Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 61-year-old woman is presented with a bilateral total ophthalmoplegia as an initial ocular symptom, caused by a midbrain hematoma. She complained of acute headache, nausea, vomiting and bilateral closure of her eyelids. Examination on admission showed meningeal irritation; mild consciousness disturbance; bilateral total ophthalmoplegia; left hemiparesis; ataxia in all extremities, more marked to the left. Computed tomography demonstrated a small hematoma in the midbrain tegmentum. Angiography demonstrated midbrain arteriovenous malformation, and she was treated conservatively. Abduction of both eyes and adduction of the left eye appeared on the next day of the ictus, and after that, improved gradually. Left ptosis had improved since one week after the ictus. Light reflex of the left pupil had seen 5 days after the ictus. At the same time, the left pupil revealed an oval-shape. Right internal ophthalmoplegia continued to exist. One year later, the right eye deviated externally, and the left deviated inferio-medially. Abduction of both eyes was normal. Infraduction of both eyes was seen, but limited on the left. Upgaze paresis remained unchanged, and adduction of the right eye was absent. Adduction of the left eye showed almost full recovery. There was right complete ptosis, but left ptosis became indefinite. These ocular findings indicated typical right oculomotor paresis plus superior rectus paresis of the left eye, which suggested a destructive lesion in the right oculomotor nucleus. Also, her left extremities showed a hemiparesis as a pyramidal tract sign (Weber's syndrome) and an ataxia as a cerebellar sign (Claude's syndrome).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Midbrain arteriovenous malformation causing bilateral total ophthalmoplegia as an initial ocular symptom--a case report]. 337 Jan 70

Mesencephalic infarcts are rarely limited to the midbrain, and usually extend rostrally to the thalamus. This fact explains why an elective palsy of the oculomotor nerve is exceedingly uncommon in brainstem infarcts. We studied 4 cases with a unilateral infarct apparently restricted to the middle mesencephalon, with intra-axial involvement of the oculomotor nerve. In 2 cases with a fascicular lesion, there was a contralateral hemiparesis or hemi-ataxia, so that it is possible to term them Weber's syndrome and Claude's syndrome. In the 2 other cases, we suggest that a nuclear syndrome of the oculomotor nerve was present, because of bilateral involvement of the rectus superior in both cases, of the levator palpebrae in one case, and of the parasympathetic pupillary fibres in the other, although the infarct was unilateral. There are several clinical variants of the intra-axial syndrome of the oculomotor nerve which can be differentiated according to the uni or bilaterality of the oculomotor palsy, the pupillary disturbances, and the type of associated neurological dysfunction. The nuclear syndrome corresponds to an infarction of the median arterial area, which is directly supplied by the most distal part of the basilar artery. The fascicular syndromes correspond to infarction of the paramedian and intermediolateral areas supplied by the first part of the posterior cerebral artery (basilar communicating or mesencephalic artery). As the paramedian thalamic arteries also originate from the basilar communicating artery, most infarcts also involve the upper midbrain and the thalamus, producing supranuclear oculomotor disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intra-axial involvement of the common oculomotor nerve in mesencephalic infarctions]. 671 14