Asterixis is a clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements. This motor disorder is myoclonus characterized by muscular inhibition (whereas muscle contractions produce positive myoclonus). Initially described in 1949 by James Foley and Raymond Adams to describe the flapping tremor they observed in liver disease, this clinical sign is not pathognomonic for any condition. However, it may indicate a serious underlying disease process.
Asterixis can be elicited on physical examination by having the patient extend their arms, dorsiflex the wrists, and spreading the fingers (similar to pushing against a wall) with their eyes closed. This is used to test for the “flap” at the wrist and is the most common method of assessment. One can also elicit asterixis at the hip joint by keeping the patient in the dorsal recumbent position (supine with their knees bent up in an outward position while the feet are flat) and allowing the knees to fall to the sides. The presence of "flapping" shows the presence of asterixis.
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The exact pathophysiology of asterixis is still unknown. Several theories suggest a role for the ascending activating systems associated with arousal, which is disturbed in encephalopathy and lesions of the thalamus and midbrain. Two types of surface electromyographic (EMG) patterns have been demonstrated in patients with encephalopathy: pure silent period (type 1) and the silent period following a brief EMG discharge (type 2). These patterns are like the EMG patterns of asterixis caused by a thalamic lesion. However, the pathophysiology of thalamic asterixis has not been definitively established.
Asterixis can either be unilateral or bilateral and is typically asynchronous, irregular and variable in frequency and amplitude. Although the clinical sign may suggest an underlying process, the clinical history of the presenting illness is fundamental in triggering further workup.
Bilateral asterixis is most commonly associated with metabolic encephalopathies, especially hepatic. The presumption in hepatic encephalopathy was that damage to brain cells due to the impaired metabolism of ammonia was predominantly related to the development of asterixis in hepatic encephalopathy, however, new research shows that ammonia level does not directly correlate with the development of this phenomenon. Bilateral asterixis may also present in patients with cardiac and respiratory failure, uremia, electrolyte abnormalities (primarily hypoglycemia, hypokalemia, and hypomagnesemia), and drug intoxication. Phenytoin intoxication is the most commonly reported drug-induced asterixis, while other drugs implicated include benzodiazepines, barbiturates, valproate, gabapentin, carbamazepine, lithium, ceftazidime, and metoclopramide.
Unilateral asterixis is usually because of focal brain lesions in the thalamus, although there have been reports of lesions in the midbrain, parietal cortex, and frontal cortex causing unilateral asterixis.
Asterixis is a significant yet poorly understood clinical sign and is part of the West Haven Criteria used to grade the severity of hepatic encephalopathy as it seems to be a relatively sensitive sign of the disease but is non-specific. Asterixis is the most widely known motor abnormality in hepatic encephalopathy. It is not present at rest, and best elicited on sustained posture. It can also be elicited by asking the patient to grip the examiner's hands tightly. It is usually bilateral but may not be bilaterally synchronous as one side may be affected more than the other. Previously thought to have been exclusively associated with hepatic encephalopathy, this phenomenon may present in different contexts. The evaluation and management depend on the underlying disease process, and one should consider a broad differential diagnosis based on clinical history. The treatment of asterixis is the treatment of the underlying pathology.
Kojovic M, Cordivari C, Bhatia K. Myoclonic disorders: a practical approach for diagnosis and treatment. Therapeutic advances in neurological disorders. 2011 Jan:4(1):47-62. doi: 10.1177/1756285610395653. Epub [PubMed PMID: 21339907]Level 3 (low-level) evidence
ADAMS RD, FOLEY JM. The neurological disorder associated with liver disease. Research publications - Association for Research in Nervous and Mental Disease. 1953:32():198-237 [PubMed PMID: 13134644]
Butz M, Timmermann L, Gross J, Pollok B, Südmeyer M, Kircheis G, Häussinger D, Schnitzler A. Cortical activation associated with asterixis in manifest hepatic encephalopathy. Acta neurologica Scandinavica. 2014 Oct:130(4):260-7. doi: 10.1111/ane.12217. Epub 2013 Dec 24 [PubMed PMID: 24372275]
Inoue M, Kojima Y, Mima T, Sawamoto N, Matsuhashi M, Fumuro T, Kinboshi M, Koganemaru S, Kanda M, Shibasaki H. Pathophysiology of unilateral asterixis due to thalamic lesion. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2012 Sep:123(9):1858-64. doi: 10.1016/j.clinph.2012.01.021. Epub 2012 Mar 15 [PubMed PMID: 22425586]
Larson AM. Diagnosis and management of acute liver failure. Current opinion in gastroenterology. 2010 May:26(3):214-21. doi: 10.1097/MOG.0b013e32833847c5. Epub [PubMed PMID: 20216412]Level 3 (low-level) evidence
Ge PS, Runyon BA. Serum ammonia level for the evaluation of hepatic encephalopathy. JAMA. 2014 Aug 13:312(6):643-4. doi: 10.1001/jama.2014.2398. Epub [PubMed PMID: 25117134]
Ninan J, Feldman L. Ammonia Levels and Hepatic Encephalopathy in Patients with Known Chronic Liver Disease. Journal of hospital medicine. 2017 Aug:12(8):659-661. doi: 10.12788/jhm.2794. Epub [PubMed PMID: 28786433]
Nayak R, Pandurangi A, Bhogale G, Patil N, Chate S. Asterixis (flapping tremors) as an outcome of complex psychotropic drug interaction. The Journal of neuropsychiatry and clinical neurosciences. 2012 Winter:24(1):E26-7. doi: 10.1176/appi.neuropsych.10110266. Epub [PubMed PMID: 22450635]