What is Asterixis?
Asterixis is a negative myoclonus characterized by brief, involuntary lapses in sustained muscle contraction leading to loss of postural tone, most commonly seen in hepatic encephalopathy but not pathognomonic for it. 1
Clinical Definition and Characteristics
Asterixis is not actually a tremor despite being called "flapping tremor"—it represents a negative myoclonus consisting of sudden, brief losses of postural tone. 1 The phenomenon manifests as arrhythmic lapses in sustained posture due to involuntary pauses in muscle contraction. 2, 3
How to Elicit Asterixis
The sign is most easily demonstrated by:
- Hyperextension of the wrists with fingers separated and spread apart 1
- Having the patient rhythmically squeeze the examiner's fingers 1
- Observing other body areas including feet, legs, arms, tongue, and eyelids 1, 2
Clinical Context and Significance
Timing in Disease Progression
Asterixis typically appears in the early to middle stages of hepatic encephalopathy, before progression to stupor or coma. 1 According to the International Society for Hepatic Encephalopathy and Nitrogen Metabolism (ISHEN) consensus, the onset of asterixis or disorientation marks the transition to overt hepatic encephalopathy. 1
Pattern Recognition
Asterixis can present in different patterns:
- Bilateral in 81.4% of cases 4
- Unilateral in 18.6% of cases 4
- May be more prominent in upper versus lower extremities depending on the underlying cause 4
Differential Diagnosis: Not Just Liver Disease
A critical pitfall is assuming asterixis is pathognomonic for hepatic encephalopathy—it can occur in multiple other conditions. 1
Common Etiologies Include:
Metabolic causes:
- Uremia (renal failure) 1, 2
- Hypercapnia (respiratory failure) 2, 3
- Hypoglycemia 2
- Electrolyte disturbances (hypokalemia, hypomagnesemia) 2
Medication-induced:
- Antiepileptic drugs (valproic acid, carbamazepine, phenytoin) 2, 3
- Levodopa, opiates, anticholinergics 2
- Benzodiazepines, lithium, clozapine 2
Structural brain lesions:
Important Clinical Pearl
Unilateral asterixis should raise suspicion for focal structural brain lesions rather than metabolic encephalopathy. 4, 5 Conversely, bilateral asterixis can rarely result from structural lesions, not just toxic-metabolic causes. 5
Pathophysiology
Neurophysiological studies localize asterixis generation to the contralateral primary motor cortex (M1, Brodmann area 4). 6 Magnetoencephalography studies demonstrate a biphasic cortical activation pattern with field reversals occurring 49 ms before and 99 ms after flap onset. 6
Clinical Implications
Asterixis is usually asymptomatic and not spontaneously reported by patients, making active examination essential in any encephalopathic patient. 3 Its presence should prompt investigation for underlying toxic or metabolic causes. 3
The sign is typically reversible upon treatment of the underlying cause. 3