Asterixis is a neurological sign characterized by the inability to maintain a sustained posture, resulting in sudden, brief lapses of muscle tone. Often referred to as “flapping tremor,” it is not a disease itself but rather a symptom indicating an underlying issue affecting the central nervous system. This involuntary movement is a specific type of negative myoclonus, caused by an interruption or pause in muscle activity rather than a sudden contraction. The appearance of this sign is a strong indicator of a metabolic or structural problem disrupting the brain’s ability to regulate posture.
Clinical Presentation and Examination
The presence of asterixis is typically detected during a clinical examination. A common technique for eliciting this sign is to have the patient extend their arms straight out, dorsiflex their wrists—as if signaling to “stop traffic”—and spread their fingers apart. This position requires a continuous, voluntary effort to maintain sustained muscle contraction against gravity.
When asterixis is present, the patient’s hands will exhibit brief, irregular, jerking movements, often described as a flapping motion at the wrist. These involuntary movements are caused by a momentary loss of muscle tone, which allows the hand to suddenly flex or drop forward. This is followed immediately by a rapid, compensatory muscle contraction to return the hand to its original position. The movement is asynchronous, meaning the flaps do not occur at the same time in both hands.
While it most commonly affects the hands and wrists, this involuntary movement can potentially involve other muscle groups, including the legs, trunk, and tongue. Asterixis is frequently bilateral, affecting both sides of the body, which suggests a widespread metabolic issue. However, a unilateral presentation can occur and often points toward a specific structural lesion in the brain, such as a stroke.
Primary Medical Conditions That Cause Asterixis
Asterixis is a hallmark of toxic-metabolic encephalopathy, where toxins or chemical imbalances accumulate and impair brain function. The most common cause is hepatic encephalopathy, which occurs in cases of severe liver failure. When the liver cannot properly metabolize waste products, toxins like ammonia build up in the bloodstream, crossing the blood-brain barrier and directly affecting neurological function.
Another significant cause is uremic encephalopathy, which results from severe kidney dysfunction and the retention of waste products, known as uremic toxins. This metabolic imbalance creates a toxic environment for the brain, leading to neurological symptoms. Similarly, respiratory failure, particularly when it leads to hypercapnia (abnormally high carbon dioxide levels in the blood), can also induce this sign.
A range of medications can also cause asterixis as a side effect, often by inducing a toxic encephalopathy. Anti-seizure medications are common culprits, with phenytoin, valproate, and carbamazepine being frequently reported. Other drugs, including barbiturates and certain benzodiazepines, are also known to trigger this sign.
Electrolyte imbalances, such as low levels of potassium or magnesium, or even high levels of magnesium, can disrupt nerve signaling and contribute to the development of asterixis. The appearance of the “flapping tremor” serves as a clinical warning sign, indicating a serious systemic derangement that requires immediate investigation.
Neurophysiological Basis of the Tremor
The mechanism underlying asterixis is rooted in a temporary failure of the motor system to maintain a sustained voluntary muscle contraction. This lapse of posture is a result of a brief, involuntary cessation of muscle activity, a phenomenon known as negative myoclonus. The problem is not with the muscle itself, but with the central nervous system’s command to the muscle.
Metabolic toxins, such as the elevated ammonia seen in hepatic encephalopathy, are thought to primarily affect the ascending activating systems in the brainstem, including the reticular formation. These brain regions are responsible for regulating the continuous flow of signals needed for postural tone and sustained movement. When these systems are poisoned, the continuous stream of excitatory impulses to the motor neurons is briefly inhibited.
This temporary inhibition leads to a silent period in the electromyography (EMG) of the muscle, causing the sudden loss of tone and the resulting downward “flap.” The subsequent, rapid return of muscle activity is a corrective reflex that attempts to re-establish the sustained posture. The widespread nature of metabolic toxicity accounts for the typical bilateral presentation.
Management of the Underlying Cause
Because asterixis is a physical sign of an underlying medical problem, there is no specific treatment directed at the movement itself. Management focuses entirely on identifying and correcting the root cause of the metabolic or structural derangement. When the underlying condition is successfully treated, the asterixis typically resolves.
For cases stemming from hepatic encephalopathy, treatment is aimed at reducing the elevated ammonia levels in the bloodstream. This often involves administering the synthetic sugar lactulose, which helps remove ammonia from the body, and the antibiotic rifaximin, which reduces the ammonia-producing bacteria in the gut.
If the sign is caused by uremic encephalopathy, the priority is to address the kidney failure. This may involve initiating or intensifying dialysis to remove accumulated toxins and correct the metabolic imbalances. In instances of drug-induced asterixis, the causative medication must be discontinued or its dosage significantly adjusted.