Cerebellum/Cranial and Peripheral Nerves

Question 1

The cerebllum regulates muscle activity across multiple joints in anticipation of and adjustment to changing mechanical forces. Describe Cb role in the context of internal vs external forces. What are interaction torques and why do they matter?

Answer 1

The cerebellum adjusts for and controls for INTERACTION TORQUES which are F=M*A.

Question 2

____ ____ is a stored set of rules that mimics systems and encompasses aspects of [internal / external / both internal and external] forces. . It estimates the interaction between ___ and ____ to yield fluid, successful, automatic movements. This control occurs [ before / during / both before and during ] movement. It is [ static / adaptive ] in the context of varying environmental demands.

Answer 2

An INTERNAL MODEL is a stored set of rules that mimics systems and encompasses aspects of INTERNAL AND EXTERNAL forces. It estimates the interaction between LIMB DYNAMICS and ENVIRONMENT to yield fluid, successful, automatic movements. This control occurs BOTH BEFORE (prediction) AND DURING ongoing movement. It is ADAPTIVE in the context of varying environmental demands.

Question 3

Visual sampling combines ___ eye movements and ____ to allow for orientation to your visual environment and bring areas of interest into focus. Visual sampling increases during ___ and ____ (movement examples).

Answer 3

Visual sampling combines SACCADIC eye movements and FIXATION to allow for orientation to your visual environment and bring areas of interest into focus. Visual sampling increases during COMPLEX TERRAIN NEGOTIATION (increased feedback reliance on visual feedback e.g. for foot placement!) and TURNING (eyes move, then head then body moves - this is predictive and continuously occurring!).

Question 4

Eye movements in visual sampling are [reactive / proactive ] (i.e. [feedforward / feedback ] ), which allows for gaze stability! Impaired ____ are shown to interact with foot placement, turning, and gait velocity. If you need to perform multiple corrective ____, you have to move more slowly to account for that!

Answer 4

Eye movements in visual sampling are PROACTIVE (i.e. they’re FEEDFORWARD, seeking info a second BEFORE the action, coordinating w/head/body movement), which allows for gaze stability! Impaired SACCADES are shown to interact with foot placement, turning, and gait velocity. If you need to perform multiple corrective SACCADES, you have to move more slowly to account for that!

Question 5

Cerebellar lesions impact control of ongoing movement because ___ (i.e. mismatch between internal model vs actual limb properties), ___, and ___ are impaired.

Answer 5

Cerebellar lesions impact control of ongoing movement because PREDICTION (i.e. mismatch between internal model vs actual limb properties), ADAPTABILITY (i.e. difficulty adapting to a change in load or environment), and PRECISION are impaired.

Question 6

To accurately predict the demands of a movement, the cerebellum has to match the internal model and actual limb properties, which are driven by the limb ___, ___, ____, and ____. When there’s a mismatch, we see ____ clinically!

Answer 6

To accurately predict the demands of a movement, the cerebellum has to match the internal model and actual limb properties, which are driven by the limb SPEED, WEIGHT, MOVEMENT MAGNITUDE / TRAJECTORY, and INERTIA. When there’s a mismatch, we see DYSMETRIA clinically!

Question 7

In individuals with Cb lesions who showed HYPERMETRIC movements, they tended to [over / under] estimate the limb inertia and start movement with a [high / low ] velocity, then overcorrect resulting in an [over/under] shoot of the movement.

In individuals with Cb lesions who showed HYPOMETRIC movements, they tended to [over / under] estimate the limb inertia and start movement with a [high / low ] velocity, then overcorrect resulting in an [over/under] shoot of the movement.

Answer 7

In individuals with Cb lesions who showed HYPERMETRIC movements, they tended to UNDERestimate the limb inertia and start movement with a LOW velocity, then overcorrect resulting in an OVERshoot of the movement.

In individuals with Cb lesions who showed HYPOMETRIC movements, they tended to OVERestimate the limb inertia and start movement with a HIGH velocity, then overcorrect resulting in an UNDERshoot of the movement.

Question 8

In cerebellar damage, we see impaired adaptability to changes in the ___ or ____. This results in a bias toward the [INTERNAL/ EXTERNAL ] model representation of limb dynamics; or, the model is “fixed” at a specific value & cannot adapt.

Answer 8

In cerebellar damage, we see impaired adaptability to changes in the LOAD or ENVIRONMENT (e.g. to internal vs external forces). This results in a bias toward the INTERNAL model representation of limb dynamics; or, the model is “fixed” at a specific value & cannot adapt.

Question 9

In cerebellar damage, we see impaired precision, which results in an [increase / decrease ] in dysmetria most notable with [single / multi] joint movemoents. These individuals [can / cannot ] use feedback (e.g. _____) to compensate, but this results in [slowed / fast ] movement.

Answer 9

In cerebellar damage, we see impaired precision, which results in an INCREASE in dysmetria most notable with MULTI joint movements. These individuals CAN use feedback (e.g. VISION ) to compensate, but this results in SLOW movement.

Question 10

Clinical features of Cb lesions include [incr/ decr] sway in quiet standing, [gait feature?],, impaired _____ (list ‘em!) eye movements, decreased ____, impaired [explicit/implicit] learning from errors & need to rely on [explicit /implicit] info, and learning/relearning balance/gait activities [is impossible / is faster / takes longer ]

Answer 10

Clinical features of Cb lesions include INCREASED SWAY in quiet standing, GAIT ATAXIA, impaired VORc, SACCADES, SMOOTH PURSUIT, VOR (which can result in dizziness, varied foot placement, less able to use visual feedback even though the Cb lesion makes you more reliant on visual feedback), decreased ADAPTABILITY (may take longer to learn balance or walk under different situations!), impaired IMPLICIT learning from errors & need to rely on EXPLICIT info (i.e. will need to think about movement, use more cognition & attention), and learning/relearning balance/gait activities TAKES LONGER.

Question 11

What is the impact of Cb dysfunction on proprioception? Are proprioceptive tests intact or impaired w/Cb lesions?

Answer 11

With a pure Cb lesion, classic proprioceptive tests should be INTACT…
BUT…a Cb lesion impairs proprioception with active, self-driven movements, which we cannot clinically test. Pt may have impaired perception of active movement outcomes.

Question 12

Impact of Cb lesion on endurance?

Answer 12

Cb lesion = pts move SLOWLY and INEFFICENTLY - they have to think about how they move! Impaired endurance can make this worse. 6MWT, monitor RPE & HDR can be helpful!

Question 13

Gait ataxia is most associated with impaired ____ NOT impaired _____.

Cerebellar lesion + balance deficits -> [gait ataxia / few gait abnormalities ]

Cerebellar lesion + LE coordination deficits but NO balance deficits -> [gait ataxia / few gait abnormalities]

Answer 13

Gait ataxia is most associated with impaired BALANCE NOT impaired LIMB COORDINATION.

Cerebellar lesion + balance deficits -> GAIT ATAXIA

Cerebellar lesion + LE coordination deficits but NO balance deficits -> FEW GAIT ABNORMALITIES!

Question 14

Anterior cerebellar lesion typically results in [low/high] velocity, [low/high] amplitude sway and [does / does not] improve with visual input.

Vestibulocerebellar lesion typically results in [low/high] frequency, [low/high] amplitude sway and [does / does not] improve with visual input.

Answer 14

Anterior cerebellar lesion typically results in HIGH velocity, LOW amplitude sway and DOES improve with visual input.

Vestibulocerebellar lesion typically results in LOW frequency, HIGH amplitude sway and DOES NOT improve with visual input - high fall risk!

Question 15

What factors contribute to increased postural sway in Cb dysfunction?

Answer 15

Increased sway due to…

• Faulty muscle scaling: hypermetric balance responses
• Exaggerated and prolonged muscle activity
• Tend to “overshoot” the initial response to an external perturbation

Question 16

CN I
Component
Function
Attachment to CNS
Cranial exit
Testing?

Answer 16

CN I - Olfactory Nerve
SENSORY
Smell (olfaction)
Attaches to CNS via telencephalon (cerebrum)
Exits cranium via the CRIBIFORM PLATE of the ETHMOID bone (fracture here w/facial trauma may injure it)
Testing = assess smell (loss of olfactory fibers & decreased smell/taste is common in older adults)

Question 17

CN II
Component
Function
Attachment to CNS
Cranial exit
Injury mechanism?
Testing?

Answer 17

CN II - Optic Nerve
SENSORY
VIsion
Attaches to CNS via diencephalon via optic chiasm
Exits cranium via the OPTIC CANAL of the SPHENOID BONE
Injury may occur via tumor (e.g. pituitary tumor) aneurysm (often internal carotid), edema, ischemia, inflammation, demyelnation, facial trauma
Test w/visual acuity: Snellen eye chart, book page, test 1 eye at a time, ?corrective lenses; confrontation/fields; color vision; fundus/optic discs

Question 18

Testing for CN II

Answer 18

• Visual acuity (snellen, Book)
• Visual fields w/confrontation
• Test color vision/color matching
  Test fundus (w/fundascope) & optic disc

Question 19

CN II - why is it unique?
Central of peripheral?
Myelin sheath is formed by [oligodendrocytes / Schwann cells]
It [is / is not] susceptible to demyelinating effects of conditions such as MS.
Fibers [stay on 1 side / decussate and cross to other side]

Answer 19

Central!!! It’s the only central cranial nerve!
Myelin sheath is formed by OLIGODENDROCYTES
It IS susceptible to demyelinating effects of conditions such as MS.
Fibers DECUSSATE - half of fibers remain ipsilateral & other half go contralateral. Specific signs of CN II damage depend on on where in the tract there is damage (think optic tract pathways)

Question 20

CN III
Component
Function

Answer 20

CN III - OCULOMOTOR
Somatic & visceral MOTOR
Somatic motor: to levator palpabrae superioris (raises eyelid)
Sup/med/inf rectus muscles
Visceral motor: constricts pupil via sphincter mm (efferent response) & accommodates eye (ciliary muscle)

Question 21

Pupillary light reflex tests the sensory component ([afferent / efferent]) which is carried by CN ___, as well as the motor component ([afferent/efferent]) which is carried by CN ___.

Answer 21

Pupillary light reflex tests the sensory component (AFFERENT) which is carried by CN II (optic), as well as the motor component EFFERENT which is carried by CN III (oculomotor).

Question 22

CN III
Attachment to CNS?
Cranial exit?
Mechanism of injury?

Answer 22

CN III - oculomotor
Attachment to CNS? MIDBRAIN
Cranial exit? SUPERIOR ORBITAL FISSURE of SPHENOID BONE
Mechanism of injury?
- trauma, tumor, infection, aneurysm increased ICP

Question 23

Which CNs exit the cranium through the superior orbital fissure of the sphenoid bone?

Answer 23

CNs that exit the cranium through the superior orbital fissure of the sphenoid bone:

• CN III (oculomotor)
• CN IV (trochlear)
• CN V1 (trigeminal)
• CN VI (abducens)

Question 24

How do you assess CN III?

Answer 24

CN III testing

• Look at symmetry of eye opening (is there ptosis?)
• Pupillary response to light (the motor component is carried by CN III) - both direct response, and consensual response on contralateral eyeball (involves CN II too); could be sluggish or absent, loss of consensual response on opposite response
• Pupil size & shape (mydriasis = blown pupil or enlarged vs other side)
• Test accommodation by focusing from far to near vision
• Visual tracking, look at EOMs
• Pt may endorse diplopia - commonly affected in PD due to impaired coordination between the two eyes, not necessarily a CN III problem

Question 25

What is mydriasis? If it is present, what does it indicate?

Answer 25

Mydriasis = blown pupil or enlarged vs other side. | Indicates CN III impairment

Question 26

``` CN IV Component Function Attachment to CNS? Cranial exit? Mechanism of injury? ```

Answer 26

CN IV - Trochlear Component - somatic motor Function - innervates superior oblique muscle to move eye inferoLATERALLY Attachment to CNS? via midbrain Cranial exit? superior orbital fissure of sphenoid bone Mechanism of injury? Trauma, infection, or tumor

Question 27

CN IV - how to test? Findings?

Answer 27

Testing: "visually track an object that is moved "down and in" Abnormal = unable to look inferomedially (though the sup oblique makes the eye look down & OUT, testing with down & IN better isolates superior oblique action from the other extraocular muscles!) May see upward drift of affected eye as pt looks down (e.g. to try to read) Pt may report visual disturbance with reading or walking down stairs Head will often tilt AWAY from involved eye

Question 28

Talk me through the superior oblique muscle! Action? How to test? What on earth is a trochlea?

Answer 28

CN IV - trochlear nerve, innervates superior oblique Action: moves eye inferoLATERALLY Test: have pt look inferoMEDIALLY (to isolate it from other extraocular muscles) If impaired, may see difficulty looking down, eye may drift up w/attempts to look down Trochlea = a pulley, which changes the direction of pull!

Question 29

CN V V1 = ___ n. (sensory/motor/both) V2 = ___ n. (s/m/b) V3 = ___ n. (s/m/b)

Answer 29

CN V: Trigeminal V1 = Opthalmic nerve (sensory) V2 = Maxillary nerve (sensory) V3 = Mandibular nerve (mixed sensory & motor)

Question 30

``` CN V1 Component Attachment to CNS Cranial Exit Injury mechanism ```

Answer 30

CN V1: Opthalmic nerve Component: general sensoryt o membranes of face, nose, and conjunctiva Attachment to CNS via PONS Cranial Exit: superior orbital fissure of sphenoid bone Injury mechanism: facial trauma, tumor, aneurysm

Question 31

How do you test CN V - V1/opthalmic nerve? - V2/maxillary nerve? - V3/mandibular nerve?

Answer 31

CN V1 /Trigeminal - V1/Opthalmic is tested via... - -> Sensation (sharp/dull or light touch) to skin of the front of the head & nose (terminates in supraorbital nerve) - -> Corneal reflex - V2/Maxillary: sensation to skin of upper jaw (terminates in infraorbital nerve) - V3/Mandibular: sensation to skin of lower jaw; activation of mm of mastication; jaw jerk reflex (terminates in mental nerve)

Question 32

``` CN V2 Component Attachment to CNS Cranial Exit Injury mechanism ```

Answer 32

CN V2: Trigeminal Nerve/Maxillary nerve Component: general sensory to skin & mucous membranes of upper jaw & maxillary teeth Attachment to CNS: via midbrain Cranial Exit: foramen rotundum of sphenoid bone Injury mechanism: facial trauma, tumor, infection, aneurysm

Question 33

``` CN V3 Component Attachment to CNS Cranial Exit Injury mechanism ```

Answer 33

CN V3: Trigeminal Nerve/Mandibular Nerve Component: 2 parts: - General sensory to lower face, mandibular teeth, and tongue - Special visceral motor (branchial motor) to all muscles of mastication, mylohyoid, anterior belly of digastric mm, tensor veli palatini (in palate), tensor tympani (in auditory canal) Attachment to CNS via PONS Cranial Exit: foramen ovale of sphenoid bone Injury mechanism: facial trauma, tumor, infection, anerysm

Question 34

Clinical findings for CN V dysfunction?

