min G: Gracilis S: Semitendinosus S: Semimembranosus

Question 435

Iliofemoral ligament

Answer 435

Y-ligament of Bigelow, strongest ligament in body Extends from AIIS to inter-trochanteric line Functions to limit extension, abduction, & ER of hip

Question 436

Ischiofemoral ligament

Answer 436

Extends from ischium behind the acetabulum to blend with the capsule Function is to limit IR of the hip

Question 437

Pubofemoral ligament

Answer 437

Extends from superior pubic ramus & joints the iliofemoral ligament Limits hip abduction

Question 438

OA of the hip

Answer 438

Limits IR first

Question 439

True leg length discrepancy

Answer 439

Measure from ASIS to medial mal (both fixed bony landmarks) True leg length has many causes, including fractures crossing epiphyseal plate in childhood or polio

Question 440

Hamstring strain

Answer 440

Normal strength hamstring:quad is 3:5 Hamstring placed under maximal stress when hip is forced into flexion & knee into extension Injuries typically occur during the eccentric phase of muscle contraction & at the myotendinous junction, most commonly in the lateral hammy

Question 441

Hip flexor strain

Answer 441

Occurs due to eccentric overload of psoas or as athlete tries to flex the fully extended hip Imaging: AP & frog leg lateral views are used to exclude bony injury such as an apophyseal avulsion fracture

Question 442

Posterior hip dislocation

Answer 442

Most common type, occurring during trauma when hip is flexed, adducted, & medially rotated , driving hip posteromedially Head of the femur is covered posteriorly by the capsule & not bone Sciatic nerve may be stretched or compressed (anterior hip dislocations may cause femoral nerve compromise) AVN in 10-20% Hip will be flexed, adducted, IR (unlike in hip fracture)

Question 443

Imaging in AVN of femoral head

Answer 443

MRI of both hips is indicated. MRI is most sensitive to early changes & is more specific than a bone scan Low signal intensity on T1 that appears as rings, wedges, or irregular configurations T2 may show a double line sign with a high signal intensity zone inside of a low signal intensity margin

Question 444

Posterior approach hip precautions

Answer 444

Total hip precautions: avoid hip flexion over 90 degrees, hip adduction past midline, & extreme hip IR A high chair height is preferred to reduce hip flexion & potential for posterior hip dislocation

Question 445

Anterior approach hip precautions

Answer 445

Avoid hip extension & ER (opposite of posterior approach)

Question 446

Inter-trochanteric fractures

Answer 446

Most common type of hip fracture Highly fragmented fractures may result in significant blood loss/hypovolemia Post-op, a leg length discrepancy may result due to comminution s/p fixation Moderately high forces are generated in this area, & a strong fixation is required Fractures may be non-displaced, displaced 2-part, or unstable 3-part

Question 447

Myositis ossificans

Answer 447

Formation of HO within muscle Ossification within an area of muscle forms from encapsulated blood 2/2 a hematoma Usually the result of repeated trauma to that area of muscle or can be due to a direct blow to the hip Quad is the most common location. Other areas: brachialis, deltoid, intercostal space, erector spinae, pec, glut U/s, heat, or repeated trauma at onset of myositis ossificans can exacerbate the process If the ossifying mass involves a nerve, related nerve impingement symptoms may occur Imaging: - Initially, XR will reveal a soft tissue mass - Calcific flocculations can develop within 2 weeks - Ossification can be seen between 2-3 weeks - Bone scan & MRI are more sensitive than XR in early stages. U/s can be helpful for office or bedside diagnosis of a hematoma & myositis ossificans Treatment: gentle ROM, prevention of contractures, strengthening involved muscles progressively. Surgery may be necessary in cases resulting in nerve entrapment, decreased ROM, or loss of function; if possible, surgery should be delayed until the lesion matures at 10-12 months. Radiation therapy can be trialed for recalcitrant symptoms

Question 448

ACL functional anatomy

Answer 448

Primary function is to limit anterior tibial translation Also prevents posterior translation of the femur & hyperextension of knee Limits IR of femur when foot is fixed & knee is locked Tightens with full extension & loosens in flexion Femoral ER loosens the ACL, & IR tightens it In flexion, it draws the femoral condyles anteriorly ACL-deficient knees create increased pressures on the posterior menisci

Question 449

PCL functional anatomy

Answer 449

Primary function is to restrain posterior tibial translation Ligament is looser in extension & tighter in flexion In extension, the PCL pulls the femur posteriorly PCL-deficient knees pace more force on the patellofemoral joint

Question 450

MCL functional anatomy

Answer 450

Has an attachment to medial meniscus In full extension, the MCL tightens to full tension. Tension is increased with abduction stress at increasing positions of flexion

Question 451

LCL functional anatomy

Answer 451

Does NOT have an attachment to lateral meniscus Restrains varus stresses. Peak stress with adduction when knee is at 70 degree flexion

Question 452

Arcuate popliteal ligament complex (APLC)

Answer 452

Provides attachment for the posterior horn of the lateral meniscus Reinforces the lateral aspect of the knee & gives posterior lateral rotary stability Also provides restraint to posterior tibial translation Its attachment can be mistaken for a tear of the posterior horn of the lateral meniscus on MRI

Question 453

Menisci of the knee

Answer 453

2 menisci (medial & lateral) are composed of crescent-shaped fibrocartilaginous tissue Deepen the articular surface area of the tibia to provide more stability for the femoral condyles & increased force dispersion to the tibial plateau Peripheral outer 1/3 of meniscus is well-vascularized. Inner 2/3 is not & cannot be surgically reparied Medial C --> longer & larger Lateral O --> covers a larger area. Jointed to the MFC by the posterior meniscofemoral ligament

Question 454

Why is anterior drawer test for knee not very sensitive?

Answer 454

Hemarthrosis, hamstring spasm, & other structures (like posterior capsule) can limit forward movement of the tibia

Question 455

What test is more sensitive: Lachman or anterior drawer?

Answer 455

Lachman

Question 456

What test has high specificity for ACL tear?

Answer 456

Pivot shift test. 5-mm of motion is considered a Grade I tear

Question 457

Treatment for meniscal tears

Answer 457

Meniscectomy: WBAT in 1-2 days Repair: NWB 4-6 weeks, followed by strengthening

Question 458

Mechanism of injury for ACL tear

Answer 458

Cutting, deceleration, & hyperextension of the knee Sudden pop & anterior knee pain with posterior lateral joint line pain

Question 459

What is the most sensitive marker for acute ACL injury?

Answer 459

Severe effusion in the 2-12 hours following injury

Question 460

Lachman test

Answer 460

May be positive but can yield a false negative in about 10% of cases. Examiner-dependent & influenced by muscle guarding Grading criteria: - Translation Grade I: <5 mm translation - II: 5-10 mm translation - III: >10 mm translation Endpoint Grade: - A: firm, sudden endpoint to passive anterior translation of tibia on fixed femur - B: absent, ill-defined, or softened endpoint to passive anterior translation of tibia on a fixed femur

Question 461

ACLR post-op rehab

Answer 461

PWB initially --> ROM to regain flexion over first 2 weeks --> progress to closed chain kinetics --> avoid open chain exercises, especially in full extension Resistive exercises between 0-45 degrees flexion is AVOIDED during first 3-6 months Lenox Hill de-rotation orthosis is used to control knee axial rotation as well as AP & medial-lateral control Sport-specific exercises at 6-12 weeks

Question 462

MCL tears

Answer 462

Opening of 5-8 mm compared to opposite side may indicate complete tear Instability in slight flexion of 30 degrees is specific for MCL injury, whereas instability in full extension may indicate injury to the MCL & posterior capsule Epiphyseal fractures may present with or without MCL tears

Question 463

Patellofemoral pain syndrome

Answer 463

Runner's/biker's knee Most common cause of anterior knee pain Overuse injury caused by repeated microtrauma, leading to peripatellar synovitis Patellar tracking problem Treatment: adjust saddle position on bicycle. Having saddle too forward or low will stress anterior knee, but too high will stress posterior knee. Minimize hyperflexion of cyclist knee in force generation phase of pedaling. Adjust rotation of cleats; anterior knee is stressed with internally rotated cleats, whereas medial knee is stress with externally rotated cleats Therapeutic exercise: - Quad strengthening, especially VMO - Short arc quad activities (0-15) used to strengthen VMO - Isotonic quad strengthening with eccentric loading occurs in a non-painful ROM - Isometric quad contractions are used - SLR for iliopsoas strengthening occurs - Stretching of hammies, ITB, adductors, & vastus lateralis - Proprioceptive exercises - Increase activity when ROM full & pain-free & strength is 80% of normal Possible surgeries (rarely needed): - Lateral release of knee capsule & retinaculum - Patellar realignment - Patellar tendon transfer - Patellectomy

Question 464

Q angle

Answer 464

Normal in females: 18 degrees, males should be 13 degrees Factors that increase Q angle: internal torsion of femur, lateral insertion of the infrapatellar tendon on the tibia, genu valgum

Question 465

Most common site of patellar tendonitis

Answer 465

Inferior pole of the patella

Question 466

Osteochondritis dissecans

Answer 466

2/2 small stresses to sub-chondral bone that disrupt blood supply to that area of bone Localized segmental area of AVN at the end of a long bone --> formation of dead sub-chondral bone covered with articular hyaline cartilage Overlying cartilage degenerates around the defect & an entire piece may detach from the rest of the bone, entering the joint space as a loose body. Usual area is MFC Other areas of involvement: distal femur, patella, elbow, talus, & distal humerus Most commonly affects adolescents Gradual onset of joint pain & irritation, synovial effusion, & buckling sensation Walking with the foot rotated outward may relieve pain To palpate the MFC, have knee flexed to 90 with pressure directed medial to the inferior pole of the patella "Shark bite" on MRI Healing of defect may occur if diagnosis is made before fragment separates --> knee must be placed at rest & NWB

Question 467

Popliteus tendonitis

Answer 467

Popliteus arises from lateral face of the LFC & inserts into the triangular area in the posterior tibia Main function is IR of the tibia (laterally rotates femur on the tibia = medially rotating the tibia with respect to the femur, depedning on which bone is fixed) Assists in unlocking knee by laterally rotating femur With the ACL, limits anterior translation of the femur Lateral knee pain with downhill activities & excessive pronation Stress to popliteus is caused by forward femoral displacement, such as running downhill Point tenderness anterior to the fibular colalateral ligament & LCL Pain with legs in figure 4 or cross-legged Treatment: may require arch supports or MEDIAL heel wedges

Question 468

Pain pattern in CECS

Answer 468

Pain will typically increase with exercise & progress as the activity increases in intensity

Question 469

What is the main predisposing factor to shin splints (MTSS)?

Answer 469

Hyperpronation

Question 470

Clinical feature of MTSS

Answer 470

Pain may improve with exercise but worsens AFTER the completion of activity & can last until next morning

Question 471

Ligaments of the ankle (lateral)

Answer 471

ATFL (primary lateral ankle ligament stabilizer), CFL, PTFL (posterior talofibular)

Question 472

Indications for surgery in lateral ankle sprains

Answer 472

Large bony avulsions, severe ligamentous damage on the medial & lateral sides of the ankle, & severe recurrent injuries

Question 473

Clinical features of tibialis posterior tendon injury

Answer 473

Insidious onset of posteromedial ankle pain increased by activity, medial hindfoot swelling, increased pain with push-off, weakness with inversion & PF, too many toes sign 2/2 collapse of medial longitudinal arch Can be a/w malignant malalignment syndrome --> broad pelvis, increased femoral anterversion, squinting patellae, excessive Q angle, & excess pronation of the foot. Hyperpronation can lead to tibialis posterior pain

Question 474

Where is there inadequate vascularization in Achilles tendon?

Answer 474

2-6 cm proximal to insertion of the tendon, which is where most ruptures occur Do not perform CSI into Achilles tendon as it may cause rupture --> decreases metabolic rate of chondrocytes & fibrocytes, weakening structural integrity of the tendon & articular cartilage

Question 475

Sinus tarsi syndrome

Answer 475

Talocalcaneal sprain Occurs via excessive foot pronation causing adduction of the talus Usually h/o arthritis: RA, gout, & seronegative spondyloarthropathies Usually h/o prior ankle injury: inversion sprain or fracture of the tibia, calcaneus, or talus Pain on anterolateral aspect of foot/ankle Diagnosis made with block into sinus tarsi. If pursuing surgical management (can be done conservatively), decompression of tunnel contents

Question 476

SPLATT procedure

Answer 476

Split Anterior Tibial Tendon Transfer Used for TA spasticity (inversion) TA tendon is split, & portion of tendon is transferred to lateral foot. Half remains attached to its site of origin, while distal end of lateral half of tendon is tunneled into the 3rd cuneiform & cuboid bones Provides an eversion force to counteract the dynamic varus deformity to provide a flat base for WB Often done along with Achilles tendon lengthening to decrease PF Over-correction is a possible complication

Question 477

Talar neck fractures

Answer 477

Shear force on the anterior lateral surface of talus --> shallow lesion Compressive force on posterior medial surface --> deep lesion MoI: eversion & DF, inversion & PF Hawkin's classification: Type I: non-displaced vertical fracture of talar neck Type II: displaced fracture of talar neck of subtalar joint with ankle joint intact Type III: displaced fracture of talar neck with dislocation of the body of the talus from the subtalar & ankle joints Complications: AVN, most commonly of the talar body. Risk increases as amount of displacement increases Fracture of the talar dome may form a subchondral fragment that can detach & become displaced in the joint space Conservative treatment: NWB, surgical is ORIF if indicated

Question 478

What is a/w plantar fasciitis?

Answer 478

Tight Achilles tendon

Question 479

What should be avoided in treatment of plantar fasciitis?

Answer 479

Do not inject anesthetic/corticosteroid into the subq tissue or fascial layer. Stay away from superficial fat pad to avoid fat necrosis Can use nighttime dorsiflexion splints if other measures fail

Question 480

Morton's neuroma

Answer 480

Irritation & degeneration of the distal interdigital nerves in the toes from the plantar nerve with eventual enlargement due to perineural fibrosis. Mass can produce pain in the web spaces between met heads Most commonly affects 3rd intermetatarsal space (between 3rd & 4th toes), followed by 2nd intermetatrsal space Females > males To examine, apply direct pressure to the interdigit web space with one hand & then apply lateral & medial foot compression to squeeze met heads together

Question 481

Hammer toe

Answer 481

Deformity of the lesser toes in which there is flexion of the PIP joint Passive extension of the MTP joint occurs when the toe is flat on the ground. DIP joint is usually not affected Caused by chronic, tight shoe wear that crowds the toes, but may be seen after trauma Treatment: - Shoe with high toe box - Shoe should be 1/2 inch longer than longest toe - HEP of passive manual stretching

Question 482

Fifth metatarsal fractures

Answer 482

Most common metatarsal to fracture Fractures at the base are classified by zone: - Zone 1: pseudo-Jones- avulsion fracture of tuberosity - Zone 2: Jones- metaphyseal-diaphyseal junction, risk of non-union - Zone 3: diaphyseal stress fractures from repetitive loading, risk of non-union Dancer's: distal shaft fracture Nutcracker: cuboid fracture March: metatarsal stress Treatment: - Jones: NWB cast for 6 weeks, ORIF if non-union occurs - Nutcracker: ORIF - March: relative rest with immobilization, cast if needed, may require surgical fixation due to increased risk of fracture displacement

Question 483

What steroid is more likely to cause tissue atrophy than methylprednisolone when injecting superficial structures?

Answer 483

Triamcinolone

Question 484

Viscosupplementation

Answer 484

HA is a large, linear glycosaminoglycan. Benefit derived from enhanced endogenous HA synthesis by synovial cells, proteoglycan synthesis by chondrocytes, anti-inflammatory effects, & analgesic effects Use caution with patients with allergy to products from birds such as feathers, eggs, or poultry

Question 485

Clinical course of LBP

Answer 485

Disability & ability to return to work generally improve in 1 month, but 1/3 may have persistent discomfort for up to a year after injury, with 20% of those reporting limitation in activity Approximately 50% resolve in 1-2 weeks Approximately 90% resolve in 6-12 weeks Approximately 85% recur in 1-2 years

Question 486

Absenteeism in regard to LBP

Answer 486

Missed 6 months --> 50% RTW Missed 1 year --> 25% RTW Missed 2 years --> 0% RTW

Question 487

Cervical uncinate processes

Answer 487

Raised spondylotic margins along the lateral aspect of the superior surface of a cervical vertebral body due to disc degeneration These raised margins approximate with the body of the superior vertebra, creating a degenerative joint known as the uncovertebral joint (joint of Luschka) Joints of Luschka limit lateral translation

Question 488

Sacral vertebrae

Answer 488

Triangular shaped bone consisting of 5 fused vertebrae (S1-S5) Four pair of foraminae (anterior & posterior), sacral promintory, sacral ala, hiatus, cornua, medial, intermediate, & lateral crests, which are analogous to spinous processes Contains sacral ligaments

Question 489

Facet joint orientation

Answer 489

Cervical: - AA & AO joints have no true facet joints due to their atypical anatomy - C3-7 facets --> frontal (coronal) plane Thoracic: frontal (coronal) plane Lumbar: sagittal plane in upper lumbar, frontal plane at L5-S1

Question 490

Intervertebral disc

Answer 490

Nucleus pulposus: viscous gel mixture of water & proteoglycans in a network of Type II collagen that braces annulus to prevent buckling Annulus fibrosis: Type I collagen fibers arranged in obliquely running lamellae that encase the nucleus pulposus & are attached to the vertebral endplates. This orientation withstands distraction forces & bending but is more susceptible to injury with torsional stresses Vertebral endplate: cartilaginous covering of the VB apophysis, forming the interface between the disc & VB (forming the top & bottom of the disc) Vascular supply: supplied by cartilaginous VB endplates; IVD's are essentially avascular by adulthood

Question 491

Innervations of IVD

Answer 491

Outer 1/3 of annulus --> sinuvertebral nerve & gray ramus communicans, both from b/l ventral rami Nucleus pulposus --> no innervation Anterolateral part of annulus --> ventral rami & gray rami communicans Posterior part of annulus --> sinuvertebral nerves (recurrent branches off the ventral rami)

Question 492

Innervations of spine/IVD

Answer 492

Ventral primary rami --> trunk musculature, plexus contributions Dorsal primary rami: - Lateral: iliocostalis, skin - Intermediate: longissimus - Medial: multifidi, rotators, interspinalis, intertransversarii, posterior spinal ligaments, Z-joints Sinuvertebral nerve: PLL, posterior disc, anterior dura, VB

Question 493

Aging effects in spine

Answer 493

Decreases: - Nuclear water content - Ratio of chondroitin:keratin - Proteoglycan molecular weight Increases: - Fibrous tissue - Cartilage cells - Amorphous tissue

Question 494

Interspinous & supraspinous ligaments

Answer 494

Run from spinous process to spinous process. The supraspinous ligament runs from C7-L3. Functions to weakly resist both spinal separation & flexion The superior continuation of the supraspinous ligament extending from occipital protuberance to C7 --> ligamentum nuchae (functions to form boundary of the deep muscle in the cervical region)

Question 495

Disc herniation

Answer 495

May initiate the release of enzyme phospholipase A2, which activates inflammatory mediators, such as leukotrienes, prostaglandins, platelet-activating factors, bradykinins, & cytokines Higher prevalence for L-spine at L4-5 or L5-S1, followed by C5-6

Question 496

Disc herniation classifications

Answer 496

Bulge: no annulus defect, disc convexity is beyond vertebral margins Prolapse: nuclear material protrudes into annulus defect Extruded: nuclear material extends to the PLL Sequestered: nuclear fragment free in the canal

Question 497

Disc herniation location

Answer 497

Central: may p/w axial spinal pain with or without radicular symptoms. Possible multiroot involvement if cauda is affected or myelopathy if SC is involved Posterolateral: more common in L-spine due to tapering of PLL. A posterolateral L4-5 herniation can impinge the L5 nerve root Lateral/foraminal: may p/w axial spinal pain with or without radicular sx. Affects the exiting root of that IV level; for example, a lateral L4-5 herniation can impinge the L4 nerve root

Question 498

Vertebral distraction for relieving nerve compression

Answer 498

Cervical: 20-30 degrees flexion with 25 lb resistance. Less flexion is required for treatment of muscle spasm Lumbar: may require increased force or a split table to overcome friction

Question 499

Chymopapain injections

Answer 499

Dissolves sub-ligamentous herniations contained by the PLL Complication/ADR: anaphylactic reaction, chronic pain, poor efficacy

Question 500

Where is LSS most common when it affects nerve roots?

