Animal models of myoclonus.

This is a comprehensive review of animal models of myoclonus with particular emphasis on posthypoxic myoclonus and other newer chemically induced models. A stimulus-sensitive myoclonus was developed by experimentally inducing cardiac arrest in rats. The etiology, pharmacology, and neurochemistry associated with this model are consistent with posthypoxic myoclonus in humans. The complex etiology of posthypoxic myoclonus and the effectiveness of diverse pharmacological therapies in this movement disorder suggest that multiple interactive neurological mechanisms are operative. The p,p'-DDT-induced animal model of myoclonus differs from posthypoxic myoclonus in terms of its neurochemical and pathophysiological mechanisms. Also, micro-injection of compounds that modulate specific neurotransmitter systems in select brain regions induces myoclonus in normal animals, suggesting that these chemically induced models may be useful in understanding the intricate neurochemical and neuroanatomical mechanisms associated with myoclonus. The experimental evidence demonstrates that these novel animal models of myoclonus have salient neurological characteristics, reasonable predictability of novel antimyoclonic agents, and pathophysiological similarities to the disorder in humans. Thus, these animal models of myoclonus have the potential to provide us with valuable information about the disorder that is not readily obtainable by other means.