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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
Q

“ideal” botox client

A
  • localized spasticity
  • cognitive ability
  • readily express pain/discomfort
  • AROM despire spasticity
  • ambulatory
  • hightly motivated
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20
Q

pre and post injection slides read
slides 32-33

A
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21
Q

T/F topical anesthesia botox causes systemic effects for generalized spasticity

A

F (oral)

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22
Q

mechanism of action - baclofen

A

inhibit relfexes at the SC level and excitatory neurotransmitter release (GABA)

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23
Q

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

A

intrathecal baclofen

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24
Q

intrathecal baclofen pump
selection criteria

A
  • 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
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25
Q

intrathecal baclofen pump CONTRAS

A
  • allergy to baclofen
  • active infection
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26
Q

baclofen pump adverse effects

A

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

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27
Q

baclofen intrathecal baclofen pump CAUTIONS FOR USE
Slide 40

A
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28
Q

slides 40-45 read

A
29
Q

advantages of ITB (intrathecal baclofen)

A

it is reversible and doesn’t cross blood brain barrier
and can fine-tune dosage

30
Q

ITB disadvantages

A
  • 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
Q

what type of motor or nerve blocks are more selective to avoid sensory nerves?

A

open

note: percutaneuous: through the skin and less selective

32
Q

effects of motor/nerve point blocks

short/long term

A

short ter: like a local anesthetic; directly proporitonal to fiber thickness
long term: protein denauration

33
Q

advantages of motor / nerve blocks

A
  • lasts ~ 6 mths
  • decreased tone allow increased functional mobility and strength
34
Q

disadvantages of motor/nerve blocks

A
  • long term axon damange
  • dysthesias
  • irritated mm
  • carcinogen (phenol)
35
Q

advantages of spinal stimulation such as cerebral ESTIM and SC ESTIM

A

better tone mgmt of UE than baclofen pump

36
Q

disadvantages of spinal stimulation such as cerebral ESTIM and SC ESTIM

A
  • dislodged cords
  • infection
  • less effective than ITB for LE tone mgmt
37
Q

neurotomies advantage and disadvantage

A

advantage: permanant change
dis: excess lesion will cause perm motor deficit, long standing pain problems, insufficient lesioning causes ineffective results

38
Q

rhizotomy

A

sensory rootlets cut
requires laminectomy or -otomy
lower thoracic / lumbar

39
Q

rhizotomy advantage and disadvantage

A

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

check slide 56

40
Q

most common tendon rlease

A

hamstring and heel cord (achilles)

41
Q

a procedure done frequently after heel cord lengthening

A

SPLATT (split anterior tib tendon transfer)
lateral aspect atached to cuboid

42
Q

peroneus longus tendon transfer from plantar medial cuneiform to

A

dorsum of navicular

43
Q

tendon lengthening: advantages and disadvantages

A
  • over lengthening
  • WBAT and AFO rigid
  • hamstrings are in a long lenght cast until full knee ext
44
Q

non-invasive tx to reduce spasticity

A
  • EMG
  • passive stretch
  • E-Stim
  • casting and splinting
  • temperature
  • meds
45
Q

PT management of spasticity

A
  • 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
Q

which muscles to stimulate and increase reciprocal inhibition of spastic muscle and increase the strength of antagonist

A

antagonist stimulation

47
Q

T/F you can over-fatigue the agonist spastic muscle

A

false it doesn’t work
that’s why you always target the antagonist muscle to allow agonistic spastic mm to relax

48
Q

if the bicep muscle is spastic, where do you stimulate?

A

triceps to allow biceps to relax

49
Q

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

A

therapeutic electrical stimulation (TES)

50
Q

contraindications to TES

A
  • primary muscle disorder
  • degenerative disease
  • behavioral
  • medical complications (arrhythmia, pacemaker, pregnant(
  • growth complications (obese or fixed contracutres)
51
Q

type of stimulation to treat the pain of spasticity

A

TENS

52
Q

use this device if we want to
- promote voluntary relaxation below thersholds
- promote voluntary active efforts

A

EMG biofeedback
works best in conjunction with PT

53
Q

which type of nonremovable cast is most successful when contracutres pesent <6 months and when patient is able to use extremity?

A

Serial/inhibitive
effective in improving contractures d/t spasticity

54
Q

static splints

A

casts, AFO

55
Q

d

dynamic splints

A

dynasplints, drop out casts

56
Q

rigit vs soft vs air-filled

A

rigid: cast, AFO
airfilled: pressure splint
soft: ACE warp, foam

57
Q

perks of air-filled pressure splints?

A
  • stimulaite proprioception
  • hold limb in inhibited posture
  • minimal stabilization
  • decrease handholds
  • very good for pain/hypersensitivity
58
Q

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

A

CIMT

59
Q

heterotopic ossification

A

abnormal formation of bone in extraskeletal soft tissue where bone doesn’t usually exist/shouldn’t exist

60
Q

most often HO locations

A

in soft tissue surrounding joints (peri-articular)

61
Q

neurogenic HO

A

traumatic CNS injury (TBI, SCI) and rarely seen in CVA or MS

62
Q

traumatic HO

A

patients with burn, amputation, fracure, joint dislocation total joint arthroplasty

63
Q

another term of HO but more often used with orthopedic injury and post-op cases
- chronic musclular trauma

A

myositis ossisficans

64
Q

most common sites for traumatic myositis ossificans are the

A

quadriceps fem
brachialis muscles

65
Q

incidence is ____ for HO

A

Variable

  • SCI (can develop up to a yr later) , TBI (especially if pt is in a PVS/COMA)
66
Q

HO risk factors

A

age and gender
severity of injury
- sex
- spasticity
- cigarette smoking
- completeness of injury
- neumonia
- pressurfe ulcers
- location or lvl of injury

67
Q

HO adverse effects

A
  • Pain
  • nerve impingement
  • joint ankylosis
  • CRPS
  • Osteoporosis
  • soft tissue infection
  • fractures
  • spasticity
  • DVT
  • Pressure injury (decubitus ulcers)
  • decreased ROM leading to contractures
68
Q

HO pt presentation

A

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
Q

HO most common sites
SCI
TBI

A

SCI: hips, knee
TBI: hip, shoulder, elbow

70
Q

initial signs/acute phase of HO

A

PAIN
- local inflammatory signs (edema,inflammation, increased temp, erythema, pain)
- decreased ROM

71
Q

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

A

2-4 weeks

note: PT may be the one to find this clinically!!

72
Q

________is gold standard to diagnose HO but recently research shows that ____may be more convenient, cost effective and safe

A

triple phase bone scintigraphy
diagnostic ultrasound

73
Q

read various methods of diagnosing HO slide 81

A
74
Q

HO Diff Dx

A
  • infection
  • cellulitis
  • DVT
  • osteomyelitis
75
Q

HO management

A
  • limit progression and maximize joint function
  • minimize risk factors (DVT, spasm, edema, infection, immobility, pressure injury)
75
Q

HO pharmacological mgmt

A

pain mgmt and spasm (NSAIDS, baclofen, botox)
radiaiton therapy to prevent conversion o fprecursor cells to bone forming cells
etc

read more slide 84

76
Q

surgery for HO goals

A
  • improve ROM
  • address joint ankylosis
  • mobility
  • spasm
  • prevent complications

options: surgical resection, soft tissue release / arthroplasty

76
Q

PT considerations for HO

A
  • too aggressive might lead to more inflammation/pain
  • consider sensation (they can’t feel as much)
  • consider pain

Neuro PT (8 decks)

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