Answer 500

L4-5 levels

Question 501

Classification of LSS

Answer 501

Central spinal stenosis: causes include facet & ligamentum flavum hypertrophy, disc herniation, epidural lipomatosis, or degenerative spondylolisthesis; C-spine AP dimensions: normal SC is 10-mm in diameter, spinal canal is 17 mm. Neuro sequelae may begin when central canal is <12 (relative stenosis) to 10 mm (absolute stenosis) Lateral recess stenosis: subdivided into 3 areas of entrapment across motion segment: - Lateral recess - Midzone (lateral/far lateral) - IVF (lateral/far lateral)

Question 502

Spinal stenosis location & borders

Answer 502

Entrance zone (lateral recess): - Borders: posterior- SAP; anterior- posterior body & disc; medial & lateral walls- open - Contents: descending nerve root - Etiology: hypertrophic facet joints - Root level: nerve root exiting below (L3-4 lateral recess involves L4 nerve root) Foraminal stenosis: mid-zone (pars region): - Borders: posterior- pars; anterior- posterior VB; medial wall- open - Contents: DRG, ventral motor root - Etiology: osteophytes under the pars - Root level: same as vertebrae (L3 pars involves L3 roots) Foraminal stenosis: exit zone (IVF): - Borders: posterior- Z-joint (inferior level); anterior- posterior disc (inferior level) - Contents: spinal nerve - Etiology: hypertrophic facet joints - Root level: one level up from the vertebrae (L4 SAP or L3-4 disc involve L3 roots)

Question 503

Etiology of spondylolisthesis

Answer 503

Class II: Isthmic --> most common type in adolescents & young adults, age 5-50 Criteria: pars fracture (subtype A), which is most common at L5-S1 or an elongation (subtype B)

Question 504

Scheuermann's disease (juvenile kyphosis)

Answer 504

Adolescent disorder of the vertebral endplates & apophysis resulting in an increased thoracic kyphosis, usually involving 3 sequential vertebrae & generally >45 degrees Imaging: XR, CT, MRI - VB wedging, irregular endplate, Schmorl's nodes with increased kyphosis angulation (Schmorl's nodes is a herniation of disc material through the vertebral endplate into the spongiosa of the VB, & vertebral wedging (~5 degrees)

Question 505

VB burst fractures

Answer 505

Compression fractures of the VB involving the anterior & middle columns of the spine from significant trauma, typically fall from height Most commonly seen in TL region Treatment is based on stability: - Stable: neurologically intact. Posterior column remains intact. <50% collapse of anterior VB height - Unstable: neuro deficits present, >50% loss of anterior VB height

Question 506

SIJ

Answer 506

Ear-shaped articulation between the sacrum & ilium that has a synovial joint anteriorly & syndesmosis posteriorly Innervated by the L4/5 dorsal ramus & lateral branches of the S1-3 (S4) dorsal rami

Question 507

VB OM & discitis

Answer 507

Embolic infection of the VB metaphysis causing ischemia, infarct, & bony destruction with disc involvement Risk factors: advanced age, DM, immunodeficiency, penetrating trauma, dental infections, GU procedures, & invasive spinal procedures Most commonly seen in L-spine with IVDA & in the TL junction with TB Staph: most common Pseudomonas: IVDA Mycobacterium tuberculi: Pott's (needs 12 months of treatment)

Question 508

Waddell's signs

Answer 508

Distraction: +SLR but negative slump (should both be +) Overreaction Regionalization Simulation: leg or lumbar pain with light axial load on skill, or presentation of lumbar pain with simultaneous pelvis & shoulder rotation in unison Tenderness

Question 509

Where is SCS placed?

Answer 509

Electrodes are placed over the area of the dorsal columns into the epidural space

Question 510

Muscles of shoulder flexion

Answer 510

Anterior deltoid Pec major, clavicular portion Biceps brachii Coracobrachialis

Question 511

Muscles of shoulder extension

Answer 511

Posterior deltoid Lat Teres major Triceps, long head Pec major, sternocostal portion

Question 512

Muscles of shoulder abduction

Answer 512

Middle deltoid Supraspinatus

Question 513

Muscles of shoulder adduction

Answer 513

Pec major Lat Teres major Coracobrachialis Infraspinatus Long head of triceps Anterior & posterior deltoid

Question 514

Muscles of shoulder IR

Answer 514

Subscapularis Pec major Lat Anterior deltoid Teres major

Question 515

Muscles of shoulder ER

Answer 515

Infraspinatus Teres minor Deltoid, posterior portion Supraspinatus

Question 516

Muscles of elbow flexion

Answer 516

Brachialis Biceps Brachioradialis Pronator teres

Question 517

Muscles of elbow extension

Answer 517

Triceps Anconeus

Question 518

Muscles of forearm supination

Answer 518

Supinator Biceps

Question 519

Muscles of forearm pronation

Answer 519

Pronator teres Pronator quadratus FCR

Question 520

Muscles of wrist flexion

Answer 520

FCR FCU Palmaris longus FDS FDP FPL

Question 521

Muscles of wrist extension

Answer 521

ECRL ECRB ECU EDC EDM EIP EPL

Question 522

Muscles of ulnar deviation of the wrist (adduction)

Answer 522

FCU ECU

Question 523

Muscles of radial deviation of the wrist (abduction)

Answer 523

FCR ECRL

Question 524

Muscles of finger flexion

Answer 524

FDP FDS Lumbricals Dorsal & palmar interossei Flexor digiti minimi

Question 525

Muscles of finger extension

Answer 525

EDC EIP EDM

Question 526

Muscles of finger abduction

Answer 526

Dorsal interossei Abductor digiti minimi

Question 527

Muscles of finger adduction

Answer 527

Palmar interossei

Question 528

Muscles of thumb flexors

Answer 528

FPB FPL Opponens pollicis Adductor pollicis

Question 529

Muscles of thumb extensors

Answer 529

EPL EPB APL

Question 530

Muscles of thumb abduction

Answer 530

APL APB

Question 531

Muscles of thumb adduction

Answer 531

Adductor pollicis

Question 532

Muscles of opposition of the thumb to 5th digit

Answer 532

Opponens pollicis FPB APB Opponens digiti minimi

Question 533

Muscles of hip flexion

Answer 533

Iliopsoas Sartortius Rectus femoris Pectineus TFL Adductor brevis/longus/magnus Gracilis

Question 534

Muscles of hip adductors (anterior)

Answer 534

Gracilis Pectineus Adductor longus/brevis/magnus

Question 535

Muscles of hip adduction (posterior)

Answer 535

Glut max Obturator externus Gracilis Long head of biceps femoris Semimem Semiten

Question 536

Muscles of hip abduction

Answer 536

Glut med Glut min

Question 537

Muscles of abductors & IR of the hip

Answer 537

TFL Sartorius Piriformis Glut max, superior fibers

Question 538

Muscles of hip extension

Answer 538

Glut max Glut med, posterior fibers Glut min, posterior fibers Piriformis Adductor magnus Hamstring muscles

Question 539

Muscles of hip ER

Answer 539

Piriformis Obturator internus Superior & inferior gemellus Obturator externus Quadratus femoris Glut max

Question 540

Muscles of knee extension

Answer 540

Rectus femoris Vastus lateralis Vastus intermedius VMO

Question 541

Muscles of knee flexion

Answer 541

Hamstrings Sartorius Gracilis Gastroc

Question 542

Muscles of medial rotation of knee

Answer 542

Semiten Semimem Sartorius Gracilis

Question 543

Muscles of lateral rotation of knee

Answer 543

Biceps femoris (long & short heads)

Question 544

Muscles of ankle dorsiflexion

Answer 544

TA EHL

Question 545

Muscles of ankle dorsiflexion & foot evertors

Answer 545

EDL Peroneus tertius

Question 546

Muscles of foot evertors & weak PF

Answer 546

Peroneus brevis Peroneus longus

Question 547

What is an innervation ratio?

Answer 547

Amount of muscle fibers belonging to 1 axon. Ratio varies depending on function of the motor unit Muscles of gross movement & greater force generated have a high ratio (axons innervating leg muscles can have a 600:1 ratio, meaning 600 muscle fibers are innervated by 1 axon) Innervation ratio of the eye muscles can be 1:1 (1 muscle fiber to 1 axon) --> finer movements

Question 548

Endoneurium

Answer 548

Connective tissue surrounding each individual axon & its myelin sheath

Question 549

Perineurium

Answer 549

Strong, protective connective tissue surrounding bundles of fascicles of myelinated & unmyelinated nerve fibers Helps strengthen the nerve & acts as a diffusion barrier Individual axons may cross from one bundle to another along the course of the nerve

Question 550

Epineurium

Answer 550

Loose connective tissue surrounding the entire nerve that holds the fascicles together & protects it from compression

Question 551

What type of nerves does EMG study?

Answer 551

Type Ia (large, myelinated) fibers

Question 552

Temperature effects on Na channels

Answer 552

Na channels normally remain open for about 25 microseconds Decrease in temp affects the protein configuration & causes a delay in opening & closing of the gates --> changes waveform appearance Although amplitude is expected to increase as a result of gates being open longer, it can still decrease due to increased temporal dispersion or phase cancellation In focal cooling, will see prolonged onset & peak latencies, increased amplitude, & decreased CV In generalized cooling, will see even longer onset & peak latencies, & even slower CV. However, amplitude is about normal because the increased temporal dispersion & phase cancellation knocks down any increase in amplitude from temp alone

Question 553

Waveform changes due to a decrease in temperature

Answer 553

Latency --> prolonged 1 ms Amplitude --> increased by 20% Duration --> increased CV --> decreased by 10 m/s Phases --> increased

Question 554

Propagation of a nerve current

Answer 554

As Na goes into the cell from a depolarization, it moves away from the membrane & spreads the current down the path of least resistance along length of the axon Affinity to flow back out through the membrane is low due to the myelin sheath covering --> potential jumps to next group of Na channels, located between the myelin to nodes of Ranvier (saltatory conduction)

Question 555

Skeletal muscle fiber

Answer 555

Cylindrical, multinucleated cell containing contractile elements composed of actin & myosin Sarcomere is a basic unit of a muscle's myofibril. Sarcomere runs from Z-line to Z-line. Its size changes during contraction M line: runs down center of sarcomere, through the middle of the myosin filaments I band: contains only thin filaments H zone: contains only thick filaments A band: contains both thin & thick filaments & is the center of the sarcomere that spans the H zone During contraction, the H zone, I band, distance between Z lines, & distance between M lines all become smaller. However, the A band's size remains constant during contraction

Question 556

Muscle fiber contraction & relaxation

Answer 556

Contraction: - An action initiated by muscle fiber depolarization - Stimulus spreads in both directions on the fiber at 3-5 m/s - Stimulus penetrates deeper into muscle through the T-tubule system, which causes Ca to be released from the SR - Ca binds to the troponin-tropomyosin complex & exposes actin's active sites - Myosin heads, powered by ATP, bind with the active sites - Actin & myosin filaments slide over each other to shorten the muscle

Question 557

Muscle fiber contraction & relaxation

Answer 557

Contraction: - An action initiated by muscle fiber depolarization - Stimulus spreads in both directions on the fiber at 3-5 m/s - Stimulus penetrates deeper into muscle through the T-tubule system, which causes Ca to be released from the SR - Ca binds to the troponin-tropomyosin complex & exposes actin's active sites - Myosin heads, powered by ATP, bind with the active sites - Actin & myosin filaments slide over each other to shorten the muscle

Question 558

Etiologies of demyelinating injuries

Answer 558

Focal compression causing a transient ischemic episode, edema, or myelin invaginations with paranodal intussusceptions

Question 559

Axonal regrowth after axonal nerve injury

Answer 559

Process of repair- axon will regrow down its original pathway toward its muscle fibers, travelling approximately 1 mm/day or 1 inch/month (35 mm/month) if the supporting connective tissue remains intact. These axons will have a decreased diameter, thinner myelin, & shorter internodal distance With reinnervation, low-amplitude, long-duration, & polyphasic potentials known as nascent potentials are formed If connective tissue is NOT in tact to guide proper nerve regrowth --> neuroma with failure to reach end organ Shorter the distance from injury to end organ, the higher the likelihood for a better prognosis

Question 560

Needle electrodes

Answer 560

If used for NCS, the waveform's amplitude & CV cannot be assessed because the needle samples only a few fibers Monopolar (what we use): 22-30 gauge Teflon-coated needle; inexpensive, omni-directional recording, less painful (Teflon decreases friction), larger recording area (2x that of concentric), records more PSW's & more abnormal activity in general. Disadvantages: requires separate reference, non-standardized tip area, Teflon can fray, may have more interference if the reference is not near recording electrode Concentric (coaxial): 24-26 gauge reference needle with a bare inner wire (active); standardized exposed area, fixed location from reference with less interference, used for quantitative EMG. Disadvantages: beveled tip so unidirectional recording, smaller recording area, MUAPs have smaller amplitudes, more painful Bipolar concentric: needle with the active & reference wires within its lumen; best for isolating MUAP with less artifact. Disadvantages: expensive & more painful Single fiber needle: needle (reference) consisting of an exposed 25 micrometer diameter wire (active); looks at individual muscle fibers, used to assess fiber type density, jitter, & fiber blocking, helpful in assessing NMJ disorders & MND. Disadvantages: not used for traditional EMG, expensive

Question 561

Anodal block

Answer 561

Theoretical local block that occurs when reversing the stimulator's cathode & anode. It hyperpolarizes the nerve, thus inhibiting the production of an AP

Question 562

What happens with volume conduction? (Stim intensity too high)

Answer 562

- Decreased conduction times & shortened latencies - Altered waveforms - Amplitudes remain unchanged

Question 563

Signal:noise ratio

Answer 563

Process of averaging improves this ratio by a factor that is the square root of the number of averages performed The # of averages must be increased by a factor of 4 to double the S:N S:N = Signal amplitude x square root of # of averages performed, then all of that divided by noise amplitude

Question 564

Types of NCS Filters

Answer 564

High-frequency filter (HFF) = Low pass Low-frequency filter (LFF) = High pass HFF (Low pass): removes signals with frequencies higher than its cutoff setting (beLOW this number can pass); affects faster portions of the waveform LFF (High pass): removes signals with frequencies lower than its cutoff setting (the high can pass). Affects slower portions of the waveform Elevating the LFF (High pass): - Reduces peak latency (but does not change onset latency) --> gets faster Reduces amplitude --> less overall getting through Changes potentials from bi to tri --> sexually gets faster Reducing the HFF (Low pass): - Prolongs peak & onset latency latency --> gets slower - Reduces amplitude --> less overall getting through - Creates a longer negative spike

Question 565

CV variations with aging

Answer 565

Newborn is 50% that of an adult 80% of adult by 1 year Adult values at 3-5 Once in 50's, CV decreases by 1-2 m/s per decade

Question 566

CV differences with temp

Answer 566

Normal is 32 C in UE & 30 C in LE CV decreases 2.5 m/s per 1 degree C dropped Once below 29 degrees C, there is a 5% decrease in CV for every degree dropped

Question 567

SNAP in relation to DRG

Answer 567

DRG is located in the IVF & contains the sensory cell body. Lesions proximal to it (injuries to sensory nerve root or to the SC) preserve the SNAP despite clinical sensory abnormalities. This is because axonal transport from the cell body to the peripheral axon remains intact. SNAPs are considered more sensitive than CMAPs in detection of an incomplete peripheral nerve injury Pre-ganglionic injury to motor fibers --> will see NCS abnormalities. But for sensory, will see above Post-ganglionic injury --> will see NCS abnormalities for both sensory & motor, since there is physical separation of the axon from the cell bodies in the DRG & the ventral portion of the SC

Question 568

Results when electrodes are <4 cm apart

Answer 568

All decrease: peak latency, amplitude, duration, rise time

Question 569

H-reflex

Answer 569

Late response analogue to a monosynaptic reflex Initiated with a SUB-MAX stim at long duration (1.0 ms), preferentially activating Ia afferent nerve fibers --> orthodromic sensory response to SC with orthodromic motor back to recording electrode Can be potentiated with agonist muscle contraction or abolished with antagonist contraction increased stimulation causing collision blocking Morphology & latency remain constant with each stim at the appropriate intensity A mean of 10 F waves can substitute for one H-reflex Typically used for S1 radic (soleus) or C7 radic (FCR) Formula: 9 + 0.5 (Leg length in cm from medial mal to pop fossa) + 0.1(age). If >60 years, add 1.8 ms Normal latency is 28-30 ms Side to side difference: Anything >0.5-1ms is significant Waveforms can still be picked up in someone with UMN lesion or even infants Limitations: - Evaluates a long neural pathway, which can dilute focal lesions & hinder specificity of injury location Can be normal with incomplete lesions - Cannot distinguish between acute & chronic lesions. Once abnormal, it is always abnormal - NOT specific --> can also be seen in generalized peripheral neuropathies, plexopathies, & UMN lesions - Can be normally abnormal in older adults

Question 570

F-wave

Answer 570

Small late motor response occurring after the CMAP, representing response from 1-5% of the CMAP amplitude Produced using a short duration, SUPRAMAX stim, which initiates an antidromic motor response to the anterior horn cells in the SC, which in turn produce an orthodromic motor response to the recording electrode Pure motor response & does NOT represent a true reflex as no synapse along the nerve pathway occurs Configuration & latency change with each stim due to activation of different groups of anterior horn cells with each stim May be helpful in polyneuropathies & plexopathies but not overly useful in radiculopathies Latency: Normal: UE: 28 ms, LE: 56 ms Side to side difference: >2 is significant in UE, >4 is significant in LE Decreased persistence (occurrence) on repetitive stim correlates with potential abnormality Can be obtained from any muscle Limitations: - Evaluates a long neural pathway, which can dilute focal lesions & hinder specificity of injury location - Only assesses motor fibers

