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In this issueof Neurology, Pappert et al. describe a model of stimulus sensitive myoclonus after cardiac arrest in the rat.1 They also investigate the potential neuropharmacology of myoclonus in their model. Whereas other investigators have implicated both NMDA and non-NMDA glutamate receptors in this syndrome,2 Pappert et al. describe the effectiveness of 5-hydroxytryptamine receptor antagonists in the myoclonus and suggest a particular role for certain subtypes of serotinergic receptors in the syndrome of posthypoxic myoclonus. The authors have thus provided a valuable lead for further study of potential therapy for myoclonus in the setting of cardiac arrest.
However, the report leaves unanswered an important mechanistic question about the etiology of “post-hypoxic” myoclonus: Is it caused by brain hypoxia or brain ischemia? The mechanism of induction of cardiac arrest used by Pappert et al. was compression of the great vessels. Po2s are not available to determine the presence or absence of hypoxia …
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