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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a rare complication after the resection of a tumor of the posterior fossa, the "one-and-a-half" syndrome. The one-and-a-half syndrome is a disturbance of horizontal eye movements in which patients have lateral gaze palsy in one direction and internuclear ophthalmoplegia in the other direction. The patient was a 54-year-old woman who developed headaches, diplopia, and blurred vision over 6 months. Computed tomographic scans and magnetic resonance imaging demonstrated an enhancing, mixed density, midline mass of the cerebellum. After a resection of the mass, an anaplastic astrocytoma, the patient complained of more severe diplopia and facial weakness. An examination disclosed a left one-and-a-half syndrome, left peripheral facial paralysis, dysarthria, dysphagia, mild left hemiparesis, dysmetria of the left upper limb, and truncal ataxia. The brain stem showed no abnormalities on postoperative computed tomographic scans. After 4 months of follow-up, the one-and-a-half syndrome had not improved, even though other signs had improved or resolved. This syndrome is caused by damage to structures within the pontine tegmentum: the medial longitudinal fasciculus, the ipsilateral paramedian pontine reticular formation, or the ipsilateral abducens nucleus. Multiple sclerosis and brain stem infarction are the most common causes of the one-and-a-half syndrome. Less frequently, it is caused by primary and metastatic tumors of the brain stem and cerebellum. Rarely, the one-and-a-half syndrome can develop postoperatively after the removal of tumors of the posterior fossa. The mechanism of pontine tegmental injury remains unknown.
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PMID:"One-and-a-half" syndrome after a resection of a midline cerebellar astrocytoma: case report and discussion of the literature. 196 11

In late 1987 there was an outbreak in Canada of gastrointestinal and neurologic symptoms after the consumption of mussels found to be contaminated with domoic acid, which is structurally related to the excitatory neurotransmitter glutamate. We studied the neurologic manifestations in 14 of the more severely affected patients and assessed the neuropathological findings in 4 others who died within four months of ingesting the mussels. In the acute phase of mussel-induced intoxication, the patients had headache, seizures, hemiparesis, ophthalmoplegia, and abnormalities of arousal ranging from agitation to coma. On neuropsychological testing several months later, 12 of the patients had severe anterograde-memory deficits, with relative preservation of other cognitive functions. Eleven patients had clinical and electromyographic evidence of pure motor or sensorimotor neuronopathy or axonopathy. Positron-emission tomography of four patients showed decreased glucose metabolism in the medial temporal lobes. Neuropathological studies in the four patients who died after mussel-induced intoxication demonstrated neuronal necrosis and loss, predominantly in the hippocampus and amygdala, in a pattern similar to that observed experimentally in animals after the administration of kainic acid, which is also structurally similar to glutamate and domoic acid. We conclude that intoxication with domoic acid causes a novel and distinct clinicopathologic syndrome characterized initially by widespread neurologic dysfunction and then by chronic residual memory deficits and motor neuronopathy or axonopathy.
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PMID:Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. 207 68

We describe 2 cases of acute encephalopathy in patients with connective tissue disease caused by small doses of ibuprofen. In addition to aseptic meningitis, both patients had altered mental status and focal neurologic signs, ophthalmoplegia in one and hemiparesis in the other. The spectrum of neurologic manifestations of ibuprofen hypersensitivity is reviewed.
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PMID:Acute central nervous system symptoms caused by ibuprofen in connective tissue disease. 221 86

The ability of cutaneous squamous cell carcinoma of the face to cause ophthalmoplegia or central nervous system dysfunction via perineural spread is not well recognized. Five patients presenting to a general neurology unit are described in whom partial or complete ophthalmoplegia developed following fifth and seventh cranial nerve involvement by cutaneous squamous cell carcinoma. Two patients subsequently developed a contralateral hemiparesis; and one, multiple cranial nerve palsies as the tumor spread centrally. Normal radiologic findings or complete healing of the primary skin lesion caused delay in the diagnosis in three of the patients. When ophthalmoplegia or central nervous system dysfunction develops as a consequence of perineural spread of cutaneous facial cancer, management is palliative.
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PMID:Perineural spread of cutaneous head and neck cancer. Its orbital and central neurologic complications. 229 96