Question 571

A-wave (axon)

Answer 571

Response evoked when you are SUBMAX (abolished when SUPRAMAX) Stim travels antidromically along the motor nerve & becomes diverted along a neural branch formed by collateral sprouting due to a previous denervation & reinnervation process Occurs between CMAP & F wave at a constant latency (M --> A --> F) Waveform represents collateral sprouting following nerve damage

Question 572

Blink reflex

Answer 572

NCS technique electrically evoking an analogue to the corneal reflex Initiated by stimulating the supra-orbital branch of the trigeminal nerve (CN V). G1 placed inferior & slightly lateral to pupil at mid-position, G2 placed just lateral to lateral canthus. For each side, the ipsilateral supra-orbital nerve is recorded over the medial eyebrow The response propagates into the pons & branches to the lateral medulla --> then branches to innervate the ipsilateral & contralateral orbicularis oculi via the facial nerve 3 responses are evaluated --> ipsilateral R1 & bilateral R2 Blink response --> a/w R2 response Latencies (normals): - R1: <13 ms - Ipsilateral R2 (direct): <40 ms - Contralateral R2 (consensual): <41 ms Afferent loop of the blink reflex is mediated by V1, which synapses with both the main sensory nucleus of CN V in the mid-pons & the nucleus of the spinal tract of CN V in the medulla. The earlier R1 potential is mediated by a di-synaptic connection between the main sensory nucleus & ipsilateral facial motor nucleus (CN VII). The later R2 responses are mediated by a multi-synaptic pathway between the nucleus of the spinal tract of CN V & both ipsilateral & contralateral CN VII. The efferent pathway for both R1 & R2 is mediated via CN VII to the orbicularis oculi muscles R1 (Early) --> through the pons R2 (Late) --> through the pons & lateral medulla R1 is affected by lesions of the: - CN V - Pons - CN VII R2 is affected by: - Consciousness level - PD - Lateral medullary syndrome - Valium - Habituation

Question 573

Synkinesis

Answer 573

Aberrant regeneration of axons can occur with facial nerve injuries, leading to reinnervation of inappropriate muscles May present as lip twitching when closing an eye or crocodile tears when chewing

Question 574

Direct facial nerve NCS (CMAP in relation to amplitude & prognosis)

Answer 574

CMAP <10% of unaffected side --> poor outcome, likely to have incomplete recovery. Recovery >1 year CMAP 10-30% of unaffected side --> fair prognosis, recovery within 2-8 months CMAP >30% of unaffected side --> good prognosis, recovery within 2 months

Question 575

Nerves most commonly used for SSEPs

Answer 575

Median for UE, tibial for LE

Question 576

What does SSEP monitor for?

Answer 576

Peripheral nerve injuries, CNS lesions such as MS, or intra-operative monitoring of spinal surgery SSEP evaluates time-locked responses of the nervous system to an external stimulus, representing function of ascending sensory pathways using an afferent potential, which travels from peripheral nerve to the plexus, root, spinal cord (posterior column), contralateral medial lemniscus, thalamus, to the somatosensory cortex Most common abnormality in MS is prolonged peak latencies (can also see amplitude reduction or absence); more common to see issues in LE During spinal cord surgery, loss of tibial nerve potentials with preservation of median nerve potentials can indicate nerve injury at the level of intervention. Anesthesia will affect SSEP potentials in both the upper & lower limbs

Question 577

Median nerve SSEP

Answer 577

N9- Erb's point (reflects brachial plexus integrity) N11- roots N13- cervicomedullary junction (nucleus cuneatus) P14- lower brainstem N18- rostral brainstem N20- primary cortical somatosensory receiving area

Question 578

Insertional activity on EMG

Answer 578

Represents discharge potentials that are mechanically provoked by physically disrupting the muscle cell membrane with a needle electrode. This is an electrical injury potential Increased insertional activity may be seen in both neuropathic & myopathic conditions In rare conditions where significant muscle atrophy has occurred, insertional activity may be decreased. Severe, acute ischemia of muscle due to vascular occlusion or compartment syndrome may also produce decreased or absent insertional activity Normal duration: 300 ms via muscle depolarization Increased insertional activity: >300-500 ms via denervation or irritable cell membrane Decreased insertional activity: via fat, fibrosis, edema, or electrolyte abnormalities

Question 579

Normal spontaneous activity: MEPP

Answer 579

Occurs spontaneously at the NMJ, referred to as endplate noise Results from the normal spontaneous exocytosis of individual quanta of ACh travelling across the NMJ, leading to a non-propagated, sub-threshold EPP Distinct small amplitude of 10-50 microvolts & monophasic negative morphology The endplate noise is due to spontaneous quanta release (100-200 quanta), which normally occurs every 5 seconds regardless of stimulus IRREGULAR baseline Seashell murmur

Question 580

Normal spontaneous activity: EPP

Answer 580

Endplate spikes due to an increased ACh release, provoked by needle irritation of the muscle fiber or synchronization of several MEPP's Results in a propagated single muscle fiber AP Hallmark sign: irregularity with negative deflection (biphasic) Sputtering fat in a frying pan

Question 581

Abnormal spontaneous activity

Answer 581

Nerve resting membrane potential becomes less negative & unstable, causing it to approach the threshhold more easily to activate an AP Abnormal via muscle fibers: - Fibs - PSWs - CRDs - Myotonic discharges Abnormal via motor unit: - Neuromyotonic discharges - Myokimia - Fasciculations

Question 582

Notes on the abnormal spontaneous activities

Answer 582

Motor fiber source Fibs & PSWs: can be seen in nerve disorders, NMJ disorders, or muscle disorders (hyperkalemic periodic paralysis, acid maltase deficiency included) CRDs: can be seen in anterior horn cell disease, chronic radic, peripheral neuropathy; muscle disorders (limb-girdle dystrophy & myxedema incldued); can be a normal variant Myotonic discharges: can be seen in chronic radic, peripheral neuropathy, myotonias (even without clinical myotonias), other muscle disorders (acid maltase deficiency & hyperkalemic periodic paralysis included); a/w Propanolol use ----------------------------------------------------------------------------- Motor unit (neural) source Fasciculations: if a/w fibs or PSWs, they care considered pathological. A/w anterior horn cell disease, tetany, Mad Cow, radic, mononeuropathy, thyrotoxicosis, or could be a normal variant Myokimic discharges: facial- MS, brainstem neoplasm, polyradiculopathy, Bell's palsy; extremity- radiation plexopathy (most common), compression neuropathy, rattle-snake venom Neuromyotonic discharges: classically seen in neuromyotonia (Isaac's syndrome); a/w muscle rippling & stiffness 2/2 irritable nerves. A/w chronic neuropathic disease, tetany, & anti-cholinesterase --------------------------------------------------------------------- Cramp discharges: NOT muscle in origin; they originate from high-frequency discharges from motor axons. A/w painful, involuntary muscle contractions & are synchronous. Etiology: electrolyte disturbances, uremia, pregnancy, myxedema, strenuous exercises, prolonged muscle contraction, liver cirrhosis, myotonia congenita, myotonic dystrophy, stiff-man's syndrome

Question 583

Firing rate

Answer 583

Number of times a MUAP fires per second, expressed in Hz Calculation: 1000/distance between 2 successive spikes in ms Normal: 20 Hz or below. Above 20 --> neuropathic process

Question 584

Recruitment frequency

Answer 584

Firing rate of the first MUAP when a second begins to fire Initiated by an increase in the force of a contraction Normal: 20 Hz or below Anything above 20 --> neuropathic This increases due to a loss of MOTOR UNITS restricting additional motor unit activation to increase contractile force. This causes the first motor unit to fire more rapidly until a second motor unit finally joins in. This shortens the interval between successive MUAPs from one motor unit

Question 585

Recruitment Interval

Answer 585

Interspike interval (in ms) between two discharges of the same MUAP when a second MUAP begins to fire Initiated by an increase in the force of a contraction Normal is about 100 ms This increases due to a loss of MUSCLE FIBERS causing a second motor unit to join in early to help increase contractile force. This occurs before the first motor unit has the opportunity to increase its firing frequency. This lengthens the interval between successive MUAPs from one motor unit

Question 586

Firing pattern of recruitment frequency vs recruitment interval in neuropathy & myopathy

Answer 586

Neuropathy: recruitment frequency increases, interval decreases Myopathy: recruitment frequency decreases, interval increases

Question 587

Recruitment ratio

Answer 587

Used to represent recruitment capabilities, especially when a patient demonstrates difficulty in controlling a contractile force Calculated by dividing the firing rate of the first MUAP by # of different MUAPs on the screen A motor unit firing at 10 Hz when 2 different MUAPs are viewed on the screen --> RR of 5 (10 Hz/2 different MUAP) Normal RR: <10

Question 588

Interference pattern

Answer 588

Qualitative or quantitative description of the sequential appearance of MUAPs It is the electrical activity recorded from a muscle during a maximum voluntary contraction, composed of recruitment + activation Activation --> ability of a motor unit to fire faster to produce a greater contractile force & is controlled by a central process Interference pattern can be decreased in CNS diseases, pain, & hysteria If a patient is asked to generate a force & only a few MUAPs are seen while the frequency (Hz) continues to remain low, it can indicate decreased activation from poor patient cooperation & is not the result of abnormal recruitment

Question 589

Interference patterns

Answer 589

Complete --> no individual MUAPS can be seen. A full screen represents 4-5 MUAPs Reduced --> some MUAPs are identified on the screen during a full contraction Discrete --> each MUAP can be identified on the screen with a full contraction Single unit --> one MUAP is identified on the screen during a full contraction

Question 590

Needle EMG for radiculopathy

Answer 590

The optimal number of muscles to screen for a cervical or lumbar radic is 6 (5 peripheral muscles & paraspinals) If 1 of the 6 is abnormal, further muscles should be evaluated Priority is placed on evaluating weak muscles Classically, Fibs or PSWs should be found in 2 different muscles innervated by 2 different peripheral nerves originating from the same root (they may not be found if the lesion is a demyelinating neuropathy, pure sensory nerve injury, chronic nerve injury, or missed by random sampling

Question 591

Cervical myotomes affected 2/2 a herniated nucleus pulposus

Answer 591

C3/4 (C2-3 + C3-4 HNP): clinical diagnosis. No discrete myotomal patterns. Innervates the posterior & lateral scalp. Patient may c/o HA. C2 & C3 become the greater & lesser occipital nerve, respecively C5 (C4-5 HNP): Rhomboids, deltoid, biceps, supraspinatus, infraspinatus, brachialis, BR, supinator, paraspinals C6 (C5-6 HNP): Deltoid, biceps, BR, supraspinatus, infraspinatus, supinator, PT, FCR, EDC, paraspinals C7 (C6-7 HNP): PT, FCR, EDC, Triceps, paraspinals C8 (C7-T1 HNP): triceps, FCU, FDP, ADM, FDI, PQ, APB, paraspinals

Question 592

Lumbar myotomes affected 2/2 a herniated nucleus pulposus

Answer 592

L2/3/4 (L1-2, L2-3, L3-4 HNP): Iliopsoas, iliacus, gracilis, adductor longus, VMO, TA, paraspinals. It is difficult to distinguish radic & alternate lesions due to only 2 major peripheral nerves L5 (Posterolateral L4-5 HNP): Glut max, glut med, TFL, TA, medial gastroc, medial hamstring, tibialis posterior, paraspinals S1 (Posterolateral L5-S1 HNP): Glut max, glut med, TFL, medial gastroc, medial hamstring, tibialis posterior, paraspinals S2/3/4 (Iatrogenic, CES, LSS): abductor hallucis, abductor digiti quinti, needle exam of the external anal sphincter. Other things to monitor: BCR, anal wink, external sphincter tone, bowel/bladder function

Question 593

Muscles with dual peripheral innervation

Answer 593

Pec major: medial & lateral pectoral nerves Brachialis: musculocutaneous & radial nerves FDP: AIN (FDP 1, 2), ulnar nerve (FDP 3, 4) Lumbricals: median & ulnar nerves FPB: median (superficial head) & ulnar (deep) nerves Pectineus: femoral & obturator nerves Adductor magnus: sciatic (tibial portion) & obturator nerves Biceps femoris: sciatic (tibial) & sciatic (peroneal) nerves

Question 594

Chronology of EDX findings

Answer 594

Time 0: decreased recruitment, decreased recruitment interval, prolonged F wave, abnormal H-reflex (S1 radic) 4 days: decreased CMAP amplitude (about 50% compared to unaffected side) in severe cases 7 days: abnormal spontaneous activity occurs first in the paraspinals. They CAN be normal IF: they become re-innervated OR the posterior primary rami are spared. Paraspinal spontaneous activity can be the only abnormal finding 10-30% of the time 2 weeks: abnormal spontaneous activity beginning in limbs 3 weeks: abnormal activity present in both the paraspinals & limbs 5-6 weeks: re-innervation occurs 6 months-1 year: increased amplitude from re-innervated motor unit. Re-innervation complete Every 3-4 months: serial EMG can be performed to monitor for reinnervation as clinically warranted

Question 595

What is the main prognostic factor in a plexopathy?

Answer 595

Distal CMAP amplitude --> represents axonal loss in these conditions Side to side comparison should be performed Paraspinals will be normal in a plexopathy (will see abnormal activity in the peripheral muscles)

Question 596

Why may you see preservation of SNAP is Klumpke palsy (C8-T1 root injury)?

Answer 596

Preservation of a SNAP may indicate a nerve root avulsion. Avulsions may be a/w this location of injury due to lack of protective support at these roots In addition, MABC sensory will be absent or reduced

Question 597

EDX findings in TOS

Answer 597

Decreased amplitudes for median CMAP, ulnar SNAP/CMAP, & MABC sensory. Median SNAP is spared Abnormal spontaneous activity occurs in median & ulnar hand muscles (lower trunk) on EMG Vascular is much more common than neurogenic (can test vascular etiology via Adson)

Question 598

Hallmark of Parsonage Turner

Answer 598

Patchy or multifocal involvement (can be bilateral in 1/3 of patients). There is severe pain at first which then resolves after a week in the shoulder/peri-scapular region followed by weakness in patchy fashion Muscles innervated by C5 & C6 are more commonly affected. Can present as mononeuropathy or plexopathy

Question 599

Neoplastic vs radiation plexopathy

Answer 599

Tumor: lower trunk, a/w Horner's syndrome, painful Radiation: upper trunk, myokymia on EMG, painless

Question 600

EDX findings of nerve root avulsion

Answer 600

Absent CMAPs with normal SNAPs Needle EMG shows absent recruitment & abnormal spontaneous activity in a myotomal distribution of the avulsed nerve root, including the paraspinals

Question 601

What does the AIN innervate (4 P's)?

Answer 601

- FPL - FDP 1 - FDP 2 - PQ

Question 602

Median nerve entrapment at Ligament of Struthers

Answer 602

A 2-cm bone spur (supracondylar process) 3-6 cm proximal to the medial epicondyle exists & is connected to the epicondyle by this ligament in 1% of the population Nerve becomes entrapped with the brachial artery under the ligament Patient may have involvement of all median nerve-innervated muscles (including PT): - Weakness in grip strength: FDS, FDP - Weakness in wrist flexion: FCR - Dull, achy sensation in distal forearm - Active benediction sign from weakness in FDS, FDP Brachial pulse may be diminished

Question 603

Median nerve entrapment at bicipital aponeurosis (lacterus fibrosis)

Answer 603

Thickening of the antebrachial fascia attaching the biceps to the ulna. Overlies the median nerve in the proximal forearm Nerve can be injured by entrapment or hematoma compression resulting from an ABG or venipuncture Presentation & EDX same as Ligament of Struthers pathology

Question 604

What muscle is usually first affected in AIN syndrome?

Answer 604

FPL (difficulty with OK sign or have difficulty forming fist because of inability to approximate the thumb & index finger due to FPL & FDP weakness)

Question 605

More sensitive studies for CTS than routine NCS/EDX

Answer 605

Comparison studies: - Identical distances between stimulator & recording electrodes for median & ulnar nerves are used - These techniques create an ideal internal control in which several variables that are known to affect conduction time are held constant, including distance/temp/age/nerve size/muscle size - Ideally, the only factor that varies in these paired median-versus-ulnar comparison studies is that the median nerve traverses the carpal tunnel & ulnar nerve does not - Therefore, any slowing of median nerve compared with ulnar can be attributed to conduction slowing through the carpal tunnel - Diagnostic yield goes from 75% to 95% when using comparison studies - These sensitive studies are considered abnormal with very small differences between median & ulnar latencies (typically 0.4-0.5 ms) Combined sensory index (Robinson index): - Maximizes sensitivity for detecting CTS without reducing specificity using a single score derived from multiple sensory tests - CSI is the sum of comparisons of sensory latencies collected with 3 established sensory tests for the study of CTS: CSI = ring diff + thumb diff + palm diff - Ring diff is the peak latency difference of the median & ulnar antidromic sensory nerve conduction to the ring finger stimulating 14-cm proximally - Thumb diff is the peak latency difference of the median & radial antidromic sensory nerve conduction to the thumb stimulating 10-cm proximally - Palm diff is the trans-palmar peak latency difference of the median & ulnar orthodromic conduction using 8-cm - Example: if latencies are 3.8 ms for median nerve conduction to ring finger & 3.4 ms for ulnar nerve conduction to the ring finger, then the ring diff is 0.4. If it was reversed, it would be -0.4. Using negative numbers helps to cancel random errors such as distance measurement --> consider ulnar or radial neuropathy if present - Upper limit of normal is 0.9. Generally, a CSI of 1.0 ms or greater would be c/w CTS. Can also diagnose CTS if any of the following occur: >0.5 for Bactrian, >0.4 for ring, or >0.3 for palm Last way to diagnose: - Take 2 nerves of the same limb (of the same type). If latency >1.0 cm between them, the more prolonged nerve is the issue - Example: median motor & ulnar motor- median is 4.0 & ulnar is 2.8 --> CTS

Question 606

Prognosis for CTS

Answer 606

Poor outcome with conservative management may occur with: - Symptoms >10 months in duration - Constant paresthesia - Positive Phalen test in <10 seconds - Weakness, atrophy - Marked prolonged latency on NCS - Abnormal spontaneous activity on EMG

Question 607

Martin Gruber anastamosis

Answer 607

- Most commonly encountered anomaly in the UE --> crossover of median-to-ulnar fibers. Involves only motor fibers; sensory fibers are spared (AIN) - Crossover usually occurs in mid-forearm, either directly from the main trunk of the median nerve or from one of its branches, most commonly from the AIN - Median fibers that have crossed over then run with the distal ulnar nerve to innervate any of the following ulnar muscles: hypothenar muscles (ADM), FDI, thenar muscles (adductor pollicis, FPB deep head), or combination - Occurs in 15-30% of population - May be unilateral or bilateral