Answer 34

CN V Trigeminal dysfunction = - Weakness/paralysis of muscles of mastication w/deviation TOWARD side of lesion (V3) - Loss of sensation to face (V1,2,3) - Los of corneal reflex (V1)

Question 35

Common causes of trigeminal nerve pathology

Answer 35

Common causes of trigeminal nerve pathology - Dental trauma - Herpes zoster - Cranial trauma - Tumors Idiopathic trigeminal neuropathy - Trigeminal neuralgia (aka Tic Douloureaux) - most commonly V2>V3>v1 distribution, cause unknown but maybe related to blood vessel or other pathology of trigeminal ganglia

Question 36

``` CN VI Component Function Attachment to CNS Cranial exit Mechanism of injury? Testing/Findings? ```

Answer 36

CN VI: Abducens Nerve Component: Somatic motor Function: Movement of eye via lateral rectus muscle Attachment to CNS: junction of pons & medulla Cranial exit: superior orbital fissure of sphenoid bone Mechanism of injury? Trauma Testing: visually track laterally Abnormal = diplopia w/far vision, unable to move eye laterally (lateral rectus palsy)

Question 37

CN VII Component Function

Answer 37

CN VII: Facial Component: Special visceral motor (branchial motor), special sensory, visceral motor Function: - Sensory: taste to anterior 2/3 of tongue & palate - Special Visceral Motor/Branchial Motor: muscles of facial expression & scalp, stylohyoid muscle, posterior belly of digastric mm, stapedius muscle - Visceral motor: lacrimal, submandibular, sublingual glands, glands of nose & palate (parasympathetic)

Question 38

``` CN VII Attachment to CNS Cranial exit Mechanism of injury? Testing/Findings? ```

Answer 38

CN VII: Facial Attachment to CNS: pons & medulla Cranial exit: a LONG course! via internal acoustic meatus of temporal bone, through facial canal of temporal bone, and ultimately out through the stylomastoid foramen of the temporal bone Mechanism of injury? trauma, inflamlmation, infection Testing/Findings? Ask pt to contract mm of facial expression, watch for symmetry (cheek puff, wrinkle forehead, close eyes, purse lips)

Question 39

CN ___ is the most commonly paralyzed motor cranial nerve! It takes up ~80% of the cross sectional area of the ___ canal, which is why it's susceptible in ___ palsy.

Answer 39

CN VII (FACIAL) is the most commonly paralyzed motor cranial nerve! It takes up to ~80% of the cross sectional area of the FACIAL canal, which is why it's susceptible in BELL'S palsy.

Question 40

Unilateral facial weakness/paralysis is commonly seen in ___ palsy. It indicates a(n) [LMN / UMN ] lesion if ipsilateral to the lesioned side, vs [LMN / UMN] lesion if contralateral to the lesioned side.

Answer 40

Unilateral facial weakness/paralysis is commonly seen in BELL'S palsy. It indicates a(n) LMN lesion if ipsilateral to the lesioned side, vs UMN lesion (e.g. CVA) if contralateral to the lesioned side (often see forehead sparing in UMN lesion due to bilateral innervation, vs no forehead sparing in LMN dz!).

Question 41

Bilateral facial weakness/paralysis is seen in ___, ____, or ___ (diseases/diagnoses).

Answer 41

Bilateral facial weakness/paralysis is seen in GUILLAIN-BARRE, MYASTHENIA GRAVIS, or LYME DZ (diseases/diagnoses).

Question 42

Abnormal findings with CN VII Facial nerve

Answer 42

- Weakness/paralysis of facial mm - Loss/excessive salvation or lacrimation (less common w/LMN injury) - Loss of taste from anterior 2/3 of tongue (less common w/LMN injury) - Difficult speech, drooling - Sensitivity to low frequency sound (stapedius muscle)

Question 43

``` CN VIII Component Function Cranial Exit CNS attachment Injury mechanism ```

Answer 43

CN VIII: Vestibulocochlear Nerve Special Sensory Vestibular division: vestibular sensation from semicircular canals, utricle, & saccule Cochlear division: special sense of hearing from spiral organ Cranial Exit: internal acoustic meatus of temporal bone CNS attachment at junction fo pons/medulla Injured w/trauma, tumor (e.g. acoustic neuroma)

Question 44

How to test for CN VIII dysfunction?

Answer 44

Test CN VIII via tests for conduction vs sensorineural hearing loss with Rinne and Weber test Also via: - Finger rub, whispered speech, watch tick, self-report

Question 45

The Rinne test assesses [conduction / sensorineural ] hearing loss. A high pitched tuning fork is placed on the ____, then once pt can no longer hear it, the still-vibrating tuning fork is placed next to the ear to test for ____. You should still be able to hear it through the air!

Answer 45

The Rinne test assesses CONDUCTION hearing loss. A high pitched tuning fork is placed on the MASTOID PROCESS, then once pt can no longer hear it, the still-vibrating tuning fork is placed next to the ear to test for AIR CONDUCTION. You should still be able to hear it through the air!

Question 46

The Weber test assesses [conduction / sensorineural ] hearing loss. A high pitched tuning fork is placed on the ____. You should be able to hear it equally through both ears!

Answer 46

The Weber test assesses SENSORINEURAL hearing loss. A high pitched tuning fork is placed on the TOP OF THE SKULL equidistant from both ears. You should be able to hear it equally through both ears! (vs pt may say one side sounds louder, which would be abnormal)

Question 47

Abnormal CN VIII findings include...

Answer 47

Tinnitus Abnormal findings on Rinne and Weber tests - warrant referral to a specialist Vestibular findings (observation of nystagmus, observation or reports of LOB or vertigo)

Question 48

``` CN IX Component Function Attachment to CNS Cranial Exit ```

Answer 48

CN IX: Glossopharyngela neve Special visceral Motor /Branchial MOTOR to stylopharyngeus muscle for swallowing Visceral MOTOR to parasympathetic to parotid gland Visceral SENSATION to parotid gland, carotid body/sinus, pharynx, middle ear Special SENSORY: taste to posteior 1/3 of tongue General SENSORY: cutaneous sensation to external ear CNS attachment via medulla Cranial exit via jugular foramen of temporal & occipital bones

Question 49

CN IX Mechanism of injury Of note, isolated CN IX lesions are [common / rare]

Answer 49

CN IX: Glossopharyngeal Mechanism of injury: it has a large extracranial position which is susceptible to trauma (fractures, stab or gunshot wounds), also via tumor Of note, isolated CN IX lesions are RARE

Question 50

CN IX testing

Answer 50

Test CN IX (glossopharyngeal) via taste to the posterior 1/3 of tongue, use tongue depressor to assess position of uvula & gag reflex, assess swallowing

Question 51

Abnormal CN IX findings include...

Answer 51

Loss of taste to posterior 1/3 of tongue Loss of sensation on affected side of soft palate Diminished gag/swallow reflex on affected side Glossopharyngeal neuralgia: often associated w/swallowing & you see in pain in back of throat, tongue, or ear

Question 52

CN ___, ___, and ___ are commonly involved together in a condition known as jugular foramen syndrome due to a ____.

Answer 52

CN IX, X, and XI are commonly involved together in a condition known as jugular foramen syndrome due to a TUMOR (or other space-occupying lesion).

Question 53

CN X | Component & Function

Answer 53

CN X: Vagus Visceral sensation: base of tongue, pharynx, larynx, trachea, bronchi, heart, esophagus, stomach, intestine to left colic flexure Visceral motor: parasympathetics to smooth muscle fo trachea, bronchi, digestive tract, cardiac muscle Branchial motor: motor to constrictor muscles of pharynx (excluding stylopharyngeus) for swallowing Special sensory: taste from epiglottis & palate Cutaneous sensory: auricle, external acoustic meatus, dura mater of posterior cranial fossa

Question 54

CN X Attachment to CNS Cranial Exit

Answer 54

CN X: Vagus nerve Attachment to CNS via medulla Cranial Exit via jugular foramen of temporal & occipital bones

Question 55

CN X | Mechanism of Injury

Answer 55

CN X Mechanism of Injury: has a large extracranial position, susceptible to trauma (fractures, stab or gunshot wounds, neck surgery) or tumor

Question 56

CN X Testing & abnormal findings Isolated CN X lesions are [rare / common ]

Answer 56

CN IX & X are commonly tested together due to similar functions Additional abnormal findings include loss of gag reflex, dysphagia, hoarseness Isolated CN X lesions are RARE - seen more in conjunction w/ CN IX, X, and XI in jugular foramen syndrome

Question 57

``` CN XI Component Function CNS attachment Cranial Exit Mechanism of Injury ```

Answer 57

CN XI: Spinal accessory nerve Somatic motor: sternocleidomastoid and trapezius CNS attachment: cranial root via the medulla, spinal root via the superior spinal cord Cranial Exit: via the jugular foramen of the temporal and occipital bones Mechanism of Injury: has a large subcutaneous extracranial position, susceptible to trauma (fractures, stab or gunshot wounds) or tumor

Question 58

CN XI testing

Answer 58

MMT to sternocleidomastoid and trapezius muscles Commonly involved al ongside CN IX, X, and XI in condition known as jugular foramen syndrome (tumor)

Question 59

``` CN XII Function/component CNS attachment Cranial Exit Mechanism of Injury Testing ```

Answer 59

CN XII: Hypoglossal Somatic motor: tongue muscles Cranial exit via hypoglossal canal MOI: least common CN injury from head trauma! Most common MOI is neck surgery Testing: protrude & retract tongue, look for deviations; observe for dysphagia, dysarthria, chewing difficulties

Question 60

Abnormal CN XII findings

Answer 60

Tongue deviation TOWARD the AFFECTED SIDE on protrusion

Question 61

Purely sensory CNs include...

Answer 61

SENSORY only: - CN I/olfactory - CN II/optic - CN VIII/vestibulocochlear

Question 62

Purely motor CNs include...

Answer 62

MOTOR only: - CN III/oculomotor - CN IV/trochlear - CN VI/abducens - CN XI/spinal accessory nerve - CN XII/hypoglossal

Question 63

Mixed sensory and motor CNs include...

Answer 63

MIXED sensory & motor CNs: - CN V/trigeminal - CN VII/facial - CN IX/glossopharyngeal - CN X/vagus

Question 64

``` Spinal nerves... [X] pairs, which include... [X] cervical [X] thoracic [X] lumbar [X] sacral [X] coccygeal ``` They are [sensory / motor / mixed]

Answer 64

``` Spinal nerves... [31] pairs, which include... [8] cervical (but recall, only 7 cervical vertibrae!) [12] thoracic [5] lumbar [5] sacral [1] coccygeal ``` They can be sensory, motor, or mixed!

Question 65

In upper cervical spine, spinal nerve exits [above/below] vertibrae, then from ___ and down, it exits [above/below] corresponding vertibrae

Answer 65

In upper cervical spine, spinal nerve exits ABOVE vertebrae, then from C8 and down, it exits BELOW corresponding vertebrae (C8 exits below C7, then T1 below T1 vertebra, etc)

Question 66

Entering the spinal cord, the dorsal ___ and the dorsal ___ ____ carry [SENSORY / MOTOR] information into the dorsal horn of [gray/white] matter of the spinal cord. The ventral ___ emerges from the ventral ___ of the spinal cord and carries [SENSORY / MOTOR] information out to the periphery. The ventral and dorsal ___s combine to create the ____. Leaving the spinal cord, the spinal nerve splits into the dorsal and ventral ___.

Answer 66

Entering the spinal cord, the dorsal ROOT and the dorsal ROOT GANGLION carry SENSORY information into the dorsal horn of GRAY matter of the spinal cord. The ventral ROOT emerges from the ventral HORN of the spinal cord and carries MOTOR information out to the periphery. The ventral and dorsal ROOTS combine to create the SPINAL NERVE. Leaving the spinal cord, the spinal nerve splits into the dorsal and ventral RAMUS.

Question 67

The spinal nerve is a [one-way / two-way] nerve. [Efferent / afferent / both efferent and afferent ] signals travel through the spinal nerve.

Answer 67

The spinal nerve is a TWO WAY nerve. BOTH EFFERENT & AFFERENT signals travel through the spinal nerve.

Question 68

The dorsal ramus is a [one-way / two-way] nerve, carrying [efferent / afferent / both efferent and afferent ] signals. Describe what (if any) sensory/motor information it carries.

Answer 68

The dorsal ramus is a TWO-WAY nerve, carrying both EFFERENT & AFFERENT (sensory & motor) signals, including: - Motor information to the muscles of the deep back - Sensory information from the skin of the back

Question 69

The ventral ramus is a [one-way / two-way] nerve, carrying [efferent / afferent / both efferent and afferent ] signals. Describe what (if any) sensory/motor information it carries.

Answer 69

The ventral ramus is a TWO-WAY nerve, carrying both EFFERENT & AFFERENT (sensory & motor) signals, including: - Motor information to the muscles of the anterior thorax & extremities - Sensory information from the skin of the anterior thorax & extremities

Question 70

Peripheral nerve connective tissue coverings are extensions of the spinal meninges. The ___ is an extension of the dura mater that surrounds the entire nerve trunk. The ____ is an extension of the arachnoid that wraps bundles of fibers into fascicles. The ___ surrounds each individual axon.

Answer 70

Peripheral nerve connective tissue coverings are extensions of the spinal meninges. The EPINEURIUM is an extension of the dura mater that surrounds the entire nerve trunk. The PERINEURIUM (inside of the nerve!) is an extension of the arachnoid that wraps bundles of fibers into fascicles. The ENDONEURIUM surrounds each individual axon.

Question 71

In myelinated peripheral nerve fibers, ___ cells are located between the [nerve connective tissue layer] and the membrane of the axon (aka the ___).

Answer 71

In myelinated peripheral nerve fibers, SCHWANN cells are located between the ENDONEURIUM and the membrane of the axon (aka the AXOLEMMA).

Question 72

Are peripheral nerves vascularized?

Answer 72

Yes! Each peripheral nerve receives an artery that penetrates THROUGH EACH connective tissue layer to give rich vascular supply

Question 73

In peripheral nerves, the motor neuron cell bodies are located in the ___. The sensory neuron cell bodies are located in the ___. The autonomic neuron cell bodies are located in the ___, ___, and ___.

Answer 73

In peripheral nerves, the motor neuron cell bodies are located in the VENTRAL HORN OF THE SPINAL CORD. The sensory neuron cell bodies are located in the PERIPHERAL/DORSAL ROOT GANGLIA. The autonomic neuron cell bodies are located in the BRAINSTEM, SPINAL CORD, and PERIPHERAL GANGLIA.

Question 74

Myelination significantly increases conduction velocity through ____ conduction of ___ at the ____. Thicker myelinated fibers conduct [faster / slower]. These are involved in [sensation type?] and serve [muscle type?] Thinner myelinated fibers conduct [faster/ slower] and transmit signals for [sensory type?] as well as [muscle type?]

