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Two cases of Claude's syndrome due to a mesencephalic infarction in the territory of the interpedoncular fossa arteries are reported. The first case had pupillary sparing while ptosis was lacking in the second case. Partial impairment of the oculomotor nerve suggests an intra-axial fascicular organization. However, the precise intra-axial pattern of the nerve is unknown in humans.
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PMID:[Paralysis of the common oculomotor nerve and contralateral cerebellar syndrome (Claude's syndrome). 2 cases caused by mesencephalic infarction]. 160 40

Spontaneous intracerebral hemorrhage rarely occurs in the mesencephalon (midbrain), though thalamic or pontine hemorrhage may extend into that location. The neurologic manifestations and outcome in patients with primary mesencephalic hemorrhage (PMH) are different from those with thalamic or pontine hemorrhage. We report 4 patients (2 men and 2 women) with nontraumatic and non-neoplastic hemorrhages confined to the mesencephalon. One young patient, a 37-year-old woman, had no detectable risk factors for stroke, and her cerebral angiogram was normal. The other 3 elderly patients (73-85 years of age) all had a history of hypertension. The neurologic manifestations of patients with PMH are characterized by disturbance of ocular movements and cerebellar signs. Two patients with tegmental hematoma showed Claude's syndrome, i.e., ipsilateral oculomotor palsy and contralateral cerebellar signs. One patient with a small central midbrain hematoma showed bilateral oculomotor palsy. Another patient with a relatively large central midbrain hematoma presented with bilateral ptosis, bilateral internuclear ophthalmoplegia, upward gaze palsy, and bilateral cerebellar signs. The prognosis after conservative treatment for our patients with PMH was good.
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PMID:[Primary mesencephalic hemorrhage: report of four cases]. 168 95

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

Claude's syndrome is a distinctive brainstem syndrome characterized by ipsilateral third cranial nerve palsy with contralateral hemiataxia and is due to an intrinsic or extrinsic lesion in the midbrain. We report a case of Claude's syndrome caused by neurocysticercosis infection. A 68 year-old Asian man was admitted to our hospital because of ataxia, left ptosis, and diplopia. Brain magnetic resonance imaging (MRI) showed a cystic lesion in the midbrain, which was surrounded by ring enhancement and peripheral edema. Neurocysticercosis infection was diagnosed by the cerebral spinal fluid study. The patient was treated with albendazole and steroids. A follow-up brain MRI three months later demonstrated the disappearance of a surrounding brain edema and rim enhancement. The most common cause of Claude's syndrome is cerebrovascular disease and malignancy. However, there is no report caused by neurocysticercosis infection. Therefore, if we encounter Claude's syndrome, we should consider neurocysticercosis infection as one of the etiologic factors.
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PMID:Claude's syndrome associated with neurocysticercosis. 2087 71

An 80-year-old man with angina pectoris abruptly developed Claude's syndrome, which consisted of left-sided partial oculomotor nerve palsy without ptosis and right-sided hemiataxia. There were no other neurological abnormalities. Cranial magnetic resonance imaging indicated an infarction of the left inferior paramedian mesencephalic artery, which may have involved the most caudal portion of the oculomotor fascicules. With anti-platelet therapy, the patient became asymptomatic within 10 days. The oculomotor fascicular arrangement in humans remains unclear. Our case suggests that in the oculomotor fascicles, the fibers to the levator palpebrae superioris may be located more in the rostral region than previously hypothesized.
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PMID:Claude's Syndrome without Ptosis Caused by a Midbrain Infarction. 2617 40