Question 608

MGA appearing on routine ulnar conduction study: pseudo-conduction block between wrist & below elbow sites

Answer 608

If the anastamotic fibers innervate the ADM: - Drop in ulnar CMAP amplitude between wrist & below-elbow stim - With stim at the wrist, the CMAP reflects all motor fibers innervating the hypothenar muscles, including those that have crossed over from the median nerve - Stim at the below-elbow site activates fewer fibers, however, as a portion of the fibers innervating the ADM originate from the median nerve & crossover in the forearm & therefore do not contribute to the CMAP - Whenever there is a >10% drop in amplitude between wrist & below-elbow sites on routine ulnar motor studies (up to 10% is considered normal 2/2 temporal dispersion), median nerve stim should be performed at the wrist & antecubital fossa while recording the hypothenar muscles. If no MGA present, there will be a small positive deflection at both sites, reflecting volume-conducted potential from median muscles. If MGA present, small positive volume-conducted potential will be present with median nerve stim at the wrist, however median nerve stim at the antecubital fossa will evoke a small CMAP over the ADM Major danger in not recognizing MGA in this situation is mistakenly interpreting findings as a conduction block in the forearm, which is an unequivocal sign of demyelination. This error is serious because presence of a conduction block at a non-entrapment site usually signifies an acquired demyelinating peripheral neuropathy

Question 609

MGA appearing on ulnar nerve conduction study recording FDI: pseudo-conduction block between wrist & below-elbow sites

Answer 609

Most common MGA occurs with crossing of median to ulnar fibers supplying the FDI. However, it usually isn't picked up because we use ADM The FDI is commonly recorded in 2 situations: - Looking for a lesion of the deep palmarmotor branch of the ulnar nerve (ulnar neuropathy at wrist) - When evaluating a suspected ulnar neuropathy at the elbow Similar pattern as if anastamotic fibers innervate the ADM with drop in amplitude >10% between wrist & below-elbow sites. However, it is more complicated to prove an MGA to FDI than it is to ADM because a CMAP is normally provoked when stimulating the median nerve at the wrist or at the antecubital fossa, recording the FDI. This is a normal finding due to volume conduction from nearby median-innervated muscles, specifically the APB, OP, & superficial head of FPB. Thus, to prove MGA to FDI, median nerve must be stimulated at the wrist & antecubital fossa while recording at FDI, looking for higher amplitude CMAP with antecubital fossa stim than with wrist stim

Question 610

MGA appearing on routine median study: increased CMAP amplitude proximally

Answer 610

Situation where median-to-ulnar crossover innervates one of the ulnar-innervated thenar muscles (adductor pollicis or deep head of the FPB) With this, recording the ADM is normal when recording routine ulnar motor studies. However, during routine median studies, CMAP amplitude is higher stimulating at the antecubital fossa than at the wrist To demonstrate that an MGA is present, must stim ulnar nerve at wrist & below-elbow while recording thenar muscles. Normally, while recording thenar muscles, ulnar stim at wrist evokes a thenar CMAP, usually with an initial positive deflection- reflects normal ulnar-innervated muscles in the thenar eminence. If no MGA present, subsequent stim of ulnar nerve at below-elbow site will evoke a CMAP potential with the same amplitude. If an MGA is present, CMAP amplitude will be substantially lower at below-elbow site than at wrist. The difference in amplitude between these two potentials approximates the contribution of the cross-over fibers

Question 611

MGA with co-existing CTS: positive proximal dip & factitiously fast CV

Answer 611

Will see positive deflection with median nerve stim at antecubital fossa recording thenar muscles & surprising fast CV in median nerve in forearm Distal median motor latency is prolonged when stimulating at wrist. However, when the median nerve is stimulated at the antecubital fossa, most fibers travel down the arm & through the carpal tunnel as usual, but some median nerve fibers bypass the carpal tunnel by traveling through the anastamosis innervating ulnar muscles Because these fibers bypass the carpal tunnel, they arrive in the hand much sooner than the median nerve fibers that are delayed through the carpal tunnel. When they depolarize their ulnar-innervated muscles, a positive deflection is seen at the thenar electrodes, indicating that a depolarization has occurred at a distance from the recording electrode Because the median fibers from the distal stim are delayed from slowing at the carpal tunnel, whereas anastamotic fibers from the proximal median stimulation arrive much sooner than expected --> time difference is artificially shortened, & the calculated CV in the forearm is surprisingly fast (>70-75 m/s) In some severe cases of CTS, the median fibers traveling through the MGA with antecubital fossa stim arrive at the thenar eminence before the fibers stimulated at the wrist because of the marked delay that occurs with wrist stim. In such cases, proximal median latency is actually shorter than distal median latency (a very unusually occurrence)

Question 612

Proximal MGA & pseudo-conduction block between above & below elbow sites on routine ulnar motor conduction studies

Answer 612

In patients with ulnar neuropathy at the elbow, one of the classic EP findings is conduction block across the elbow, whereby a drop in CMAP amplitude is seen between below & above elbow sites during routine ulnar motor studies Very rarely, the crossover fibers of the MGA are very proximal In these cases where the below-elbow stim might happen BELOW the MGA, MGA might result in mistaken diagnosis of ulnar neuropathy Take home point: always look for an MGA in any patient that is diagnosed with ulnar neuropathy by conduction block across the elbow without any other supporting abnormalities

Question 613

Accessory peroneal nerve

Answer 613

Most common anomalous innervation in LE Involves innervation of EDB. This is the muscle usually recorded during routine peroneal motor conduction studies & normally innervated only by deep peroneal nerve Patients with this anomaly to EDB display medial portion of EDB supplied by deep peroneal as usual, but lateral portion is supplied by an anomalous motor branch originating from the superficial peroneal nerve Recognized during routine peroneal motor studies. If an anastamosis is present, CMAP amplitude recording EDB is higher when stimulating at below-fibular neck & lateral pop foss sites than at ankle If present, APN originates from the distal aspect of the superficial peroneal nerve & travels down the lateral calf, posterior to the lateral mal. If stim is performed posterior to the lateral mal while recording EDB, a small CMAP will be evoked if an APN is present; otherwise, no potential would be seen

Question 614

What is Riche-Cannieu (all ulnar hand) protective against?

Answer 614

CTS

Question 615

Dorsal ulnar cutaneous nerve (DUC)

Answer 615

Branch of the ulnar nerve that does now travel through Guyon's canal (arising 5-8-cm proximally) & is normal in a distal ulnar neuropathy at the wrist but abnormal in more proximal compressions

Question 616

Ulnar neuropathy at guyon's canal

Answer 616

Entrapment at the wrist can take on several patterns: - Pure motor affecting only the deep palmar motor branch - Pure motor affecting the deep palmar & hypothenar motor branches - Motor & sensory (proximal canal lesion) - Pure sensory involving only the sensory fibers to the volar 4th & 5th fingers (rare) Shea's classification: Type 1: involvement of the deep ulnar branch, hypothenar, & sensory Type 2: involvement of the deep ulnar motor branches Type 3: involvement of the superficial ulnar sensory branch

Question 617

Muscles innervated by radial nerve BELOW spiral groove

Answer 617

BR, ECRL, posterior cutaneous nerve of forearm

Question 618

What does radial nerve split into & where?

Answer 618

At the lateral epicondyle, it splits into a motor (PIN) & sensory (superficial radial nerve) branch

Question 619

PIN-innervated muscles

Answer 619

ECRB, supinator, EDC, EDM, ECU, APL, EPL, EPB, EIP

Question 620

Monteggia fracture

Answer 620

Can cause PIN syndrome at arcade of frohse/supinator Fracture of the proximal 1/3 of the ulna & dislocation of the radial head. Typically occurs from a FOOSH with forearm locked in pronation

Question 621

Anatomy of the suprascapular nerve

Answer 621

Passes through the posterior triangle of the neck & runs beneath the trap to the superior margin of the scapula Runs through the suprascapular notch, which is covered by the transverse scapular ligament & branches to innervate the spinoglenoid notch to innervate the infraspinatus

Question 622

Suprascapular neuropathy

Answer 622

Only peripheral nerve injury at the trunk level Most commonly involved nerve in neuralgic amyotrophy Can be injured from trauma, including forced scapular protraction, penetrating wounds, traction from a massive RTC tear, stinger/Erb's palsy, compression from spinoglenoid ganglions, hematoma, suprascapular or spinoglenoid notch entrapment, or paralabral cyst Activities involving exaggerated shoulder movements, including sports with repetitive overhead throwing/hitting such as volleyball, baseball, & lacrosse may also injure the nerve. Volleyball more commonly injures branches to the infraspinatus muscle Injury to the nerve at the suprascapular notch results in weakness in both supraspinatus & infraspinatus muscles. Nerve injury at the spinoglenoid notch will result in weakness only in the infraspinatus muscle Patient may p/w weakness in abduction (SSp) and/or ER (infraspinatus) of the GHJ NCS: SNAP not available, CMAP abnormal EMG: abnormal activity in the infraspiantus only if entrapment is at the spinglenoid notch or both SSp & IS muscles if nerve entrapment is at the suprascapular notch

Question 623

Does medial or scapular winging result in increased winging with shoulder abduction?

Answer 623

Lateral scapular winging (trap injury via spinal accessory) Medial scapular winging (serratus via long thoracic) results in decreased winging with shoulder abduction

Question 624

Treatment for scapular winging

Answer 624

Treatment of serratus anterior/injury to long thoracic nerve (SALT): acute stage- pain reduction & ROM exercise; intermediate stage- passive stretching of the rhomboids, levator scap, & pec minor; late stage- strengthening exercise of all shoulder girdle muscles, including trap Treatment of trap palsy/injury to spinal accessory nerve: involves PT to adequately strengthen adjacent muscle groups, including rhomboids & levator scap Surgical repair with a dynamic muscle transfer recommended if patient fails conservative treatment

Question 625

Diabetic amyotrophy

Answer 625

Most common cause of femoral neuropathy. Proximal diabetic neuropathy is distinct from other types of distal diabetic peripheral neuropathies AKA lumbosacral radiculoplexus neuropathy, as it can involve the plexus & nerve roots, as well as peripheral nerves. Predominantly affects the lumobsacral plexus Believed to result from a multifocal immune-mediated microvasculitis. Nerve is believed to be injured from an abnormality of the vaso-nervorum due to DM Nerve biopsy shows multifocal nerve fiber loss suggesting ischemic injury & perivascular infiltrate Noted to occur after marked weight loss Typically affects an older group of diabetics, more frequently males, usually >50 years. Most patients have T2DM Begins with severe unilateral pain in the lumbar region or proximal LE, which commonly spreads to the contralateral side within weeks to months. Patients then develop weakness & atrophy of the proximal > distal LE musculature Patient may c/o assymetric thigh pain, knee extension weakness (quadriceps), & atrophy. Loss of the patellar reflex may also occur Self-limited condition, but the recovery process is gradual & occurs over a period of months. There are some patients who are left with residual LE weakness

Question 626

Sciatic nerve anatomy

Answer 626

Exits the pelvis through the greater sciatic foramen between the lesser trochanter & ischial tuberosity Sciatic nerve is comprised of a tibial (medial portion of the nerve) & peroneal (lateral portion). Travels as one unit up to the pop fossa where it splits into peroneal & tibial division Sciatic nerve muscle innervation in the thigh: - Peroneal division innervates the short head of the biceps femoris - Tibial division innervates long head of the biceps femoris, semiten, semimem, adductor magnus (also innervated by obturator)

Question 627

NCS findings in acquired vs hereditary neuropathies

Answer 627

Acquired: conduction block present, focal slowing present, increased temporal dispersion Hereditary: no conduction block, diffuse slowing, normal temporal dispersion

Question 628

Norepinephrine synthesis & release

Answer 628

Norepinephrine is the primary neurotransmitter for post-ganglionic sympathetic adrenergic nerves. It is synthesized inside the nerve axon, stored within vesicles, then released by the nerve when an AP travels down the nerve. Details: - AA Tyrosine is transported into the sympathetic nerve axon - Tyrosine is converted to DOPA by tyrosine hydroxylase - DOPA is converted to dopamine by DOPA decarboxylase - Dopamine is transported into vesicles then converted to norepinephrine by dopamine b-hydroxylase - An AP traveling down the axon depolarizes the membrane & causes Ca to enter the axon - Increased intracellular Ca causes the vesicles to migrate to the axonal membrane & fuse with the membrane, which permits the norepinephrine to diffuse out of the vesicle into the extracellular space - Norepinephrine binds to the post-junctional receptor & stimulates the effector organ response

Question 629

Sympathetic skin response

Answer 629

Means of evaluating the unmyelinated, sympathetic nerve fibers of the PNS For median nerve testing using standard electrodes, E1 can be placed on the palm & E2 on the dorsum of the hand. The median nerve is stimulated at the wrist & elbow at the usual locations. Stimulation occurs over several minutes, & irregular stim intervals are required to prevent nerve habituation Stimulus sources are electrical, coughing, noises, breathing, or tactile Current: 10-20 mA with a pulse width of 0.1 ms Sweep speed: 500 ms/cm LFF: 0.5 Hz HFF: 2000 Hz UE CV: 1.6 m/s LE CV: 1.0 m/s

Question 630

Anal sphincter activity in healthy individuals

Answer 630

EMG recording of the external anal sphincter has continuous activity at rest There is a brief contraction in response to rapid rectal distention, & a preserved or increased activity during a prolonged substantial rectal distention during defecation

Question 631

What is considered an abnormality on repetitive nerve stimulation (RNS)?

Answer 631

>10% decrease in amplitude from the 1st to 5th waveform These are studies in which a repeated supramaximal stimulation of a motor nerve is performed Progress from ADM/APB --> deltoid --> trap --> orbicularis oculi

Question 632

Post-activation facilitation vs post-activation exhaustion vs pseudofacilitation

Answer 632

Post-activation facilitation: after a decrement is noted with low-rate repetitive stimulation, a 30- to 60-second isometric contraction or tetany-producing stimulation (50 Hz) should be performed. PAF demonstrates a repair in CMAP amplitude with an immediate follow-up low-rate repetitive stim because of an improvement in NM transmission Post-activation exhaustion: this response is seen as a CMAP amplitude decreases. It occurs with a low-rate repetitive stimulation performed every minute for 5 minutes after an initial 30- to 60-second isometric contraction. The greatest drop-off is between 2 & 4 minutes. This test should be used if a decrement does not p/w the initial low-rate repetitive stimulation, but a diagnosis of a NMJ disorder is suspected Pseudofacilitation: this is a normal reaction & demonstrates a progressive increase in CMAP amplitude with high-rate repetitive stimulation or voluntary muscle contraction. It represents a decrease in temporal dispersion due to increased synchronicity of muscle fiber contraction. The waveforms produced maintain a constant area under the curve though the amplitude appears increased because the duration is decreased

Question 633

Difference among NMJ disorders in relation to RNS

Answer 633

MG: normal or reduced CMAP amplitude. RNS- >10% decrement noted between first and 4th-5th stimulation. 20-50% improvement with PAF. PAE observed 2-4 minutes after maximal voluntary contraction LEMS: decreased CMAP amplitude. RNS- >10% decrement in amplitude. >100% improvement with PAF. A train of 5 stimuli every 5 minutes to monitor for decrease should be done for PAE Botulism: decreased CMAP amplitude. >10% decrement in amplitude, or variable changes. >40% improvement with PAF. Absent PAE

Question 634

Single fiber EMG

Answer 634

Monitors the parameters of single muscle fiber AP's Useful if repetitive stimulation of at least 3 muscles is normal & an abnormal diagnosis is still suspected Most sensitive test for NMJ disorders, but has low specificity Abnormalities can be a/w NMJ disorders, MND, & peripheral neuropathies Parameters: fiber density, jitter, & blocking

Question 635

SFEMG: fiber density

Answer 635

Represents the number of single fibers belonging to the same motor unit within the recording radius of the electrode Determined by dividing the number of single muscle AP's at 20 sites by 20 FD of 1.5 is normal. Anything higher than this represents a denervation & reinnervation process

Question 636

SFEMG: jitter

Answer 636

During voluntary contraction, a small variation exists between the inter-potential discharges of two muscle fibers belonging to the same motor unit. This variation is normally 10-60 microseconds. Considered abnormal if longer than this Disorders of NM transmission affect the safety factor & cause a delay in the time for an EPP to reach threshold for a muscle fiber AP, which increases the jitter between 2 neighboring muscle fibers. Reinnervation through collateral sprouting after a nerve injury can also cause a delay. The immature NMJs have poor activation, resulting in increase jitter in the first month Seen in conditions including ALS, NMJ disorders, axonal neuropathies, & myopathies

Question 637

SFEMG: blocking

Answer 637

Abnormality that occurs when a single muscle fiber AP fails to appear. Occurs if the jitter becomes >100 microseconds Typically resolves in 1-3 months, after reinnervation has completed. However, increased jitter may take approximately 6 months to resolve

Question 638

Difference between paramyotonia & myotonia

Answer 638

Paramyotonia: muscle stiffness brought on by repeated muscle contraction or exercise Myotonia: warm-up period of repeated muscle contraction alleviates the muscle stiffness

Question 639

Conditions seen in Type I vs Type II fiber atrophy

Answer 639

Type I fiber atrophy: myotonic dystrophy, nemaline rod myopathy, fiber type disproportion Type II fiber atrophy: steroid myopathy, MG, deconditioning

Question 640

Kennedy disease

Answer 640

Spinal & bulbar muscular atrophy A/w tongue scalloping Expanded CAG repeat on first exon of androgen receptor gene X-linked disorder Various endocrine abnormalities (DM, testicular atrophy, gynecomastia, oligospermia, ED)

Question 641

Incidence & prevalence of SCI in US

Answer 641

Incidence: 54 cases per 1 million (17,700 cases a year) Prevalence: 300K

Question 642

What is the average age of injury for SCI?

Answer 642

43 years

Question 643

Most common cause of SCI

Answer 643

MVC *Although falls is most common after 45 years

Question 644

What type of SCI is most common?