Answer 74

Myelination significantly increases conduction velocity through SALTATORY conduction of ACTION POTENTIALS at the NODES OF RANVIER. Thicker myelinated fibers conduct FASTER. These are involved in PROPRIOCEPTIVE SENSE (e.g. to muscle spindle & golgi tendon organ) and serve SKELETAL MUSCLE FIBERS (via alpha motor neurons) Thinner myelinated fibers conduct SLOWER and transmit signals for PAIN, TEMPERATURE, AND TOUCH as well as AUTONOMIC SIGNALS TO AND FROM THE GANGLIA TO SMOOTH MUSCLE

Question 75

Age related changes to PNS - Perineurium and epineurium [thin / thicken ] - Endoneurium gets ___ with increased ___ content - Overall [increased / decreased ] number of [myelinated / unmyelinated / both] fibers - [Ventral (motor) / dorsal (sensory) ] root fibers are more affected. - We see generalized deterioration of the ___

Answer 75

- Perineurium and epineurium THIN - Endoneurium gets FIBROTIC with increased COLLAGEN content - Overall DECREASED number of BOTH myelinated and unmyelinated fibers - VENTRAL (MOTOR) root fibers are more affected than dorsal (sensory) root fibers. - We see generalized deterioration of the MYELIN SHEATH (likely r/t decreased protein synthesis as we age)

Question 76

Age related changes to PNS (continued) - ___ may occlude vessels supplying nerves, leading to a loss of ___ and development of ___ - Dysfunction of the ___ nervous system, including decline of sympathetic control of ___ , which leads to decreased ___ healing - Decreased ___ synthesis leads to deterioration of ___ with shorter internode distances, leading to decreased nerve conduction velocity

Answer 76

Age related changes to PNS (continued) - ATHEROSCLEROTIC PLAQUES may occlude vessels supplying nerves, leading to a loss of NERVE FIBERS and development of PERIPHERAL NEUROPATHIES - Dysfunction of the AUTONOMIC nervous system, including decline of sympathetic control of DERMAL VASCULATURE (leads to decreased WOUND healing) - Decreased PROTEIN synthesis leads to deterioration of MYELIN with shorter internode distances, leading to decreased nerve conduction velocity

Question 77

Peripheral nerve injuries can be the result of ___, ___, or ___ injuries. From least involved to most involved (based on what structures are affected), we call these ___, then ___, then ___.

Answer 77

Peripheral nerve injuries can be the result of ISCHEMIA, COMPRESSION, or STRETCH (ie traction) injuries; transection can also occur. From least involved to most involved (based on what structures are affected), we call these NEURAPRAXIAS, then AXONOTMESIS, then NEUROTMESIS.

Question 78

Neurapraxia involves segmental ___. It is the [mildest / most severe] type of nerve injury and involves a [permanent /transient ] conduction block usually as a result of [ischemia / compression / stretch ]. It slows or blocks the action potential, and connective tissue coverings of the nerve [remain intact / are severed]. When this occurs in the setting of disease (e.g. MS), we call this a ___. Muscle typically [atrophies / does not atrophy] because action potentials are normally above and below the site of injury. Schwann cells can become ____ active to repair. We [ do / do not] see axonal/Wallerian degeneration. Prognosis/timing?

Answer 78

Neurapraxia involves segmental DEMYELINATION. It is the MILDEST type of nerve injury and involves a TRANSIENT conduction block usually as a result of COMPRESSION. It slows or blocks the action potential, and connective tissue coverings of the nerve REMAIN INTACT. When this occurs in the setting of disease (e.g. MS), we call this a MYELINOPATHY. Muscle typically DOES NOT ATROPHY because action potentials are normally above and below the site of injury. Schwann cells can become MITOTICALLY active to repair. We DO NOT see axonal/Wallerian degeneration. Prognosis is GOOD! Expect a GRADUAL & FULL RECOVERY of symptoms in DAYS to WEEKS.

Question 79

Axontomesis involves ____ degeneration. The ___ is damaged but __ ___ coverings remain intact. This most commonly occurs as a result of [compression / stretch / ischemia ], such as ____, but can also happen as a result of __ or ___ type injuries. It leads to ___ and ___. You get degeneration distal to site of the injury where the ___ breaks down, which is known as ____ ___ and begins with in ___ hours/days post-injury. Repair is [impossible / possible] as long as the ___ ___ ___ is intact. New axons sprout from damaged ___, but the [proximal / distal / proximal and distal ] end(s) of the ____ ___ ___ MUST be intact for healing to take place. Prognostically, we expect healing over the course of [days/ weeks/ months/ years] [without / with possibility of / with definite] residual deficits.

Answer 79

Axontomesis involves AXONAL degeneration. The AXON is damaged but CONNECTIVE TISSUE coverings remain intact. Most common via COMPRESSION, (e.g. CARPAL TUNNEL), but can also happen as a result of STRETCH or BLUNT TRAUMA type injuries. It leads to INFARCTION AND NECROSIS. You get degeneration distal to site of the injury where the AXON breaks down, known as WALLERIAN DEGENERATION and begins within 12 HOURS post-injury. Repair is POSSIBLE as long as the NERVE CELL BODY is intact. New axons sprout from damaged AXON, but PROXIMAL AND DISTAL ends of NEURAL TISSUE TUBE must be intact for healing to take place. Can also happen in stretch or blunt trauma type injuries. Prognostically, we expect healing over the course of WEEKS TO MONTHS WITH THE POSSIBILITY OF residual deficits.

Question 80

Neurotmesis is most severe ___ loss, involving complete severance of the ___ and disruption of one to all of the three ___ ___ coverings. This is common in [compression / stretch / ischemia / trauma], such as ____, ____, and ___-type injuries. Axonal continuity is [maintained / lost], resulting in ___ ____ distal to the site of injury. Muscle fibers innervated by the axon [remain intact / atrophy slowly / atrophy rapidly], which is a process known as ___ ___, with irreversible damage after [X timeframe]. Recovery [involves spontaneous reattachment of / generally requires surgical intervention to reattach ] the proximal & distal ends of the ____, otherwise a ___ will often form. Once the axon has distal contact with the ___ or __ ___, _____ can then begin. Repair process begins with sprouting of a new ___ ___ as new ____ is synthesized. ____ degrade waste tissues, facilitating axonal entry into tissue. ___ and ___ cues guide ___ through the [epineurium / perineurium / endoneurium]. Growth rate is typically ____/day or ___/month. Residual deficits are [uncommon / likely / definite].

Answer 80

Neurotmesis is most severe AXONAL loss, involving complete severance of the AXON and disruption of 1, 2, or all 3 of the CONNECTIVE TISSUE coverings. This is common in TRAUMA such as GUNSHOT, STAB WOUNDS, and AVULSION-TYPE injuries. Axonal continuity is LOST, resulting in WALLERIAN DEGENERATION distal to the site of injury. Muscle fibers innervated by the axon atrophy RAPIDLY, a process known as DENERVATION ATROPHY, after 2 YEARS, those muscle fibers actually undergo irreversible damage. Recovery generally requires SURGERY to reattach the proximal & distal ends of the ENDONEURIUM, otherwise a NEUROMA will often form. Once the axon has distal contact with the MUSCLE or SENSORY RECEPTOR, MYELINATION can then begin. Repair process begins with sprouting of a new GROWTH CONE as new CYTOPLASM is synthesized. PROTEASES degrade waste tissues, facilitating axonal entry into tissue. CHEMICAL and TACTILE cues guide filopodia through ENDONEURIUM. Growth rate is typically 1mm/day or 1"/month. Residual deficits are LIKELY.

Question 81

Clinical manifestations of peripheral nerve injuries follow those typical of [UMN/LMN] injuries: - [flaccid paralysis / spasticity ] of muscles distal to the site of the lesion. - Rapid ____ of involved musculature - [preservation / loss of ] sensory function distal to the site of the lesion.

Answer 81

Clinical manifestations of peripheral nerve injuries follow those typical of LMN injuries: - FLACCID PARALYSIS of muscles distal to the site of the lesion. - Rapid ATROPHY of involved musculature - LOSS OF sensory function distal to the site of the lesion.

Question 82

Neurapraxia (1st degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.

Answer 82

Neurapraxia (1st degree): involves ONLY Myelin. Associated with MINOR COMPRESSION injury. There is a conduction BLOCKAGE (though not conduction failure). We see PROFOUND motor loss lasting days to weeks, but no muscle wasting. Normal to minimal sensory involvement.

Question 83

Axonotmesis (2nd degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.

Answer 83

Axonotmesis (2nd degree) involves the myelin AND axon. Associated with SEVERE COMPRESSION/crush injury. There is a conduction FAILURE. We see COMPLETE motor loss and NO or PARTIAL sensory loss.

Question 84

Neurotmesis (3rd degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.

Answer 84

Neurotmesis 3rd degree involves the MYELIN, AXON, and ENDONEURIUM. Associated with TRANSECTION, LACERATION, or CHEMICAL injury. There is a conduction FAILURE. We see COMPLETE motor loss and COMPLETE sensory loss.

Question 85

Neurotmesis (4th degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.

Answer 85

Neurotmesis 4th degree involves the MYELIN, AXON, ENDONEURIUM, and PERINEURIUM. Associated with TRANSECTION, LACERATION, or CHEMICAL injury. There is a conduction FAILURE. We see COMPLETE motor loss and COMPLETE sensory loss.

Question 86

Neurotmesis (5th degree): involves what structures? Typical etiology/injury type? There is a conduction [ blockage/ failure]. We see [complete / partial / no] motor loss and [complete / partial / no] sensory loss.

Answer 86

Neurotmesis 4th degree involves the MYELIN, AXON, ENDONEURIUM, PERINEURIUM, and EPINEURIUM (all the layers). Associated with TRANSECTION, LACERATION, or CHEMICAL injury. There is a conduction FAILURE. We see COMPLETE motor loss and COMPLETE sensory loss.

Question 87

Prevalence of peripheral neuropathy is estimated at ___% in the general population and ___% in those over 55 years of age. There [is only one etiology /are multiple etiologies ] which present with a [consistent/ varied] clinical picture. If you see [acute / chronic] onset, [slow / rapid ] progression, and [mild / moderate / severe ] disability, you need to refer to a specialist.

Answer 87

Prevalence of peripheral neuropathy is estimated at 2.5% in the general population and 8% in those over 55 years of age. There ARE MULTIPLE ETIOLOGIES which present with a VARIED clinical picture. If you see ACUTE onset, RAPID progression, and SEVERE disability, you need to refer to a specialist.

Question 88

Prevalence of peripheral neuropathy is estimated at ___% in the general population and ___% in those over 55 years of age. There [is only one etiology /are multiple etiologies ] which present with a [consistent/ varied] clinical picture. If you see [acute / chronic] onset, [slow / rapid ] progression, and [mild / moderate / severe ] disability, you need to refer to a specialist given concern for something like ____.

Answer 88

Prevalence of peripheral neuropathy is estimated at 2.5% in the general population and 8% in those over 55 years of age. There ARE MULTIPLE ETIOLOGIES which present with a VARIED clinical picture. If you see ACUTE onset, RAPID progression, and SEVERE disability, you need to refer to a specialist given concern for something like GUILLAN BARRE SYNDROME, which is a medical emergency given risk for respiratory failure.

Question 89

PNS disorders are classified into two categories: neuropathies involve a pathological condition confined to the ___, whereas myopathies involve a pathological condition confined to the ___.

Answer 89

PNS disorders are classified into two categories: neuropathies involve a pathological condition confined to the NERVE, whereas myopathies involve a pathological condition confined to the MUSCLE.

Question 90

Peripheral nerves can be impaired at varied sites. For motor nerves? (4) For sensory nerves? (3)

Answer 90

Peripheral nerves can be impaired at varied sites. For motor nerves? Motor neuron cell body, axon motor end plate, and muscle fiber For sensory nerves? Cell body in the DRG, axon, and sensory receptor

Question 91

Difference between mononeuropathy vs polyneuropathy?

Answer 91

Mononeuropathy: one peripheral nerve is affected Polyneuropathy: several peripheral nerves are affected

Question 92

Causes of neuropathies

Answer 92

Potential causes of neuropathies: Genetic (e.g. hereditary disorders like Charcot-Marie Tooth) Metabolic/endocrine (e.g. Diabetic neuropathy) toxic exposures (e.g. lead neuropathy) inflammatory (e.g. GBS) Trauma (including repetitive motions (e.g. for carpal tunnel), critical illness) paraneoplastic (i/s/o cancer or chemotherapy) Also could be caused by - Myasthenia gravis (neuromusc dz leading to various levels of skeletal muscle weakness) - Botulism - Vitamin & nutritional deficiencies (Vitamin E and Niacin, which are crucial to nerve health)

Question 93

In peripheral neuropathies, the [shortest / longest] nerves are commonly affected first, leading to [proximal / distal] symptoms initially which then extend [proximally/ distally]. [Sensory / motor ] symptoms usually appear first (though not always!). [Upper / lower] extremity nerves are commonly involved first, leading to dysesthesias and parasthesias in [what parts of the body?]. Onset of motor weakness leads to symptoms of muscle weakness and [hypertonicity /hypotonicity and flaccidity].

Answer 93

In peripheral neuropathies, the LONGEST nerves are commonly affected first, leading to DISTAL symptoms initially which then extend PROXIMALLY. SENSORY symptoms usually appear first (though not always!). LOWER extremity nerves are commonly involved first, leading to dysesthesias and parasthesias in the FEET. Onset of motor weakness leads to symptoms of muscle weakness and HYPOTONICITY / FLACCIDITY (AKA LMN symptoms).

Question 94

Common nerve entrapment syndromes (aka entrapment neuropathies) List in format of nerve / syndrome name. Median n. / ___ or ____ Brachial plexus & subclavian a. / ___ Tibial n. / ___ Ulnar n. / ____ Facial n. (CN VII) / ___

Answer 94

Median n. / CARPAL TUNNEL SYNDROME or PRONATOR TERES SYNDROME Brachial plexus & subclavian a. / THORACIC OUTLET SYNDROME Tibial n. / TARSAL TUNNEL SYNDROME Ulnar n. / TARDY ULNAR PALSY Facial n. (CN VII) / BELL'S PALSY

Question 95

Carpal tunnel syndrome involves entrapment of what nerve?

Answer 95

Carpal tunnel syndrome = | Median n.

Question 96

Pronator teres syndrome involves entrapment of what nerve?

Answer 96

Pronator teres syndrome = Median n.

Question 97

Thoracic outlet syndrome involves entrapment of what nerve and artery?

Answer 97

Thoracic outlet syndrome = Brachial plexus & subclavian a.

Question 98

Tarsal tunnel syndrome involves entrapment of what nerve?

Answer 98

Tarsal tunnel syndrome = Tibial n.

Question 99

Tardy ulnar palsy involves entrapment of what nerve?

Answer 99

Tardy ulnar palsy = Ulnar n.

Question 100

Bell's palsy involves entrapment of what nerve?

Answer 100

Bell's palsy = CN VII Facial nerve

Question 101

Signs and symptoms of nerve entrapment syndrome will dependent on 4 things: (1) ___ (2) ___ (3) ___ (4) ___

Answer 101

Signs and symptoms of nerve entrapment syndrome will dependent on 4 things: (1) the NERVE affected (2) LOCATION of the pathology along the nerve (3) SEVERITY of the compression (4) DURATION of the compression

Question 102

The underlying mechanism of a nerve entrapment syndrome is ___ to the nerve, causing a temporary block of the ___. If compression persists, segmental demyelination (aka a [neuropraxia / axontomesis / neurotomesis ] ) and/or axonal degeneration (aka [neuropraxia / axonotmesis / neurotomesis ] ) can follow.

Answer 102

The underlying mechanism of a nerve entrapment syndrome is ISCHEMIA to the nerve, causing a temporary block of the ACTION POTENTIAL. If compression persists, segmental demyelination (aka a NEUROPRAXIA ) and axonal degeneration (aka AXONOTMESIS) can follow.

Question 103

Charcot-Marie Tooth disease is a hereditary [motor / sensory / both] neuropathy. It is the most commonly inherited disorder of these nerves. It initially involves the ___ nerve followed by the muscles of the ___ and ___. It is [rapidly / slowly] progressive and leads to weakness of the [which muscle group(s)?] and ___ type gait.

