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Neuromuscular Practice > Week 4.8 Spasticity management 2 > Flashcards

Week 4.8 Spasticity management 2 Flashcards

1
Q

what is the most common oral mediation for TBI and SCI

A

baclofen

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2
Q

what are the side effects of baclofen

A

horsiness, dizziness and weakness

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3
Q

what are the cons of oral medications

A

effects ebb and flow
must take on a schedule
sedating side effects must ween off

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4
Q

what are some of the pros of oral medications

A

non-invasive
non-permeant
effective management or positive signs
inexpensive

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5
Q

the clinical usefulness of oral medications are limited by

A

side effects

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6
Q

do oral meds have a lot of high evidence,

A

no

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7
Q

we choose medications based on…

A

side effect profiles

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8
Q

should oral meds be the first line of treatment

A

no

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9
Q

what is chemical neurolysis:

A

phenol or alcohol applied to the nerve via injection with EMG guidance. causes demyelination of the axon, and can last up to 6 months.

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10
Q

what is a neuromuscular blockade

A

Botox, injected into the, muscles, binds to presynaptic cholinergic nerve terminal and blocks the release of ACH

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11
Q

what are the advantages of chemical neurolysis

A

better effect on larger muscles and the cost is minimal

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12
Q

what are the disadvantages of chemical neurolysis

A

difficult procedures, risk of sensory complications, muscles become fibrotic after many injections.

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13
Q

what are the advantages of neuromuscular blockade

A

less painful easier to perform, no sensory side effects, and not permanent.

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14
Q

what are the disadvantages of neuromuscular blockage

A

only reinfect every 3 months, not permanent, cost and you might develop antibodies

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15
Q

what is an intrathecal baclofen (ITB)

A

right into the SC, much less medications

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16
Q

how does and ITB work

A

baclofen is diffused into the CSF in the intrathecal space, there is a catheter attached to the pump

17
Q

mechanism of action of the ITB

A

presynaptic inhibition, GABA b receptor agonist

18
Q

What kind of reflexes does the ITB inhibit

A

mono and polysynaptic reflexes.

19
Q

what are the advantages of ITB

A

reversible, easy to titrate, fewer side effects, impoverished function and ease of care

20
Q

what are the disadvantages of ITB

A

mechanical complication, and you need refills every 3 months and its costly.

21
Q

what is the benefits of the ITB for post–stroke hypertonia

A

improved FIM, SIP, AS, no adverse effect on strength in unaffected limbs.

22
Q

what is the ITB CPG

A

for those who did not respond or tolerate other interventions, can use them 3-6 months after stroke. you need the optimal dosage.

23
Q

compare intrathecal with oral

A

intrathecal: lower dose needed and less side effects

Oral: low blood brain barrier penetration, high systemic absorption and low CNS absorption, lack of preferential distribution in the SC, adverse effects: sedation

24
Q

what kind of orthopedic surgeries can we do for soft tissue

A

selective percutaneous myofascial lengthening,
lengthening
tendon release or transfers.

25
Q

what are some skeletal procedures we can do

A

osteotomies and fusions

26
Q

what neurological interventions can we do

A

selective dorsal rhizotomy, with selective destruction of problematic nerve roots (spastic roots), and lesioned.

27
Q

what are general and reversible management things for spasticity

A

oral therapy and ITB

28
Q

what are general and permanent managements

A

SDR

29
Q

Reversible and focal

A

BTX-A

30
Q

permanent and focal

A

surgery

31
Q

what can we use to treat focal spasticity in MS

A

BoNT-A and exercise,

32
Q

review paper of rehab procedures in spasticity management showed the integration of…

A

meds and rehab

33
Q

rehab therapies after BoNT-A for limb spasticity

A

ergometer cycling, E-STIM, CIMT, task specific motor earning and exercise programs with the BoNT-A.

34
Q

what assumption do we make about spasticity and what does this mean

A

assume that spasticity is a direct cause of disordered movement,, an we assess it in resting limbs, and associate it with movement disorders.

35
Q

is there a direct causation between spasticity and function

A

no

36
Q

what can we manipulate when treating spasticity

A

task and enviro to make the demands less,

biomechanical constraints of the individual and decrease the DOF

37
Q

how can diagnose spasticity vs. MSK Contracture

A

tardieu scale, end feels, lidocaine block and an eval under anesthesia

38
Q

what must be treated prior to surgical interventions for contractions.

A

spasticity

Neuromuscular Practice (40 decks)

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