Answer 644

C5 overall most common T12 overall most common cause of paraplegia Incomplete tetraplegia --> incomplete para --> complete para --> complete tetra

Question 645

Return to work post SCI

Answer 645

1 year: 12-18% 5 years: 25% 10 years: 35%

Question 646

Causes of death in SCI population

Answer 646

- Acute phase: respiratory disorders are the leading cause, with PNA being most common. Heart disease ranks 2nd, followed by septicemia (usually a/w pressure injuries, urinary tract, or respiratory infections) & CA GU diseases (like renal failure) were the leading cause of death >40 years ago, but this has declined dramatically, most likely due to advances in urology Suicide risk: rate is 3x higher than for non-injured. Risk is highest in first 6 years after injury, for people with paraplegia, if AIS A-C, & for non-Hispanic whites

Question 647

Spinal cord anatomy

Answer 647

Located in upper 2/3 of the vertebral column Terminal portion --> conus medullaris, which becomes cauda at the L1-2 vertebral levels Spinal cord has white matter surrounding an inner core of gray matter. The white matter consists of nerve fibers, neuroglia, & blood vessels. The nerve fibers form spinal tracts, which are divided into ascending, descending, & inter-segmental tracts

Question 648

Long tracts of the spinal cord

Answer 648

Lateral corticospinal: pyramidal, deep lateral column - Motor: theorized to have motor fibers running medial (cervical, thoracic) to lateral (sacral) - Descending pathway Anterior corticospinal: medial ventral column - Motor: neck & trunk movements - Descending pathway Lateral spinothalamic: ventrolateral column - Pain & thermal sensation - Ascending pathway Ventral spinothalamic: ventral column - Tactile sensation of crude touch & pressure - Ascending pathway Spinocerebellar: superficial lateral column - Muscular position & tone, unconscious proprioception - Ascending pathway Dorsal columns: fasciculus gracilis (medial dorsal column), fasciculus cuneatus (lateral dorsal column) - FG: proprioception from the leg- light touch, vibration - FC: proprioception from the arm- light touch, vibration - Ascending pathway

Question 649

Lateral corticospinal tract (descending pathway)

Answer 649

Main motor tracts for controlling voluntary muscle activity Origin is the pre-central gyrus of the frontal lobe of the brain. Axons descend through the internal capsule to the medulla 80-90% of axons cross-over (decussate) to contralateral side at the pyrimidal decussation in the medulla. Nerve fibers then descend in the lateral white columns of the SC (lateral corticospinal tracts). At each level of the SC, the axons from the lateral tract peel off & enter the gray matter of the ventral horn to synapse with secondary neurons The remaining 10-20% of axons that do not decussate/travel in the anterior (ventral) corticospinal tracts. The axons of the ventral tract then crossover at the corresponding level of muscles that they innervate Both tracts travel from the pre-central gyrus to the ventral horn as uninterrupted neurons & are terms UMN, while the secondary neurons that they synapse on are termed LMN

Question 650

Spinocerebellar tracts (ascending pathway)

Answer 650

Transmit unconscious proprioception (muscle proprioceptive, stretch, tension fibers) from the IPSILATERAL side of the body to the brain

Question 651

Lateral spinothalamic tracts (ascending pathway)

Answer 651

Transmit pain & temp from the CONTRALATERAL side of the body to the brain Pain & temp sensory fibers enter the SC & synapse in the dorsal horn of the gray matter. The fibers cross-over to the contralateral side of the SC within 1-3 vertebral segments, ascend in the lateral spinothalamic tracts to the contralateral thalamus, & then ascend in the internal capsule to the post-central gyrus of the cerebral cortex A lesion of the lateral spinothalamic tract will result in loss of pain-temperature sensation CONTRALATERALLY below the level of the lesion

Question 652

Dorsal (posterior) columns

Answer 652

Transmit proprioception, fine touch, & vibration sense from the IPSILATERAL side of the body to the brain These sensory fibers synapse at the DRG & immediately ascend into the ipsilateral dorsal white columns They travel up the medulla, at which point they decussate. Fasciculus gracilis & cuneatus synapse in the medulla & form a bundle called the medial lemniscus, which ascends to the post-central gyrus A lesion of the posterior columns --> loss of proprioception & vibration ipsilaterally below the level of the lesion

Question 653

Artery of Adamkiewicz

Answer 653

Provides the major blood supply to the lumbar & sacral cord. Generally arises from the left intercostal or lumbar artery at the levels of T9-L3 & provides the major blood supply to the lower two-thirds of the SC

Question 654

Lower thoracic region of SC

Answer 654

Referred to as watershed area because there are fewer radicular arteries that supply the mid-thoracic region of the SC This area (T4-6) is most affected when there is low blood flow to the SC (like clamping aorta intra-op)

Question 655

Cervical flexion/extension injuries

Answer 655

Flexion/axial loading (burst/compression fracture) - Stable if ligaments remain intact - Compression fracture with fragmentation of VB & projection of bony spicules into canal - Most common level: C5 Flexion/rotation injury (unilateral facet dislocation): - Unstable if PLL disrupted - VB <50% anteriorly displaced on XR - Likely to be incomplete SCI if SC is compromised - Most common level: C5-6 Flexion (bilateral facet dislocation) - Unstable if PLL is disrupted - VB displaced >50% anteriorly on XR - Anterior dislocation of C-spine with SC compression/compromise - More likely to result in complete SCI - Most common level: C5-6 Hyper-extension (central cord): - Stable; ALL may be disrupted - Hyper-extension of C-spine, UE weaker than LE - Likely to be incomplete injury - Most common level: C4-5

Question 656

NMO (Neuromyelitis optica) AKA Devic's disease

Answer 656

Fairly uncommon disease of CNS that affects optic nerves & SC, causing a combination of optic neuritis & transverse myelitis Marked female predominance Often mimics MS, also immune-mediated Clinically, the myelopathy is more severe in NMO than in MS, & on MRI the lesions tend to be more longitudinal (>3 spinal segments). These lesions can lead to weakness or complete paralysis, painful spasms, sensory loss, & bowel/bladder dysfunction. Optic neuritis can cause blindness in one or both eyes Most of these lesions cause permanent deficits, although some flare-ups can be reversible Treatment: IV glucocorticoids followed by plasmapheresis if not responsive to steroids. IVIg also can be considered Long-term immunosuppression has become standard --> Rituximab, mycophenylate, mofetil, or azathioprine

Question 657

Extradural spinal tumors

Answer 657

Largely comprised of spinal mets & primary bony tumors. Extradural mets account for up to 95% of spinal lesions Highest incidence between 40-65 years Majority of cases involve T-spine, followed by L-spine & then C-spine Most common primary malignancies with spinal mets are lung, breast, & prostate as well as lymphoma Major presenting symptoms are non-specific & include local or radicular pain with or without motor weakness, sensory changes, as well as loss of sphincter control. Radicular pain is usually unilateral in the C- & L-spines but bilateral with thoracic lesion Pain is worse with movement & worse at night

Question 658

Completeness of injury based on radiological findings

Answer 658

Complete: bilateral cervical facet dislocations, TL flexion-rotation injuries, trans-canal GSW Incomplete: cervical spondylosis with a fall, unilateral facet joint dislocation, non-canal penetrating GSW/stab injury

Question 659

Hangman fracture (C2 burst)

Answer 659

Usually bilateral from an abrupt deceleration injury (MVC with head hitting windshield) Most often stable with only transient neuro findings Treatment: external orthosis (Halo is first-line). Unstable fracture will require surgery

Question 660

Chance fracture

Answer 660

Transverse fracture of the T- or L-spine from posterior to anterior through the SP, pedicles, & VB Usually affects T12, L1, or L2 Lap belt injury, a/w falls/crush injury with acute hyper-flexion of the thorax Tend to be stable & seldom a/w neuro compromise unless significant amount of translation occurs

Question 661

How many key sensory dermatomes are there on AISA?

Answer 661

28 on each side

Question 662

How many key myotomes are there on AISA?

Answer 662

10 on each side

Question 663

What is the NLI?

Answer 663

Most caudal segment of the SC with both normal sensory & motor function >/= 3/5 with cephalad segments graded 5/5 on both sides of the body Motor & sensory levels are the same in <50% of complete injuries In cases where there is no key muscle available (cervical levels at & above C4, T2-L1, & sacral levels below S2), the NLI is that which corresponds to the sensory level, if testable motor function above that level is also normal

Question 664

Sacral sparing

Answer 664

Presence represents at least partial structural continuity of the white matter long tracts There is better prognosis for motor & sensory return the level of injury as well as the possibility of return of bowel/bladder function in a person with sacral sparing relative to persons without sacral sparing

Question 665

AIS Impairment scale

Answer 665

A: no motor or sensory is preserved in S4-5 B: Sensory but not motor function is preserved below the NLI & at the most caudal sacral segments S4-5 (light touch or pinprick at S4-5 or DAP) AND no motor function is preserved >3 levels below the motor level on either side of the body C: Motor function is preserved at the most caudal sacral segments (S4-5) on VAC OR the patient meets criteria for secondary incomplete status with sparing of motor function >3 levels below the ipsilateral motor level on either side of the body. This includes key or non-key muscle functions >3 levels below the motor level to determine motor incomplete status. For AIC C --> <50% of key muscle functions below NLI has a muscle grade of 3 or more D: Motor incomplete status as defined previously, with 50% or more of key muscle functions below the NLI having a muscle grade of 3 or more

Question 666

Central cord syndrome

Answer 666

Most common incomplete SCI syndrome Motor weakness in UE > LE with variable loss of sensation, bowel, & bladder function Predominantly a white matter lesion May occur at any age but is more common in older patients with cervical spondylosis who sustain a cervical hyper-extension injury, usually from a fall Recovery: LE's recover first & to a greater extent --> bladder recovery --> proximal UE recovery --> intrinsic hand function Age <50 is a favorable prognostic indicator

Question 667

Brown Sequard syndrome

Answer 667

Results from a lesion that causes a relative hemi-section of the SC Rare injury (2-4% of all traumatic SCI) A/w with stabbing but can occur from other causes (like MVC) At level of lesion: - Ipsilateral flaccid paralysis (anterior horn cells) - Ipsilateral loss of all sensory modalities Below level of lesion: - Ipsilateral paralysis (corticospinal tract) - Ipsilateral loss of light touch & proprioception (dorsal columns) - Contralateral loss of pain & temp (spinothalamic) Overall --> ipsilateral motor & proprioceptive loss & contralateral loss of pain & temp

Question 668

Anterior cord syndrome

Answer 668

Lesion affecting the anterior 2/3 of the SC while preserving the posterior columns Can occur from flexion injuries, direct injury to the anterior SC from bone fragments or disc herniation, or anterior spinal artery lesions Results in: - Variable loss of motor function (corticospinal tract) - Variable loss of pain, temp, & pinprick sensation (spinothalamic tract) - Preservation of proprioception, light touch, & deep pressure sensation (dorsal columns) Motor recovery is poor compared to other incomplete syndromes

Question 669

CES

Answer 669

Injuries below L1-2 vertebral levels affecting the cauda equina (nerve rootlets), which innervate the lumbar & sacral segments Cauda is comprised of spinal nerve rootlets, which are peripheral nerves, & would result in LMN signs & symptoms Results in motor weakness & atrophy of the LE's (L2-S2) with neurogenic bowel & bladder (S2-4), sexual dysfunction, & areflexia below level of lesion (including absence of anal wink/BCR) Has a better prognosis relative to UMN injuries for recovery, most likely due to fact that the nerve roots (peripheral nerves) are more resilient to injury & are more likely to regenerate

Question 670

Functional outcomes after SCI

Answer 670

Most important factors in determining functional outcome are the motor level & AIS classification Highest level that can live independently without the aid of an attendant is a C6 complete tetra (extremely motivated) C7 is the usual level for achieving independence

Question 671

Levels to remember in SCI

Answer 671

T6 and above --> at risk for BP dysregulation --> orthostatic hypotension & AD T8 & above --> temp8ture --> cannot regulate & maintain normal body temp. Central temp regulation in the brain is located in the hypothalamus

Question 672

Orthostatic hypotension in SCI

Answer 672

Transient reflex depression caused by a lack of sympathetic outflow & triggered by tilting the patient upright to >60 degrees Mechanism: - Upright position causes decrease in BO - Aortic & carotid baroreceptors sense decrease in BO (would usually increase sympathetic outflow in neurologically intact individual); however, efferent pathway interrupted following SCI - Brainstem unable to send message through SC to cause sympathetic outflow & vasoconstriction of splanchnic bed to increase BP - Orthostasis lessens with time due to development of spinal postural reflexes which allow for vasoconstriction due to improved autoregulation of cerebrovascular circulation in the presence of perfusion pressure Management: - Reposition: Trendelenberg/recliner WC - Elastic stocking/abdominal binder - Accommodation (use of tilt table) - Increase fluid intake - Pharm: salt tab 1g QID, Midrodrine (alpha-1 agonist) 2.5-10 mg TID, Florinef 0.05-1.0 mg qD, Droxidopa 100 mg TID (careful because once orthostasis improves, at risk for AD)

Question 673

Autonomic dysreflexia

Answer 673

Syndrome of massive imbalanced reflex sympathetic discharge in patients with SCI above the splanchnic outflow (T5-L2). Secondary to the loss of descending central sympathetic control & hypersensitivity of receptors below the level of the lesion Noxious stimulus increases sympathetic reflex spinal release --> regional vasoconstriction causes a marked rise in arterial BP --> increases PVR, increases CO, increases BP --> aortic & carotid baroreceptors respond to increased BP & relay impulses to vasomotor center in brainstem --> impulses via vagus nerve that can lead to bradycardia (not effective in combatting the increased BP) (bradycardia not always seen & may actually see tachycardia/tachy-arrhythmias) Brainstem is unable to send messages through the injured SC to decrease sympathetic outflow & allow vasodilation of splanchnic bed to decrease BP Onset occurs after spinal shock & may appear within 2-4 weeks post-injury. If it is going to occur, usually occurs within first year of injury for first time More commonly occurs in complete injuries Most common causes: - Bladder (#1) - Bowel: fecal impaction - Abdominal emergency, etc Elevated BP --> systolic BP >20 mmHg above baseline Spinal anesthesia is recommended during delivery with SCI at T6 or above Predisposes the patient to cardiac dysrhythmias (like AF) by altering the normal pattern of repolarization of the atria, making the heart susceptible to re-entrant type arrhythmias

Question 674

Does the bladder wall have baroreceptors?

Answer 674

No!

Question 675

What does bladder activation of A1 adrenergic receptors produce?

Answer 675

Contraction of the internal sphincter at the base of the bladder & prostatic urethra, preventing leakage --> promotes storage

Question 676

What does bladder activation of B3 adrenergic receptors produce?

Answer 676

Relaxation of body of bladder to allow expansion --> promotes storage

Question 677

Post-SCI urologic function & management

Answer 677

Acutely, patients in spinal shock p/w an areflexic bladder, which retains urine. This can last from 1 week to many months, but most cases resolve in 2-12 weeks Indwelling catheter, especially while IVF are administered IC program can begin once patients no longer receiving IVF, UOP has stabilized (<100 mL/hr), & ~2-3 L/day fluid restriction can be maintained. Best started q4h with goal volume <500 mL

Question 678

What is spinal shock?

Answer 678

Temporary loss or depression of all spinal reflex activity below the level of the lesion, although this may not occur in all patients

Question 679

Detrusor-sphincter dyssynergia

Answer 679

Up to 85% of SCI patients develop this Occurs via neurologic injury between pontine micturition centers & sacral (S2-4) centers --> lack of coordinated regulation of bladder function Can lead to above normal bladder pressures determined on urodynamics & should be treated to minimize renal dysfunction Result: small, overactive, spastic bladder (detrusor hyperreflexia), tight, spastic internal sphincter (sphincter hyperactivity), failure to empty & high voiding pressures if able to empty any If not treated --> vesicoureteral reflux, increased volumes, colonized infected stagnant urine, high-pressure voiding against a closed sphincter with risk of VUR Treatment: anti-cholinergic meds to prevent long-term complication of VUR & quiet bladder wall contractions, IC, botox to detrusor wall, alpha-blockers to open bladder neck, sphincterotomy

Question 680

Abnormal bladder anatomy

Answer 680

Bladder wall hypertrophy causes the course of the distal ureter to become progressively perpendicular to the inner surface of the bladder. The vesicoureteral junction then becomes incompetent, permitting reflux of urine During relaxation of the bladder, the ureter pumps urine into the bladder like normal The valve cannot close during bladder contraction given the perpendicular orientation of the distal ureter to the inner surface of the bladder. As such, urine is forced up the ureter to the kidney & hydronephrosis can result Reflux can be further complicated by acute or chronic pyelo with progressive renal failure Congenital abnormalities of the ureters, including posterior placed ureteral orifices & severe trabeculation disrupting the posterior bladder wall, have been a/w VUR after SCI

Question 681

Asymptomatic UTIs in SCI

Answer 681

When managed with IC or indwelling foley, not treated. Exceptions: patients undergoing invasive procedures, presence of VUR, or growth of urease-producing organisms (Proteus, Pseudomonas, Klebsiella, Providentia, E. coli, staph epidermidis Urea-splitting organisms produce struvite calculi made of ammonium & mag phosphate

Question 682

Prevention of UTIs

Answer 682

Use of ppx abx to prevent UTIs after SCI is not supported Some complications can be prevented by adequately draining the bladder at pressures <40 cm H20, either by IC (in conjunction with the use of anti-cholinergic meds) or by timely surgical relief of outflow obstructions that would not otherwise respond to meds Vit C supplementation & methenamine salts can be used as acidifying agents to discourage bacterial growth

Question 683

Most common urinary tract complication in neurogenic bladder

Answer 683

Earliest changes --> irregular, thickened bladder wall & small diverticuli

Question 684

Rate of ejaculation after SCI

Answer 684

Varies depending on the location & nature of the neurological injury 5-15% of men with complete UMN lesions & 18% with complete LMN lesions have ejaculations %'s are higher with incomplete injuries

Question 685

Electroejaculation

Answer 685

Sperm retrieval for those unable to ejaculate Performed if penile vibratory stimulation (done at home) is unsuccessful Medical supervision is required. May lead to AD

Question 686

Why do men have poor semen quality after SCI?

Answer 686

- Stasis of prostatic fluid - Testicular hyperthermia - Recurrent UTI's - Abnormal testicular histology - Changes in hypothalamic-pituitary-testicular axis - Possible sperm antibodies - Type of bladder management - Long-term use of various medications

Question 687

What causes afferent signals to travel via the pudendal nerve into S2-4 segments in women during sex?

Answer 687

Stimulation of the genital region, including clitoris, labia majora & minora

Question 688

Is the likelihood of pregnancy changed after SCI in women?

Answer 688

No! Fertility is unimpaired (although may have amenorrhea in first 6-12 months after injury, but this goes away)

Question 689

What may be the only clinical manifestation of labor?

Answer 689

Autonomic dysreflexia

Question 690

What is treatment of choice for AD during pregnancy?

Answer 690

Epidural anesthesia extending to T10 level Epidural should continue for at least 12 hours after delivery or until AD resolves

Question 691

Colonic dysfunction in SCI patient

Answer 691

In an UMN lesion such as an SCI, the GI system can be affected by loss of sympathetic & parasympathetic input at the transverse & descending colon, resulting in decreased fecal movement Fecal impaction & constipation are the most common complications during recovery

Question 692

Gastrocolic reflex

Answer 692

Contraction of the colon occurring with gastric distention When feasible, SCI patients should be instructed to perform their bowel programs 20-30 minutes after a meal Increased colonic activity occurs in the first 30-60 minutes after a meal (usually within 15 mins)

Question 693

Rectocolic reflex

Answer 693

Occurs when rectal contents stretch the bowel wall reflexively, relaxing the internal anal sphincter & leading to left colonic contraction Suppositories & digital stimulation cause the bowel wall to stretch & take advantage of the reflex Reflex can be manipulated by digital stimulation of the rectum Digital stim --> gently inserting a gloved, lubricated finger into the rectum & slowly rotating finger clockwise in a circular motion until relaxation of the bowel wall is felt or stool/flatus passes (approximately 1 minute)

Question 694

Most common cause of emergency abdominal surgery in chronic SCI patients

Answer 694

Cholecystitis

Question 695

When does pancreatitis typically occur in the SCI patient?

