Perverted Head Impulse Test in Cerebellar Ataxia

Jeong, Seong-Hae; Kim, Ji-Soo; Baek, In Chul; Shin, Jong Wook; Jo, Hyun-Jin; Lee, Ae Young; Kim, Jae-Moon

doi:10.1007/s12311-013-0480-0

Cited by 16 publications

(6 citation statements)

References 12 publications

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“…Thus, one should suspect a central pathology if a patient with acute vertigo and spontaneous nystagmus exhibits normal HIT [ 13 ]. A refixation saccade in a different plane (i.e., vertical catch-up saccade after horizontal rotation) also suggests a central lesion [ 41 - 43 ]. However, bedside HIT may be negative when the vestibular deficits are partial [ 44 ] or the covert saccades complement the vestibular deficits [ 39 ].…”

Section: Acute Spontaneous Dizziness/vertigomentioning

confidence: 99%

Approach to dizziness in the emergency department

Jung

Kim

2015

Clin Exp Emerg Med

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Acute dizziness/vertigo is among the most common causes for visiting the emergency department. The traditional approach to dizziness starts with categorizing dizziness into four types: vertigo, presyncope, disequilibrium, and nonspecific dizziness. However, a recently proposed approach begins with classifying dizziness/vertigo as acute prolonged spontaneous dizziness/vertigo, recurrent spontaneous dizziness/vertigo, recurrent positional vertigo, or chronic persistent dizziness and imbalance. Vestibular neuritis and stroke are key disorders causing acute prolonged spontaneous dizziness/vertigo, but the diagnosis of isolated vascular vertigo has increased by virtue of developments in clinical neurotology and neuroimaging. However, a well-organized bedside examination appears more sensitive than brain imaging in diagnosing strokes presenting with acute dizziness/vertigo. A detailed history is vital to diagnose recurrent spontaneous dizziness/vertigo since confirmatory diagnostic tests are usually unavailable. Isolated positional vertigo is usually caused by benign paroxysmal positional vertigo, which can be treated at the bedside. In recent years, marked progress has occurred in the evaluation/management of acute dizziness/vertigo. However, even with developments in imaging technology, the diagnosis of acute dizziness/vertigo largely relies on bedside examination.

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Section: Acute Spontaneous Dizziness/vertigomentioning

confidence: 99%

Approach to dizziness in the emergency department

Jung

Kim

2015

Clin Exp Emerg Med

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“…Conversely, in cerebellar disorders HIT is mostly normal, but horizontal (compensatory) or downward (perverted) corrective saccades have been described during horizontal HIT. 3,4 Instead, our patient showed reversed (paradoxical) corrective saccades in the same direction of head rotation during bedside HIT. This paradoxical response should be considered an additional bedside cerebellar sign and may be useful in detecting cerebellar dysfunction.…”

Section: Discussionmentioning

confidence: 57%

Hypomagnesemia-induced cerebellar syndrome: a case report

Betti,

Cornacchini,

Pastorelli

et al. 2024

JOENTR

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Magnesium is the second most abundant intracellular cation after potassium and is involved in over 600 enzymatic reactions that are essential for life. Hypomagnesemia (serum magnesium concentration <1.8 mg/dL (< 0.70 mmol/L)), is longstanding known to cause many clinical disorders: other electrolyte abnormalities, life-threatening arrhythmias and various neurological manifestations, from muscle cramps and myopathy, to vertigo, nystagmus, depression, acute confusional state and seizures. In the last few years some case reports have highlighted the possible existence of a peculiar hypomagnesemia induced cerebellar syndrome (HiCS). Here we present a clinical case of a 74-years-old man with severe hypomagnesemia presenting with vomiting, gait instability, diffuse tremor, associated with neuro-otological signs of cerebellar dysfunction and a MRI hyperintense lesion at cerebellar nodulus with clinico-radiological resolution after magnesium repletion.

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“…Previous reports proposed that apositive head impulse test with preserved caloric response is most likely due to cerebellar flocculus dysfunction, considering the findings of previous studies related to the high-frequency VOR. [6][7][8][9] This ocularmotorfindingis meaningful in that it expands the neurotolgical findings of AxD. While no structural lesions were identified in the flocculus on brain MRI, cervicomedullary atrophy with intramedullary signal changes suggests broader implications for the functional integration within the medulla and cerebellum.…”

mentioning

confidence: 56%

Adult-Onset Alexander Disease With Late-Presenting Vestibulopathy: A Case Report

Chang,

Jeong,

2024

JMD

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Alexander disease (AxD) is a progressive astrocytic leukodystrophy, primarily attributed to autosomal dominant or de novo mutations in the GFAP gene. 1 AxD presents differently across age groups, including infantile, juvenile, and adult subtypes, each with its own set of symptoms and prognoses. Adult-onset AxD accompanies bulbar symptoms, ataxia, autonomic dysfunction, and gait disturbance, while juvenile and infantile onset show cognitive

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Perverted Head Impulse Test in Cerebellar Ataxia

Cited by 16 publications

References 12 publications

Approach to dizziness in the emergency department

Approach to dizziness in the emergency department

Hypomagnesemia-induced cerebellar syndrome: a case report

Adult-Onset Alexander Disease With Late-Presenting Vestibulopathy: A Case Report

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