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Neuro PT > Lecture 5: spasticity and HO > Flashcards

Lecture 5: spasticity and HO Flashcards

1
Q

muscle tone

A
  • resistance to stretch in resting
  • flacid (completely lacking resistance), hypotonic (abnormally low resistance), normal, hypertonia
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2
Q

2 versiona of hypertonia are?

A

1. spasticity (velocity dependent)
2. rigidity (velocity independent)

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3
Q

what is spasticity?
is the neural input underactive or overacitve?

A

velocity dependent resistance
overactive nerual input to muscle causing excessive muscle contraction

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4
Q

T/F paients with medical conditins like stroke, SCI, UMN, TBI, CP and Parkinsons may present with spasticity

A

FALSE (parkinsons - rigidity)

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5
Q

DTR scale

A

0 no response
1+ sluggish or diminshed
2+ active or expected response
3+ brisker than expected, slight hyperactive
4+ brisk, hyperactive with intermitent or transient clonus

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6
Q

without ____, contractures should be entirely preventable

A

spasticity
note: spasticity and paralysis significantly contribute to contractures but are NOT sole cause. without spasm, contractures should be entirely preventable

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7
Q

contracture

A

chronic loss of PROM of a joint becuase of structural changes in non-bony tissue

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8
Q

how might spasticity be helpful?

A
  • may assist w/ posture and mobility
  • maintain mm mass and bone mineralization
  • reduce dependent edema
  • prevents DVT
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9
Q

ashworth scale for grading spasticity

A

1 No increase in tone
2 slight increase in tone, giving a “catch when moved in flexion or extension
3 more marked increase in tone but affected parts easily flexed
4 considerable increase in tone; passive movement difficult
5 rigid flexion/extension

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10
Q

MODIFIED ashworth scale

A

0 no increase in tone
1 slight increase in muscle tone mainfested by a catch and release or by minimal resistance at the end of ROM during flexion/extension
1+ slight increase in tone manifested by a catch followed by minimal resistance throughout remainder (less than half) of the ROM
2 more marked increase in muscle tone through most of the ROM but the affected part(s) easily moved
3 considerable increase in muscle tone, passive movement difficult
4 rigid in flexion and extension

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11
Q

with modified ashworth sclae, avoid starting your test at

A

end range

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12
Q

clinicians prefer which scale to measure spasticity, Tardieu or MAS?

A

Tardieu

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13
Q

tardeu measures 3 things

A

velocity of stretch
quality of stretch
angle of muscle reaction

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14
Q

Velocity of stretchy

A

V1: slow as possible
V2: speed of limb falling with gravity
V3: as fast as possible

V1 PROM, V2/3 for spasticity

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14
Q

Tardieu: Quality of muscle reaciton (X)

A

0: no resistance through full PROM
1: slight resistance through full PROM with no clear catch
2: clear catch at precise angle followed by release
3: fatigable clonus (<10 sec when maintaining pressure) at precise angle
4: unfatigable clonus at precise angle

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14
Q

Angle of muscle reaction (Y) measured from 0 deg position

A

R1= PROM till catch point
R2= full PROM

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14
Q

MEDICAL MANAGEMENT OF SPASTICITY

A
  • Botulinum toxin A
  • baclofen
  • nerve / motor point block
  • spinal or cerebral electral stimulation
  • peripheral neurotomy
  • rhizotomy
  • tendon release with / without transfer
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15
Q

how does botox work?
which fibers recover faster?

A

blocks acetylcholine relase
slow twitch fibes recover faster than fast twitch

relaxation diminishes as formation of new junctions occur

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15
Q

Penn spasm scale

A
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15
Q

self-report measure of impact of spasticiy on social, psychologoical, daily activities, need for assistance, positive impact, intervention, social embarrassment

A

PRISM
patient reported impact of spasticity emasure

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16
Q

an importnat advantage of botox is the fact that it can be

read slide 28

A

injected for selective muscle paralysis
and
no dysthesia

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16
Q

effects of botox is seen

A

witin 24 - 72 hours with peak effects at 4-5 days and lasts 8-12 weeks
effective in reducing spasticity

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17
Q

BOTOX contraindications

A

neuromuscular transmission disease
inflammation at projected injection site
pregnancy
children under 2 yr

