Asterixis, more colloquially referred to as flapping tremor, is not actually a tremor but rather a negative myoclonus. This movement disorder is characterized by an inability to maintain a position, which is demonstrated by jerking movements of the outstretched hands when bent upward at the wrist (which can be similar to a bird flapping its wings, hence the name "flapping tremor"). [1][2]
The tremor is caused by abnormal function of the diencephalic motor centers in the brain, which regulate the muscles involved in maintaining position. Asterixis is associated with various encephalopathies due especially to faulty metabolism.[3] The term derives from the Greeka, meaning "not" and stērixis, meaning "support" or "stable position".
Asterixis is normally asymptomatic and found during clinical examination for other reasons, but more rarely it can also be the leading symptom.[4] Usually there are brief, arrhythmic interruptions of sustained voluntary muscle contraction causing brief lapses of posture, with a frequency of 3–5 Hz. It is bilateral, but may be asymmetric. Unilateral asterixis may occur with structural brain disease.[5]
To elicit the sign the patient should be asked to hold constant posture against gravity. This can be done by extending the arms at 90° to the body and extending the wrists with the fingers spread. This position should be held for at least 30 seconds and in that duration the examiner should look for intermittent loss of posture in fingers, wrists or arms.[4]
Hepatic encephalopathy (for which the term was firstly described). The inability of the liver to metabolize ammoniatourea damages the brain cells. The cause is thought to be predominantly related to abnormal ammonia metabolism.[6]
Structural brain problems, like haemorrhage and neoplasia, which usually cause contraleteral one-sided asterixis.
Some drugs, particularly phenytoin (when it is known as phenytoin flap). Other drugs implicated include benzodiazepines, salicylates, barbiturates, valproate, gabapentin, lithium, ceftazidime, and metoclopramide.
R.D. Adams and J.M. Foley first described asterixis in 1949 in patients with severe liver failure and encephalopathy.[8] Initially Foley and Adams referred to asterixis simply as "tremor" but realized that they needed a more appropriate term. On a literature search they found a poorly described phenomenon in similar patients mentioned by German physicians called “jactitations” but the reference was vague. Foley consulted Father Cadigan, a Jesuit classics scholar, who suggested “anisosterixis” (an "negative"–iso "equal"–sterixis "firmness") but Foley shortened this to asterixis due to the former being too difficult to pronounce. They introduced the term in 1953 by way of a medical abstract and later Adams solidified its medical use as he was an author and editor of the widely influential Harrison's Principles of Internal Medicine.[9]
^Zackria, Rasiq; John, Savio (2021), "Asterixis", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID30571066, archived from the original on 2022-06-01, retrieved 2021-03-12
^Adams RD, Foley JM. The neurological changes in the more common types of severe liver disease. Trans American Neurology Association 1949; 74: 217–219.
^Pal G, Lin, Laureno R. Asterixis: a study of 103 patients. Metabolic Brain Disease [serial online]. September 2014;29(3):813–824.