Answer 103

Charcot-Marie Tooth disease is a hereditary MOTOR AND SENSORY neuropathy. It is the most commonly inherited disorder of the sensory and motor nerves. It initially involves the PERONEAL nerve followed by the muscles of the FOOT and LEG. It is SLOWLY progressive and leads to weakness of the DORSIFLEXORS AND EVERTORS and STEPPAGE type gait.

Question 104

Charcot-Marie Tooth disease subtypes include: CMT-1: causes mutations in the ____ responsible for ___ in the peripheral nerves. We see extensive demyelination with a ___ ___ "bulb" formation which is palpable. CMT-2: affects the ___ ___ ___ and the ___ of the lumbar levels.

Answer 104

Charcot-Marie Tooth disease subtypes include: CMT-1: causes mutations in the PROTEINS responsible for SCHWANN CELL MYELINATION in the peripheral nerves. We see extensive demyelination with a SCHWANN CELL "bulb" formation which is palpable. CMT-2: affects the ANTERIOR HORN CELLS and the DRG of the lumbar levels.

Question 105

The most common metabolic neuropathy is ___ neuropathy, the severity of which is dictated by ___ control. it involves progressive [nerve / muscle ] fiber loss and atrophy. Neural function deteriorates, causing [central / peripheral] sensory and motor loss. Usually occurs in a [proximal / distal ] [symmetrical / asymmetrical] pattern. It has many subclinical forms which depend on the nerve(s) involve. It can be caused by changes in the ___, altered ___ synthesis, and reduced concentrations of __ ___ ___.

Answer 105

The most common metabolic neuropathy is DIABETIC neuropathy, the severity of which is dictated by GLYCEMIC control (ie severity of diabetes) it involves progressive NERVE fiber loss and atrophy. Neural function deteriorates, causing PERIPHERAL sensory and motor loss. Usually occurs in a DISTAL SYMMETRICAL pattern. It has many subclinical forms which depend on the nerve(s) involve. It occurs because of changes in the VASCULATURE, altered ATP synthesis, and reduced concentrations of NERVE GROWTH FACTOR.

Question 106

Diabetic neuropathy is an important risk factor for ___ breakdown and amputation. Impaired tactile, vibratory, and proprioceptive sense leads to altered ___ patterns, impaired __, and increased risk for ___. It is well-documented that ___ and ___ can benefit glycemic control. Weight bearing exercise can help, based on the ___ ___ ___ which states that Physical stress theory = changes in physical stress causes predictable changes in biological tissues to allow for adaptation (as long as the stress is not too much, which could lead to tissue ___ or __). Important to monitor for ___ and __ in this population.

Answer 106

Diabetic neuropathy is an important risk factor for SKIN breakdown and amputation. Impaired tactile, vibratory, and proprioceptive sense leads to altered GAIT patterns, impaired BALANCE, and increased risk for FALLS. It is well-documented that DIET and EXERCISE can benefit glycemic control. Weight bearing exercise can help, based on the PHYSICAL STRESS THEORY which states that PHYSICAL STRESS causes predictable changes in biological tissues which allow for adaptation (as long as the stress is not too much, which could lead to tissue INJURY or DEATH). Important to monitor SKIN INTEGRITY & DEFORMITIES in this population.

Question 107

Guillan Barre syndrome is an ____ neuropathy characterized by ___ ___ and [hyper / hypo / a]reflexia. It is believed to be an immune-mediated disorder preceded by an infection (e.g. ___, ___ __ virus, ____, or ___ infections). It involves an ____ reaction which causes ___-mediated demyelination. ____ is the go-to safe and effective treatment. Most people will recover, but ___% will have permanent neurological deficits. GBS is considered a medical emergency because of the risk of ___ failure.

Answer 107

Guillan Barre syndrome is an INFLAMMATORY neuropathy characterized by FLACCID PARALYSIS and AREFLEXIA. It is believed to be an immune-mediated disorder preceded by an infection (e.g. INFLUENZA, EPSTEIN BARR virus, CYTOMEGALOVIRUS, or BACTERIAL infections). It involves an AUTOIMMUNE reaction which causes ANTIBODY-mediated demyelination. IMMUNOGLOBULINS are the go-to safe and effective treatment. Most people will recover, but 20% will have permanent neurological deficits. GBS is considered a medical emergency because of the risk of RESPIRATORY failure.

Question 108

Complex regional pain syndrome (AKA ___ ___ ____) can occur following ___% of all injuries. It involves reflex neurogenic ___ and commonly results in [sensory / motor / autonomic] changes. Average age of onset is ___ years. Injury at one somatic level initiates ___ efferent activity that affects [the same / multiple ] segmental levels. Diagnosed based on history & clinical exam. Tends to affect females {< / > / = ] males.

Answer 108

Complex regional pain syndrome (AKA REFLEX SYMPATHETIC DYSTROPHY, CRPS SUBTYPE I) can occur following 5% of all injuries. It involves reflex neurogenic INFLAMMATION and commonly results in SENSORY, MOTOR, AND AUTONOMIC changes. Average age of onset is 30 years. Injury at one somatic level initiates SYMPATHETIC efferent activity that affects MULTIPLE segmental levels. Diagnosed based on history & clinical exam. Often related to surgery or injury. Tends to affect females GREATER THAN males (3:1)

Question 109

Acute CRPS symptoms

Answer 109

Acute CRPS symptoms | Limb is PAINFUL, WARM, RED, EDEMATOUS

Question 110

Later CRPS symptoms

Answer 110

Later CRPS symptoms: Limb is PAINFUL, COLD, PALE,ATROPHIC skin with DYSTONIA and TREMOR being common. Can also see loss of strength or ROM in affected joints.

Question 111

In CRPS, we see a cycle of pain and swelling after an initial injury, which leads to pain information being sent to the ___ for interpretation. ___ ___ convey input to the ____ nervous system neurons which send impulses, triggering ___ . That leads to ___ and increased ___, which starts the cycle again and the cycle perpetuates itself. Clinical evidence of dysfunction [in what part of the brain? ]which correlates with the extent of allodynia in CRPS 1, vs more global changes in the __ in CRPS 2!

Answer 111

In CRPS, we see a cycle of pain and swelling after an initial injury, which leads to pain information being sent to the CNS for interpretation. SPINAL INTERNEURONS convey input to the SYMPATHETIC nervous system neurons which send impulses, triggering VASOSPASM. Vasospasm leads to SWELLING and increased PAIN, which starts the cycle again and the cycle perpetuates itself. Clinical evidence of PARIETAL CORTEX dysfunction which correlates with the extent of allodynia in CRPS 1, vs more global changes in the CORTEX in CRPS 2!

Question 112

Diseases/conditions frequently associated with peripheral neuropathies include: - Common? (4) - Frequently associated with... (5) - Less common? (7)

Answer 112

Diseases/conditions frequently associated with peripheral neuropathies include: - Common? DIABETES (60-70%), AUTOIMMUNE DISORDERS, i/s/o CHEMOTHERAPY, DYSPROTEINEMIC DISORDERS - Frequently associated with... DISC HERNIATION, ARTHRITIS, JOINT DISLOCATIONS, TENDONITIS, OTHER BONE AND SOFT TISSUE CHANGES - Less common? (7) CHRONIC KIDNEY DZ, LIVER INFECTIONS, LOW VIT B12 LEVELS, POOR BLE CIRCULATION, UNDERACTIVE THYROID GLAND, TRAUMA, TUMORR

Question 113

Compression injuries are a type of a peripheral nerve injury, and can result from __, ___, ___, or ___. Excessive compression can result in ___ of the neural tissue.

Answer 113

Compression injuries are a type of a peripheral nerve injury, and can result from ISCHEMIA, FRICTION, SHEARING, or INFLAMMATION. Excessive compression can result in ISCHEMIA of the neural tissue.

Question 114

After nerve damage, describe the regeneration process.

Answer 114

(1) Damage occurs, the axon is separated/severed. (2) Macrophages will dispose of the degenerate axon and myelin sheath. (3) Wallerian degeneration occurs at the distal end (4) Schwann cells and endoneurium support regeneration at the proximal end (5) Connection with the target muscle is lost, leading to muscle atrophy and fibrosis (6) Axonal sprouting occurs (7) As the connected axon matures, function is restored

Question 115

Factors affecting nerve recovery: - Age of patient; [older/younger] is better - Location of injury: better recovery if injury is more [proximal / distal] - [Sharp cuts vs crush injuries] are better - If ____ is preserved - If there is a favorable orientation of the nerve [epi / peri / endo] neurium repair

Answer 115

Factors affecting nerve recovery: - Age of patient (YOUNGER is better) - Location of injury: better recovery if injury is more DISTAL - SHARP CUTS are better than crush injuries - If VASCULARITY is preserved - If there is a favorable orientation of the nerve EPIneurium repair

Question 116

Signs/symptoms of neuropathies include... - Early symptoms: (7) - Progressed symptoms: (9) - Of note, pure autonomic problems are [rare / common]

Answer 116

- Early symptoms of neuropathies include: Pain, numbness, tingling, burning sensations, pins and needles sensation, pricking, stabbing, sensitivity to touch - Progressive symptoms of neuropathies include: Weakness, loss of mm mass, digestive problems, dizziness/balance problems, difficulty walking/moving muscles, decreased skin integrity (i.e. foot ulcers, changes in hair or nails), decreased sweating, loss of DTR, muscle twitching - Of note, pure autonomic problems are RARE (but make sure you screen for orthostasis)

Question 117

Initial lab values with work up / diagnostics of peripheral neuropathies... Secondary/additional labs include... Other tests...

Answer 117

Initial labs: - CBC (looking for infectious cause) - Metabolic panel - ESR (looking for vasculitis) - Fasting blood glucose, HgbA1c (looking for DM) - TSH (looking for thyroid abnormalities) - Vitamin B12 Secondary/additional labs include... - SPEP (serum protein immunofixation electrophoresis - BUN/Cr - CMP (liver/kidney abnormalities) - Paraproteins (immune dysfunction) - UA/heavy metal screen - ANA Other tests... - Autonomic testing - Nerve biopsy - CSF collection (can give useful info in GBS) - Imaging (MRI) - Quantitative Sensory Testing (QST)

Question 118

Pending results of initial lab panels, electrodiagnostics may also be used in the diagnostic work-up of peripheral neuropathies. Two primary electrodiagnostic studies include ___ and ___.

Answer 118

Pending results of initial lab panels, electrodiagnostics may also be used in the diagnostic work-up of peripheral neuropathies. Two primary electrodiagnostic studies include NERVE CONDUCTION STUDIES and CLINICAL ELECTROMYOGRAPY (EMG).

Question 119

Nerve conduction studies measure the degree of damage in [large / small] peripheral nerve fibers. They aide in differentiating between degeneration of the ___ vs the ___. Two types include the ___ and the ___.

Answer 119

Nerve conduction studies measure the degree of damage in LARGE peripheral nerve fibers. They aide in differentiating between degeneration of the MYELIN vs the AXON. Two types include the NERVE CONDUCTION VELOCITY TEST (NCV) and the SENSORY NERVE ACTION POTENTIALS (SNAP).

Question 120

A nerve conduction velocity (NCV) test assesses motor action potentials (CMAP). Specifically, it looks at the following: - __ and ___ of the AP at each site - ___ in signal arrival to each site - Conduction ___ between sites - ___ ____ latencies

Answer 120

A nerve conduction velocity (NCV) test assesses motor action potentials (CMAP). Specifically, it looks at the following: - AMPLITUDE and DURATION of the AP at each site - LATENCY in signal arrival to each site - Conduction VELOCITIES between sites - F WAVE latencies

Question 121

Clinical electromyography (EMG) records electrical activities of the ___ at rest and with contraction. These are helpful in differentiating between __ and ___ disorders.

Answer 121

Clinical electromyography (EMG) records electrical activities of the MUSCLES at rest and with contraction. These are helpful in differentiating between NERVE and MUSCULAR disorders.

Question 122

[ Clinical EMG / Nerve conduction studies ] aides in measuring the degree of damage and differentiating between myelin and axon degeneration. [ Clinical EMG / Nerve conduction studies ] aides in differentiating between muscle and nerve disorders.

Answer 122

NERVE CONDUCTION STUDIES aide in measuring the degree of damage and and differentiating between myelin and axon degeneration. CLINICAL EMG aides in differentiating between muscle and nerve disorders.

Question 123

Neurapraxia: Findings on nerve conduction studies? Findings on EMG? Recovery timing?

Answer 123

Neurapraxia: Findings on nerve conduction studies? Normal signal DISTAL to lesion, ABNORMAL signal across lesion Findings on EMG? NORMAL/DECREASED recruitment. NO fibrillation. NO fasiculations. Recovery timing? <=3 months to full recovery

Question 124

Axonotmesis: Findings on nerve conduction studies? Findings on EMG? Recovery timing?

Answer 124

Axonotmesis: Findings on nerve conduction studies? Conduction mimics neurapraxia for 4-5 days until Wallerian degeneration occurs. REDUCED CMAP and SNAP (motor and sensory action potentials). ABSENT motor conduction. Findings on EMG? ABNORMAL activity. We see FIBRILLATIONS and FASCULATIONS, with decreased recrutiment, and fast firing Recovery: ~1"/month

Question 125

Neurotmesis: Findings on nerve conduction studies? Findings on EMG? Recovery timing?

Answer 125

Neurotmesis: Findings on nerve conduction studies? Conduction mimics axonotmesis initially, but does NOT demonstrate recovery. Reduced or ABSENT SNAP/CMAPs (sensory and motor action potentials) Findings on EMG? Abnormal activity. +fibrillations. Motor unit loss Recovery timing? Grade III: <1"/month and slowed by scar tissue blockage of nerve growth Grade IV: Requires surgical intervention Grade V: Permanent damage

Question 126

Challenges with electrodiagnostic testing: - No reliable means of studying [proximal / distal ] [sensory/motor] nerves - Nerve conduction studies can be normal in patients with [large / small ] fiber neuropathies - BLE sensory responses can be absent in [patient population?] without injury

Answer 126

Challenges with electrodiagnostic testing: - No reliable means of studying PROXIMAL SENSORY nerves - Nerve conduction studies can be normal in patients with SMALL fiber neuropathies (remember, they best assess large fiber neuropathies) - BLE sensory responses can be absent in ELDERLY PATIENTS without injury

Question 127

Integumentary signs on exam which may contribute to differential diagnosis of peripheral neuropathies?

