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Original Article
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Tilt Suppression of the Post-rotatory Nystagmus in Cerebellar Nodular Lesions
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Sun Young Oh, Kwang Dong Choi, Jung Eun Kim, Ja Won Koo, Ji Soo Kim
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J Korean Bal Soc. 2007;6(2):161-166.
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Abstract
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- Background and Objectives: Head tilt at the end of step rotation about a vertical axis decreases the time constant (TC) of the post-rotatory nystagmus, which is known as tilt-suppression of the vestibulo-ocular reflex (VOR). Tilt suppression of the VOR is mediated by the cerebellar nodulus and ventral uvula and is eliminated after surgical ablation of those structures. However, studies on the tilt suppression of the VOR have been sparse in humans with cerebellar lesions.
Materials and Methods: Five patients with circumscribed cerebellar lesions involving the nodulusor ventral uvula underwent recording of spontaneous and positional nystagmus, and the VOR. To evaluate tilt suppression of the VOR, the participants pitched their head forward at the end of step rotation about a vertical axis both in the clockwise and counter-clockwise directions.
Results: The VOR gain was increased in a patient with infarction in the territory of the medial posterior inferior cerebellar artery while the gain of visually enhanced VOR was normal in all the patients. The time constants of perand post-rotatory nystagmus was increased in a patient with increased VOR gain and the tilt suppression of the post-rotatory nystagmus was impaired in two patients, either uni- or bilaterally. Spontaneous downbeat and central positional nystagmus were frequently accompanied.
Conclusions: Nodular lesion may impair tilt suppression of the VOR. Measurement of tilt suppressive effect of the VOR may provide a valuable tool for evaluating the nodular dysfunction.
Case Report
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Isolated nodular infarction and vestibular neuritis
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Hyung Lee, Yong Won Cho
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J Korean Bal Soc. 2003;2(2):237-240.
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Abstract
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- An isolated nodular infarction presenting as an isolated vertigo with unidirectional, gaze-fixed nystagmus has not been previously reported. We reported a patient with cerebellar infarction who presented with purely isolated vertigo, ipsilesional, spontaneous nystagmus, and contralesional axial lateropulsion without usual symptoms or signs of cerebellar dysfunction. An MRI of the brain showed a small infarct selectively involving the nodulus. A pure vestibular syndrome in our patient may be explained by an ipsilateral involvement of nodulo-vestibular inhibitory projection to vestibular nucleus. Clinicians should be aware of the possibility of a nodulus infarction in patients with an acute vestibular syndrome, even if the pattern of nystagmus and lateropulsion is typical of vestibular neuritis.