Cholinesterase Inhibitors

Cholinesterase inhibitors interfere with the hydrolysis of acetylcholine at the cholinergic synapses. Peripherally active agents have been the mainstay of myasthenic treatment until the advent of immunosuppressive therapy in the 1960s. Pyridostigmine bromide and neostigmine bromide are the most commonly used cholinesterase inhibitors. Pyridostigmine bromide is preferred because it has fewer gastrointestinal side effects and a longer duration of action.

Side effects of cholinesterase inhibitors result from overstimulation of the cholinergic system at the level of the muscarinic receptors of the smooth muscle, the nicotinic receptors of the skeletal muscle, the autonomic glands, and the CNS. Signs of cholinergic excess include nausea, abdominal cramps, excessive secretions, and bronchospasm. This syndrome is distinct from myasthenia gravis and is usually diagnosed accurately. However, because overstimulation can lead to subsequent depolarization blockade and enhanced weakness, exacerbation of myasthenia and cholinergic crisis can be dangerously confused. In situations in which there is a question of too much or too little cholinesterase inhibition, edrophonium (Tensilon) given in 1-mg increments may be helpful. More likely, however, admission to an intensive care unit for transient cessation of cholinesterase inhibition is needed to elucidate whether the dose should be raised or lowered.

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It has been suggested that chronic administration of cholinesterase inhibitors may damage the neuromuscular junction. This concern is based in part on the chronic effects on the neuromuscular junction known to occur in animals after large doses of prostigmine and reported decrease in improvement after thymectomy when the use of cholinesterase inhibitors increased. Nevertheless, the latter was a retrospective review, and therefore, there is no evidence that would discourage the use of cholinesterase inhibitors to treat myasthenia gravis when needed. y

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