Asterixis is an involuntary movement disorder that signals an underlying neurological or metabolic problem. It is characterized by an inability to maintain a sustained posture, which results in brief, irregular lapses of muscle contraction. The disorder is a clinical sign often associated with conditions causing widespread brain dysfunction, but it is not a diagnosis in itself.
Defining the Physical Manifestation
Asterixis is a disorder of motor control, not a true tremor, and is formally classified as a type of negative myoclonus. The term “negative” refers to the sudden, momentary loss of muscle tone rather than an active muscle contraction. These brief interruptions in muscle activity cause the body part to briefly relax before the patient rapidly corrects the posture.
To observe the characteristic movement, a physician will typically ask the patient to extend their arms straight out, dorsiflex the wrists (as if stopping traffic), and spread the fingers. After a few seconds, the hands of a person with asterixis will suddenly drop or “flap” forward at the wrist, then quickly return to the extended position. This bilateral and asynchronous movement usually occurs at a frequency of 3 to 5 Hertz. Although most commonly seen in the wrists, asterixis can also affect other body parts, including the tongue, jaw, or legs.
Primary Underlying Causes
The presence of asterixis most frequently suggests toxic-metabolic encephalopathy, where toxins or imbalances in the bloodstream interfere with normal brain function. The most common cause is Hepatic Encephalopathy, which occurs when the liver is unable to effectively metabolize and remove toxins. This leads to an accumulation of substances like ammonia, which then travel to the brain and disrupt neural activity.
Other major causes include Uremic Encephalopathy, arising from kidney failure where uremic toxins build up in the blood, and Respiratory Encephalopathy, caused by severe respiratory failure resulting in excessive retention of carbon dioxide (hypercapnia). Asterixis may also be triggered by specific electrolyte imbalances, such as low levels of potassium (hypokalemia) or magnesium (hypomagnesemia). Certain medications, particularly anticonvulsants like phenytoin and valproate, are also known to cause drug-induced encephalopathy. While bilateral asterixis is linked to these metabolic issues, a one-sided presentation can sometimes signal a structural brain lesion, such as a stroke or tumor, typically in the thalamus or midbrain.
The Neurological Mechanism
Asterixis is a lapse of posture that results from a temporary, involuntary pause in the muscle’s electrical activity, known as a silent period. This pause is caused by a temporary dysfunction in the neural circuits responsible for maintaining sustained muscle contraction. Specifically, it involves the motor centers in the diencephalon and the brainstem reticular formation, which regulate posture and muscle tone.
In conditions like hepatic encephalopathy, the buildup of circulating metabolic toxins, such as ammonia, crosses the blood-brain barrier. Ammonia interferes with inhibitory neurotransmission by enhancing the activity of the gamma-aminobutyric acid (GABA) system in the brain. This heightened inhibitory tone disrupts the normal function of the brain’s ascending activating systems, which are responsible for arousal and the continuous signaling needed to sustain posture.
Diagnosis and Management Approach
The initial step in diagnosis is confirming the physical sign of asterixis through the clinical examination maneuver of sustained arm and wrist extension. Once the characteristic flapping movement is observed, the clinical focus shifts immediately to identifying the underlying cause, as the symptom is a marker of a serious systemic problem. The diagnostic workup involves extensive laboratory testing to assess the function of the organ systems most commonly implicated.
Physicians will order blood tests to check liver function, kidney function, and arterial blood gas levels to detect carbon dioxide retention. Electrolyte panels are also performed to look for imbalances such as hypoglycemia or hypokalemia.
Management of asterixis is synonymous with treating the root metabolic disorder, not the movement itself. For example, in hepatic encephalopathy, treatment focuses on reducing ammonia levels in the bloodstream, often using medications like lactulose or rifaximin. If the cause is medication-related, the drug dosage is adjusted or the drug is discontinued. The asterixis is generally reversible and resolves once the underlying toxic or metabolic condition is successfully corrected.