Answer 695

Most commonly within 1 month from injury

Question 696

Metabolic complications in SCI

Answer 696

Hypercalciuria Hypercalcemia Osteoporosis Fractures CV Disease Hyperglycemia & metabolic syndrome

Question 697

Metabolic complications in SCI: hypercalciuria

Answer 697

Immobilization & reduced body weight bearing result in uncoupling of normal mechanism responsible for maintaining bone, promoting bone resorption, & hyeprcalciuria Vit D & PTH are NOT involved

Question 698

Metabolic complications in SCI: hypercalcemia

Answer 698

Treat both sx & asx as prolonged hypercalcemia can cause nephrocalcinosis Restriction of dietary Ca is unnecessary; 1,25-dihydroxy Vit D levels already are low, suppressing intestinal absorption of Ca Restriction of Vit C may be a good idea Give IVF to help pee out Ca Pamidronate can be used to inhibit osteoclast-mediated resorption & reduces osteoclast viability. The drug is administered as a single IV infusion & rapidly lowers serum Ca within 3 days. Serum Ca then falls to nadir within 1 week & may remain normal for several weeks or longer. Can repeat if needed. IVF can be discontinued 2-3 days after Pamidronate is completed Other meds: Didronel (Etidronic acid), calcitonin

Question 699

Metabolic complications in SCI: osteoporosis

Answer 699

Rapidbone loss occurs below level of injury & primarily at load-bearing sites FES may help

Question 700

Metabolic complications in SCI: fractures

Answer 700

Knee (distal femur & proximal tibia) is the most common site Risk factors: prior fragility fracture, family history of fracture, female gender, age (bimodal: 10 years), BMI <19, paraplegia, motor complete SCI, alcohol intake >5 servings per day Fractures are usually non-op with soft padded splints (well-padded knee immobilizer for femoral supracondylar, femoral shaft, & proximal tibial fractures; well-padded ankle immobilizer for distal tibial fractures) With non-op management, patient can sit within a few days. Callus formation --> 3-4 weeks. ROM is initiated at 6-8 weeks, with WB delayed for a longer period

Question 701

Metabolic complications in SCI: CV disease

Answer 701

Low HDL, high LDL, high CRP Tetras & complete injuries have higher risk Higher prevalence of insulin resistance, DM, metabolic syndrome

Question 702

Metabolic complications in SCI: hyperglycemia & metabolic syndrome

Answer 702

Both FES & arm ergometry (high-intensity target HR 70-80% of max HR predicted) have increased glucose tolerance & reduced lipid profile in SCI

Question 703

Most frequent complications in SCI

Answer 703

PNA, atelectasis, vent failure. Most common in first year following injury but persist throughout life. Within first 15 years, respiratory illnesses comprise 20-25% of all deaths Diaphragm (innervated by C3-5) is major muscle of inspiration contributing 65% of VC Primary muscles of expiration to help clear secretions: rectus, transversus abdominus, internal & external obliques (T4-L2), & intercostal muscles of the lower rib cage (T6-12) For persons with neurologically complete injuries with high cervical injuries, reported rates of successful weaning from MV: - 0% at C1 - 0-30% C2 - 25-50% C3 - 77-83% C4

Question 704

What is the leading cause of death among chronic SCI patients?

Answer 704

PNA

Question 705

What type of lung disease do tetraplegics develop?

Answer 705

Restrictive All volumes shrink, except residual volume If VC <1L --> consider MV Once VC 15-20 mL/kg, can usually wean off vent

Question 706

When to MV SCI patient

Answer 706

- VC <1L - ABG shows increasing PCO2 (>50 mmHg) or decreasing PO2 (<50 mmHg) - Severe atelectasis

Question 707

Weaning from ventilator in SCI

Answer 707

Useful indices: - Maximum inspiratory pressure -20 cm H2O or more negative - VC >10-15 mL/kg ideal weight (can use larger TV target but must keep plateau pressures <30 cm H2O to prevent atelectasis) & patient must not have ARDS Method for highest success rates for weaning off MV: progressive free breathing, with or without the use of PEEP 5 cm H2O or less

Question 708

Potential benefits of pacing for ventilation compared to MV

Answer 708

Improved quality of life, engagement of patient's own breathing muscles, improved level of comfort, improved speech, restoration of olfactory sensation, increased mobility, reduced anxiety & embarrassment, elimination of vent noise, & reduced overall costs

Question 709

Signs of pacemaker failure for ventilation

Answer 709

Sharp chest pain, SOB, absence of breath, erratic pacing

Question 710

Most common joints to experience HO in SCI

Answer 710

Hip (anteromedial aspect) >> knee/shoulder/elbow

Question 711

Onset of HO in SCI

Answer 711

1-3 months s/p injury is most common; peaks at 2 months Can still present after 6 months. When it occurs after 1 year, usually a/w an acute fracture, DVT, or pressure injury (usually with benign course)

Question 712

Gold standard for DVT diagnosis in SCI

Answer 712

LE venogram

Question 713

What is the leading cause of death in acute SCI?

Answer 713

PE

Question 714

Gold standard for PE diagnosis in SCI

Answer 714

Pulmonary arteriogram

Question 715

Duration of DVT ppx in SCI

Answer 715

Incomplete SCI & ambulating injured patients: can continue until discharge, but can be continued if soon after injury or other co-morbidities present Complete SCI: 8 weeks post-injury if uncomplicated Complete, complicated SCI: 12 weeks post-injury or until discharge from rehab (if >12 weeks). Complicated: LE fracture, history of thrombosis, CA, HF, obesity, >70 years old

Question 716

General uses for e-stim or FES in SCI

Answer 716

1. As exercise to avoid complications of muscle inactivity 2. As a means of producing extremity motion for functional activities - FES can be used to provide a CV conditioning program - Increase muscle bulk, strength, & endurance - Produce motion for UE activity, bladder function, standing, & ambulation

Question 717

Pain in the SCI patient

Answer 717

There are NO consistent associations between presence of pain & SCI characteristics Nociceptive --> from bone, ligaments, muscle, skin, other organs Neuropathic --> from peripheral or central neural tissue damage Shoulder is most commonly affected joint (nociceptive)

Question 718

Incidence of CTS in SCI patients

Answer 718

Between 20-65% with persons with paraplegia, who are more affected than tetras Due to recurrent stress from transfers, WC propulsion, & pressure relief. Padded glove use may decrease the trauma of WC propulsion 25% of people have bilateral UE involvement

Question 719

Post-traumatic syringomyelia/cystic myelopathy

Answer 719

Lesion progresses in a cephalad & caudad direction. As the lesion progresses & compromises more nerve fibers, symptoms may become more apparent Most common presenting symptom is pain --> aching or burning, often worse with coughing, sneezing, straining, & usually in sitting (rather than supine) position Earliest sign is ascending loss of DTRs Ascending sensory loss is also common. Dissociated sensory loss (impaired pain & temp sensation but intact touch, etc) Weakness occurs but rarely in isolation Diagnosis: MRI with gad is gold standard

Question 720

Tendon transfer by spinal level

Answer 720

C5: BR --> ECRB: restores wrist extension; deltoid --> triceps: provides elbow extension C6: Moberg "key grip" procedure: restores lateral or "key" grip to improve grooming, eating, writing, desktop skills; BR (or other active muscles) --> FPL (or other finger flexors) to restore lateral pinch (FPL) or grasp (finger flexors), which provides better function & preferable to Moberg procedure; posterior deltoid --> triceps- recommended prior to hand reconstruction (or simultaneously); re-routing of biceps around radial neck- correct supination contracture of forearm that may occur in C5 & C6 motor injuries C7: BR --> FPL to restore thumb function; ECRL or FCU --> FDP to restore finger flexion C8: intrinsic minus or "claw hand" may be addressed with lumbrical bar, preventing hyper-extension of MCPs to improve function; this surgery is rarely indicated

Question 721

Incidence of dual diagnosis

Answer 721

Between 25-75%

Question 722

Incidence of depression in SCI

Answer 722

Occurs in 20-45% of those injured & usually occurs within first month Suicide rate for injured people is 3-5x the age- & sex-specific rate in the US Leading cause of death in individuals with SCI in the youngest age groups

Question 723

Pressure injuries

Answer 723

Most common location in SCI within first 2 years is the sacrum, followed by ischium, heels, & trochanters In children, the occiput is the most frequent site

Question 724

NPUAP staging of pressure injuries

Answer 724

Stage I: intact skin with localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. Blanchable erythema or changes in sensation, temp, or firmness may precede visual changes. Color changes do NOT include purple or maroon discoloration Stage II: partial-thickness loss of skin with EXPOSED DERMIS. Wound bed is viable, pink/red, moist, & may also present as an intact or ruptured serum-filled blister. Adipose & deeper tissues are NOT visible. Granulation tissue, slough, & eschar are NOT present Stage III: Full-thickness loss of skin, in which ADIPOSE is visible in the ulcer & GRANULATION TISSUE & EPIBOLE (rounded wound edges) are often present. SLOUGH and/or ESCHAR may be visible, but will not obscure extent of tissue loss. Depth varies; areas of significant adiposity can develop deep wounds. UNDERMINING & TUNNELING may occur. Fascia, muscle, tendon, ligament, cartilage, and/or bone are NOT exposed Stage IV: Full-thickness skin & tissue loss with EXPOSED or DIRECTLY PALPABLE FASCIA, MUSCLE, TENDON, LIGAMENT, CARTILAGE, or BONE in the ulcer. SLOUGH & ESCHAR may be visible. EPIBOLE, UNDERMINING, and TUNNELING often occur Unstageable: Full-thickness skin & tissue loss in which extent of tissue damage within the ulcer is obscured by slough or eschar. A stable eschar (dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed

Question 725

Risk factors for developing pressure injuries

Answer 725

Persistent pressure & shear forces

Question 726

Mechanisms of developing a pressure injury

Answer 726

Local soft tissue ischemia results due to prolonged pressure over bony prominences that exceed supra-capillary pressure Ischemia: a/w hyperemia in surrounding tissue, increased local O2 consumption occurs Pressure: prolonged pressure over bony prominences, exceeding supra-capillary pressure continuously for 2 or more hours, resulting in occlusion of the microvessels of the dermis with subsequent tissue ischemia. Muscle is more susceptible to pressure ischemia than skin Friction (shearing): removes corpus striatum of skin

Question 727

Prevention of pressure injuries

Answer 727

Decrease duration of pressure forces --> patient should initially be turned & positioned q2h Pressure relief (weight shifting) & repositioning should be done for >2 minutes at a time, every 15-30 mins when sitting

Question 728

What has been shown to significantly increase tendon extensibility?

Answer 728

Combined heat & stretching

Question 729

Contraindications to heat therapy

Answer 729

Ischemia (arterial insufficiency) --> metabolic requirement of the limbs is increased with the use of heat; for every 10 degrees F increase in skin temp, there is a 100% increase in metabolic demand Scar tissue --> elevation of temp increases tissue's metabolic demand. Scar tissue has inadequate vascular supply & is unable to provide an adequate vascular response when heated, which can lead to ischemic necrosis

Question 730

Which conversion technique is the only to produce superficial heat?

Answer 730

Radiant heat (infrared lamps) Light energy (non-thermal) is absorbed through the skin & converted to superficial heat Distance from the lamp to skin is usually 45-60 cm (18-24 inches). Most lamps work as heat sources, & their heating effectiveness decreases with the square of their distance from the body (1/r2) Used in patients who cannot tolerate the weight of hot packs Precautions: general heat precautions, light sensitivity (dermal photo-aging), & skin drying. Use with photosensitizing meds

Question 731

Where is absorption greatest when using U/s as a deep heating modality?

Answer 731

At the bone-muscle soft tissue interface

Question 732

U/s indications for deep heating modality

Answer 732

Bursitis, tendinitis (calcific), MSK pain, degenerative arthritis & contracture (adhesive capsulitis, shoulder peri-arthritis, hip contracture) to maintain a prolonged stretch & increase ROM; when used to address small joints like fingers/toes, must be done underwater but only if water is degassed, subacute trauma. Less established: scar tissue (keloids), post-herpetic neuralgic pain, plantar warts

Question 733

U/s contraindications for deep heating modality

Answer 733

General heat contraindications, near brain/cervical ganglia/spine, laminectomy sites (can cause SC heating), near the heart or reproductive organs, near pacemakers (may cause thermal or mechanical injury to the pacemaker), near tumors, gravid or menstruating uterus, at infection sites, on contact lenses/eyes (fluid-filled cavity with risk of cavitation & heat damage), skeletal immaturity (open epiphysis can be affected with decreased growth due to thermal injury, THA or TKA with PMMA or high-density polyetyhlene (high coefficient of absorption- more than soft tissue; prosthesis may loosen due to unstable cavitation in the cement), arthroplasties

Question 734

U/s prescription for deep heat modality

Answer 734

Frequency: 0.8-1.1 MHz Intensity: 0.5-2.0 W/cm2 (max should be 3.0) For tendinitis/bursitis, average intensity used is 1.2-1.8 W/cm2, which generates temperatures up to 115F in deep tissues

Question 735

Shortwave diathermy for deep heat modality

Answer 735

Produces deep heating through the conversion of radio wave electromagnetic energy to thermal energy Most commonly used frequency is 27.12 MHz (11 m wavelength) Provides heat over a larger area as well as deep heat to 4-5 cm depth. Preferentially heats low impedance tissues --> skeletal muscle, blood, synovial fluid, so good choice if deep muscle heating is primary goal Inductive coil method: produces high temps in water-rich tissues (superficial muscles, skin) via a coiled magnetic field (induction coil); body acts as a receiver & eddy currents are induced in tissues in its field; applicators are in the form of cables or a drum. Indicated when heat to more superficial muscles or joints with minimal superficial tissue is desired; muscle tends to become warmer than fatty tissue Condensor method: produces high temps in water-poor tissues (fat, bone) with low conductivity via rapid oscillation of an electrical field. Treatment area is placed between 2 capacitor plates to which the shortwave output is applied. Body acts as an insulator in a series circuit. Indicated for subq adipose tissue & superficial muscle, more effect in deep joints (like the hip)

Question 736

Microwave diathermy for deep heat modality

Answer 736

Conversion of microwave electromagnetic energy to thermal energy Frequencies: 915 MHz (33 cm wavelength) - 2,456 MHz (12 cm) Do not penetrate tissues as deeply as U/s or SWD Preferentially heats fluid-filled cavities

Question 737

Summary of deep heating modalities (diathermy)

Answer 737

Options: U/s, SWD, microwave diathermy. All are conversion U/s: sound waves, frequency 0.8-1.1. MHz, heats at 8-cm depth (deepest penetration) SWD: radio waves, freq 27.12 MHz, heats at 4-5 cm depth. Indications: chronic prostatitis, refractory PID, myalgia, back spasms Microwave: micro waves, freq 915-2,456 MHz, superficial heat: 1-4 cm depth. Indications: superficial heat for muscles & joints, speed resolution of a hematoma

Question 738

Therapeutic cold techniques

Answer 738

Decrease spasticity due to: - Decreased muscle spindle activity: decreased firing rates of Ia & II afferent fibers - Decreased golgi tendon organ activity: decreased firing rates of Ib afferent fibers Evaporation: vapocoolant sprays used for spray & stretch techniques to treat myofascial & MSK pain

Question 739

Ultraviolet radiation for therapeutic modality

Answer 739

Wavelength of 2000-4000 A. Bactericidal wavelength is 2,537 A Produces a non-thermal photochemical reaction with resultant alteration of DNA & cell proteins Physiologic effects: bactericidal on motile bacteria, increased vascularization of wound margins, hyperplasia & exfoliation, increased Vit D production, excitation of Ca metabolism, tanning Precaution: scar, atrophic skin Dosage: prescribed as the minimal exposure time required to cause erythema on the volar surface of the forearm --> measured in minimal erythema dosage (MED). The MED subsides in 24 hours. Usual initial prescription is in the dose of 1-2 MED & kept <5 2.5 MED: exposure produces a second-degree erythema in 4-6 hours with pain & subsides in 2-4 days followed by desquamation 5 MED: 3rd degree erythema in 2-4 hours with local edema, pain, & followed by local desquamation 10 MED: 4th degree erythema with superficial blister Treatment can be given 2-3x/week

Question 740

Goeckerman's technique

Answer 740

Psoriasis treatment --> coal-tar ointment is applied to the skin prior to UV treatment

Question 741

How does TENS provide pain control?

