Head-shaking nystagmus in lateral medullary infarction

Choi, Kwang-Dong; Oh, Sun-Young; Park, S. H.; Kim, J. H.; Koo, Ja-Won; Kim, J. S.

doi:10.1212/01.wnl.0000260224.60943.c2

Cited by 120 publications

(100 citation statements)

References 24 publications

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“…Patients with complete infarction in the lateral medulla commonly show mixed horizontal, vertical, and torsional nystagmus, but horizontal nystagmus may be ipsi-or contralesional, and the vertical components may be upbeat or downbeat. 37 However, the prominent downbeat nystagmus in most patients with RVAO can be hardly explained by unilateral ischemia of the lateral medulla. Furthermore, absence of other neurological symptoms or signs does not support ischemia of the dorsolateral medulla in RVAO, although a greater vulnerability to ischemia of the vestibular nucleus than other brain stem structures has been suggested previously.…”

Section: Strokementioning

confidence: 99%

Rotational Vertebral Artery Occlusion

Choi

Choi²,

Kim³

et al. 2013

Stroke

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Background and Purpose-To elucidate the mechanisms and prognosis of rotational vertebral artery occlusion (RVAO). Methods-We analyzed clinical and radiological characteristics, patterns of induced nystagmus, and outcome in 21 patients (13 men, aged 29-77 years) with RVAO documented by dynamic cerebral angiography during an 8-year period at 3 University Hospitals in Korea. The follow-up periods ranged from 5 to 91 months (median, 37.5 months). Most patients (n=19; 90.5%) received conservative treatments. Results-All the patients developed vertigo accompanied by tinnitus (38%), fainting (24%), or blurred vision (19%).Only 12 (57.1%) patients showed the typical pattern of RVAO during dynamic cerebral angiography, a compression of the dominant vertebral artery at the C1-2 level during contralateral head rotation. The induced nystagmus was mostly downbeat with horizontal and torsional components beating toward the compressed vertebral artery side. None of the patients with conservative treatments developed posterior circulation stroke, and 4 of them (21.1%) showed resolution of symptoms during the follow-ups. Conclusions-RVAO has various patterns of vertebral artery compression, and favorable long-term outcome with conservative treatments. In most patients with RVAO, the symptoms may be ascribed to asymmetrical excitation of the bilateral labyrinth induced by transient ischemia or by disinhibition from inferior cerebellar hypoperfusion. Conservative management might be considered as the first-line treatment of RVAO. (Stroke. 2013;44:1817-1824.)

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Section: Strokementioning

confidence: 99%

Rotational Vertebral Artery Occlusion

Choi

Choi²,

Kim³

et al. 2013

Stroke

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“…The examiner pitched the patient's head forward by $30 to bring the horizontal semicircular canals into the plane of stimulation. The patient's head was then grasped firmly with both hands, and shaken horizontally in a sinusoidal fashion at a rate of 2.8 Hz with an approximate amplitude of AE 10 for 15 s (Choi et al, 2007b).…”

Section: Oculographymentioning

confidence: 99%

“…However, only a few studies have investigated head-shaking nystagmus in central vestibulopathies (Walker and Zee, 1999;Minagar et al, 2001;Kim et al, 2005;Choi et al, 2007b;Moon et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Gaze-Evoked and Perverted Head-Shaking Nystagmus in a Patient with Polycythemia Vera

Kim¹,

Song²,

Jeong³

et al. 2017

Res Vestib Sci

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Horizontal head-shaking may induce nystagmus in peripheral as well as central vestibular lesions. While the patterns and mechanism of head-shaking nystagmus are well established in peripheral vestibulopathy, they require further exploration in central vestibular disorders. To define the characteristics and mechanism of head-shaking nystagmus in central vestibulopathies, we investigated spontaneous nystagmus and head-shaking nystagmus in 72 patients with isolated cerebellar infarction. Spontaneous nystagmus was observed in 28 (39%) patients, and was mostly ipsilesional when observed in unilateral infarction (15/18, 83%). Head-shaking nystagmus developed in 37 (51%) patients, and the horizontal component of head-shaking nystagmus was uniformly ipsilesional when induced in patients with unilateral infarction. Perverted head-shaking nystagmus occurred in 23 (23/37, 62%) patients and was mostly downbeat (22/23, 96%). Lesion subtraction analyses revealed that damage to the uvula, nodulus and inferior tonsil was mostly responsible for generation of head-shaking nystagmus in patients with unilateral posterior inferior cerebellar artery infarction. Ipsilesional head-shaking nystagmus in patients with unilateral cerebellar infarction may be explained by unilateral disruption of uvulonodular inhibition over the velocity storage. Perverted (downbeat) head-shaking nystagmus may be ascribed to impaired control over the spatial orientation of the angular vestibulo-ocular reflex due to uvulonodular lesions or a build-up of vertical vestibular asymmetry favouring upward bias due to lesions involving the inferior tonsil.

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“…37 Vibration-induced nystagmus is recorded by applying a vibration stimulator to the forehead and both mastoids.…”

Section: 29mentioning

confidence: 99%