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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied clinical manifestations of sixteen patients with cerebellar infarcts diagnosed by MRI. In fourteen of them, the stroke developed abruptly with vertigo, which continued for several days. At the early stage of illness, ataxia was obscure. But after vertigo and nausea disappeared, nine cases showed truncal ataxia, while limb ataxia was found in only five. Their vertigo was rotatory and aggravated by head movement. Gaze-evoked nystagmus was observed in only 5 cases. Four patients preferred to take unilateral posture since they experienced less vertigo. The side of their lesions was the lower side of their posture. Limb ataxia was more frequent in SCA-involving cases than in SCA-non involving cases (3 out of 6 vs 2 out of 10, respectively). On the other hand, headache was more frequent in PICA-involving cases than in PICA-non-involving cases (6 out of 11 vs 1 out of 5, respectively). Ataxic gait was seen more in medial branch-involving cases than medial branch non-involving cases (5 out of 6 vs 4 out of 10, respectively). One patient died due to obstructive hydrocephalus.
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PMID:[A study of MRI and clinical neurology in acute cerebellar infarcts]. 939 54

Vestibular syndromes are one of the commonest paroxysmal disorders in our clinical practice. These consist of vertigo, oculomotor abnormalities (nystagmus), postural changes and nausea/vomiting. Vertigo can be classified as real vertigo and dizziness, based upon the presence of clinical rotatory perception. In order to diagnose a responsible lesion for various central and peripheral vestibular syndromes, we have to carefully observe nystagmus in patients with acute vertigo. Gaze-evoked nystagmus is the most important nystagmus in patients with the central vestibular syndromes. The finding is easily found at the bed side examination. In order to keep a velocity-position neural signal such as gaze holding, the neural structure to hold and maintain the neural command for a saccade is hypothesized and this has been called as the brainstem neural integrator, which sends tonic-step commands for eccentric gaze. If this fails then the integrator becomes leaky and the eyes drift back to the central position. This movement necessitates corrective saccades, hence gaze-evoked nystagmus will ensue. Vertical nystagmus such as primary position upbeat or downbeat nystagmus is also seen only in the central vestibular syndromes. The detection and diagnosis of these characteristic nystagmus are essential for primary clinicians who care patients with acute vertigo.
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PMID:[Overview: diagnosis of vestibular syndromes]. 2227 89