181. Flapping Tremor: Unraveling Asterixis-A Narrative Review

Article type: Literature Review

Article title: Flapping Tremor: Unraveling Asterixis-A Narrative Review 

Journal: Medicina

Year: 2024

Authors: Jamir Pitton Rissardo, Sara Muhammad, Venkatesh Yatakarla, Nilofar Murtaza Vora, Paras Paras, and Ana Letícia Fornari Caprara

E-mail: jamirrissardo@gmail.com

ABSTRACT

Asterixis is a subtype of negative myoclonus characterized by brief, arrhythmic lapses of sustained posture due to involuntary pauses in muscle contraction. We performed a narrative review to characterize further asterixis regarding nomenclature, historical aspects, etiology, pathophysiology, classification, diagnosis, and treatment. Asterixis has been classically used as a synonym for negative myoclonus across the literature and in previous articles. However, it is important to distinguish asterixis from other subtypes of negative myoclonus, for example, epileptic negative myoclonus, because management could change. Asterixis is not specific to any pathophysiological process, but it is more commonly reported in hepatic encephalopathy, renal and respiratory failure, cerebrovascular diseases, as well as associated with drugs that could potentially lead to hyperammonemia, such as valproic acid, carbamazepine, and phenytoin. Asterixis is usually asymptomatic and not spontaneously reported by patients. This highlights the importance of actively searching for this sign in the physical exam of encephalopathic patients because it could indicate an underlying toxic or metabolic cause. Asterixis is usually reversible upon treatment of the underlying cause.

Keywords: asterixis; anisosterixis; mini-asterixis; myoclonus; hyperkinetic; encephalopathy; drug induced; movement disorder

Full text available at:

https://www.mdpi.com/1648-9144/60/3/362

DOI

https://doi.org/10.3390/medicina60030362

Citation

Rissardo JP, Muhammad S, Yatakarla V, Vora NM, Paras P, Caprara ALF. Flapping Tremor: Unraveling Asterixis—A Narrative Review. Medicina 2024; 60:362.

Figure 1. Schematic diagram of the sensory-motor control. CPGs, central pattern generators; GPi, globus pallidus internus; LRST, lateral (medullary) reticulospinal tract; MRST, medial (pontine) reticulospinal tract; PM, premotor cortex; PPNc, caudal region of pedunculopontine nucleus; PPNr, rostral region of pedunculopontine nucleus; SMA, supplementary motor area; SRT, spinoreticular tract; STN, subthalamic nucleus; and VST, vestibulospinal tract.

Figure 2. Neurological assessment of asterixis of the upper and lower limbs.

Figure 3. Lesions already reported in the motor pathway associated with asterixis. The references are according to the area affected in the motor pathway. Notably, the individuals had contralateral motor symptoms at the location of the lesions.

Figure 4. Pathophysiology of hepatic encephalopathy and asterixis. The development of asterixis in hepatic encephalopathic individuals is probably multifactorial, and it can associate with hyperexcitability of motor cortical areas. Abbreviations: NH3, ammonia; NH4+, ammonium cation.

Table 1. Positions for examination of asterixis proposed by Pal et al. [7].

Table 2. Asterixis classification based on the severity proposed by Pal et al. [7].

Table 3. Bilateral asterixis secondary to focal brain lesions.

Table 4. Unilateral/asymmetric asterixis associated with contralateral brain lesion.

Table 5. Classification of hepatic encephalopathy (the West Haven criteria) based on Basile et al. [59].

Table 6. Drug-induced asterixis.

Table 7. Clinical clues in asterixis.