Answer 127

``` Pulse assessments Skin temp of BLEs Skin ulcers/cellulitis -> DM Alopecia -> hypothyroid, lupus Mess lines -> arsenic, thallium Clubbing -> inflammatory lung dz White nails -> polyneuropathy Edema in joints -> (could lead to compression of peripheral nn) spinal stenosis, disc herniation, compression fx ```

Question 128

The PNS connects the ___ and the ___ to the __ , ___, and ___.

Answer 128

The PNS connects the BRAIN and the SPINAL CORD to the SENSORY RECEPTORS, MUSCLE, and GLANDS

Question 129

The PNS consists of two primary divisions: the ___ and ___ nervous system.

Answer 129

PNS consists of SOMATIC and AUTONOMIC nervous system

Question 130

The somatic nervous system is a division of the [CNS / PNS]. It is an [afferent / efferent ] system and acts to transmit [what kind of signals, to what end destinations?]

Answer 130

The somatic nervous system is a division of the PNS. It has both AFFERENT and EFFERENT components. Afferent signals are the sensory signals which come from the skin, bones, joints, and tendons. It also acts to send EFFERENT motor signals to the muscle (voluntary or involuntary!)

Question 131

The autonomic nervous system is a division of the [CNS / PNS]. It is an [afferent / efferent ] system and acts to transmit [what kind of signals, to what end destinations?]

Answer 131

The autonomic nervous system is a division of the PNS. It has both AFFERENT and EFFERENT components. Afferent signals come from autonomic nerves from the internal organs. It also acts to send EFFERENT signals via autonomic nerves to the internal organs and skin.

Question 132

A peripheral nerve is a bundle of nerve ___, which range in diameter from ___ to ___ micrometers. They conduct electrical impulses through the axons & dendrites to communicate. They can actually stretch to ___% their length to accommodate tension! ___ cells form a thin cytoplasmic tube around each fiber and further wrap larger fibers in a ___ sheath.

Answer 132

A peripheral nerve is a bundle of nerve FIBERS, which range in diameter from 0.3 to 22 micrometers. They conduct electrical impulses through the axons & dendrites to communicate. They can actually stretch to 150% their length to accommodate tension! SCHWANN cells form a thin cytoplasmic tube around each fiber and further wrap larger fibers in a MYELIN sheath.

Question 133

3 layers of connective tissue surrounding nerve

Answer 133

(from out to in) Epineurium Perineurium Endoneurium

Question 134

The [endoneurium / perineurium / epineurium ] surrounds individual nerve fibers. It houses ___ that feed nutrients and O2 to the nerve.

Answer 134

The ENDONEURIUM surrounds individual nerve fibers. It houses BLOOD CAPILLARIES that feed nutrients and O2 to the nerve.

Question 135

The [endoneurium / perineurium / epineurium ] binds axons into fascicles.

Answer 135

The PERINEURIUM binds axons into fascicles. Goal is to protect the contents.

Question 136

The [endoneurium / perineurium / epineurium ] is a fibrous outermost layer (sheath) which binds ___ into the nerve. Nutrients [do / do not ] diffuse across this layer.

Answer 136

The EPINEURIUM is a fibrous outermost layer (sheath) which binds FASCICLES into the nerve. NO diffusion occurs across the epineurium.

Question 137

The circulatory system that supplies the peripheral nerves is termed the ____ ___. It consists of [extrinsic / intrinsic / both extrinsic and intrinsic ] arteries and capillaries that provided a redundant supply of O2 via robust system of ___. We see large external vessels approach a peripheral nerve and run [parallel / perpendicular] to it. Then, intervals of smaller vessels are divided off to the epineural layer then into ____ to supply the peri- and endo-neurium. [Positive / negative / both positive and negative ] tissue pressure exists to support homeostasis. If blood flow is reduced, it may result in pain in [which body parts?] and eventual muscle __ and __.

Answer 137

The circulatory system that supplies the peripheral nerves is termed the VASA NERVORUM. It consists of BOTH EXTRINSIC AND INTRINSIC arteries and capillaries that provided a redundant supply of O2 via robust system of ANASTOMOSES. We see large external vessels approach a peripheral nerve and run PARALLEL to it. Then, intervals of smaller vessels are divided off to the epineural layer then into ANASTOMOSES to supply the peri- and endo-neurium. POSITIVE tissue pressure exists to support homeostasis. If blood flow is reduced, it may result in pain in HANDS AND FEET and eventual muscle WEAKNESS and WASTING (similar to with prolonged vasculitis).

Question 138

Three types of peripheral nerves in terms of myelination: (consider size & myelinated vs not)

Answer 138

Three types of peripheral nerves in terms of myelination: Large MYELINATED Small MYELINATED Small UNmyelinated

Question 139

Large myelinated fibers are responsible for [proprioceptive / non-proprioceptive ] sensory as well as ___. These are [fast/slow]!

Answer 139

Large myelinated fibers are responsible for PROPRIOCEPTIVE sensory (JOINT POSITION, VIBRATION, MUSCLE SPINDLE AFFERENTS) as well as MOTOR. These are fast!

Question 140

Small myelinated fibers are responsible for [proprioceptive / non-proprioceptive ] sensory as well as ___.

Answer 140

Small myelinated fibers are responsible for NON-proprioceptive sensory (LIGHT TOUCH, PAIN, TEMP) as well as AUTONOMIC.

Question 141

Small unmyelinated fibers are responsible for ___ sensation as well as ___.

Answer 141

Small unmyelinated fibers are responsible for PINPRICK sensation as well as PAIN AND TEMP.

Question 142

Injury to myelin results in: - (muscle changes?) - "___" sensations - [increased /decr/ absent ] DTRs - Autonomic changes including fluctuations in ___ and ___

Answer 142

Injury to myelin results in: - MUSCLE WEAKNESS AND WASTING - "TINGLING" sensations - DECREASED OR ABSENT DTRs - Autonomic changes including fluctuations in HR and BP

Question 143

Recall, cranial nerves are [central / peripheral] - exceptions??

Answer 143

Recall, cranial nerves are PERIPHERAL- except CN I AND CN II EMERGE FROM THE DIENCEPHALON so really they're central (CN II is definitely central, it's wrapped in oligodendrocytes, susceptible to CNS degenerative diseases like MS, etc.)

Question 144

Peripheral nerves originate largely from the spinal cord and are broken down into plexuses. Name the 4 biggies.

Answer 144

``` Peripheral nerves originate largely from the spinal cord and are broken down into plexuses. Cervical plexus (spinal accessory n., greater occipital n., facial n., cutaneous nn.) Brachial plexus (Axillary, radial, median, musculocutaneous, and ulnar nn.) Lumbar plexus (Femoral and obturator nerves) Sacral plexus (Sciatic n., Common fibular n., Tibial n., Superior and inferior gluteal nerves) ```

Question 145

Name the large nerves associated with the cervical plexus.

Answer 145

``` Cervical plexus: Spinal accessory n. Greater occipital n. Facial n. Cutaneous nerves ```

Question 146

Name the large nerves associated with the brachial plexus.

Answer 146

Brachial plexus nerves: | Axillary, radial, median, musculocutaneous, and ulnar nn.

Question 147

Name the large nerves associated with the lumbar plexus.

Answer 147

Lumbar plexus nerves: | Femoral and obturator nerves

Question 148

Name the large nerves associated with the sacral plexus.

Answer 148

``` Sacral plexus nerves: Sciatic n. Common fibular n. Tibial n. Superior and inferior gluteal nerves ```

Question 149

Peripheral neuropathies affect ~___% of the general population, with increased prevalence with age (~___% of those >55 yo). Both genders are affected, though symptoms are unique to the individual.

Answer 149

Peripheral neuropathies affect ~2.4% of the general population, with increased prevalence with age (~8% of those >55 yo). Both genders are affected, though symptoms are unique to the individual.

Question 150

The Neuropathic Pain Scale (NPS) measures ten specific qualities associated with neuropathic pain. A score over ___ is indicative of neuropathic pain, and a score of less than ____ indicates non-neuropathic pain. MCID: ___% reduction occurs that a change occurred after 6wks intervention.

Answer 150

The Neuropathic Pain Scale (NPS) measures ten specific qualities associated with neuropathic pain. A score over 5.53 is indicative of neuropathic pain, and a score of less than 5.53 indicates non-neuropathic pain. MCID: 33% reduction occurs that a change occurred after 6wks intervention.

Question 151

Measures of neuropathic pain include... (5)

Answer 151

Neuropathic Pain Scale (NPS) Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) Scale DN4 Pain Questionnaire Neuropathic Pain Questionnaire (NPQ) Neuropathic Pain Symptom Inventory (NPSI)

Question 152

Sensory exam for peripheral neuropathies should include what specific tests? What is the most sensitive and specific combination of testing?

Answer 152

MOST sensitive and specific combo is MONOFILAMENT and VIBRATION testing. Include light touch, sharp dull, vibration, proprioception. Might also include temperature and deep pressure.

Question 153

Sensory vibration testing [improves / declines ] with age. Deficits in vibration sense are often detected [earlier / later]. % of adults >65yo with absent vibration? % of adults >75yo with absent vibration?

Answer 153

Sensory vibration testing DECLINES with age. Deficits in vibration sense are often detected EARLIER than other sensory deficits. 25% of adults >65yo have absent vibration vs 30% of adults >75yo!

Question 154

[Monofilament / Vibration ] testing assesses protective sensation.

Answer 154

MONOFILAMENT testing assesses protective sensation.

Question 155

Monofilament testing is done with a ___ (size?) monofilament which, when deflected, creates ___grams of force at the site. This assesses nerves which rely on the [DCML / spinothalamic ] pathway. You want to touch the filament to the site for only ___ seconds (from initial contact to filament deflection). What sites do you test to show peripheral neuropathy with 90% accuracy? What do you do if there is a scar, callous, or ulcer?

Answer 155

Monofilament testing is done with a 5.07 monofilament which, when deflected, creates 10 GRAMS of force at the site. This assesses nerves which rely on the DCML pathway. You want to touch the filament to the site for only 1-2 seconds (from initial contact to filament deflection). Sites to test to show peripheral neuropathy with 90% accuracy: (test order randomly!) Plantar great toe Plantar met heads ~1, 3, and 5 Can also test plantar aspects of toe 3 and 5, mid arch, plantar 5th met head, plantar heel, and dorsal webspace between toes 1 and 2. Assess near the SIDE of and NOT directly ON any scar, callous, or ulcer.

Question 156

Peripheral neuropathies may be accompanied by autonomic symptoms, including [early / late ] satiety, [impact on sexual fxn?], [positional tolerance?], and ___ abnormalities. Pure autonomic signs/symptoms are [common / uncommon and warrant further neuro w/u]

Answer 156

Peripheral neuropathies may be accompanied by autonomic symptoms, including EARLY SATIETY, IMPOTENCE, ORTHOSTATIC HYPOTENSION, and SWEAT abnormalities. Pure autonomic signs/symptoms are UNCOMMON and warrant further neuro w/u

Question 157

What could be the impact of postural changes on peripheral nerve dysfunction?

Answer 157

Postural changes could increase risk for nerve entrapment

Question 158

Standardized tests and measures that can be used in balance/postural control assessment in individuals with peripheral neuropathies include... (6)

Answer 158

Tests and measures for balance in peripheral neuropathy: TUG Mini-BESTest (measures across all contexts of postural control!) mCTSIB (Modified Clinical test of sensory interaction on balance) Four Square Step Test (FSST; stepping over threshold, stepping in different directions) Functional Gait Assessment (FGA) Dynamic Gait Index (DGI)

Question 159

Examples of provocation tests for peripheral neuropathies or entrapment syndromes...

Answer 159

Spurling's (Cervical nerve root pain) Tinel's sign (used to eval/monitor progress of spontaneous regeneration of sensory axons, but poor Sn & Sp) Neurodynamic testing (e.g. Femoral Nerve Test, SLR, Upper and Lower Limb Nerve Tension Tests) - putting pt in positions to provide tension on nerve, as well as nerve's ability to slide/glide within tissue

Question 160

Participation measures/disability scales in periperpheral neuropathies include... (3)

Answer 160

Overall Neuropathy Limitations Scale (ONLS) Neuropathy Disability Scale (NDS) Neuropathy Impairment Score in Lower Limbs (NIS-LL)

Question 161

When considering exam findings for a peripheral nerve presentation, what aspects of presentation should you consider/be asking yourself?

Answer 161

Clinical Reasoning... - Is a neuropathy actually present? - What is the pattern of nerve invovlement - symmetric/asymmetric? If symmetric, is it proximal or distal? - Any CN involvement? - What is the fiber type involved (motor, sensorimotor, sensory only, small fiber/autonomic) - Acute or chronic? - How does it affect function?

Question 162

Neuropathy-related exam findings which are red flags and warrant referral to specialist include... - [acute / chronic] onset with [slow / rapid ] progression - [sensory / motor] predominant - [singular focus / multifocal] and [known/unknown] cause - [mono/poly] radiculoneuropathies - [Mild / severe] autonomic involvement

Answer 162

Neuropathy-related exam findings which are red flags and warrant referral to specialist include... - ACUTE onset with RAPID progression - MOTOR predominant - MULTIFOCAL and UNKNOWN cause - POLYradiculoneuropathies - SEVERE autonomic involvement

Question 163

Differential diagnosis for neuropathies includes... - ___ neuron disease - Disorders of the ___ junction - ___pathy - ____pathy - Disorders of the ___ (long tract)

Answer 163

Differential diagnosis for neuropathies includes... - MOTOR neuron disease - Disorders of the NEUROMUSCULAR junction - MYOpathy (primary muscle tissue dz) - MYELOpathy (nerve compression within spinal cord) - Disorders of the ___ (long tract)

Question 164

Interventions to assist with controlling inflammation when this is driving peripheral neuropathies: (1) Remove the ___! (2) RICE - with "rest" defined as the absence of [the offending stimulus / the absence of movement]. Can also prescribe selective motions as well as use/modification of ____ or ___. (3) _ Manual therapy such as ___ or ___ (4) Encourage [early motion / initially limited activity] - this decreases ____ that would be associated with rest and prevents ligamentous "___" (5) Medications - what is PT's role?

Answer 164

Interventions to assist with controlling inflammation when this is driving peripheral neuropathies: (1) Remove the STIMULUS! (2) RICE - with "rest" defined as the absence of THE OFFENDING STIMULUS! Can also prescribe selective motions as well as use/modification of ASSISTIVE/ADAPTIVE EQUIPMENT (e.g. assistive devices, wrapping techniques to control edema, etc) or ORTHOTICS. (3) Manual therapy such as NERVE FLOSSING (e.g. with median, ulnar, radial, or sciatic nerve injuries with entrapment/compression problems) or NERVE GLIDES (4) Encourage EARLY MOTION- this decreases MUSCLE ATROPHY that would be associated with rest and prevents ligamentous "CREEPING" (5) Medications - what is PT's role? be aware of what the meds are, coordinate PT interventions around peak dose and/or potential side effects (and monitor for side effects e.g. myopathies i/s/o steroids!)

Question 165

Biophysical agents for management of neuropathies - Cryotherapy - Thermotherapy by way of ___ or __ - Mechanical: via ____ (sound) or ____ (compression) - Electromagnetic: via ___ (electrical stim), ____ (light), or ___ (electromagnetic sources)

Answer 165

Biophysical agents for management of neuropathies - Cryotherapy - Thermotherapy by way of ULTRASOUND or DIATHERMY - Mechanical: via ULTRASOUND (sound) or INTERMITTENT PNEUMATIC COMPRESSION or WRAPPING (compression) - Electromagnetic: via HIGH VOLT or TENS (electrical stim), LASER (light), or SHORT-WAVE DIATHERMY (electromagnetic sources)

Question 166

Evidence demonstrates positive results for use of Transcutaneous Electrical Nerve Stimulations (TENS) for ___ relief, with complete relief in ___% of patients (and best result when combined with amitriptyline). Parameters for use include [mono / bi]phasic, with ___msec pulse duration, amplitude of ___mA or less. Pts can self-select frequency of ___-___pps. Perform for ___ minutes/day for ___ weeks. Recent studies show that a combo of both high and low frequency may yield better therapeutic benefits! Recall, high frequency addresses pain at the ___-control mechanism, vs low frequency addresses more via the ___-type mechanism.

Answer 166

Evidence demonstrates positive results for use of Transcutaneous Electrical Nerve Stimulations (TENS) for PAIN relief, with complete relief in 36% of patients (and best result when combined with amitriptyline). Parameters for use include BIPHASIC, with 4 msec pulse duration, amplitude of 35 mA or less. Pts can self-select frequency of 2 -70 pulses/sec (pps). Perform for 30 minutes/day for 4 weeks. Recent studies show that a combo of both high and low frequency may yield better therapeutic benefits! Recall, high frequency addresses pain at the GATE-control mechanism, vs low frequency addresses more via the OPIOID-type mechanism.

