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Blepharospasm and other manifestations of involuntary muscle spasm can be disabling and, in the case of large muscles, painful. Contraction of skeletal muscle is triggered by exocytotic release of acetylcholine (ACh) from motor nerves in response to calcium influx at the nerve ending. Release of ACh can be reduced or blocked by botulinum toxin, which interferes with the fusion of nerve ending ACh vesicles with the nerve ending membrane (see text). Depend-ing on dosage, botulinum blockade has an average duration of 1 to 3 months.
Achilles J. Pappano, PhD
In late morning, a coworker brings 43-year-old JM to the emergency department because he is agitated and unable to continue picking vegetables. His gait is unsteady, and he walks with support from his colleague. JM has difficulty speaking and swallowing, his vision is blurred, and his eyes are filled with tears. His coworker notes that JM was working in a field that had been sprayed early in the morning with a material that had the odor of sulfur. Within 3 hours after starting his work, JM complained of tightness in his chest that made breathing difficult, and he called for help before becoming disoriented. How would you proceed to evaluate and treat JM? What should be done for his coworker?
Acetylcholine-receptor stimulants and cholinesterase inhibitors make up a large group of drugs that mimic acetylcholine (cholinomimetics) (Figure 7–1). Cholinoceptor stimulants are classified pharmacologically by their spectrum of action, depending on the type of receptor—muscarinic or nicotinic—that is activated. Cholinomimetics are also classified by their mechanism of action because some bind directly to (and activate) cholinoceptors whereas others act indirectly by inhibiting the hydrolysis of endogenous acetylcholine.