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18
Q

“extreme” botox client

A
  • non localized spasticity
  • decreased cognition/motivation
  • decreased sensory/kinetetic awareness
  • contracture
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19
"ideal" botox client
- localized spasticity - cognitive ability - readily express pain/discomfort - AROM despire spasticity - ambulatory - hightly motivated
20
pre and post injection slides read slides 32-33
21
T/F topical anesthesia botox causes systemic effects for generalized spasticity
F (oral)
22
mechanism of action - baclofen
inhibit relfexes at the SC level and excitatory neurotransmitter release (GABA)
23
if pt can't tolerate oral baclofen, they can take this version where it doesn't reach the systemic circulation or brain - fewer side effects - imporves voluntary mm control
intrathecal baclofen
24
intrathecal baclofen pump selection criteria
- severe spasticity (Ashworth greater or equal 3) - not depend on spasticiy for function - movement disorders not main problem - less invasive modalities are unacceptable - goals identified, therapy available, family capable - >1 yr since injury, >4 y/o
25
intrathecal baclofen pump CONTRAS
- allergy to baclofen - active infection
26
baclofen pump adverse effects
risk of pump malfunction rapid cessation causes side effects like confusion, delirium, seizure, fever risk of disinhibition overdose if pump malfuncitons causes disorientaiton, weakness, N/V, etc
27
baclofen intrathecal baclofen pump CAUTIONS FOR USE Slide 40
28
slides 40-45 read
29
advantages of ITB (intrathecal baclofen)
it is reversible and doesn't cross blood brain barrier and can fine-tune dosage
30
ITB disadvantages
- need to replace the unit - **csf** leak - **infection** - refills 3/12 **increase tolerance overtime (Tachyphylaxis/tolerance)** - difficult to help UEs without overdoing it with LEs because of catheter placement - **battery life** only 3-5 yrs - can see it in thin pt
31
what type of motor or nerve blocks are more selective to avoid sensory nerves?
open note: percutaneuous: through the skin and less selective
32
effects of motor/nerve point blocks short/long term
short ter: like a local anesthetic; directly proporitonal to fiber thickness long term: protein denauration
33
advantages of motor / nerve blocks
- lasts ~ 6 mths - decreased tone allow increased functional mobility and strength
34
disadvantages of motor/nerve blocks
- long term axon damange - dysthesias - irritated mm - carcinogen (phenol)
35
advantages of spinal stimulation such as cerebral ESTIM and SC ESTIM
better tone mgmt of UE than baclofen pump
36
disadvantages of spinal stimulation such as cerebral ESTIM and SC ESTIM
- dislodged cords - infection - less effective than ITB for LE tone mgmt
37
neurotomies advantage and disadvantage
advantage: permanant change dis: excess lesion will cause perm motor deficit, long standing pain problems, insufficient lesioning causes ineffective results
38
rhizotomy
sensory rootlets cut requires laminectomy or -otomy lower thoracic / lumbar
39
rhizotomy advantage and disadvantage
a: perm changes at the segmental lvl d: infection, bleeding, CSF leak, motor nerve issue, Bowel and Bladder, temp sensory loss, hospitilization, over-weakeneing of mm needed for ambulation and transfers, and more ## Footnote check slide 56
40
most common tendon rlease
hamstring and heel cord (achilles)
41
a procedure done frequently after heel cord lengthening
SPLATT (split anterior tib tendon transfer) lateral aspect atached to cuboid
42
peroneus longus tendon transfer from plantar medial cuneiform to
dorsum of navicular
43
tendon lengthening: advantages and disadvantages
- over lengthening - WBAT and AFO rigid - hamstrings are in a long lenght cast until full knee ext
44
non-invasive tx to reduce spasticity
- EMG - passive stretch - E-Stim - casting and splinting - temperature - meds
45
PT management of spasticity
- stertching and ROM ex to reduce tightness and maintain joint flexibility (stretch for a long time like 20-30 min) - strength training of agonist and antagonists to improve function and counteract imbalances d/t spasticity
46
which muscles to stimulate and increase reciprocal inhibition of spastic muscle and increase the strength of antagonist
antagonist stimulation
47
T/F you can over-fatigue the agonist spastic muscle
false it doesn't work that's why you always target the antagonist muscle to allow agonistic spastic mm to relax