Question 167

FREMS (aka ___ ___ ___ ___ ___) has also been shown to help with pain as well as results on ___, ___, and ___ testing. This is done with a [high / low] voltage, [mono / bi] phasic current and rhythmic delivery with a [consistent / variable ] pulse frequency, pulse duration, and amplitude.

Answer 167

FREMS (aka FREQUENCY RHYTHMIC ELECTRICAL MODULATION SYSTEMS) has also been shown to help with pain as well as results on VIBRATION PERCEPTION TESTING, MONOFILAMENT TESTING, and NERVE CONDUCTION VELOCITY (which lasted at least 4 months!) testing. This is done with a HIGH voltage, BIPHASIC current and rhythmic delivery with a VARIABLE pulse frequency, pulse duration, and amplitude.

Question 168

What does the research say about the use of e-stim for nerve regeneration?

Answer 168

Research isn't that strong, but several studies reported axonal regeneration for both sensory and motor neurons after 1 hour of LOW frequency (20 pps) stim x2 weeks. ...but needs more research, largely animal studies under experimental conditions right now.

Question 169

What does the research say about the use of ultrasound for nerve regeneration?

Answer 169

Research isn't strong, largely limited to animal studies but does show some positive benefit of ultrasound for nerve recovery with US <1.0W / CM^2 (ultrasound >1.0W/CM^2 can actually retard recovery). The clinical research in humans is mostly in Carpal Tunnel Syndrome, showing positive results to improve SYMPTOMS for mild to moderate symptoms, but not much re: regeneration.

Question 170

What does the research say about the use of laser therapy for nerve regeneration?

Answer 170

Current evidence DOES support use of low level laser therapy for nerve regneration. It augments and enhances the body's natural process for healing via increased metabolic activity of the fibroblasts, endothelial cells, osteoclasts, and neurons which yields increased axonal sprouting- and thereby decreases pain. It's promising, but needs more evidence in human models.

Question 171

Targeted sensorimotor training (SMT) which progresses from [order the following: functional / static / dynamic] induces [peripheral / supraspinal ] reorganization and results in regeneration of ___ structures after injury. We also see decreased __ excitability, diminished prevalence of injury, improved ___ and ___, and increased mobility.

Answer 171

Targeted sensorimotor training (SMT) which progresses from STATIC -> DYNAMIC -> FUNCTIONAL and induces SUPRASPINAL reorganization and results in regeneration of NEUROMUSCULAR structures after injury. We also see decreased REFLEX excitability, diminished prevalence of injury, improved PROPRIOCEPTION and BALANCE, and increased mobility.

Question 172

Whole-body vibration (WBV) has been found to improve ___, impact ___ reduction, improve postural ___, and reduce ___. Additionally, it has an effect on ___ skeletal muscles.

Answer 172

Whole-body vibration (WBV) has been found to improve GAIT, impact PAIN reduction, improve postural SWAY, and reduce FALLS. Additionally, it has an effect on DECONDITIONED skeletal muscles.

Question 173

Tai Chi has been found to improve (6), stabilize ___, and reduce ___.

Answer 173

Tai Chi has been found to improve BALANCE, GAIT, MUSCLE STRENGTH, FLEXIBILITY, COORDINATION, and STAMINA. It stabilizes JOINTS, and reduces FALLS.

Question 174

Recommended strength/conditioning parameters in those with peripheral neuropathies? Precaution? - Progressive resistance training of __-___% of 1RM, ___x/week for ____ sets - Aerobic training at least ___x/week of __-___% HRMax, ____ minutes. Benefits include increased blood supply to ___ and increased ___ and ___ delivery to the mitochondria. Impact of trophic changes?

Answer 174

Recommended strength/conditioning parameters in those with peripheral neuropathies? BUT must know cause of the injury and that it is not progressive in nature (e.g. GBS) before starting strength/ conditioning. - Progressive resistance training of 60-80% of 1RM, 2-3x/week for 1-2 sets - Aerobic training at least 3x/week of 60-85% HRMax, 10-20 minutes. Benefits include increased blood supply to PERIPHERAL NERVES and increased O2 and GLUCOSE delivery to the mitochondria. Impact of trophic changes? Consider WB vs NWB activity i/s/o other wounds etc to not make things worse!

Question 175

What does the research say about the role of e-stim in strengthening? - In normally innervated but weak skeletal muscle? - In denervated muscle or muscle awaiting re-innervation (due to peripheral nerve injury)?

Answer 175

What does the research say about the role of e-stim in strengthening? - Evidence SUPPORTS NMES (in adjunct with HEP to strengthen) for increasing strengthening, volitional recruitment, and muscle re-education in NORMALLY innervated but weak skeletal muscle - ...but it is CONTROVERSIAL in denervated muscle or muscle awaiting re-innervation (due to peripheral nerve injury) - literature is contradictory, some studies show positive results, others not as clear. Cochrane review says we can't confirm or refute, so it's up o you as a clinician! Needs more evidence.

Question 176

Medical management of peripheral neuropathies - what meds do we commonly see? (Duh, depends on root cause of the neuropathy, but go with it...) Any surgical interventions?

Answer 176

Medical management of peripheral neuropathies - what meds do we commonly see? (Duh, depends on root cause of the neuropathy, but go with it...) - Analgesics - Antiepileptic meds - Antidepressants - Capsaisin - Lidocaine - Management of blood sugars - Meds to alter immune system for autoimmune dz - Vitamins - Hormones (e.g. thyroid) Any surgical interventions? e.g. with Neurotmeses Grades IV-V, we see nerve repair, graft, or transfers

Question 177

Diabetic polyneuropathies are [an uncommon / the most common] complication of DM, affecting __-__% of patients with DM, though only __-__% are symptomatic. These are typically [chronic / acute], [length / non-length] dependent [sensory/ motor / sensorimotor] peripheral neuropathies. Typically, these become symptomatic over many years of chronic prolonged [hyper / hypo] glycemia in Type [1 /2] diabetes. Vs in type [1 / 2] diabetes, these can become apparent after only a few years of poor glycemic control.

Answer 177

Diabetic polyneuropathies are THE MOST COMMON complication of DM, affecting 30-66% of patients with DM, though only 10-15% are symptomatic. 11-26% are limited by neuropathic pain, can be quite debilitating. These are typically CHRONIC LENGTH-dependent SENSORIMOTOR peripheral neuropathies. Typically, these become symptomatic over many years of chronic prolonged HYPERGLYCEMIA in Type 1 diabetes. Vs in type 2 diabetes, these can become apparent after only a few years of poor glycemic control.

Question 178

There are a few theories regarding the pathophysiology of diabetic polyneuropathies. Differentiate between the Polyol Pathway Theory ; Microvascular Theory ; and the Non-enxymatic Glycosylation Theory.

Answer 178

There are a few theories regarding the pathophysiology of diabetic polyneuropathies. Differentiate between the following: - Polyol Pathway Theory: this pathway is normally a 2-step metabolic pathway that converts glucose -> sorbitol -> fructose. This elevates blood glucose concentrations which creates nerve damage. - Microvascular Theory: changes to microvasculature including thickening of capillary basement membranes and hypertrophy of endothelial cells, as well as erythrocyte and platelet abnormalities -> changes in O2 and nutrient distribution and uptake by the peripheral nerve - Non-enxymatic Glycosylation Theory: a sugar molecule (glucose of fructose) binds to a protein or lipid molecule without the controlling action fo an enzyme -> elevated glucose concentrations -> nerve damage We have no idea which theory is most accurate. Bummer.

Question 179

Diagnosis of diabetic peripheral neuropathy is made by a combination of a patient's medical ___, lab tests (with the goal being to rule [in/out] other causes of neuropathies), electrodiagnostics (including __ and ___), ___ imaging (to measure skin ___), as well as the ____ Score (standardized test; i.e. Michigan, NIS-LL)

Answer 179

Diagnosis of diabetic peripheral neuropathy is made by a combination of a patient's: - medical HISTORY, - Lab tests (with the goal being to rule OUT other causes of neuropathies), electrodiagnostics (including NERVE CONDUCTION STUDIES (NCS) and ELECTROMYOGRAPHY (EMS)) - DOPPLER imaging (to measure skin PERFUSION) - QoL scales, e.g. DIABETIC NEUROPATHY Score (standardized test; i.e. Michigan, NIS-LL - helps to classify severity)

Question 180

Differential diagnoses for diabetic neuropathies? (11)

Answer 180

Ddx for Diabetic neuropathies: - EtOH-related neuropathies - Amyloid polyneuropathy - Chronic Inflammatory Demyelinating Polyradiculopathy - Chronic Myelogenous Lukemia (CML - Neurosarcoidosis - Nutritional neuropathy - Spinal cord tumors - Toxic neuropathy - Uremic neuropathy - Vasculitic neuropathy - Vitamin B12 deficiency *Up to 50% of patients with DM have additional diagnoses which could account for neuropathies - the most common is an inherited neuropathy or neuropathy from EtOH toxicity

Question 181

Clinical presentation of Diabetic Peripheral Neuropathies include primary [sensory / motor] changes - usually insidious in onset in a ___-___ distribution in the [proximal/distal] extremities. Sensory changes can positive or negative (e.g. feeling additional ___, vs absent sensation). Later, you will see [sensory / motor] involvement - what type of a pattern does this follow? It is also common to see some autonomic changes (though rarely autonomic changes alone) - might see ___, ___, and ___ systems involved as well as in the sweat glands.

Answer 181

Clinical presentation of Diabetic Peripheral Neuropathies include primary SENSORY changes - usually insidious in onset in a STOCKING-GLOVE distribution in the DISTAL extremities. Sensory changes can positive or negative (e.g. feeling additional TINGLING/BURNING, vs ABSENT sensation). Later, you will see MOTOR involvement - can be DISTAL OR PROXIMAL or MORE FOCAL weakness, sometimes occuring along the sensory neuropathy but sometimes different! Depends which nerves are affected and which muscles they innervate. It is also common to see some autonomic changes (though rarely autonomic changes alone) - might see CARDIOVASCULAR, GASTROINTESTINAL, and GENITOURINARY systems involved as well as in the sweat glands.

Question 182

Symmetrical polyneuropathies include (4)

Answer 182

Symmetrical polyneuropathies include: - Distal symmetrical sensorimotor polyneuropathy** (most common!) - Small-fiber neuropathy - Diabetic autonomic neuropathy (though again, purely autonomic diabetic neuropathy is rare) (**sometimes see a combo of all of the above 3!) - Diabetic neuropathic cachexia (profound quick weight loss)

Question 183

Asymmetrical neuropathies include (5)

Answer 183

Asymmetrical neuropathies include: - Cranial mononeuropathies - Somatic mononeuropathy - Diabetic thoracic radiculoneuropathy - Diabetic radiculoplexus neuropathy - Charcot neuropathy (changes at the joint, often subtalar joint, can see subluxation/dislocation)

Question 184

Small fiber neuropathic involvement - [Superficial / deep] pain - [Normal / lost] reflexes - [Normal strength / muscle wasting] - [Burning sensations / numbness, "pins and needles," and tingling] - [+ / -] autonomic dysfunction - [changes in thermal perception?] - [changes in vibratory function?] - Electrophysiologically [ heightened / silent] - [changes in nerve conduction velocities?] - Leads to [morbidity and mortality / decreased balance, function, increased fall risk]

Answer 184

Small fiber neuropathic involvement - SUPERFICIAL pain - NORMAL strength and reflexes - BURNING SENSATIONS - AUTONOMIC dysfunction - ALTERED thermal perception - Vibration INTACT - Electrophysiologically SILENT - Nerve conduction velocities INTACT - Leads to MORBIDITY AND MORTALITY

Question 185

Large fiber neuropathic involvement - [Superficial / deep] pain - [Normal / lost] reflexes - [Normal strength / muscle wasting] - [Burning sensations / numbness, "pins and needles," and tingling] - [+ / -] autonomic dysfunction - [changes in thermal perception?] - [changes in vibratory function?] - Electrophysiologically [ heightened / silent] - [changes in nerve conduction velocities?] - Leads to [morbidity and mortality / decreased balance, function, increased fall risk]

Answer 185

Large fiber neuropathic involvement - DEEP pain - LOSS OF reflexes - MUSCLE WASTING - NUMBNESS, "pins and needles," and TINGLING - NO autonomic dysfunction - Thermal perception INTACT - IMPAIRED VIBRATION - Electrophysiologically FINE - IMPAIRED nerve conduction velocities - Leads to DECREASED BALANCE, function, increased FALL RISK

Question 186

Medical interventions for diabetic peripheral neuropathies involve: - Tight ___ control (in Type I DM, this decreased risk of neuropathy by 60% in 5 years!) - Pain management via medications (4 primary ones) - Treatment of ___ dysfunctions - Surgical intervention for subsequent ___ ___ - [frequency?] sensorimotor screening recommended for pts with DM - history alone is [an accurate report / insufficient] to identify peripheral neuropathies. Screening should involve assessing ___ and ___, as well as __ and ___.

Answer 186

Medical interventions for diabetic peripheral neuropathies involve: - Tight GLYCEMIC control (Cochrane Review: in Type I DM, this decreased risk of neuropathy by 60% in 5 years!) - Pain management via medications: PREGABALIN, GABAPENTIN, SODIUM VALPROATE, TRANSDERMAL LIDOCAINE - Treatment of AUTONOMIC dysfunctions - Surgical intervention for subsequent ___ FOOT ULCERS - ANNUAL sensorimotor screening recommended for pts with DM - history alone is INSUFFICIENT to identify peripheral neuropathies. Screening should involve assessing LIGHT TOUCH (MONOFILAMENT) and VIBRATION, as well as DTRs and SUPERFICIAL PAIN (PINPRICK). * You're not going to reduce nerve involvement, but you can minimize risk for progression and secondary effects

Question 187

Length-dependent neuropathies, which are common in DM, often result in the typical stocking-glove sensory symptoms, however we can also see changes to the ___ secondary to the ___ and ___ nerves being affected.

Answer 187

Length-dependent neuropathies, which are common in DM, often result in the typical stocking-glove sensory symptoms, however we can also see changes to the ANTERIOR TRUNCAL WALL (2-4cm bilaterally from midline) secondary to the DISTAL INTERCOSTALS and ABDOMINAL SENSORY NERVES nerves being affected.

Question 188

In diabetic neuropathies, strength training attenuates ___ deficits, prevents ___ loss, improves __, ___, and ___. Aerobic conditioning improves ___ fitness, improves ___ control, and decreases ___.

Answer 188

In diabetic neuropathies, strength training attenuates motor deficits, prevents motor loss, improves coordination, neural control and gait. Aerobic conditioning improves CV fitness, improves glycemic control, and decreases HTN.

Question 189

Guillain-Barre Syndrome (syndorme not dz because we don't know the cause!) is an ___ disease affecting the [CNS / PNS]. It is usually triggered by a ___ or ___. Most individuals reach the most severe neurological state around ___ [hours/days/weeks/months] after onset of symptoms. GBS is the most common cause of [acute / chronic], non-traumatic neuromuscular paralysis. It manifests typically as [ascending / descending ] [sensory / motor / both sensory and motor] paralysis. Sensory symptoms tend to be distal [ < / > / = ] proximal with [increased / diminished / absent] reflexes. Febrile? Dysautonomia occurs in ___ % of cases. 85-90% of cases occur in [what parts of the world?], and the incidence is ~ ___/100,000 cases. Age groups or race/ethnicity affected? Men vs women?

