Cognitive Deficits Associated with Essential Tremor34
Classic Concept of Essential Tremor
Essential Tremor: New Findings
Cognition in Patients with Essential Tremor
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At the end of the 20th century, essential tremor was considered to be a monosymptomatic condition that was distinct from other disorders associated with tremor, such as dystonia, PD and myoclonus.[13,57] This classic concept of essential tremor maintained that the condition was not caused by structural changes within the CNS.[10] In the past decade, however, this concept has been challenged. Studies indicate that many patients with essential tremor also experience subtle neurological deficits that are considered to result from cerebellar dysfunction, such as tandem gait ataxia, bradykinesia, and dysfunctional hand-eye coordination and ocular movements, among others.
Within the past decade, patients with essential tremor have also been shown to experience cognitive impairments and mood disorders (mainly depression). The cognitive deficits are typically mild, and are a common feature of this condition. The observations that both essential tremor and the cognitive deficits associated with this disorder are typically progressive, patients with this condition have an increased risk of dementia,[36,37] and the majority of essential tremor cases have evidence of cerebellar pathology has changed the concept of essential tremor completely. In fact, it might be more appropriate to consider essential tremor to be a neurodegenerative disorder.
Most cases of essential tremor probably occur as a result of cerebellar pathology (Purkinje cell loss and degeneration with evidence of 'torpedos' and gliosis). In a subgroup of patients, however, the condition might be caused by brainstem pathology, including locus coeruleus nuclei cell loss associated with Lewy body inclusions.[44] Neuroimaging studies have shown that cerebellar dysfunction is evident in some patients with essential tremor. In such situations, the mild cognitive and mood disorders could be manifestations of subclinical CCAS, and could result from damage to neural networks that require coordinated activity in the cerebellum, the sensorimotor cerebral cortex, and the dorsolateral prefrontal, parietal-temporal and limbic cortices.[109-111] The knowledge acquired during the past decade needs further evidence from clinical and basic neuroscience studies before essential tremor can be classified as a neurodegenerative cerebellar disorder.