Asterixis is a disorder of motor control characterized by irregular myoclonic lapses of posture affecting various parts of the body independently. These lapses are caused by involuntary 50- to 200-msec silent periods appearing in muscles (even antagonistic groups of muscles) which are tonically active. That is, the silent periods and postural lapses occur in muscles that have been contracting for a time whether or not there has been slow shortening or lengthening but probably do not occur during or immediately after a sudden movement at a joint. What constitutes a sudden as opposed to a slow movement remains to be defined. When bilateral asterixis is present, one cannot rule out the possibility of a focal lesion (see Table 2), but it is almost always due to a metabolic encephalopathy (with a wide variety of possible causes). Unilateral asterixis is due to a localized lesion, perhaps otherwise not clinically evident, in the contralateral cerebral hemisphere. This episodic dysfunction within neural circuits which are normally concerned with maintenance of sustained or tonic muscle contraction may be released by focal lesions only in specific CNS areas (such as ventrolateral thalamus) or by a more generalized neurochemical imbalance (metabolic encephalopathies of various kinds). The system, a lesion or metabolic dysfunction which produces asterixis, is presumably an anatomically and/or pharmacologically distinct one; asterixis is not the result of a nonspecific disorder any more than are seizures. Presumably, those aspects of each of the different factors (e.g., subdural hematomas, drugs, electrolyte imbalance, cerebrovascular accidents, intracerebral tumors) that may produce asterixis or a seizure are mediated through some fundamental neuronal or neural systems process. To label asterixis or seizures nonspecific results of CNS disorders or results of nonspecific CNS disorders may be simply to avoid confronting our ignorance of the specific pathophysiologic mechanisms involved. Although the anatomy, neurochemistry, and physiologic function of this asterixogenic system remain to be elucidated, observations that asterixis may be caused by discrete anatomic or pharmacologic (e.g., phenytoin) lesions should tell us something important about mechanisms underlying sustained muscle contraction in humans. Unfortunately clinicoanatomic correlations alone cannot provide precise answers because even those reasonably focal vascular lesions that cause asterixis are too gross to permit localization or identification of the neural systems involved.(ABSTRACT TRUNCATED AT 400 WORDS)