Answer 741

Placebo effect --> 30-35% Gate Control Theory (Melzack & Wall) - Attempts to account for mechanisms by which non-noxious stimuli can modulate pain sensation (how non-painful stimuli can suppress pain) - TENS stimulates large Ia myelinated (delta) afferent nerve fibers --> stimulate substantia gelatinosa in the SC, closing the gate on pain transmission to Lissauer's tract (posterior lateral tract of pain & temp), & ultimately to the thalamus. Pain signals can be blocked at the SC before they are transmitted to the brain

Question 742

Conventional TENS

Answer 742

High frequency, low intensity stim --> most effective Pain relief begins in 10-15 minutes & stops shortly after removing stimulation Useful for neuropathic pain

Question 743

Clinical use of NMES

Answer 743

Strengthens muscles & maintains muscle mass after immobilization Benefits: has been shown to potentially increase muscle mass, stroke volume, & CO, as well as reduce venous pooling. Also shown to potentially improve cardiorespiratory fitness

Question 744

Physiologic effects of therapeutic massage

Answer 744

Reflex vasodilation with improvement in circulation Assist in venous blood return from periphery

Question 745

Effleurage

Answer 745

Gliding, rhythmic strokes of the hand over the skin in a distal to proximal direction; performing gently & slowly results in muscle relaxation, whereas performing at a faster pace will increase stimulation Deeper strokes result in more mechanical effects on circulatory & deep myofascial system: relieving pain, increasing lymphatic drainage, & reducing vascular congestion a/w specific conditions

Question 746

Petrissage

Answer 746

Kneading technique in which the muscle tissue is pinched with the fingers & lifted from its underlying origin; increases circulation & tissue pliability, & reduces edema & adhesions. Other variations: wringing, rolling, or shaking techniques

Question 747

Tapotement

Answer 747

Percussion Helps with desensitization, allows clearing of secretions, & improves circulation. Used for chest physiotherapy in conjunction with postural drainage

Question 748

Soft tissue mobilization

Answer 748

Forceful massage of the fascia muscle system. Massage is done with the fascia muscle in a stretched position rather than relaxed or shortened. Used for reduction of contractures

Question 749

Physiologic effect of traction

Answer 749

Vertebral joint distraction --> elongation of the C-spine of 2-20 mm can be achieved with 25 lb or more of tractive force

Question 750

Contraindications to C-spine traction

Answer 750

Cervical ligamentous instability (RA, Down syndrome, Marfan syndrome, achondroplasia, EDS), infectious process of the spine, cervical spinal stenosis with significant cord compromise, AA subluxation with SC compromise, vertebrobasilar insufficiency

Question 751

Amount of spinal traction required

Answer 751

C-spine: distraction requires >25 lbs. Weights >50 lbs do not provide an advantage L-spine: posterior vertebral distraction >50 lbs is needed; for anterior separation >100 lbs is needed Effect of friction between treatment table & body should be counterbalanced before true traction of the spine is accomplished A pull equal to about 1/2 weight of the body part treated is needed to overcome friction. For lower body, this is ~25% of the total body weight. Another option is using a split table, which eliminates the lower body segment friction Regardless of the effect of friction, another 25% or more of body weight is needed to cause vertebral separation

Question 752

Muscle physiology

Answer 752

Skeletal muscle fibers contain hundreds-thousands of myofibrils, each subdivided into units of contraction called sarcomeres Sarcomere is composed of contractile proteins, actin & myosin, that lie parallel to the axis of the fiber. Muscle shortening is produced by coordinated movement of the thin (actin) & thick (myosin) filaments within the myofibrils Actin filaments attach to the outer margins of the sarcomere (Z line) & the myosin filaments are located centrally Sarcomere is measured from Z line to Z line During muscle rest, the filaments overlap a little. The A band runs the length of the thick (myosin) filament), with continuous overlap except at the center (H zone). The I band is composed of thin (actin) filaments that remain bare throughout the outermost portion of the sarcomere Thick & thin filaments are linked to each other via cross bridges that arise from the myosin molecule. During muscle contraction, an increasing amount of myosin overlap is observed. Contraction results in the Z lines approaching each other, shrinking the H zone & I band Transient muscle fiber shortening takes place whenever an AP is generated & travels through the sarcolemma (muscle fiber cell membrane)

Question 753

Relationship between force generation & velocity during eccentric, concentric, & isometric contractions

Answer 753

Greatest force is generated with: Fast eccentric contractions > slow eccentric contractions > isometric contractions > slow concentric contractions Fast concentric contractions generate the least force

Question 754

Plyometric exercises

Answer 754

Training technique designed to increase muscular power & explosiveness (hopping, box jumps, forward hurdle hops) Should be used as an advanced level of exercise in carefully selected patients such as athletes who want to return to high demand functional activities. Exercises are intended to mimic motions used in sports Uses short, explosive movements that cause alternating eccentric & concentric muscle contractions. Increased elastic energy is stored in the eccentric phase, resulting in a more powerful concentric contraction Increased risk of injury due to high-intensity load on muscles

Question 755

Aquatic exercises

Answer 755

Pool-based therapy takes advantage of buoyancy & viscosity of water Buoyancy: weight of a patient can be reduced in proportion to water depth. Being chest deep has a decreased WB load of 40% of total body weight Viscosity: allows for increased resistance to movement equal to the force exerted by the patient. Resistance also decreases in proportion to the speed of movement Improvements can last up to 2 years after participation

Question 756

Biofeedback

Answer 756

Technique of using visual & audio equipment to reveal & translate normal & abnormal internal physiologic events in order to teach patient to manipulate otherwise involuntary events Various types. Training requires potential for voluntary control & ability to follow commands Clinical applications: CVA, SCI, TBI, chronic pain, urinary/fecal incontinence management, sports-related muscle strengthening. Also used in CP, MS, dystonia, dyskinesis, peripheral nerve denervation, & Raynaud's Types: EMG, pressure/force, position, temp/peripheral blood flow, BP, respiratory, sphincter control training Although EMG biofeedback has been studied & is used extensively in CVA rehab, it has less efficacy when there are major sensory deficits, especially severe deficits in proprioception. Additionally, proprioceptive deficits, marked spasticity, & receptive aphasia correlate with lower functional improvements when using biofeedback. This is more evident in UE training than LE training

Question 757

Effects of extended bedrest: muscle

Answer 757

Immobilization decreases strength by 1.0-1.5% daily. Strength can decrease as much as 20-30% during only 1 week of bedrest. 5 weeks of total inactivity costs 50% of the previous muscle strength. A plateau is reached at 25-40% of original strength. One contraction per day of max strength is enough to prevent this decrease Percentage of muscle mass lost per week is ~5-10%

Question 758

Effects of extended bedrest: bone & joints

Answer 758

Lack of stress & tension on the bone through WB & muscle pull on the bone cause osteopenia. Hypercalcemia develops. Calcium is excreted in urine & feces starting at 2-3 days after immobilization, peaking at 3-7 weeks. After activity is resumed, Ca levels remain high for 3 weeks, reaching normal values at 5-6 weeks

Question 759

Effects of extended bedrest: cardiac

Answer 759

Reduction in blood & plasma volumes Redistribution of body fluids leads to postural hypotension. Venous blood pooling occurs in the legs. In addition, beta-adrenergic sympathetic activity is increased CV efficiency is decreased: patients develop an increased resting HR & decreased SV. HR increases 0.5 beats/minute/day, leading to immobilization tachycardia & abnormal HR with minimal or sub-max workloads. SV decrease may reach 15% within 2 weeks of bedrest due to blood volume changes & venous pooling in LE. Also a decrease in VO2 max that can occur as early as 3-5 days Increased risk of thromboembolism due to decrease in blood volume & increased coagulability

Question 760

FIM score

Answer 760

Documents severity of disability, measures activity limitations, & documents outcomes of rehab treatment as part of a uniform data system Consists of 18 items organized under 6 categories (ordinal scale): - Self-care (eating, grooming, bathing, UB dressing, LB dressing, toileting) - Transfers - Sphincter control - Locomotion - Communication - Social cognition (interaction, problem-solving, memory) Graded in each category on scale of 1 (total assistance required) to 7 (complete independence)

Question 761

Physiologic effects of aging: cardiac

Answer 761

Progressive decline in max HR --> decreased chronotropic response to adrenergic stim Increased LV end-systolic volume & decreased EF with exercise. When added to a decreased HR, CO during exercise is more dependent on an increased SV by with higher end diastolic volumes CO decreases with aging Rate of diastolic early filling is decreased. More dependent on late filling through atrial contraction. Patients are more susceptible to AF or atrial tachycardia as well as CHF VO2 max decreases regardless of level of activity, but more physically active patients have smaller decreases than sedentary patients Progressive, gradual increases in systolic & diastolic BP --> decreased arterial elasticity Decreased baroreceptor sensitivity is a/w orthostatic hypotension. Diminished reflex tachycardia with position change, in a/w blunted plasma renin activity & reduced vasopressin & angiotensin II levels. Decreased baroreceptor sensitivity is also a/w cough & micturition syncope syndromes. Meds to monitor for causing orthostatic hypotension: anti-hypertensives, levodopa, phenothiazines, TCAs

Question 762

Physiologic effects of aging: pulmonary

Answer 762

Decreased VC Decreased PO2 --> linear decline a/w mild degree of impaired gas exchange NO change in PCO2 or pH Decreased FEV1. This decreases consistently at 30 mL/year Decreased maximum minute ventilation --> stiffening of rib cage, weakening of intercostal muscles, small airway narrowing due to decreased elastic recoil Increase in residual volume & functional reserve capacity related to loss of elastic recoil of the lung tissue No change in total lung capacity High incidence of PNA

Question 763

Physiologic effects of aging: renal

Answer 763

Digitalis toxicity in the elderly is commonly 2/2 impaired renal function. Toxicity manifests with cardiac dysrhythmias, anorexia, n/v, abdominal pain, fatigue, depression, drowsiness, lethargy, HA, confusion, & ocular disturbances NSAIDs can also cause injury to kidneys with most common finding being pre-renal azotemia. In settings where the renal blood flow is dependent on the activity of vasodilating prostaglandins, NSAIDs can precipitate ARF. In states of prostaglandin inhibition, patients develop hypo-reninemic hypo-aldosteronism

Question 764

Physiologic effects of aging: GI

Answer 764

Dysphagia --> age-related changes in swallowing physiology & age-related diseases are pre-disposing factors for dysphagia in the elderly

Question 765

Physiologic effects of aging: hearing

Answer 765

Presbyacusis --> loss of ability to perceive or discriminate sounds as one ages. Age of onset & pattern may vary

Question 766

TCAs in elderly

Answer 766

Nortriptyline (Pamelor) is preferred due to fewer anticholinergic effects, decreased sedating effect, & causes less orthostatic hypotension (which is a result of alpha-1 blockade) Amitryptiline (Elavil) should be used in agitation in elderly

Question 767

Benefits of pulmonary rehab

Answer 767

- Improvement in exercise tolerance, symptom-limited O2 consumption, work output, & mechanical efficiency - Exercise increases arterial venous O2 (AVO2) difference by increasing O2 extraction from arterial circulation - Reduction in dyspnea & RR at rest & at various levels of activity - Improvement in general QoL, decreased anxiety & depression, as well as improvement in the capacity to perform ADLs - Improvement in ambulation capacity - Decreased hospitalization rates/reduced healthcare resource utilization - Focus on conditioning peripheral musculature to improve efficiency & reduce stress on heart & lungs

Question 768

Who benefits the most from a pulmonary rehab program?

Answer 768

Respiratory limitation of exercise at 75% of predicted maximum O2 consumption Obstructive airway disease with FEV1 <2000 mL or FEV1/FVC <60% Restrictive lung disease or pulmonary vascular disease with carbon monoxide diffusion capacity <80% of predicted value

Question 769

Classification of functional pulmonary disability: Moser classification

Answer 769

1 --> normal at rest, dyspnea on strenuous exertion 2 --> normal ADL performance, dyspnea on stairs/inclines 3 --> dyspnea with certain ADLs, able to walk 1 block at slow pace 4 --> dependent with some ADLs, dyspnea with minimal exertion 1-4 --> NO dyspnea at rest 5 --> housebound, dyspnea at rest, in need of assistance with most ADLs

Question 770

Active muscle during inspiration

Answer 770

Diaphragm, innervated by phrenic nerve Contraction of diaphragm increases the volume & decreases intra-thoracic pressure --> decrease in intra-thoracic pressure relative to atmospheric pressure --> inspiration

Question 771

Lung voume definitions

Answer 771

Vital capacity (VC) --> greatest volume of air that can be exhaled from the lungs after maximum inspiration Forced vital capacity (FVC) --> VC measured with the patient exhaling as rapidly as possible Maximal mid-expiratory flow rate --> average flow rate, between 25-50% of FVC Total lung capacity (TLC) --> amount of gas within the lungs at the end of maximal inspiration Tidal volume (TV) --> amount of gas moved in normal resting inspiratory effort Functional residual capacity (FRC) --> amount of gas in lungs at end of normal expiration Residual volume (RV) --> amount of gas in the lungs at end of maximal expiration Maximal voluntary ventilation --> max volume of air exhaled in a 12-second period in liters per second Maximal static inspiratory pressure (PI max) --> static pressure measured near residual volume after maximum expiration Maximal static expiratory pressure (PE max) --> static pressure measured near total lung capacity after maximal inspiration Minute volume --> volume of gas inhaled or exhaled per minute

Question 772

Maximal O2 consumptions

Answer 772

Expired gases during maximal exercise are collected & analyzed for O2 content VO2 max: maximal volume of O2 that can be utilized in 1 minute during maximal or exhaustive exercise VO2 max is measured in mL of O2 in 1 minute per kg of body weight Fick equation: VO2 max = (HR x SV) x AVO2 difference So, increasing amount of O2 that gets extracted from arteries increases VO2 max Individual VO2 max is dependent on body weight, age (peak is ~20 years), sex (values for females are 70% of males), & inherent genetics (the most important) Training or the presence of pathological conditions can affect this potential Endurance exercise training increases VO2 max, CO, & physical work capacity of untrained healthy individuals

Question 773

COPD

Answer 773

C/b increased airway resistance due to bronchospasm, which may result in air trapping, low maximum mid-expiratory flow rate, & normal to increased compliance Possible V/Q mismatching resulting in hypoxemia Can be a/w increased airway resistance, impaired expiratory airflow, & respiratory muscle fatigue. Flattening of the diaphragm seen on CXR due to increased total & residual lung volumes

Question 774

Types of COPD

Answer 774

Chronic bronchitis Emphysema CF Asthma

Question 775

COPD: emphysema

Answer 775

Distention of air spaces distal to the terminal non-respiratory bronchioles with destruction of alveolar walls, 2/2 unimpeded action of neutrophil-driven elastase Destruction of the alveolar wall elasticity --> loss of lung recoil, leading to excessive airway collapse on exhalation & chronic airflow obstruction Decreased gas exchange surface area of the lung (alveolar membranes in a/w V/Q mismatch causes hypoxemia) Chronic increase in pulmonary vascular resistance in the presence of pulmonary tissue hypoxia can lead to severe pulmonary artery hypertension & RV heart failure O2 is the only proven therapy that improves mortality in hypoxemic patients

Question 776

COPD: CF

Answer 776

AR disease involving the chloride ion channels found in exocrine glands. Respiratory involvement is caused by failure to adequately remove secretions from the bronchioles, resulting in widespread bronchiolar obstruction & subsequent bronchiectasis, overinflation, & infection Aerobic exercise for CF patients helps to increase sputum expectoration. Patients have increased ciliary beat with improved mucous transport Aerobic exercise also improves exercise capacity & respiratory muscle endurance, & reduces airway resistance by facilitating expectoration of retained secretions Chest PT can help to mobilize airway secretions

Question 777

SMA syndrome

Answer 777

3rd part of the duodenum is intermittently compressed by overlying SMA --> GI obstruction Predisposing factors: - Rapid weight loss (decrease in protective fatty layer) - Prolonged supine position, most common in tetraplegia - Spinal orthosis - Flaccid abdominal wall causes hyperextension of the back Symptoms: post-prandial n/v, bloating, abdominal pain Diagnosis: upper GI series demonstrates abrupt duodenal obstruction to barium Treatment: typically conservative - Eat small, frequent meals in upright position - Lie in left lateral decubitus after eating - Metocopramide (Reglan) to stimulate motility of upper GI tract (primarily stomach) - Rarely requires surgery. If conservative treatment fails, surgical duodenojejunostomy should be performed Any condition that decreases the normal distance between the SMA & aorta may result in compression of the duodenum --> nutcracker effect

Question 778

General guidelines to assessing functional limitations of COPD patients based on PFTs

Answer 778

When the predicted FEV1 is close to 4L, the patient should NOT have a h/o significant exercise impairment Impairment usually develops when FEV1 falls below 3L/second, but is variable - FEV1 between 2-3L/second --> mild exercise limitation, able to walk long distances but not at high speed - FEV1 between 1-2L/second --> moderate degree of exercise impairment, intermittent rest periods are required to walk significant distances or to climb stairs - FEV1 <1L/second --> severe exercise impairment, very short-distance ambulation

Question 779

Restrictive lung disease

Answer 779

Impaired lung ventilation due to loss of normal elastic recoil of the lungs or chest wall, can be a/w respiratory muscle dysfunction or stiffness of chest wall or lung tissue itself, thereby resulting in increased work to breathe A/w variable levels of hypercapnia or hypoxia Almost all lung volumes are decreased & flow rates are increased owing to loss of compliance

Question 780

Causes of restrictive lung disease

Answer 780

Intrinsic lung disease (stiffness of lung tissue) --> can lead to pHTN, RV hypertrophy, & cor pulmonale; examples are sarcoid, asbestosis, silicosis, & IPF Extrinsic lung disease (stiffness of chest wall) NM diseases --> DMD, ALS, GBS, MG; weakness of respiratory muscles impairs the bellowing activity of the chest wall, limiting ventilatory capacity & causing hypoventilation Thoracic deformities --> if scolitoic angle >90, patients have dyspnea; if >120, will have hypoventilation & may have cor pulmonale Pleural disease Ankylosing spondylitis --> limited expansion of chest wall Cervical SCI Obesity Surgical removal of lung tissue

Question 781

DMD pulmonary effects

Answer 781

X-linked recessive Atelectasis 2/2 hypoventilation & PNA can occur No clear guidelines have been established for determining the point at which vent support should be instituted in patients with DMD, but suggestions: - Dyspnea at rest - 45% predicted VC - Maximal inspiratory pressure <30% of expected - Hypercapnia

Question 782

PFT volume changes

Answer 782

Normal changes noted with age: decreased VC, maximal voluntary ventilation, FEV1 (decreases at a rate of 30 mL/year, PO2. NO change in TLC or PCO2. Will see INCREASE in RV & FRC Obstructive lung disease: air trapping occurs. Limitation in expiration before air is fully expired. Flattening of diaphragm is increased. Impaired gas exchange as a result of air trapping leads to respiratory muscle fatigue. Decreases in VC, FEV1 (decreases 45-75 mL/year), maximal voluntary ventilation, & FVC. INCREASE in RV, FRC, TLC Restrictive lung disease: all volumes are decreased. Increased stiffness of lung & elastic work of breathing. Decreases in VC, TLC, RV (although this is increased in cervical SCI), FRC, FVC, maximal voluntary ventilation. FEV1 is NORMAL

Question 783

What PFT should be followed in ALS?