Answer 189

Guillain-Barre Syndrome (*fun fact! It's termed a "syndrome" not a "disease" because we don't know the cause!) is an AUTOIMMUNE disease affecting the PNS. It is usually triggered by a ACUTE BACTERIAL or VIRAL INFECTION. Most individuals reach the most severe neurological state around 8 DAYS after onset of symptoms. GBS is the most common cause of ACUTE, non-traumatic neuromuscular paralysis. It manifests typically as ASCENDING SENSORY AND MOTOR paralysis. Sensory symptoms tend to be distal OVER proximal with DIMINISHED OR ABSENT REFLEXES. NO FEVER at onset (but hx of flu-like symptoms ~2 weeks before onset of sensorimotor symptoms). Dysautonomia occurs in 15% of cases. 85-90% of cases occur in the USA and EUROPE, and the incidence is ~ 0.8 - 1.89 (roughly 1-2 people)/100,000 cases. Affects all age groups and race/ethnicity. affectedMore common in MEN than WOMEN (3:2 ratio men to women).

Question 190

GBS is most often preceded by a __ or ___ illness (in ~2/3 cases), which generally occurs ___-___ weeks prior to onset of weakness. The immune response of body attacks nervous system - the ___ cells are the primary target. Damage to these result in changes in conduction including disrupted propagation of the ___ ___, [slowed / faster/ unchanged / absent] conduction velocity, dysynchrony of conduction, or a conduction ___. Approximately ___% of patients have myelin loss, and ___% have axonal loss.

Answer 190

GBS is most often preceded by a RESPIRATORY or GASTROINTESTINAL illness (in ~2/3 cases), which generally occurs 2-4 weeks prior to onset of weakness. The immune response of body attacks nervous system - the SCHWANN cells are the primary target. Damage to these result in changes in conduction including disrupted propagation of the ACTION POTENTIAL, SLOWED conduction velocity, dysynchrony of conduction, or a conduction BLOCK. Approximately 80% of patients have myelin loss, and 20% have axonal loss.

Question 191

Types of GBS...differentiate between the following - Acute inflammatory demyelinating polyneuropathy (AIDP): involves primary demyelination of [sensory / motor / both] nerves. Most common in [what parts of the world?]. - Acute axonal motor neuropathy and - Acute axonal motor and sensory neuropathy: these involve degeneration of the [myelin / axon / both] and have a [better / poorer] prognosis, increased frequency of ___ symptoms. These make up __-__% of all cases. - Miller-Fisher Syndrome: this is characterized by ___, ___, and ___. It is a [common / rare] and [more focal / more global] form, accounting for __% of cases.

Answer 191

Types of GBS...differentiate between the following - Acute inflammatory demyelinating polyneuropathy (AIDP): involves primary demyelination of SENSORY AND MOTOR nerves. Most common in US AND EUROPE (85-90% of cases) - Acute axonal motor neuropathy and - Acute axonal motor and sensory neuropathy: these involve degeneration of the MYELIN + AXON and have a POORER prognosis, increased frequency of RESPIRATORY symptoms. These make up 5-10% of all cases. - Miller-Fisher Syndrome: this is characterized by AREFLEXIA, ATAXIA, and OPTHALMOPLEAGIA. It is a RARE and MORE FOCAL form, accounting for 5% of cases.

Question 192

Diagnostic criteria for GBS REQUIRES [static / progressive] [symmetric / asymmetric] weakness in at least one ___, as well as [hyper / hypo / a] reflexia. The following are also SUPPORTIVE of the diagnosis of GBS: -

Answer 192

Diagnostic criteria for GBS REQUIRES PROGRESSIVE SYMMETRIC weakness in at least one LIMB, as well as HYPOREFLEXIA or AREFLEXIA. Of note, it is NOT ALWAYS an ascending paralysis, but that is most often what we see. The following are also SUPPORTIVE of the diagnosis of GBS: - <4 weeks of progressive symptoms - SENSORY findings - can be sensitive to touch, buzzing/tingling, generally peripheral (can sometimes include face or trunk). - Involvement of the CRANIAL nerves (in 45-75% of cases! Often will see FACIAL NERVE involvement, +/- oculomotor or oralpharyngeal invovlement) - Impaired AUTONOMIC function (changes in BP, changes in cardiac output, arrhythmias or dysrhythmias, occasional orthostasis) - Elevated CSF PROTEIN - CSF cell count < 10 mm^3 - Demyelination on EMG testing - Recovery of signs/symptoms

Question 193

What is the role of electrodiagnostic studies in GBS?? - Nerve conduction velocity (NCV) studies are most supportive of the diagnosis in the [early / plateau / late] stages, around the [#] day, as this can detect [early / late ] [re / de]myelination. It is the most reliable predictor of ___, when testing is repeated around ___ weeks. Findings on NCV include abnormal nerve conduction studies of [premature / prolonged / absent] latency responses. - EMG can be used to determine the integrity of the ___ ___.

Answer 193

What is the role of electrodiagnostic studies in GBS?? - Nerve conduction velocity (NCV) studies are most supportive of the diagnosis in the EARLY stages, around the FOURTH day, as this can detect EARLY DEMYELINATION (to support diagnosis). It is the most reliable predictor of PROGNOSIS (when repeated 4-6 weeks). Findings on NCV include abnormal nerve conduction studies of PROLONGED or ABSENT latency responses. - EMG can be used to determine the integrity of the MOTOR UNITS.

Question 194

What exam findings may increase a GBS patient's risk for needing mechanical ventilation?

Answer 194

``` Impaired respiratory mm strength Impaired cough efficacy or difficulty clearing secretion Decreased vital capacity Changes in tidal volume Impaired O2 sats ```

Question 195

Pulmonary function tests (PFTs) are key in determining if an individual with GBS may need ventilation or early intubation. Neuromuscular respiratory function is compromised in __-___% of GBS patients. Early intubation in patients with autonomic dysfunction is indicated if: - ____ ___ ___ is <20 mL/kg - Maximal ____ pressure is >30 cm H20 - Maximal ___ pressure is <40 cm H2O. If PFTs do not improve over [#] weeks, tracheostomy is usually indicated. PTs should be monitoring ___ efficacy, ability to manage secretions, changing in __ or __, and progression of __.

Answer 195

Pulmonary function tests (PFTs) are key in determining if an individual with GBS may need ventilation or early intubation. Neuromuscular respiratory function is compromised in 17-30% of GBS patients. Early intubation in patients with autonomic dysfunction is indicated if: - FORCED VITAL CAPACITY is <20 mL/kg - Maximal INSPIRATORY pressure is >30 cm H20 - Maximal EXPIRATORY pressure is < 40 cm H2O. If PFTs do not improve over TWO weeks, tracheostomy is usually indicated. PTs should be monitoring COUGH efficacy, ability to manage secretions, changing in BREATHING or SPEAKING, and progression of WEAKNESS.

Question 196

Pain and GBS: ___% of individuals report pain at some point during course of disease and recovery. Can be disabling! Pain is typically described as a muscle __, or ___ pain. It is [symmetrical / asymmetrical], involves [large / small] bulk muscles more [distal / proximal]. Pts may complain of severe __ or ___ to touch, worse [during the day / at night]. May see different types/locations of pain including... (6). What meds do they typically use for pain management? What can PTs do to help with pain?

Answer 196

Pain and GBS: 72% of individuals report pain at some point during course of disease and recovery. Can be disabling! Pain is typically described as a muscle ACHING, or THROBBING pain. It is SYMMETRICAL involves LARGE bulk muscles more PROXIMAL. Pts may complain of severe BURNING or HYPERSENSITIVITY to touch, worse AT NIGHT. May see different types/locations of pain including... PARESTHESIAS, DYSESTHESIAS, AXIAL and RADICULAR PAIN, JOINT PAIN and MYALGIAS. Typical meds: Acetaminophen, NSAIDS; oral, parenteral, and IV opioids Tricyclic antidepressants Carbamazepine (tegretol) and gabapentin both have evidence for acute pain management, and are also often used for long term management PT pain management: positioning, thermal modalities, sensory integration/management of parasthesias, TENS (for neuropathic pain, in the chronic phase)

Question 197

Acute phase of GBS involves [slow / rapid] progression of symptoms until they peak/nadir around __-___ weeks. What % of patients reach nadir by different time points?

Answer 197

``` Acute phase of GBS involves RAPID progression of symptoms until they peak/nadir around 2-4 weeks. 50% nadir within 1 week 70% nadir by 2 weeks 80% by 3 weeks 98% by 4 weeks ```

Question 198

Plateau phase of GBS involves [further decline / stability / improvement ] of symptoms. How long does it last?

Answer 198

Plateau phase of GBS involves STABILITY of symptoms. May last only DAYS, but can last MONTHS.

Question 199

Recovery phase of GBS involves gradual [improvement/ decline / stability] of symptoms, though the time frame is individualized. Most patients show gradual recovery of muscle strength __-__ weeks after plateau, but sensory disturbances and fatigue can persist for ___.

Answer 199

Recovery phase of GBS involves gradual IMPROVEMENT of symptoms, though the time frame is individualized. Most patients show gradual recovery of muscle strength 2-4 weeks after plateau, but sensory disturbances and fatigue can persist for YEARS *Consider also the cognitive/psych adjustments that occur in the setting of the above.

Question 200

Medical management of GBS focuses on 2 key approaches: pharmacological interventions and symptom management/attenuating recovery. There [is / is not] a cure. Pharmacologically, they start with ___-therapy based treatments within the first 1-2 weeks, specifically ____ to assist with fighting and preventing infections; 5 days of treatment is shown to accelerate recovery! You may also see use of __ or ___ exchange, completed on <=5 consecutive days, which may be more effective than no treatment. What's the role of corticosteroids? Goal is also to decrease risk for life-threatening secondary effects. What do we and medical team monitor and do to support this?

Answer 200

Medical management of GBS focuses on 2 key approaches: pharmacological interventions and symptom management/attenuating recovery. There IS NOT a cure. Pharmacologically, they start with IMMUNE-therapy based treatments within the first 1-2 weeks, specifically IVIG (INTRAVENOUS IMMUNOGLOBINS) to assist with fighting and preventing infections; 5 days of treatment is shown to accelerate recovery! You may also see use of PLASMAPHERESIS or PLASMA exchange, completed on <=5 consecutive days, which may be more effective than no treatment. LITTLE EVIDENCE to support that corticosteroids reduce overall inflammation and nerve damage; they're really not used for this anymore. Goal is also to decrease risk for life-threatening secondary effects. Monitoring vitals, skin integrity, heparin + support stockings for DVT prophylaxis, psychosocial support, ?ventilator needs

Question 201

Tests and measures for GBS: Body Structure/Function - Muscle performance via ... (3) - ROM via ___ - Sensory integrity via ___ - Pain with use of ___ or ___ - Ventilation/gas exchange via ___, ___ assessment, and looking at breathing ___ - Aerobic capacity - Postural control via the ___

Answer 201

Tests and measures for GBS: Body Structure/Function - Muscle performance via MMT/DYNAMOMETRY (if early on, might not want to test resistance, maybe just look AROM against gravity), 5xSTS, %1RM - ROM via goniometry - Sensory integrity via MONOFILAMENT - Pain with use of VAS (both MSKL and neuropathic pain) or BODY CHART (consider type of pain, pain at different times of day, impact on fxn, etc) - Ventilation/gas exchange via AUSCULTATION, COUGH assessment, and looking at breathing PATTERN - Aerobic capacity - Postural control via the MiniBESTest (looks across the 6 contexts of balance)

Question 202

Tests and measures for GBS: Activity Level | Post acute care, can look at... (6)

Answer 202

Tests and measures for GBS: Activity Level Post acute care, can look at... - Level of assistance - 10MWT - TUG - 2 or 6MWT - 2 min step test (a good alternative if pt can't do 2 or 6MWT) - Functional balance measures via: DGI/FGA

Question 203

Tests and measures for GBS: Participation... (3)

Answer 203

Tests and measures for GBS: Participation... (3) - Fatigues Severity Scale: 9 items, measures severity of fatigue and effect on a person's lifestyle in a variety fo disorders (ranges from 1 = strongly disagree to 7 = strongly agree) - GBS Disability Scale: 7-point rating level of global disability from healthy (0) -> able to walk with a stick (3) -> death (6) - Overall Disability Scale: indicates UE and LE functional tasks scored on range of 0 (no signs of disability) to 12 (severe disability). Can be self-scored or done by interview. Reliable, valid, and responsive to change across spectrum of care.

Question 204

PT management in the acute phase of GBS includes focus on...

Answer 204

Acute GBS PT management: - Maintaining ROM, splinting as appropriate, positioning in bed - Minimize pain (via modalities, positioning, ROM) - Maintain skin integrity - Pulmonary function and airway clearance (positioning, deep breathing/coughing) - Functional training (increase upright tolerance; if doing any strengthening, should be low reps, low weight, MONITOR FATIGUE!) - Balance training - Adaptive equipment

Question 205

Exercise with GBS depends on phase of recovery - overload during the ___ phase can lead to further damage (rather than the intended exercise-induced hypertrophy). Focus on ___ training and tasks. What is the role of targeted strength training?

Answer 205

Exercise with GBS depends on phase of recovery - overload during the RE-INNERVATION phase can lead to further damage (rather than the intended exercise-induced hypertrophy). Focus on FUNCTIONAL training and tasks. Sub-maximal strength training is appropriate as RECOVERY begins. Needs to be NON-fatiguing, with rest breaks - has not shown adverse effects.

Question 206

In GBS, [maximal / sub-maximal] strength training is appropriate [during acute phase / during plateau phase / as recovery begins]. Strengthening that is [fatiguing / non-fatiguing] with rest-breaks has not demonstrated adverse effects. Recommendations vary depending on phase of recovery: - Subacute phase (MMT >=3/5, but fatigues): aim for [#?] set(s) at __-__% 1RM with careful monitoring. Chronic (>=3/5 with no complaints of overwork): follow ____ guidelines: __-__% 1RM, [#]x/week, focus on major muscle groups Considerations: monitor closely for symptoms of ____! - Objective testing of strength (monitor for unusual weakness ___-___h post exercise) - Monitor for subjective c/o soreness (___ or increased ___)

Answer 206

In GBS, SUB-MAXIMAL strength training is appropriate as RECOVERY begins. Strengthening that is NON-FATIGUING with rest-breaks has NOT demonstrated adverse effects Recommendations vary depending on phase of recovery: - Subacute phase (MMT >=3/5, but fatigues): aim for MORE THAN 1 set at 60-70% 1RM with careful monitoring. Chronic (>=3/5 with no complaints of overwork): follow ACSM guidelines: 60-80% 1RM, 2-3x/week, focus on major muscle groups Considerations: Evaluate for symptoms of OVERWORK - Objective testing of strength (monitor for unusual weakness 24-48h post exercise) - Monitor for subjective c/o soreness (DOMS, increased PARESTHESIAS)

Question 207

Aerobic training in GBS depends on phase of recovery: - Subacute: aim for ___-___ intensity, __-__% HRMax or an RPE of __-__. Frequency of __-__x/week for __-__ min duration. - Chronic: aim for __-__ intensity, at __-__% HRMax, RPE of __-__ Need ongoing education to pt re: monitoring for ___ and signs of ___!

