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Chapter 21 Neuromuscular Disorders
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Disorders associated with movement; difficult conditions to treat
Muscle spasms: involuntary contractions of a muscle or group of muscles
o The muscles become tightened and develop a fixed pattern of resistance,
resulting in diminished level of functioning
Causes of Muscle Spasms
o Associated with excessive use of and local injury to the skeletal muscle
o Overmedication with antipsychotic drugs
o Epilepsy
o Hypocalcemia
o Pain
o Debilitating neurological disorders
Patients with muscle spasms may experience inflammation, edema, and pain at the
affected muscle, loss of coordination, and reduced mobility
Muscle locks in the contracted state
Tonic spasm: A single, prolonged contraction
Clonic spasm: multiple, rapidly repeated contractions
Pharmacologic & Nonpharmacologic Treatment
o Nonpharmacologic measures may include
 Immobilization of the affected muscle
 Application of heat/cold
 Hydrotherapy
 Ultrasound
 Supervised exercises
 Massage & manipulation
o Pharmacologic measures for muscle spasms include
 Analgesics
 Anti-inflammatory agents
 Centrally acting skeletal muscle relaxants – relieve symptoms of
muscular stiffness and rigidity
o Help improve mobility
o goals = minimize pain and discomfort, increase ROM, & improve ability
to f(x) independently
Centrally acting skeletal muscle relaxants – muscle relaxants generate their effects by
inhibiting motor neurons within the brain/spinal cord; origin of drug action is within
the CNS
Treating Muscle Spasms @ the CNS level
o Inhibiting upper motor neuron activity, causing CNS depressant effects, or
altering simple spinal reflexes
o Antispasmodic drugs
 Baclofen- similar to GABA; inhibits neuronal activity within the
brain; reduce muscle spasms in patients with MS, cerebral palsy, or
spinal cord injury; wide safety margin
 Advers effects = drowsiness, dizziness, weakness & fatigue
 Tizanidine – alpha2-andrenergic agonist; inhibits motor neurons
mainly @ the spinal cord; as efficacious as baclofen
Chapter 21 Neuromuscular Disorders
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Adverse effects = drowsiness, hallucinations, dry mouth,
fatigue, dizziness, and sleepiness
 Benzodiazepines – inhibit both sensory & motor neuron activity by
enhancing the effects of GABA
 Adverse effects = drowsiness and ataxia (loss of
coordination)
Spasticity: a condition in which certain muscle groups remain in a continuous stat of
contraction, usually resulting from damage to the CNS
o Mild to severe pain, exaggerates deep tendon reflexes, and muscle spasms,
scissoring (involuntary crossing of the legs), and fixed joints
Causes & Treatment of Spasticity
o Results from damage to the motor area of the cerebral cortex that control
muscle movement
o Etiologies = neurologic disorders, severe head injuries, spinal cord injury
or lesions, and stroke
o Dystonia: a chronic neurologic disorder, characterized by involuntary
muscle contraction that forces body parts into abnormal occasionally
painful movements or postures
o Types of treatment
 Muscle stretching helps prevent contractures
 Muscle group strengthening exercises
 Repetitive-motion exercises for improvement of accuracy
 Surgery to release tendons or to sever the nerve-muscle pathway
has occasionally been used
o Drugs effective in treatment
 Antispasmodics that act at the level of the CNS, neuromuscular
junction, or muscle tissue
Direct-Acting Antispasmodics – dantrolene (Dantrium); produce an antispasmodic
effect at the level of the neuromuscular junction and skeletal muscle
Treating Muscle Spasms directly @ the Muscle Tissue
o Dantrolene
 relieves spasticity by interfering with the release of Ca2+ ions in the
skeletal muscle
 If the release of Ca2+ is blocked, muscle tension will be reduced
o Botulinum
 A toxin that is an unusual drug because in higher doses it = a
poison
 Clostridium botulinum = bacterium responsible for food poisoning
 It produces its effects by blocking the release of acetylcholine from
cholinergic nerve terminals
 Drawbacks – delayed and limited effects; treatment is mostly
effective within 6 weeks and lasts only 3-6 months; painful
because it is injected directly into the muscle
Blocking the effect of Acetylcholine at the Receptor
o Neuromuscular blockers: bind to nicotinic receptors located on the
surface of skeletal muscle fibers
Chapter 21 Neuromuscular Disorders
o Nicotinic blocking agents interfere with the binding of acetylcholine
which prevents voluntary muscle contraction
o Nicotinic blocking agents are cholinergic
o Neuromuscular blocking agents
 Nondepolarizing blockers – compete with acetylcholine for the
receptor; as long as agents interfere with the binding of Ach,
muscles remain relaxed
 Depolarizing blockers – bind to Acetylcholine receptor & produce
a state of continuous depolarization; this action 1st results in small
fasciculations (brief repeated muscle movements), followed by
relaxation if muscle fibers
 Relaxation is short lived until charges across the muscle
membrane are restored (repolarization)
o Neuromuscular blocking agents are DIFFERENT from Ganglionic
blocking agents
o Ganglionic Blocking Agents – target the autonomic nervous system
 Acetylcholine does bind to nicotinic receptors
 The resulting actions are involuntary and do not involve skeletal
muscle contraction
 Dampen parasympathetic tone
 Produce effects like increased heart rate, dry mouth, urinary
retention, and reduced GI activity
 Dampen sympathetic tone
 Resulting in reduced sweating & less norepinephrine being
released from the postsynaptic nerve terminals
o Classic example of a nondepolarizing blocker = tubocurarine
 Used to relax the muscles of patients being prepared for longer
surgical procedures
 Concerns = over-relaxation of muscles
o Depolarizing agents are used primarily to relax the muscles of the patients
receiving electroconvulsive therapy (ECT) & for shorter surgical
procedures
 Succinylcholine = prototype depolarizing blocker
 Adverse effects = persistent paralysis, elevated blood levels of K+,
malignant hyperthermia, and postoperative muscle pain