Functional Mobility and Postural Control in Essential Tremor

Parisi, Sarah L.; Héroux, Martin E.; Culham, Elsie; Norman, Kathleen E.

doi:10.1016/j.apmr.2006.07.255

Cited by 70 publications

(89 citation statements)

References 39 publications

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“…Difficulties with gait and balance have been repeatedly reported to occur in patients with ET, 7-9 and, on a functional level, this can lead to reduced mobility and perhaps more near-falls and falls. 37 However, the proportion of patients with ET and controls who died from hip or femoral fractures was similar in this series. Of interest is that death from pneumonia occurred in five times as many cases as controls.…”

Section: Discussionmentioning

confidence: 71%

A population-based study of mortality in essential tremor

et al. 2007

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Section: Discussionmentioning

confidence: 71%

A population-based study of mortality in essential tremor

et al. 2007

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“…Cerebellar-like problems, with abnormalities in tandem gait and balance, have been repeatedly described in ET patients [28][29][30][31][32]; in some patients, this ataxia can be marked, and the full extent of the problem has not been mapped [33]. Intention (i.e., "cerebellar") tremor of the arms occurs in approximately one half of ET patients [34]; furthermore, in 10 % of ET patients, intention tremor also involves the head (i.e., neck) [32,35].…”

Section: Additional Supporting Evidencementioning

confidence: 99%

Linking Essential Tremor to the Cerebellum: Neuropathological Evidence

Louis

2015

Cerebellum

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A fundamental question about essential tremor (ET) is whether its associated pathological changes and disease mechanisms are linkable to a specific brain region. To that end, recent tissue-based studies have made significant strides in elucidating changes in the ET brain. Emerging from these studies is increasing neuropathological evidence linking ET to the cerebellum. These studies have systematically identified a broad range of structural, degenerative changes in the ET cerebellum, spanning across all Purkinje cell compartments. These include the dendritic compartment (where there is an increase in number of Purkinje cell dendritic swellings, a pruning of the dendritic arbor, and a reduction in spine density), the cell body (where, aside from reductions in Purkinje cell linear density in some studies, there is an increase in the number of heterotopic Purkinje cell soma), and the axonal compartment (where a plethora of changes in axonal morphology have been observed, including an increase in the number of thickened axonal profiles, torpedoes, axonal recurrent collaterals, axonal branching, and terminal axonal sprouting). Additional changes, possibly due to secondary remodeling, have been observed in neighboring neuronal populations. These include a hypertrophy of basket cell axonal processes and changes in the distribution of climbing fiber-Purkinje cell synapses. These changes all distinguish ET from normal control brains. Initial studies further indicate that the profile (i.e., constellation) of these changes may separate ET from other diseases of the cerebellum, thereby serving as a disease signature. With the discovery of these changes, a new model of ET has arisen, which posits that it may be a neurodegenerative disorder centered in the cerebellar cortex. These newly emerging neuropathological studies pave the way for anatomically focused, hypothesis-driven, molecular mechanistic studies of disease pathogenesis.

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“…In recent years, perception of ET as a pure tremor disease has been challenged due to the observation that severely affected patients exhibit a broader spectrum of motor dysfunction like ataxia in reach-to-grasp hand movements [2,3] and abnormalities in tandem gait [4,5]. A cerebellar gait disorder in advanced ET has also been confirmed with more subtle and objective tests [4,[6][7][8][9][10]. The majority of studies focused on tandem gait, consistently report a greater number of mis-steps [4,5,[8][9][10] and increased step width [4,8].…”

Section: Introductionmentioning

confidence: 98%