Answer 207

Aerobic training in GBS depends on phase of recovery: - Subacute: aim for LOW to MODERATE intensity, 40-60% HRMax or an RPE of 12-13. Frequency of 3-5x/week for 20-30min duration. - Chronic: aim for MODERATE TO HIGH intensity, at 60-80% HRMax, RPE of 14-17 Need ongoing education to pt re: monitoring for FATIGUE and signs of OVERWORK!

Question 208

Prognosis in GBS: The ___ Score is a good predicator if pt will be independent and ambulatory after ___ months, when scored at [#days/weeks] post admission. Indicators of a poorer prognosis include: - [older/younger] age at onset, particularly age [>/

Answer 208

Prognosis in GBS: The ERASMUS GBS OUTCOMES SCORE {EGOS)/MODIFIED EGOS Score is a good predicator if pt will be independent and ambulatory after SIX months, when scored at 1-2 WEEKS post admission. Indicators of a poorer prognosis include: - OLDER age at onset, particularly age >60 - Need for VENTILATORY support - RAPID onset < 7 days prior to admission - Distal motor response amplitude reduction to <20% of normal - History of GI illness, particularly if +DIARRHEA

Question 209

Outcomes in GBS: - ~___% have respiratory failure requiring ventilation - Persistent disability in __% of patients, persistent fatigue in __% of patients - Death rate is between __-__% of patients - increases markedly with age, usually in ventilator-dependent individuals

Answer 209

Outcomes in GBS: - ~25% have respiratory failure requiring ventilation - Persistent disability in 20% of patients, persistent fatigue in 67% of patients - Death rate is between 4-15% of patients - increases markedly with age, usually in ventilator-dependent individuals

Question 210

Bell's Palsy is the most common acute [mono / poly] neuropathy, which is a [UMN/LMN] palsy, usually [unilateral/bilateral]. It affects the ___ nerve, and we see inflammation of the ___ ganglion in the facial canal between the labyrinth and tympanic segments leading to compression which causes impaired "___" flow from edema of the nerve within the ___ canal, which results in ischemia, and demyelination of the nerve. Increasing evidence suggests the main cause is reactivation of the latent ___ virus in the cranial nerve ganglia. Typically has a [rapid/slow] onset and evolution over [X time frame]. May be associated with acute neuropathies of cranial nerves __-___, but is also 2.5 more likely to occur in pts with a ___, ___, or __. Diagnosis via clinical exam and occasionally with ___; also will do MRI or CT to ___.

Answer 210

Bell's Palsy is the most common acute MONOneuropathy, which is a LMN palsy, usually UNILATERAL (R side more often affected than L). Occurs at any age, but generally age 15-60, M=W. It affects the FACIAL nerve (CN VII), and we see inflammation of the GENTICULATE ganglion in the facial canal between the labyrinth and tympanic segments leading to compression which causes impaired "AXOPLASMIC" flow from edema of the nerve within the FALLOPIAN canal, which results in ischemia, and demyelination of the nerve. Increasing evidence suggests the main cause is reactivation of the latent HERPES SIMPILEX virus TYPE 1 in the cranial nerve ganglia. Typically has a RAPID onset and evolution IN UNDER 48HRS May be associated with acute neuropathies of cranial nerves V-X, but is also 2.5 more likely to occur in pts with a FAMILY HISTORY, DIABETES, or IMMUNODEFICIENCY (e.g. with HIV), as well as women who are pregnant, in HTN, tumors, Lyme dz, and i/s/o tumors. Diagnosis via clinical exam and occasionally with EMG; also will do MRI or CT to r/o PRESSURE ON THE NERVE as well as other central causes of presentation.

Question 211

Differential diagnosis of facial paralysis... - A supranuclear cause, e.g. ____, would result in paralysis to the [upper half / lower half / entirety] of the face. You see loss of ____, but preservation of ___. - An infranuclear cause affects [the upper half/ the lower half / the entire] face. You see loss of ___ and __ _ movements, inability to ___, and loss of __. Examples include ...(5).

Answer 211

Differential diagnosis of facial paralysis... - A supranuclear cause, e.g. CVA, would result in paralysis to the LOWER HALF of the hemi face (due to bilateral innervation of forehead!). You see loss of NASOLABIAL FOLDS and +DROOPING OF LOWER LIP, but preservation of FOREHEAD AND BROW movements. - An infranuclear cause affects THE ENTIRE (hemi)face. You see LOSS OF FOREHEAD AND EYE MOVEMENTS, INABILITY TO CLOSE EYES, +DROOPING EYELIDS, NASOLABIAL FLATTENING, and +DROOPING OF LOWER LIP. Examples include: - Bell's palsy - Trauma - Varicell Zoster Virus / Ramsay Hunt Syndrome - Otitis media - Parotid land tumor

Question 212

Clinical exam findings in Bell's palsy include: - Weakness of the ___ muscles - Poor ___ closure - Aching of the __ or __ (in 60%) - Altered ___ - Hyperacusis (30%), meaning ___ - Tingling or numbness of the ___/___, mostly [unilateral/bilateral] - Epiphoria, meaning ___ - Pain to __ or __ - Any vision changes? - Synkinesis, meaning ___

Answer 212

Clinical exam findings in Bell's palsy include: - Weakness of the FACIAL muscles - Poor EYELID closure - Aching of the EAR or MANDIBLE (in 60%) - Altered TASTE - Hyperacusis (30%), meaning SENSITIVTY TO CERTAIN PITCH SOUNDS - Tingling or numbness of the CHEEK/MOUTH, mostly UNILATERAL * ** Of note, pt may c/o numbness/tingling, but sensation should be intact!! *** - Epiphoria, meaning IMPAIRED TEAR DRAINAGE RESULTING IN TEARS OUTFLOWING ONTO FACE - OCULAR PAIN or EARACHE - BLURRED VISION - Synkinesis, meaning with voluntary muscle activation (e.g. smile) you see involuntary contraction of other muscles (e.g. associated eye squinting)

Question 213

Treatment of Bell's Palsy: - Role of corticosteroids? - Role of antivirals (aka acyclovir)? - Role of Botox? - Role of surgical intervention?

Answer 213

Treatment of Bell's Palsy: - Role of corticosteroids? A tapered dose of Prednisone is thought to reduce edema around the facial nerve, but it's controversial, shows only small benefits in adults. - Role of antivirals (aka acyclovir)? Animal studies show improved recovery when using antivirals + corticosteroids - Role of Botox? Can be used to reduce overactive or uncoordinated muscles (e.g. orbicular mm of eye., platysma in the neck, mentalis) - Role of surgical intervention? Rare, but will occasionally see: - - Surgical decompression fo CN VII at the entrance to the meatal foramen where the labrythine segment and geniculate ganglion reside. - - Nerve anastomosis (done after 6 months) - - Muscle tendon transfer (temporalis mm) - controversial, reserved for intractable cases

Question 214

What is the "Bell Phenomenon" on clinical exam of Bell's Palsy?

Answer 214

"Bell Phenomenon" = you see upward diversion of the eye with attempted eyelid closure in an individual with Bell's Palsy

Question 215

The House-Brackmann Scale is used to grade the degree of facial nerve damage in Bell's Palsy. It is graded from I-VI (I = [normal / no movement], VI = [normal / no movement]). Categories include: (4)

Answer 215

The House-Brackmann Scale is used to grade the degree of facial nerve damage in Bell's Palsy. It is graded from I = NORMAL to VI = ASYMMETRICAL/NO MOVEMENT. Categories include: - Overall APPEARANCE/resting tone, FOREAHEAD movement, EYE closure, and MOUTH movement.

Question 216

PT interventions with Bell's Palsy focus on [strengthening / coordination] of appropriate facial movement/muscles and ___ overactive muscles. Techniques include (6). Also some good effects from kinesiotaping in neurofacilitation as well as managing __ and __. Additionally, may need education/intervention surrounding eye protection via use of eye ___ or ___, taping eye closed when ___, or consideration of eyelid __.

Answer 216

PT interventions with Bell's Palsy focus on OVERALL COORDINATION of appropriate facial movement/muscles and INHIBITING overactive muscles. Techniques include: FINGER KNEADING, TAPPING, FRICTION, VIBRATION, STROKING, INHIBITORY TECHNIQUES Also some good effects from kinesiotaping in neurofacilitation as well as managing EDEMA AND PAIN. Additionally, may need education/intervention surrounding eye protection via use of eye PATCH or EYEDROPS, taping eye closed when SLEEPING or consideration of eyelid WEIGHTS (in chronic cases). PT can help with speeding along recovery.

Question 217

PT and Bell's Palsy: what is the evidence for... - Low level laser therapy (LLLT)? - Electrical Stimulation? - Dry needling?

Answer 217

PT and Bell's Palsy: what is the evidence for... - Low level laser therapy (LLLT)? Protocol of 830nm wavelength, power output of 100Mw, and frequency of KHz. Applied to 8 points of the affected side of face 3x/week over 6 weeks. - Electrical Stimulation? Some studies/cases found possible increase in the already overractive/synkinetic muscles (not desirable). Some studies did have +results, but needs further research re: effective dosage and length of intervention. - Dry needling? Evidence to suggest that accupuncture decreases inflammatory factors, improves blood flow to the facial nerve, strengthens the immune system, and facilitates remyelination

Question 218

Bell's palsy prognosis: total recovery depends on ____. 10-20% of patients are left with residual facial ___, involuntary __, or persistent ___. BUT! ___-___% of patients will recover completely within __ months! 50-60% of cases improve within __ weeks.

Answer 218

Bell's palsy prognosis: total recovery depends on AMOUNT OF DAMAGE TO THE NERVE. 10-20% of patients are left with residual facial WEAKNESS, involuntary MOVEMENTS, or persistent LACRIMATION. BUT! 80-90% of patients will recover completely within SIX months! 50-60% of cases improve within THREE weeks.

Question 219

Neuro screen: first, observe! - Observe for posture and general symmetry - Look for clues to LMN involvement such as __ and __ - Look for cues re: basal ganglia involvement such as ___, __, __, and __

Answer 219

Neuro screen: first, observe! - Observe for posture and general symmetry (e.g. with arm movement while walking) - Look for clues to LMN involvement such as MUSCLE ATROPHY and MUSCLE FASCICULATIONS - Look for cues re: basal ganglia involvement such as INVOLUNTARY MOVEMENTS, TREMORS, BRADYKINESIA, and HYPOKINESIA, DYSKINESIAS/ HYPERKINESIAS

Question 220

``` Grading reflexes: 0 = ___ 1+ = ___ 2+ = ____ 3+ = ____ 4+ = ___ ``` Recall that DTRs from __-___ are normal unless they are asymmetric OR if there is a dramatic difference between UE/LE.

Answer 220

Grading reflexes: 0 = ABSENT 1+ = DIMINISHED 2+ = NORMAL/AVERAGE 3+ = BRISKER THAN AVERAGE, but not necessarily indicative of dz 4+ = VERY BRISK, HYPERACTIVE, may hav CLONUS Recall that DTRs from 1+ to 3+ are normal unless they are asymmetric OR if there is a dramatic difference between UE/LE.

Question 221

Deep Tendon Reflexes - give nerve roots associated with each of the following: - Biceps - Brachioradialis - Triceps - Patella - Achilles

Answer 221

Deep Tendon Reflexes - give nerve roots associated with each of the following: - Biceps: C5-6 - Brachioradialis: C6-7 - Triceps: C6, 7, 8 - Patella: L3-4 - Achilles: S1-2

Question 222

``` Give the primary nerve root for the following MMT tests/myotomes Biceps Wrist extensor Triceps Finger flexors Finger abduction Hip flexor Knee extensor Ankle DF Great toe extension Ankle PF ```

Answer 222

``` Give the primary nerve root for the following MMT tests/myotomes: Biceps C5 Wrist extensor C6 Triceps C7 Finger flexors C8 Finger abduction T1 Hip flexor L2 Knee extensor L3 Ankle DF L4 Great toe extension L5 Ankle PF S1 ```

Question 223

Common injuries which precede CRPS include...

Answer 223

``` Fractures (represent 44-46% of cases) Crush injuries sprain & strains Surgery falls contusions immobilization Cerebral vascular injuries burns venipuncture neuroma electrical shock PPM placement Mastectomy Insidious onset Neurodegenerative dz ```

Question 224

Per the Budapest Criteria (2010), three criteria must be present for clinical diagnosis of CRPS: - Pain which is ____ to any inciting event - Needs at least 1 symptom in 3 of the 4 following categories: - --Sensory: __ or __ - --Vasomotor: ____ asymmetry, changes in skin ___, or asymmetry - --Sudomotor/edema: ___, changes in ___, or asymmetry - -- Motor/trophic: decreased ___ or motor dysfunction including __, __, or ___; or ___ changes

Answer 224

Per the Budapest Criteria (2010), three criteria must be present for clinical diagnosis of CRPS: - Pain which is DISPROPORTIONATE to any inciting event - Needs at least 1 symptom in 3 of the 4 following categories: - --Sensory: ALLODYNIA or HYPERESTHESIA - --Vasomotor: TEMPERATURE asymmetry, changes in skin COLOR, or asymmetry - --Sudomotor/edema: EDEMA, changes in SWEATING, or asymmetry - -- Motor/trophic: decreased ROM or motor dysfunction including WEAKNESS, TREMOR, DYSTONIA; or TROPHIC changes With the above, 2 or more signs and 2 or more symptoms = Sn = 0.94

Question 225

Treating CRPS: Goal is to guide ____! - Start [immediately / after acute phase / later] post injury or before surgery - Use sensory __ and touch ___ exercises. - Watching other hand moving normally to activate __ neurons - Laterality or R/L identification - ___ therapy - Patient needs to be dedicated to the cause!

Answer 225

Treating CRPS: Goal is to guide PLASTICITY! - Start IMMEDIATELY post injury or before surgery - Use sensory IMAGERY and touch IMAGERY exercises - start with non-threatening imagery, progress as tolerated. Called "graded motor imagery" - helps with pain and lasts for up to ~6 months! - Watching other hand moving normally to activate MIRROR neurons - Laterality or R/L identification (to reorganize body scheme!) - MIRROR therapy - Patient needs to be dedicated to the cause!

Question 226

In phantom limb pain, this is often secondary to impaired ___ and smudging in the homunculus.

Answer 226

In phantom limb pain, this is often secondary to impaired PROPRIOCEPTION and smudging in the homunculus.

Question 227

Mirror therapy with phantom limb pain: - Put the [involved / uninvolved ] side in front of the mirror. Make the hands look like each other, so cover up all ___ and remove __. - Tell patient to look at [the / the image of the ... in the mirror] [involved limb / uninvolved limb ]. Start just by viewing the extremity, then try movement of the non involved side in the mirror. [Do / do not ] attempt movement of the involved side too soon. Aim for ___-___ time sessions of no longer than __-__ minutes, [x/week] [duration and # of weeks].

Answer 227

Mirror therapy with phantom limb pain: - Put the UNINVOLVED side in front of the mirror. Make the hands look like each other, so cover up all TATTOOS and remove JEWELRY. - Tell patient to look at THE IMAGE OF THE UNINVOLVED LIMB. Start just by viewing the extremity, then try movement of the non involved side in the mirror. DO NOT attempt movement of the involved side too soon. Aim for 6-10x/day, no longer than 10-15 minutes, DAILY FOR AT LEAST 2 WEEKS (but adjust this for your patient...may be able to tolerate more!)