This is a comprehensive review of animal models of myoclonus with part
icular emphasis on posthypoxic myoclonus and other newer chemically in
duced models. A stimulus-sensitive myoclonus was developed by experime
ntally inducing cardiac arrest in rats. The etiology, pharmacology, an
d neurochemistry associated with this model are consistent with posthy
poxic myoclonus in humans. The complex etiology of posthypoxic myoclon
us and the effectiveness of diverse pharmacological therapies in this
movement disorder suggest that multiple interactive neurological mecha
nisms are operative. The p,p'-DDT-induced animal model of myoclonus di
ffers from posthypoxic myoclonus in terms of its neurochemical and pat
hophysiological mechanisms. Also, microinjection of compounds that mod
ulate specific neurotransmitter systems in select brain regions induce
s myoclonus in normal animals, suggesting that these chemically induce
d models may be useful in understanding the intricate neurochemical an
d neuroanatomical mechanisms associated with myoclonus. The experiment
al evidence demonstrates that these novel animal models of myoclonus h
ave salient neurological characteristics, reasonable predictability of
novel antimyoclonic agents, and pathophysiological similarities to th
e disorder in humans. Thus, these animal models of myoclonus have the
potential to provide us with valuable information about the disorder t
hat is not readily obtainable by other means. (C) 1996 Wiley-Liss, Inc
.