48
if the bicep muscle is spastic, where do you stimulate?
triceps to allow biceps to relax
49
what type of stimulation do you use on general spasticity that interferes with function, requiring a special type of TENS that needs a certification, used at night during peak secretion of GH and for the want of healthier mm? subthershold stimulation to sensory nn
therapeutic electrical stimulation (TES)
50
contraindications to TES
- primary muscle disorder - degenerative disease - behavioral - medical complications (arrhythmia, pacemaker, pregnant( - growth complications (obese or fixed contracutres)
51
type of stimulation to treat the pain of spasticity
TENS
52
use this device if we want to - promote voluntary relaxation below thersholds - promote voluntary active efforts
EMG biofeedback works best in conjunction with PT
53
which type of nonremovable cast is most successful when contracutres pesent <6 months and when patient is able to use extremity?
Serial/inhibitive effective in improving contractures d/t spasticity
54
static splints
casts, AFO
55
# d dynamic splints
dynasplints, drop out casts
56
rigit vs soft vs air-filled
rigid: cast, AFO airfilled: pressure splint soft: ACE warp, foam
57
perks of air-filled pressure splints?
- stimulaite proprioception - hold limb in inhibited posture - minimal stabilization - decrease handholds - very good for pain/hypersensitivity
58
for mgmt of spastcity, PT should use ____ method for promoting the use of affected limbs and improve motor function which can indirectly reduce spasticity by increasing VOLUNTARY control
CIMT
59
heterotopic ossification
abnormal formation of bone in extraskeletal soft tissue where bone doesn't usually exist/shouldn't exist
60
most often HO locations
in soft tissue surrounding joints (peri-articular)
61
neurogenic HO
traumatic CNS injury (TBI, SCI) and rarely seen in CVA or MS
62
traumatic HO
patients with burn, amputation, fracure, joint dislocation total joint arthroplasty
63
another term of HO but more often used with orthopedic injury and post-op cases - chronic musclular trauma
myositis ossisficans
64
most common sites for traumatic myositis ossificans are the
quadriceps fem brachialis muscles
65
incidence is ____ for HO
Variable - SCI (can develop up to a yr later) , TBI (especially if pt is in a PVS/COMA)
66
HO risk factors
age and gender severity of injury - sex - spasticity - cigarette smoking - completeness of injury - neumonia - pressurfe ulcers - location or lvl of injury
67
HO adverse effects
- Pain - nerve impingement - joint ankylosis - CRPS - Osteoporosis - soft tissue infection - fractures - spasticity - DVT - Pressure injury (decubitus ulcers) - decreased ROM leading to contractures
68
HO pt presentation
any joint below the level of lesion rarely affecting peripheral joints like wrist, ankle, hand, foot may also affect incisions, kidney, uterus, corpora cavernosum and GI tract
69
HO most common sites SCI TBI
SCI: hips, knee TBI: hip, shoulder, elbow
70
initial signs/acute phase of HO
**PAIN** - local **inflammatory** signs (edema,inflammation, increased temp, erythema, pain) - decreased **ROM**
71
patient presents ____ weeks later of HO with firm region that's hard to palpate. jont ROM may become further restricted serum alkaline phosphatase levels increase and stay eelvated with new bone formation
2-4 weeks note: PT may be the one to find this clinically!!
72
________is gold standard to diagnose HO but recently research shows that ____may be more convenient, cost effective and safe
triple phase bone scintigraphy diagnostic ultrasound
73
read various methods of diagnosing HO slide 81
74
HO Diff Dx
- infection - cellulitis - DVT - osteomyelitis
75
HO management
- **limit progression** and maximize joint function - **minimize risk factors** (DVT, spasm, edema, infection, immobility, pressure injury)
75
HO pharmacological mgmt
pain mgmt and spasm (NSAIDS, baclofen, botox) radiaiton therapy to prevent conversion o fprecursor cells to bone forming cells etc ## Footnote read more slide 84
76
surgery for HO goals
- improve ROM - address joint ankylosis - mobility - spasm - prevent complications | options: surgical resection, soft tissue release / arthroplasty
76
PT considerations for HO
- too aggressive might lead to more inflammation/pain - consider sensation (they can't feel as much) - consider pain

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