Post-hypoxic myoclonus is a form of myoclonus frequently caused by cardiac arrest. Development of an animal model may facilitate understanding of the condition and its treatments. We describe an animal model of post-hypoxic myoclonus developed in our laboratory through cardiac arrest, initially induced by chemical and later by mechanical obstruction of major cardiac vessels. These animals respond to valproate, clonazepam and 5-hydroxytrytophan reminiscent of its human counterpart. We review their behavioral, pharmacological and neuropathological features. Therapy developed for myoclonus in this model may be helpful for myoclonus from other etiologies such as corticobasal degeneration, Lewy-body disorders, Creutzfeld-Jacob disease, Alzheimer's disease.