Asterixis is characterized by flapping tremors. It can be unilateral or bilateral and presents as irregular, sudden, and brief losses of muscle tone (negative myoclonus).
Patients can be evaluated for asterixis by holding the arms extended with the wrists dorsiflexed and fingers spread. Patients will demonstrate flapping tremors at the wrist. A silent period of 50-200 ms is seen between each "flap".
During the physical examination of a patient with asterixis, their hand will fall and rapidly be corrected to its starting position. This is called a corrective reflex movement.
Hyperammonemia is thought to be the main causative factor of asterixis. However, the exact pathophysiology is still not well understood.
Metabolic encephalopathies are associated with asterixis, especially liver disease, which can lead to hepatic encephalopathy.
Hepatic encephalopathy occurs due to the inability of the liver to metabolize ammonia. It is thought that brain damage from hyperammonemia leads to asterixis.
Another metabolic encephalopathy that is associated with asterixis is kidney disease. Other diseases or disorders that may cause asterixis are respiratory failure (hypoxia and/or hypercapnia), hypoglycemia, Wilson's disease, urea cycle disorders, drugs (most often antiepileptics), and structural brain abnormalities (such as hemorrhage, infarct, neoplasia, viral encephalitis, and cerebral toxoplasmosis).
Kidney failure lead to the inability to excrete nitrogenous waste products, which results in excessive urea in the body. The brain may be affected, resulting in asterixis in these patients.
Management of asterixis is achieved by treating the underlying disorder (e.g. liver or renal disease).
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