A rare case of systemic lupus erythematosus (SLE) associated with lateral medullary syndrome and unilateral internuclear ophthalmoplegia was reported. A 15 year old girl was admitted to Kyushu University hospital on 2 September in 1987 because of vertigo, occular symptom, and sensory disturbance. She had noted vertigo since 28 August. On admission she had nystagmus, left Horner syndrome, sensory disturbance of left hemiface and right limbs and trunk and mild hemiparesis of right limbs. She also had a discoid erythema behind the left ear, butterfly rash on her cheek. She developed right internuclear ophthalmoplegia on 6 September. Investigations revealed biological false positive of serological test for syphilis, positive antinuclear antibodies, and prolonged APTT. Peripheral blood cell count and erythrocyte sedimentation rate were normal. There was no proteinuria. Computed tomography and magnetic resonance imaging failed to detect any lesions in the brain. Cerebrospinal fluid cell count was 20/3 and Ig-G index was 17.1%. Her neurological signs were thought to be related to SLE. Lupus anticoagulant might be responsible for the development of impairment of central nervous system (CNS). She was treated with prednisolone, initial dose of 40mg, and the symptoms and signs were improved quickly. Early diagnosis and treatment for SLE with CNS involvement is primarily important.
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PMID:[A case of systemic lupus erythematosus associated with lateral medullary syndrome and unilateral internuclear ophthalmoplegia]. 250 Oct 49

Acute enlargement of pituitary adenomas due to haemorrhage or ischaemic necrosis in the tumour was described as "pituitary apoplexy" by Brougham et al. in 1950. Since then, more than 200 cases have been reported, but--especially in the German literature--the syndrome has caught only little attention. Therefore, in a series of 12 own patients, typical findings and clinical characteristics are demonstrated and the literature is discussed. 9 patients had a haemorrhage into the tumour, 3 an acute ischaemic necrosis. The guiding symptom was the acute onset with ophthalmoplegia (11 of 12 patients). Only in one case the adenoma was known before the apoplexy. Other symptoms were headache, blurred vision, drowsiness and, in severe cases, hemiparesis, coma, and hypothalamic disorder. Most important is the acute endocrinological substitution with hydrocortisone; this may be life-saving. Neuroophthalmological recovery depends on early operation: cases of oculomotor palsy require an operation within the first 2 weeks after the acute event. An emergency operation is required only by an acute amaurosis. In general there will be enough time for careful clinical endocrinological and radiological investigations.
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PMID:[Acute hemorrhage and ischemic necroses in hypophyseal tumors: hypophyseal apoplexy]. 259 99

Internuclear ophthalmoplegia has been infrequently described in patients with systemic lupus erythematosus. We report a 23-year-old woman with lupus who presented with bilateral internuclear ophthalmoplegia and skew deviation. Additional neurologic findings included dysarthria, hemifacial weakness, hemiparesis, and dysmetria. Computed tomography of the patient's brainstem was unremarkable while magnetic resonance scanning demonstrated two areas of infarction. Magnetic resonance imaging is superior to computed tomography in both neuroradiographic study of the brainstem as well as evaluation of patients with neurologic complications of lupus.
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PMID:Bilateral internuclear ophthalmoplegia in systemic lupus erythematosus. 295 86

Seven cases of compromised pituitary fossa at the conventional skull X-ray, who had the final diagnosis of giant aneurysm of the intracavernous portion of the carotid artery (6 cases) and one of the anterior communicating artery, are reported. The main findings were: headache (7/7), complex ophthalmoplegia involving the III, IV and VI cranial nerves (5/7), compromised V cranial nerve (4/7) and eyeball pain (4/7). Other manifestations were: meningeal signs (2/7), unilateral blindness (1/7), hemiparesis (1/7), cacosmia (1/7) and inferior bitemporal quadrantanopsia (1/7). Five patients with intracavernous carotid artery aneurysm showed benefits with progressive occlusion of the internal carotid artery at the cervical level. One died before surgery. The case with anterior communicating artery aneurysm improved after its surgical clipping. Our data, in accord with the literature, support the conclusion that the differential diagnosis of aneurysms in the parasellar region remains a very difficult task. The accurate final diagnosis requires cerebral angiography and the surgical treatment with progressive occlusion at the cervical portion of the internal carotid artery has a relatively low risk with promising results.
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PMID:[Giant parasellar aneurysm simulating pituitary tumor]. 324 75

Paramedian infarction in the region of the thalamus and upper midbrain may produce a wide range of neuro-ophthalmological, behavioural and motor abnormalities. The paramedian arteries arise from the first part of the posterior cerebral artery, also known as the basilar communicating artery. The particular arterial topography and its anatomical variation may result in unusual combinations of clinical signs, and infarction may be bilateral in some cases. Diagnosis is often aided by CT scanning and magnetic resonance imaging. Both atherosclerotic occlusion and embolism are thought to be responsible for these particular syndromes. We describe 3 cases that illustrate some of the various clinical features and underlying anatomical vascular arrangements which may be seen in this condition. Thalamic dementia was present in one case with evidence of bilateral thalamic infarction. A complex ophthalmoplegia and hemiparesis were seen in another case, and the third case had a combination of thalamic dementia and ophthalmoplegia.
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PMID:Paramedian thalamic and midbrain infarction: the 'mesencephalothalamic syndrome'. 326 52

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


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