PTE 731: exam 4

what are skeletal muscle relaxants?

drugs used to treat conditions associated with hyper-excitable skeletal muscles (aka spasticity and muscle spasms)

what is the goal of prescribing skeletal muscle relaxants?

to normalize muscle excitability without a profound decrease in muscle function

what is spasm?

sudden, involuntary, localized contraction of a muscle/group of muscles 

• caused by muscle trauma, inflammation, nerve root, irritation, metabolic insult 

what is spasticity?

velocity-dependent increase in muscle tone due to loss of UMN inhibitory control 

• caused by CVA, TBI, SCI, MS, CP

what’s the difference between the pathophysiology of spasm and spasticity?

spasm: peripheral response to muscle insult (LMN injury) resulting in alpha-MA overactivity

spasticity: peripheral response to CNS loss of control (UMN injury) resulting in loss of inhibitory control over reflexes → hyperactivity of reflex arc

_________ treat spasms via decreasing excitatory interneuronal transmission which facilitates CNS inhibition. 

Spasmolytics

________ treats spasticities via increasing inhibitory neurotrasmission (GABA/Alpha-2) which facilitates CNS inhibition.

Antispasticity A’s

list some examples of spasmolytics.

• cyclobenzaprine (flexeril)

• diazepam (valium)

• methocarbamol (sloma)

• metaxalone (skelaxin)

• orphenadrine (norflex)

list some examples of antispasticity a’s.

• baclofen (lioresal)

• diazepam (valium)

• gagpentin (neurontin)

• tizanidine (zanaflex)

anti-spasm: cylobenzaprine (flexeril)

MOA: TCA-like structure adds to anticholinergic properties

SEs: sedation, anticholinergic

PT: schedule at end of dosage; monitor balance and vital signs; elderly alert

anti-spasm: diazepam (valium)

MOA: GABA-A enhancer

SEs: sedation, ataxia, cognitive slowing, tolerance, dependence, and addiction

PT: short-term use; fall risk; emphasize transfer safety

anti-spasm: metaxalone (skelaxin)

MOA: ?

SEs: less sedation, nausea/vomiting, rare chance of hypatotoxicity or anemia

PT: monitor for drowsiness; schedule at end of dose; monitor for liver symptoms

anti-spasm: orphenadrine (norflex)

MOA: antimuscarinic

SEs: sedation, anticholinergic

PT: use caution with elderly and heart patients; monitor for confusion, tachycardia, falls 

anti-spastic: baclofen (lioresal)

MOA: GABA-B enhnacer

SEs: drowsiness, fatigue, confusion, muscle weakness, hypotonia, withdrawal symptoms

PT: monitor for strength and tone; avoid abrupt cessation

anti-spastic: tizanidine (zanaflex)

MOA: alpha-2 agonist

SEs: sedation, dizziness, dry mouth, hypotension, bradycardia, and rare chance of hepatotoxicity

PT: monitor blood pressure and strength; transfer precautions; ensure hydration

which two drugs are used to treat spasticity but do not facilitate CNS inhibition?

1. botulism toxin (botox)

2. dantrolene (dantrium)

explain the mechanism of action for botox.

botox destroys the fusion proteins, thereby preventing Ach laden vesicles from binding and releasing Ach into the synapse → no muscle contraction available

what are the two types of botox?

1. type A botox

2. type B myobloc

which type of botox is favored and why?

type A botox because it has a higher immunogenicity, chemically more stable, longer duration, and less painful

what are the adverse effects of receiving botox?

possibility of rash, laryngospasm, wheezing, systematic paralysis, and if it enters the bloodstream = respiratory failure

explain the mechanism of action for dantrolene.

prevents calcium release from the sarcoplasmic reticulum resulting in complete relaxation of the muscle fibers