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

Until such time as results of more rigorous studies are available, the morbidity rates for thyroid dysfunction cited here must suffice. The 1955 to 1956 outpatient "incidence" for England and Wales was 1.1 per 1,000 for thyrotoxicosis and 1.7 per 1,000 for myxedema (18). United States in-patient "incidence" for 1971 was 0.16 per 1,000 for thyrotoxicosis and 0.13 per 1,000 for myxedema (25). The 1935 to 1967 average annual incidence of Graves' disease for females in Olmsted County, Minnesota, was 30.5 per 100,000 (10). Well over 50% of hyperthyroid patients have clinical evidence of mild or moderate muscle weakness. Usually this weakness is proximal, and electro-myography and muscle biopsy confirm the existence of myopathic process (Table 11). Severe muscular weakness of acute onset is relatively rare and is encountered in approximately 1% of hyperthyroid patients (11,17,40). Ophthalmoplegia and psychosis are reported 4% and 2% of patients, respectively (17). Myasthenia gravis, although well publicized, is estimated to occur in less than 1% of patients (3,30). TPP is virtually nonexistent in the West; in the Orient it is reported in 2 to 8% of hyperthyroid patients and is 20 to 60 times more frequent in the hyperthyroid male than in the hyperthyroid female (Table 12). The neurologic symptomatology of myxedema is more extensive, and agreement among the various series is poor. The only unselected series addressing itself to neuromuscular manifestations of myxedema that is suitable for citation is that of Scarpalezos et al. (36). This comprehensive study was done without apparent patient selection, and it reported 2% of patients with definite carpal tunnel syndrome, 6% with myopathy, and 18% with polyneuropathy (Table 13). Reported percentages of hypothyroid patients found to have neurologic manifestations of cerebellar dysfunction are extremely diverse: ataxic gait was reported in 5 to 32% (6,7,12,27) of patients and dysdiadochokinesia in 6 to 52% (7,12,27). Psychosis is encountered in 2 to 5% (6,14,17,27,39) of myxedematous patients, memory loss in 23 to 55% (6,14,27), and coma in less than 1% (27).
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PMID:Neurologic complications of thyroid dysfunction. 74 45

Total external ophthalmoplegia was observed in five patients consequent to the oral or intravenous administration of phenytoin. Coincident with the ophthalmoplegia, the state of consciousness varied from drowsiness to coma and the blood levels of phenytoin ranged from 36 to 55 mug per milliliter. Initially, the eyes were fixed in midposition, and oculocephalic and oculovestibular stimulation failed to evoke either horizontal or vertical eye movements. The return of vestibulo-ocular responsiveness lagged behind the return of consciousness and other reflex activity. The mechanism underlying this ophthalmoplegia may be related to the ability of phenytoin to potentiate inhibitory synapses in the vestibulo-oculomotor pathway which utilize gamma aminobutyric acid, and to increase the discharge rate of Purkinge cells which exert an inhibitory influence on the same structures.
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PMID:Phenytoin-induced ophthalmoplegia. 82 68

The authors present an extremely rare case of aspergillosis of the central nervous system (CNS) causing subarachnoid hemorrhage (SAH). A 78-year-old female developed facial pain, progressive deterioration in left visual acuity, and left total ophthalmoplegia. Computed tomography demonstrated a heterogeneously enhanced mass extending from the sphenoid sinus to the left cavernous sinus and left orbit, and angiography showed luminal narrowing and irregularity of the left internal carotid artery at its siphon. Biopsy of the left orbital and sphenoid sinus mass resulted in the diagnosis of Aspergillus granuloma. Despite combined administration of amphotericin-B and 5-FC, she became comatose from brainstem infarction and finally, suddenly died. Postmortem examination revealed massive SAH due to a ruptured mycotic aneurysm of the basilar artery. Aspergillosis of the CNS is a growing problem with the wider use of immunosuppressants and antibiotics. To the authors' knowledge, however, only 13 cases of CNS aspergillosis causing SAH have been reported. The prognosis is absolutely bad, with all patients dying from rupture of major intracranial arteries such as the internal carotid artery and basilar artery. Early diagnosis and vigorous chemotherapy are important.
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PMID:Aspergillosis of the central nervous system causing subarachnoid hemorrhage from mycotic aneurysm of the basilar artery--case report. 170 41