Answer 783

FVC --> best prognostic indicator for non-invasive ventilation Once below 50% of predicted --> risk of imminent respiratory failure & need for vent If symptoms begin with limb weakness, the disorder may progress to respiratory failure in 2-5 years Earliest changes noted are decreases in maximum inspiratory & expiratory muscle pressures, followed by reduced VC & maximum breathing cpacity When VC falls to 25 mL/kg, the ability to cough is impaired

Question 784

Pulmonary changes in C 5 tetra

Answer 784

Diaphragm remains intact & expiratory muscles are paralyzed Patients retain approximately 60% of their inspiratory capacity & ventilate well, but have weak cough & difficulty clearing secretions during respiratory infections All volumes are greatly reduced because of limited expansion of the chest wall (although with increased RV) In SCI patients, the abdominal contents sag due to greater strength of the diaphragm relative to weakness of the abdominal wall muscles. This decreases diaphragmatic excursion & the VC in the sitting position. This improves with use of abdominal binder One goal of pulmonary rehab for these patients is to increase VC

Question 785

Rehab of the COPD patient: pharmacologic optimization prior to rehab program

Answer 785

For dyspnea & to decrease exacerbations of COPD: - Inhaled anti-cholinergics (ipratropium, umeclidinium bromide, tiotropium) --> block muscarinic receptors - Short-acting inhaled beta-2 agonists Young patients with moderate asthma, who have tried B2 agonists during exercise as well as mast cell stabilizers or leukotriene inhibitors, may benefit from theophylline use for EIA/bronchospasm

Question 786

Rehab of the COPD patient: supplemental O2 use

Answer 786

Recommended for patients who desat during exercise. Use if exercise-induced SaO2 falls below 90% Benefit of home O2: reduction of polycythemia, improvement in pHTN, reduction of the perceived effort during exercise, prolongation of life expectancy, improvement in cognitive function, reduction in hospital needs, decreased BP & pulse in patients with COPD who have increased sympathetic activity & reduced baroreflex sensitivity

Question 787

Rehab of the COPD patient: training in controlled breathing techniques

Answer 787

Used to reduce dyspnea, reduce work of breathing, & improve respiratory muscle function & pulmonary function parameters Different types may be used in patients with obstructive pulmonary disease & restrictive disease Diaphragmatic breathing benefits: increased TV, decreased FRC, & increase in maximum O2 uptake Pursed lip breathing: - Patient inhales through nose for a few seconds with mouth closed, then exhales slowly for 4-6 seconds through pursed lips. Expiration lasts 2-3x as long as inspiration - By forming a wide, thin slit with the lips, the patient creates an obstruction to exhalation, slowing the velocity of exhalation & increasing mouth pressure - Benefits: prevents air trapping due to small airway collapse during exhalation & promotes greater gas exchange in the alveoli. Increases TV & reduces dyspnea & work of breathing in COPD patients. When added to diaphragmatic breathing, it reduces the RR & can improve ABGs

Question 788

Rehab of the COPD patient: secretion mobilization techniques (positions for postural drainage)

Answer 788

Commonly used position is Tberg (feet higher than head) in supine or prone To drain upper lobes: patient is sitting up - Exceptions: right anterior segment- place patient supine, lingular- place patient in lateral decubitus Tberg, both posterior segments- place patient prone To drain the right middle & lower lobes: lateral decubitus Tberg - Exceptions: superior segment of lower lobe- place patient prone with butt elevated, posterior lower segment- place patient prone Tberg with butt elevated, anterior segment- supine Tberg Precautions: COPD patients can only tolerate up to 25 degree tilt Avoid in: pulmonary edema, CHF, HTN, dyspnea, abdominal problems- hiatal hernia, obesity, recent food ingestion, abdominal distension Side-lying contraindications: axillofemoral bypass graft, MSK pain (like rib fractures)

Question 789

Postural changes in COPD

Answer 789

Not only help with secretion mobilization but also affect work of breathing by changing the mechanical load on respiratory muscles & O2 supply/consumption in these areas Mechanical load: weight of the pulmonary tissue also contributes to overall pressure on the most dependent alveoli. The dependent alveoli expand in size when changing from sitting to supine, increasing ventilation at base of lung Blood flow: difference in blood flow distribution is based on the pressure affecting the capillaries Zone 1 (top): good ventilation, bad perfusion Zone 2 (middle): ventilation & perfusion are fairly equal Zone 3 (base): most-gravity dependent region of the lung where pulmonary artery pressure > pulmonary venous pressure > alveolar pressure --> perfusion > ventilation When changing from sitting to supine, venous pressure increases in relation to arterial pressure in dependent areas of the lung

Question 790

Rehab of the COPD patient: secretion mobilization techniques (chest therapy program peri-operatively)

Answer 790

Pre-op & post-op chest therapy program: - Decreases incidence of PNA - Reduces probability of developing post-op atelectasis following thoracic & abdominal surgery

Question 791

Rehab of the COPD patient: instruction on reconditioning exercises

Answer 791

Aerobic exercise in patients with CF: exercises involving the trunk muscles (sit ups), swimming, jogging) Patients with CF that participate in a structured running program show significant improvements in exercise capacity, respiratory muscle endurance, & a reduction in airway resistance. Also see increased sputum expectoration & an improvement in lung function after several weeks of strenuous regular aerobic exercise

Question 792

Uses of glossopharyngeal breathing (controlled breathing technique for restrictive lung disease)

Answer 792

Enables patient to breathe without MV (up to 4 or more hours if the lungs are normal; if lungs are affected, may only tolerate minutes). This time off the ventilator can be used to transfer to different types of aids Improves volume of voice & rhythm of speech, allowing patient to shout Helps prevent micro-atelectasis Allows patient to take deeper breaths for more effective cough Improves or maintains pulmonary compliance

Question 793

Use of non-invasive ventilation for restrictive lung disease: positive pressure body ventilator

Answer 793

Intermittent abdominal pressure ventilator (IAPV) Examples: Pneumobelt (BachBelt), exsufflation belt - Abdominal corset containing a battery-operated rubber air sac is cyclically inflated & deflated by a portable vent that delivers 2.5 L of air at a time. When the air sac inflates, it compresses the abdomen, causing the diaphragm to move upwards & assist with expiration - With cessation of air flow, the sac empties & the diaphragm descends due to gravity, causing inhalation. Inhalation is mostly passive & dependent on gravity --> only useful in sitting or standing. A trunk angle of 30 degrees or more from horizontal is necessary for it to be effective, but 75 degrees is optimal - Device is worn from the xiphoid to above pelvic arch. Cycles are 40% inspiration & 60% expiration. About 250-1,200 mL of TV can be provided - This is the most useful mode of ventilation for wheelchair-bound patients with <1 hour of vent-free time during the day - Benefits also include liberating the mouth & hands for other activities - Contraindicated in severe scoliosis & severe obesity. Patient should have a mobile abdomen - Not useful in patients with decreased pulmonary compliance or increased airway resistance - Most beneficial when used during the day in addition to nocturnal non-invasive IPPV. Inspiration may be supplemented by the use of available inspiratory muscles and/or glossopharyngeal breathing

Question 794

Use of non-invasive ventilation for restrictive lung disease: positive & negative pressure body ventilator

Answer 794

Rocking bed - Rocks the patient along a vertical axis (15-30 degrees from the horizontal) utilizing gravity to assist ventilation - When the head of the bed is up, inspiration is assisted by using gravity to pull the diaphragm down --> negative pressure - With head down, exhalation assist is obtained. Cephalad movement of the abdominal contents pushes the diaphragm up with production of positive pressure - Used for patients with diaphragm paralysis with some accessory muscle function - Benefits: prevents venous stasis, improves clearance of bronchial secretions, weight-shifting prevents pressure ulcers, benefits bowel motility, easy to apply - Disadvantages: heavy (not portable), not effective in patients with poor lung or chest wall compliance or in those with increased airway resistance

Question 795

Fenestrated vs non-fenestrated tubes

Answer 795

Fenestrated: - Good for patients who are able to speak & require only intermittent ventilatory assistance Non-fenestrated: - If patient wants to talk, a one-way talking valve may be used on the trach tube. These devices open on inhalation & close during exhalation to produce phonation

Question 796

Talking trach tubes versus speaking valves

Answer 796

Speaking trach tubes --> Portex Talk tube, Bivona Fome-cuff with side-port airway connector, Communi-Trach - Used in alert & motivated patients, who require an inflated cuff for ventilation & who have intact vocal cords & ability to mouth words - Distinguishing characteristic of talking trach's is that the cuff remains inflated at all times so patient is able to speak while maintaining a closed system for ventilation - Talking tach's contain a gas line with an external thumb port. When the thumb port is occluded, gas passes through the larynx via small holes above the inflated cuff, allowing patient to speak - Quality of speech is altered (lower pitch, coarser, low whisper) & some patients may not be able to produce adequate voice even with practice. Patients need to speak short sentences (because constant flow through the vocal cords can cause the voice to fade away) - Patient requires manual dexterity & some strength to occlude the external port One-way speaking valves (Passy-Muir speaking valve, Olympic Trach Talk) - PMV is the only valve that has a biased, closed position; opens only on inspiration - All the other valves are open at all times until they are actively closed during expiration (when enough force is placed) - Air is directed into the trachea & up through the vocal cords, creating speech as air passes through oral & nasal chamber - Requires less work- opening & closing the valve is not needed - Indications: patient awake/alert/attempting to communicate, medically stable & able to exhale efficiently & completely around the tracheostomy tube/upper airway, able to tolerate complete cuff deflation, able to tolerate speaking valve trial - Contraindications: unconscious/comatose patients, vocal cord paralysis in adducted position, inflated trach tube cuff of any kind, foam-filled cuffed trach tubes (may cause airway obstruction), severe airway obstruction, laryngeal stenosis, or tracheal stenosis

Question 797

Speaking valve trial

Answer 797

Cuff must be completely deflated when PMV is on. Failure to deflate can cause immediate respiratory distress. Uncuffed trach tube is recommended Assess vitals --> monitor breathing sounds (should remain same after PMV placement); decreased breath sounds or prolonged expiratory phase indicate possible airway obstruction --> slowly deflate cuff & allow patient to adjust to this --> proceed with PMV placement

Question 798

Trach suctioning complications

Answer 798

Bleeding, infection, atelectasis, hypoxemia, CV instability (dysrhythmias & in extreme cases cardiac arrest & death), elevated ICP, lesions to tracheal mucosa

Question 799

Which phase of the cardiac rehab program is the convalescent stage following hospital discharge?

Answer 799

Phase II This period is the most closely monitored phase of rehab

Question 800

Exercise physiology

Answer 800

Total O2 consumption (VO2) --> O2 consumption of the whole body. Corresponds to work of the peripheral skeletal muscles rather than myocardial muscles Aerobic capacity (VO2 max) --> maximum O2 consumption that an individual can achieve during exercise. As person increases exercise, VO2 increases in a linear fashion until it levels off & reaches a plateau despite further increases in the workload. This is the aerobic capacity of the individual. Usually expressed in mL of O2 consumed per kg of body weight per minute (mL O2/kg/min). Provides good measure of dynamic work capacity as well as CV fitness. Provides info regarding prognosis in patients with heart disease & can assist in evaluating work resumption after recovery. Treadmill or leg cycle ergometer testing is primarily used to estimate VO2 max Myocardial O2 consumption (MVO2) --> actual O2 consumption of the heart (like myocardial workload). Can be measured directly with cardiac cath. In a clinical setting, can use rate pressure product (AKA double product) to estimate this value = SBP x HR Fick equation: VO2 max = CO x AVO2 difference Metabolic equivalent (MET) --> ratio of working metabolic rate to basal (resting) metabolic rate. 1 MET is 3.5 mL O2 consumed per kg of body weight per minute. 1 MET is the energy consumption while at basal metabolic rate (seated rest)

Question 801

Outcomes of cardiac rehab services

Answer 801

Improvement in exercise tolerance Improvement in symptoms Improvement in blood lipid levels Reduction of cigarette smoking Improvement in psychosocial well-being & stress reduction Reduction in mortality Safety

Question 802

Graded exercise testing

Answer 802

Assesses the patient's ability to tolerate increased physical stress. Can be used for diagnostic, prognostic, & therapeutic application, with or without addition of radionuclide or echo Cardiac rehab professions usually use these as functional rather than diagnostic tools Can also provide useful info when applied to risk stratification models. Allow establishment of appropriate limits & guidelines for exercise therapy & the assessment of functional change over time Sub-maximal graded exercise testing is recommended for inpatients & prior to outpatient cardiac rehab programs These may be sub-maximal or maximal relative to patient effort in addition to common indications for stopping the exercise test. Endpoint criteria for sub-maximal testing may include HR limits, perceived exertion, & pre-determined MET levels Most of the ADLs in the home environment require <4 METs AHA suggests a HR limit of 130-140 bpm for patients not on BB agents, or a Borg Rating of Perceived Exertion of 13-15 as additional criteria for low level testing (serves as baseline for ambulatory exercise therapy). Frequency of the test should be relative to the patient's clinical course rather than a fixed schedule

Question 803

Exercise testing protocols

Answer 803

Can use treadmill, cycle, or arm ergometer LE amputees can use arm ergometers Treadmill testing provides a more common form of physiologic stress (like walking), in which subjects are more likely to attain a slightly higher VO2 max & peak HR Cycle ergometer has the advantage of requiring less space & generally is less costly than the treadmill. Minimized movements of the arm & thorax facilitate better quality EKG recording & BP monitoring To perform a stress test in an AKA, an upper extremity ergometer is used Balke-Ware protocols that increase metabolic demands by 1 MET per stage are appropriate for high-risk patients with functional capacity <7 METs

Question 804

Bruce protocol

Answer 804

Metabolic demands of >2 METs per stage may be appropriate for low-intermediate risk patients with functional capacity >7 METs Bruce protocol allows 2-3 METs per stage with stable patients with functional capacities of 10 METs Pharm stress testing in debilitated patients for whom exercise testing cannot be performed has been used to evaluate ischemia. The data from this CANNOT be used in exercise presumption

Question 805

Physical activity program & associated METs

Answer 805

Slow walk --> 2-3 METs (2 mph) Regular speed walk --> 3-4 METs (3 mph) Very brisk walk --> 5-6 METs (4 mph) Sex --> 3-4 METs (if reaching 5-6 METs on stress testing without ischemia or arrhythmias, can resume normal sexual activities without risk Outdoor work (shovel snow, spade soil) --> 7 METs Jog --> 9 METs (5 mph)

Question 806

Sex after MI

Answer 806

Cleared after 2 weeks Intercourse is as physically intense as climbing 2 flights of stairs Intercourse with familiar partners in a known environment requires 4 METs

Question 807

Target HR for exercise intensity

Answer 807

HR range based on the clearance HR. There are 3 main methods of measuring target HR: 1. Clearance HR method 2. Age-predicted method 3. Karvonen method Target HR is 70-85% of the maximum HR Clearance HR is the clinical maximum HR attained on stress test - For the CARDIAC patient, max HR is obtained based on max HR achieved on exercise stress test (clearance HR) --> 70% of max HR attained on exercise stress test - For HEALTHY patient, the max HR is gotten via age-predicted formula (220-age), but still using the 70-85% of that number; has the potential for over & underestimating the actual exercise intensity; can place patients with heart disease at risk for exercise-induced CV complications Karvonen method uses the subject's potential HR increase & assumes that the resting HR represents zero intensity - Target HR = 0.70 to 0.85 (max HR - resting HR) + resting HR - Useful for those on chronic BB or with abnormally high resting HR

Question 808

Borg Scale of Ratings of Perceived Exertion

Answer 808

Linear scale of rating from 6-20. Valid indication of physical exertion & correlates linearly with HR, ventricular O2 consumption, & lactate levels The new exerciser can proceed with exercise to level 13 (somewhat hard) provided they have been given clearance to do so from the exercise stress test AHA suggests a HR limit of 130-140 bpm for patients not on BB, or Borg RPE of 13-15 as an additional point criteria for low-level testing 6: no exertion at all 9: very light 11: light 13: somewhat hard 15: hard (heavy) 17: very hard 19: extremely hard 20: max exertion

Question 809

Duration & frequency of exercise

Answer 809

ACSM recommends that in order to develop & maintain comprehensive physical fitness, healthy adults need to engage in: - Moderate cardio-respiratory exercise for 30 minutes or more for 5 or more days a week - Vigorous cardio-respiratory exercise 20 minutes or more 5 or more days a week or combination of moderate-vigorous exercise to achieve a TEE of 500-1000 MET minutes per week - Resistance & neuromotor exercise involving balance, agility, & coordination 2-3 days a week. Adults can benefit from exercising in amounts less than recommended Cardio-respiratory aerobic exercise: - Freq: >/= 5 days/week of moderate exercise or 3 or more days per week of vigorous exercise, or a combo on 3-5 days or more per week - Intensity: moderate and/or vigorous intensity for most adults; light-to-moderate intensity exercise may be beneficial in de-conditioned patients - Time: 30-60 minutes per day (150 minutes per week) of purposeful moderate exercise or 20-60 minutes per day (75 minutes per week) of vigorous exercise, or a combination - Type: regular, purposeful exercise that involves major muscle groups & is continuous & rhythmic in nature - Volume: increase steps to 2000 or more daily to reach 7000 or more per day - Pattern: may be performed in one continuous session per day or broken up into 10 minutes or more to get to desired duration & volume. <10 minutes may be helpful in very de-conditioned people - Progression Resistance exercise: each major muscle group should be performed on 2-3 days per week Flexibility: 2-3 days a week or more Neuromotor exercise training: 2-3 days a week or more; balance, agility, coordination, & gait. Proprioceptive exercise training (tai chi, yoga) ACSM recommends that exercise intensity be prescribed within a range of 70-85% of maximal HR, 50-85% of VO2 max, or 60-80% of maximal METs. Lower intensities elicit a favorable response in low-fit individuals, inpatients, & people with MSK pain

Question 810

Orthotopic heart transplant

Answer 810

Consists of over 99% of all cardiac transplants Orthotopic bicaval technique is the preferred method & makes up 75% of all OHT --> donor heart is excised with intact RA & a long segment of the SVC. Donor heart LA is sutured to the stump of the 4 pulmonary veins in the recipient. The superior & inferior vena cavae are sutured to the recipient atrial cuff & the great arteries are anastamosed

Question 811

Heterotopic heart transplant

Answer 811

Less than 1% of all heart transplants Recipient heart is left in place to assist the donor heart

Question 812

Physiologic response after heart transplant

Answer 812

Transplanted hearts are denervated & lack vagal innervations & central regulation (parasympathetic tone) --> lack vagal inhibition to the SA node --> resting tachycardia of 100-110 bpm Loss of sympathetic innervation results in circulating catecholamines acting on the chronotropic response --> delayed HR response to exercise. Peak HR is 20-25% lower than controls Patients have HTN 2/2 renal effects of calcineurin inhibitors & prednisone from maintenance medication regimens. Diastolic dysfunction may be present in some patients Altogether result in reduced work output & O2 by 1/3 compared to controls Summary: catecholamine-induced inotropy is reported during peak dynamic exercise in denervated patients - High resting HR due to parasympathetic denervation - Lower peak exercise HR - Resting HTN is common, caused in part by the renal effects of anti-rejection meds - Slower return to resting HR post-exercise - At maximum effort, the work capacity, CO, SBP, & VO2 are lower After transplant, the 1-year survival is 90%. 5-year is 70%. 20-year is 20% Accelerated atherosclerosis occurs following transplantation

Question 813

Exercise prescription for heart transplant patient

Answer 813

Standard HR guidelines are NOT used Intensity of exercise is based on the following: - Borg RPE scale 11-14 - Percentage of VO2 max or maximum workload performed on stress test - Anaerobic threshold - Duration, frequency, & types of exercise follow the same principles as those with other types of cardiac problems During exercise testing, heart transplant patients with cardiac ischemia do not present with typical symptoms of angina. Instead, EKG changes & other symptoms should be followed

Question 814

How does exercise improve PAD & walking economy?

Answer 814

By increasing bio-mechanical & metabolic efficiency

Question 815

How do amputees compensate for the increase in energy consumption with ambulation?

Answer 815

By using slower speeds to keep the rate of energy expenditure stable

Question 816

Energy cost of ambulation for the amputee

Answer 816

Based on the % increase above the cost of normal ambulation at 3 METs No prosthesis with crutches --> 50% increase --> 4.5 METs Unilateral BKA with prosthesis --> 9-28% increase --> 3.3-3.8 METs Unilateral AKA with prosthesis --> 40-65% increase --> 4.2-5.0 METs Bilateral BKA with prosthesis --> 41-100% increase --> 4.2-6.0 METs Unilateral BKA + contralateral AKA --> 75% increase --> 5.3 METs Bilateral AKA with prosthesis --> 280% increase --> 11.4 METs Unilateral hip disarticulation --> 82% increase --> 5.5 METs Hemipelvectomy with prosthesis --> 125% increase --> 6.75 METs