Asterixis is a neurological sign indicating the temporary inability to maintain a fixed body posture, often referred to as a “flapping tremor.” This involuntary movement is not a disease itself but rather a manifestation of an underlying dysfunction, typically one that affects the brain’s metabolism or structure. The term derives from Greek roots meaning “not supported” or “unstable position.” Recognizing this sign is important because it alerts medical professionals to a potentially serious metabolic or toxic imbalance that requires immediate investigation and treatment.
Clinical Presentation and Physical Examination
The classic presentation of asterixis involves the hands and wrists, where the movement is most readily observed. To elicit the sign, a clinician instructs the patient to extend their arms straight out in front of them with their wrists bent backward, or dorsiflexed, and their fingers spread. This specific posture demands sustained contraction from the extensor muscles of the wrist.
After holding this position for a short time, typically around 30 seconds, a patient with asterixis will exhibit brief, jerky, and irregular downward movements of the hands. The hand immediately returns to the original extended posture, creating a characteristic “flapping” motion, hence the common nickname. While the hands are the most common site, asterixis can also be observed in other areas that require sustained posture, such as the feet, tongue, and jaw.
Primary Medical Conditions Linked to Asterixis
The presence of bilateral asterixis is a strong indicator of a toxic or metabolic encephalopathy, a generalized disorder affecting brain function. The most common cause is hepatic encephalopathy, a complication of severe liver disease where the liver is unable to properly filter toxins. This failure leads to a buildup of substances, particularly ammonia, that cross the blood-brain barrier and interfere with neurotransmission.
Another frequent cause is uremia, which stems from severe kidney failure where waste products accumulate in the blood. This buildup of toxins impairs normal brain function. Respiratory failure, especially when it leads to hypercapnia (excess carbon dioxide retention), also commonly causes asterixis. The resulting acid-base imbalance disrupts the central nervous system’s environment.
Less common causes include severe electrolyte disturbances, such as low levels of magnesium or potassium, and certain medications. Several anticonvulsant drugs, including valproic acid and phenytoin, have been documented to induce asterixis, often by affecting ammonia metabolism. In rare instances, unilateral asterixis may be a sign of a structural brain lesion, such as a stroke or tumor, typically located in the thalamus or midbrain.
The Physiological Mechanism of the Tremor
The underlying mechanism of asterixis is not a traditional tremor caused by alternating muscle contractions, but rather a form of “negative myoclonus.” This means the movement is caused by a brief, involuntary cessation of muscle activity, a sudden pause in the sustained contraction required to hold the posture. This temporary loss of muscle tone lasts for a short period, generally between 50 and 200 milliseconds.
When the postural muscles temporarily relax, gravity pulls the hand downward, creating the initial part of the “flap.” The brain quickly attempts to compensate for this sudden lapse of tone, causing a rapid, jerky muscular contraction that returns the hand to its original position. The metabolic toxins associated with the underlying diseases are thought to disrupt the motor pathways, specifically affecting the brain’s diencephalic motor centers.
Diagnostic Steps and Treatment Focus
Once asterixis is identified during a physical examination, the immediate medical priority is to determine the precise underlying cause. The diagnostic process centers on a series of laboratory tests designed to assess the function of the body’s major filtering and regulatory systems. These tests include comprehensive liver function panels, blood ammonia levels, kidney function tests to check for uremia, and arterial blood gas analysis to assess for carbon dioxide retention.
Treatment for asterixis is entirely dependent on correcting the primary disorder; there is no specific medication to treat the sign itself. For hepatic encephalopathy, treatment focuses on reducing ammonia levels, often using medications like lactulose or antibiotics. If the cause is kidney failure, management may involve dialysis to remove the accumulated toxins. Asterixis is typically reversible, and the movement will resolve as the metabolic or toxic imbalance is successfully corrected.