2014
DOI: 10.1016/j.ncl.2014.07.001
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Toxic-Metabolic, Nutritional, and Medicinal-Induced Disorders of Cerebellum

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Cited by 19 publications
(16 citation statements)
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“…In cerebellar lesions, pHSN may be ascribed to disruption of the central pathways from the anterior semicircular canals due to flocculus and paraflocculus lesions, which are known to send their inhibitory fibres to the floccular target neurons in the anterior canal VOR pathway (and less to the posterior canal VOR pathway) [11][12][13][14]. Therefore, lesions involving the flocculus/paraflocculus may disinhibit anterior canal projections and cause upward eye drift.…”
Section: Discussionmentioning
confidence: 99%
“…In cerebellar lesions, pHSN may be ascribed to disruption of the central pathways from the anterior semicircular canals due to flocculus and paraflocculus lesions, which are known to send their inhibitory fibres to the floccular target neurons in the anterior canal VOR pathway (and less to the posterior canal VOR pathway) [11][12][13][14]. Therefore, lesions involving the flocculus/paraflocculus may disinhibit anterior canal projections and cause upward eye drift.…”
Section: Discussionmentioning
confidence: 99%
“…The classic triad of WE consists of confusion, ataxia, and eye movement abnormalities. 10 A diagnosis of WE constitutes a medical emergency, and prompt treatment is required to avoid death or the development of Korsakoff's syndrome. Symptoms of Korsakoff's syndrome include profound deficits in anterograde and retrograde memory as well as confabulation.…”
Section: Discussionmentioning
confidence: 99%
“…5 Reversible acute dizziness or vertigo due to medication side effects or toxicity from overdosage is typical with central nervous system (CNS)-acting agents that have a brainstem or cerebellar predilection, such as antiepileptic drugs (especially phenytoin, carbamazepine, and phenobarbital), benzodiazepines, and lithium. 6 Anticonvulsants are perhaps most likely to mimic a true AVS presentation with severe persistent vertigo, dizziness, or ataxia in combination with pathologic nystagmus, 7,8 although similar presentations have also been reported for other medications, such as amiodarone. 9 Acute alcohol intoxication produces dizziness by both central and peripheral mechanisms.…”
Section: Pharmacologic Toxicity and Withdrawalmentioning
confidence: 98%
“…9 Acute alcohol intoxication produces dizziness by both central and peripheral mechanisms. 6,10 The resultant nystagmus can therefore be of a mixed type but is most commonly a direction-changing, gaze-evoked horizontal nystagmus (ie, beats to the right when looking right, beats to the left when looking left), as with other brainstem and cerebellar intoxicants, that results from impairment of central gaze-holding pathways. Alcohol use can also cause dizziness via other mechanisms such as thiamine deficiency (discussed later) and chronic cerebellar degeneration, although the last two mechanisms generally lead to a more chronic presentation, unless there is intercurrent medical illness.…”
Section: Pharmacologic Toxicity and Withdrawalmentioning
confidence: 99%