Part 3 - Muscle Relaxants Flashcards
Muscle Relaxants Primary Goals
Selectively decrease skeletal muscle excitability
Muscle Relaxants Primary Uses
Muscle Spasms and spasticity
Muscle Spasms
Usually injury to mm or peripheral nn causing tonic contraction
Spasticity
CNS lesion that causes an exaggerated stretch reflex. Often velocity dependent.
Types of agents used to treat muscle spasms
Centrally acting anti-spasm drugs
Diazapam (Valium)
Centrally acting anti-spasm drugs
Diverse group
Used commonly in back and neck spasms; other ortho injuries
Common Central antispasm drugs
Carisoprodol Chlorzoxazone Cyclobenzaprine Metaxalone Methocarbarbamol Orphenadrine Citrate
Centrally-acting anti-spasm drugs primary effect
Strong sedatives
Carisoprodol MOA
Enhances GABA inhibition in brain
Cyclobenzaprine MOA
Might increase serotonin in the brainstem
Antispasm drugs bottom line
Short term use for acute spasms
Patients may decide to take at bedtime
Combine with aggressive PT
Should be discontinued ASAP
Diazepam (Valium)
Developed originally as an antianxiety drug
Works in CNS to increase inhibitory effects of GABA
GABA Receptor
Has binding sites for GABA, Benzo, Barbituates
Chloride channel in the center
Chloride is normally inhibitory
Valium keeps GABA bound longer
Valium effects
Increases GABA mediated inhibition of alpha motor neuron
Less excitation leads to muscle relaxation
Used in spasms and spasticity, but causes sedation
Long-term use limited by tolerance and dependence
Agents used to treat spasticity
Diazepam Baclofen Alpha-2 agonists Gabapentin Dantrolene Botulinum toxin
Baclofen
Synthetic GABA
Stimulates GABA receptors in cord
Decreases excitation of alpha motor neuron
Can be administered intrathecally
Intrathecal Baclofen
Used in severe spasticity
Catheter and pump deliver drug to subarachnoid space
May decrease spasticity with less drug, fewer side effects
Intrathecal baclofen signs of OD
Decreased respiration
Decreased cardiac function
Stupor
Coma
Intrathecal baclofen signs of withdrawal
Fever
Confusion
Hallucinations
Seizures
Alpha-2 agonists
Primarily tizanidine
Stimulates alpha-2 receptors located on spinal interneurons
Causes inhibition of interneurons; decrease excitation on alpha motor neuron
Efficacy similar to oral baclofen but less generalized mm weakness
Gabapentin (Neurontin)
Developed as antiseizure drug
Inhibits Ca++ entry presynaptic terminal; decreased release of glutamate
Used primarily in MS, SCI.
May cause sedation, dizziness, ataxia
Dantrolene Sodium (Dantrium)
Only direct-acting muscle relaxant
Inhibits release of calcium from skeletal mm SR
Problems with liver toxicity; esp women over 35
Botulinum toxin
Muscle paralytic...Injected locally for severe spasms such as torticollis Increased use in spasticity 7 serotypes, 2 used clinically -Type A (Botox, Dysport, Xeomin) -Type B (Myobloc)
Botulinum toxin MOA
Inhibits release of ACh at skeletal neuromuscular junction by eating connection proteins so no exocytosis of ACh
Botulinum toxin antispasticity effects
Injected into selected muscle Relaxation occurs within 3 to 7 days; lasts 2 to 3 months Reduces spastic dominance -Increases residual function -Improved ADL, braces fit better, etc
Botulinum toxin effects
BTX may be transported to CNS (retrograde transmission)
May produce carry-over & long term effects on activity in cord and brain
Limitations of botulinum toxin
Local irritation at injection site
Potential for antibody production
Must limit total dose
Botulinum toxin total dose
300-400 Units/tx Type A
2500-5000 Units/Tx Type B
BTX signs of OD
Drooping eyes
Difficulty speaking/swallowing
General muscle weakness
Respiratory distress
Muscle relaxants rehabilitation concerns
Generalized weakness
Sedation
Possible drastic change in spasticity over relatively short time span
