Essential tremor

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Essential tremor (ET) is a slowly progressive neurological disorder whose most recognizable feature is a tremor of the arms that is apparent during voluntary movements such as eating and writing.[1] This type of tremor is often referred to as "kinetic tremor." The tremor may also occur in the head (neck), jaw and voice as well as other body regions, with the general pattern being that the tremor begins in the arms and then spreads to these other regions in selected patients. Women are more likely to develop the head tremor than are men.[2][3] Other types of tremor may also occur, including postural tremor of the outstretched arms, intentional tremor of the arms and rest tremor in the arms.[4] Some patients may have unsteadiness and problems with gait and balance that are above and beyond that due to normal aging.[5][6] In addition to these motor problems, a variety of non-motor features have recently been linked with ET. These include anxiety and depressive symptoms as well as cognitive difficulty.[7] Recent studies have demonstrated that late-onset ET (onset > age 65) may be associated with an increased risk of developing dementia.[8] ET is one of the most common neurological diseases, with a prevalence of approximately 4% in persons age 40 and older and considerably higher among persons in their 60s, 70s, 80s, and 90s.[9][10] Aside from enhanced physiological tremor, it is the most common type of tremor and one of the most commonly observed movement disorders.[11] Essential tremor was also previously known as "benign essential tremor", but the adjective "benign" has been removed in recognition of the sometimes disabling nature of the disorder. Although often mild, patients with severe tremor have difficulty performing many of their routine activities of daily living.[12][13]

Contents

Cause

The underlying etiology is not clear but many cases seem to be familial.[14] It has been estimated that approximately one-half of the cases are due to a genetic mutation and the pattern of inheritance is most consistent with autosomal dominant transmission. As of yet, no genes have been identified but genetic linkage has been established with several chromosomal regions.[15][16] A number of environmental factors, including toxins, are also under active investigation and these may play a role in disease etiology.[17] In terms of pathophysiology, clinical, physiological and imaging studies point to an involvement of the cerebellum and/or cerebellothalamocortical circuits.[18] Recent postmortem studies have demonstrated the presence of degenerative changes in the ET brain, with these changes including Purkinje cell axonal swellings and Purkinje cell loss in the majority of cases and brainstem Lewy bodies in the remainder. These studies suggest that the disease is both heterogeneous and degenerative. In other words, ET might be a family of degenerative diseases rather than a single disease.[19][20]

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