Development of Asterixis
Asterixis develops through a loss of postural tone resulting in negative myoclonus, most commonly caused by metabolic encephalopathies (particularly hepatic encephalopathy), medications, renal dysfunction, pulmonary insufficiency, or structural brain lesions including stroke.
Pathophysiological Mechanism
Asterixis is fundamentally a negative myoclonus consisting of loss of postural tone rather than a true tremor 1. The mechanism involves:
- Intermittent lapses in sustained muscle contraction required to maintain posture, creating the characteristic "flapping" appearance 1
- Disruption of neural pathways that maintain tonic muscle activity, though the precise anatomical substrate remains incompletely understood 2
- The phenomenon can be elicited in any muscle group requiring sustained postural tone, including wrists, fingers, feet, legs, arms, tongue, and eyelids 1
Primary Etiologies
Metabolic Encephalopathies
Hepatic encephalopathy is the classic and most common cause 1:
- Asterixis appears in early to middle stages of hepatic encephalopathy, before progression to stupor or coma 1
- The International Society for Hepatic Encephalopathy and Nitrogen Metabolism uses the onset of asterixis (along with disorientation) as a defining criterion for overt hepatic encephalopathy 1
- Results from accumulation of neurotoxic substances (particularly ammonia) that impair neural function 1
Other metabolic causes include 2:
- Uremic encephalopathy (renal failure)
- Pulmonary insufficiency with hypercapnia
- Electrolyte disturbances
Medication-Induced
Various medications can precipitate asterixis through effects on neural transmission or metabolic pathways 2. This represents a common and potentially reversible cause in hospitalized patients 2.
Structural Brain Lesions
Asterixis can result from focal brain pathology 2:
- Stroke affecting specific brain regions involved in motor control 2
- Intracranial mass lesions including malignancy 2
- Subdural hematoma 2
- Epidural abscess 2
When caused by structural lesions, asterixis may be unilateral (18.6% of cases), providing localizing value, whereas metabolic causes typically produce bilateral asterixis (81.4% of cases) 2.
Clinical Patterns and Presentation
Distribution Patterns
Asterixis manifests in varied anatomical distributions 2:
- Some patients demonstrate easier elicitation in upper extremities
- Others show predominant involvement of lower limbs
- Unilateral or asymmetric patterns suggest structural rather than metabolic etiology 2
Examination Technique
The classic method to elicit asterixis involves 1:
- Hyperextension of the wrists with fingers separated and extended
- Rhythmic squeezing of the examiner's fingers
- Observation for brief lapses in sustained posture creating a "flapping" motion 1
Important Clinical Caveats
Asterixis is not pathognomonic for any single condition and occurs across multiple disease states 1. The presence of asterixis should prompt:
- Evaluation for hepatic encephalopathy in patients with known or suspected liver disease 1
- Assessment of renal function, pulmonary status, and medication review 2
- Consideration of structural brain lesions, particularly when asterixis is unilateral or accompanied by focal neurological signs 2
The pattern of asterixis (bilateral versus unilateral, upper versus lower extremity predominance) provides diagnostic clues to the underlying etiology and should be carefully documented 2.