Glucocorticoids improve acute dizziness symptoms following acute unilateral vestibulopathy

Batuecas‐Caletrío, Ángel; Yáñez-González, Raquel; Sánchez-Blanco, Carmen; Pérez, Pedro Blanco; González-Sánchez, Enrique; Sanchez, Luis Alberto Guardado; Kaski, Diego

doi:10.1007/s00415-015-7918-x

Cited by 22 publications

(65 citation statements)

References 24 publications

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“…Bilateral vestibulopathy (BVP) is a chronic vestibular syndrome defined by bilaterally impaired vestibulo-ocular reflex, variably involving semicircular canal (SCC) and otolith function ( 1 ), as typically assessed by individual SCC head impulse test (HIT) ( 2 , 3 ) and vestibular evoked myogenic potential ( 4 ), respectively. Peripheral lesions, such as gentamicin vestibulotoxicity, autoimmune inner ear diseases, bilateral Meniere’s disease, and bilateral vestibular schwannomas are well recognized in BVP ( 5 , 6 ). Central lesions, however, are increasingly recognized to affect SCC and otolith function bilaterally, thus potentially mimicking BVP ( 7 – 11 ).…”

Section: Introductionmentioning

confidence: 99%

Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy

Chen

Hálmagyi

2018

Front. Neurol.

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Bilateral vestibulopathy (BVP), which is due to peripheral lesions, may selectively involve certain semicircular canal (SCC). Recent eye movement recordings with search coil and video head impulse test (HIT) have provided insight in central lesions that can cause bilateral and selective SCC deficit mimicking BVP. Since neurological signs or ocular motor deficits maybe subtle or absent, it is critical to recognize central lesions correctly since there is prognostic and treatment implication. Acute floccular lesions cause bilateral horizontal SCC (HC) impairment while leaving vertical SCC function unaffected. Vestibular nuclear lesions affect bilateral HC and posterior SCC (PC) function, but anterior SCC (AC) function is spared. When both eyes are recorded, medial longitudinal fasciculus lesions cause horizontal dysconjugacy in HC function and catch-up saccades, as well as selective deficiency of PC over AC function. Combined peripheral and central lesions may be difficult to distinguish from BVP. Anterior inferior cerebellar artery stroke causes two types of deficits: 1. ipsilateral pan-SCC deficits and contralateral HC deficit and 2. bilateral HC deficit with vertical SCC sparing. Metabolic disorders such as Wernicke encephalopathy characteristically involve HC but not AC or PC function. Gaucher disease causes uniform loss of all SCC function but with minimal horizontal catch-up saccades. Genetic cerebellar ataxias and cerebellar-ataxia neuropathy vestibular areflexia syndrome typically do not spare AC function. While video HIT does not replace the gold-standard, search coil HIT, clinicians are now able to rapidly and accurately identify specific pattern of SCC deficits, which can aid differentiation of central lesions from BVP.

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Section: Introductionmentioning

confidence: 99%

Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy

Chen

Hálmagyi

2018

Front. Neurol.

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“…A 2015 retrospective study by Batuecas‐Caletrio et al, consisting of 76 patients diagnosed with acute VN, compared glucocorticoid treatment on admission to nonglucocorticoid treatment . Each patient had caloric testing and completed a dizziness handicap inventory (DHI) upon admission to the hospital and moments before discharge.…”

Section: Literature Reviewmentioning

confidence: 99%

“…Dizziness Handicap Inventory scores were also noted to be significantly lower at discharge ( P < .001) and with a shorter length of hospital stay (2.18 ± 1.5 days compared to 3.6 ± 1.7 days, P = .002) compared to the nonglucocorticoid arm. The authors did not explore long‐term outcomes …”

Section: Literature Reviewmentioning

confidence: 99%

“…1 A 2015 retrospective study by Batuecas-Caletrio et al, consisting of 76 patients diagnosed with acute VN, compared glucocorticoid treatment on admission to nonglucocorticoid treatment. 5 Each patient had caloric testing and completed a dizziness handicap inventory (DHI) upon admission to the hospital and moments before discharge. Patients receiving glucocorticoids demonstrated a significantly lower canal paresis at discharge (P < .001) and a marked reduction in nystagmus intensity (P = .03) compared to the nonglucocorticoid arm.…”

Section: Literature Reviewmentioning

confidence: 99%

“…The authors did not explore long-term outcomes. 5 The reviewed data present several limitations. These studies show heterogeneity with respect to how the trials were conducted in inclusion and exclusion criteria for VN, the difference in corticosteroid treatment regimens, and the clinical outcomes measured by each study (Table I).…”

Section: Literature Reviewmentioning

confidence: 99%

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