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Terms in this set (26)
Spasticity epidemiology in SCI, Stroke, MS
40-78% SCI, 19-42% Stroke, 85% MS
Motor control pathway from cortex to muscle
Premotor planning area/Motor cortex --> Internal capsule --> decussate in medullary pyramids --> corticospinal tract (UMN) --> interneurons and ventral horn LMN (alpha MN to NMJ for contraction, Gamma to intrafusal fibers for lengthening info)
Muscle spindle and Golgi tendon roles
Spindle: Activated by gamma MN, relay info about muscle lengthening (not shortening) via 1a afferents
Golgi: Receptors for muscle tension (lengthening and shortening) via 1b
Passive stretch -> MS and G activated Active contraction ->G only
What is 1a reciprocal inhibition?
Innate inhibition of antagonist muscle when agonist contracts (1a have excitatory connections to muscles they originate in and to synergistic muscles and inhibitory interneurons of antagonists)
1b nonreciprocal inhibition
Golgi firing --> interneuron activation of agonist alpha MN and facilitation of antagonist muscles
Prevents musclotendinous injury by causing ceiling effect to contraction
What causes spasticity
-Loss of supraspinal influence --> exaggerated reflexes
-Cocontraction and out of phase firing --> loss of normal recruit/decruit patterns
-Impaired reciprocal inhibition
-Decreased presynaptic 1a inhibition --> increased alpha MN firing
-Decreased nonreciprocal inhibition from GTO
-Increase in Renshaw cell inhibition --> decr recip inhib
Name 4 clinical spasticity assessments
MAS (and MMAS)
Modified Tardieu scale
SCATS (Spinal cord assessment tool for spastic reflexes)
Triple spasticity scale (stroke)
Name 3 patient reported assessment scales
Penn spasm frequency scale
PRISM (pt report impact spas measure)
SCI Spasticity Evaluation Tool
Name 6 non pharmacologic treatments for spasiticity
1. Decr noxious stimulation
2. Positioning (avoid scissoring, windswept, frogleg; encourage 90deg at hips and knees in WC)
3. Stretch (brief -> short lasting, Chronic (splints and orthotics) -> longer lasting)
4. Physical modalities (cooling and heating)
6. Whole body vibration, TCMS, Extracorporeal shockwave
BZD MOA, t1/2, SE
GABAa --> opens Cl- channels --> hyperpolarization --> decr mono and polysynaptic reflexes and incr presyn inhib. Best in SCI/MS.
Diazepam used most common, t1/2 20-80 hrs
Addiction, withdrawal, ataxia, weakness, cog impair, hypotension, resp depr, CNS depr
Baclofen MOA, t1/2, SE
GABAb receptor agonist and presynaptic inhib GABAb receptors. Best for SCI and MS.
T1/2 is 5 hrs. Eliminated by kidney
Sedation, hypotension, weakness, nausea, dizziness, hallucinations, lower sz threshold
Dantrolene MOA, t1/2, SE
Inhibit Ca++ release from sarcoplasmic reticulum during muscle contraction. Also acts on Gamma MN to decr muscle spindle sensitivity. Good for stroke, BI.
Liver toxicity in 1%, weakness, flushing, paresthesias, nausea, diarrhea
Clonidine MOA, t1/2, SE
Imidazoline derivitive. Central acting Alpha2 adrenergic agonist. 1. Acts on locus coeruleus (NE production center) to decr tonic facilitation. 2. Enhances presynaptic inhibition. Cleared by kidneys (and some by liver)
Oral: Peaks in 3hrs and t1/2 5-20hrs (40 if renal impairment). Transdermal is more consistent.
Bradycardia, depression, lethargy, syncope, hypotension. Can impair motor recovery after ABI.
Tizanidine MOA, t1/2, SE
Imidazoline derivative. Alpha2 agonist --> increases presynaptic inhibition of Gamma motor neurons and decr excitatory amino acids
2.5hr half life (cleared by liver and excreted by kidneys)
15% DC rate: drowsiness 50%. Dry mouth, fatigue, dizzy, hotn, weakness, n/v. Check liver enzymes.
Botox MOA, types, SE
Enters presynaptic nerve terminal --> light chain detaches and cleaves SNARE proteins --> prevents ACh release. May also act more proximally in MU and CNS via axonal transport. Decr recurrent inhib. Blocks ACh release between Renshaw cells. May attenuate maladaptive cortical reorg.
BotoxA targets SNAP25. Botox B targets synaptobrevin (Myobloc only). More pure toxins --> less immunogenicity --> secondary nonresponse rare. Still rec every 3 mo. Try another if one inneffective.
Local inj (bleeding), transient weakness, infx, remote spread (esp for cervical dystonia) --> dysphagia, URI-like sx, reports of botulism.
Phenol and ethanol MOA and SE
Denature proteins --> destroy tissue. Perineural phenol causes decr spasticity without weaness.
ITB procedure, SE
LP --> 50ug baclofen, if no response increase up to 100ug. If response, starting dose 2x effective bolus over 24 hrs
Replace device q7yrs, infx, csf leak, pump dysfunx --> withdrawal and sz.
Other intrathecal agents
Morphine: use as drug holiday from baclofen
Clonidine: improved spas control and gait speed, decr detrusor hyperactivity
Surgical procedures for spasticity
Osteotomy, capsulotomy, myotomy
Tendon lengthening (SPLATT - split anterior tendon transfer for excessive inversion during swing), achilles lengthening
Usual dosage of Botoxper muscle (range)? Max dosage for first tx?
Botox onset and duration
Onset 24-72hrs up to 7days. Peak in 4to 6 weeks. Lasts 2 to 6 months.
Sx/Tx of baclofen overdose
Tx with physostigmine to reverse respiratory depression. 10-20% dose reduction usually resolves sx.
Sx of baclofen withdrawal
Rebound spasticity --> rigidity --> rhabdo/mult system failure
Caution with Botox in what 3 pt groups?
ALS, MG, LEMS
involuntary patterned muscle contractions often associated with twisting movements or abnormal posture
Modified Ashworth Scale
Describe 1-4 scale
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