A case of fungal aneurysm associated with presumed Tolosa-Hunt syndrome is reported. A 57-year-old man was admitted to our hospital with complaints of left blepharoptosis, headache and weight loss. Neurological examination revealed left ophthalmoplegia without facial hypesthesia. Visual acuity was normal. Laboratory studies showed raised ESR, 4+ glycosuria, and a blood sugar of 351mg/dl. Computerized tomography (CT) scan and left carotid angiography were considered normal. Left orbital venography showed no filling of the left cavernous sinus. Diabetic ophthalmoplegia was suspected by a neurologist. The patient was treated with insulin therapy, but visual acuity worsened, and hypesthesia was noted in the first and second divisions of the left trigeminal nerve. Subsequent CT scan demonstrated a high density lesion, which was homogeneously enhanced, in the left cavernous portion and the superior orbital fissure. The patient was presumed of Tolosa-Hunt syndrome, and prednine therapy (30mg/day) was started. On the second day after the administration of prednine, hypesthesia of the first and second division of the left trigeminal nerve improved. After 9 days of prednine therapy, the patient suddenly complained of severe headache, and lapsed into a coma. Massive hemorrhage with subarachnoid hemorrhage was recognized on the CT scan, with a marked midline shift to the right. The hematoma was immediately removed. A ruptured cerebral aneurysm was found at the bottom of the hematoma. The aneurysm was located in the distal portion of the left middle cerebral artery. Aneurysm clipping with external decompression and bilateral ventricular drainage was performed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A fungal aneurysm in a patient with presumed Tolosa-Hunt syndrome]. 185 58

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

Wernicke's encephalopathy should be considered as a possible diagnosis in comatose and hypothermic patients. The classic triad of confusion, ophthalmoplegia (or nystagmus) and ataxia may be absent, and the history of alcohol abuse or other causes of thiamine deficiency may be unknown. Left untreated, acute Wernicke's encephalopathy has a 17 percent mortality rate. Since the morbidity from Wernicke's encephalopathy is potentially reversible with parenteral thiamine, and large doses of thiamine can be given without documented ill effects, it is recommended that all comatose or hypothermic patients, as well as those with more classic presentations of Wernicke's encephalopathy, be given parenteral thiamine before administration of glucose.
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PMID:Wernicke's encephalopathy. 218 37

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

A 63-year-old man suddenly fell in a state of apparent coma. An electroencephalogram (EEG) performed at a local hospital revealed the maintenance of a reactive alpha rhythm over the posterior regions of the scalp, allowing a diagnosis of alert coma. The persistence of minimal degrees of alertness and ability to communicate made the clinical picture classifiable as a "locked-in" syndrome (LIS). Bilateral ptosis and complete ophthalmoplegia oriented towards a total mesencephalic form of LIS. Computed tomography (CT) and magnetic resonance imaging (MRI) of the brain showed pathological findings at mesencephalic level. Such findings were insufficient to explain the clinical picture.
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PMID:Total mesencephalic "locked-in" syndrome. A case report and review of the literature. 270 Aug 40

Traumatic carotid-cavernous sinus fistula is an uncommon situation resulting from severe trauma, with less than 40 cases having been reported. It is usually associated with a skull base, frontal or mid-facial fracture, but it may also be a spontaneous phenomenon of congenital, infective or degenerative origin. The blood shunts from the internal carotid to the cavernous sinus resulting in pulsating exophthalmos, orbital headache, pain, orbital or frontal bruit, loss of visual acuity, diplopia, ophthalmoplegia and the differential diagnosis should include superior orbital fissure syndrome, orbital apex syndrome and cavernous sinus thrombosis. Several modes of treatment have been proposed. We were recently faced with such a case, who had sustained fractures of the facial skeleton and developed the fistula despite an initial non-contributory angiogram. The patient remained in a permanent coma.
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PMID:Traumatic carotid-cavernous sinus fistula. 320 64

We report a survival patient with hemorrhage in the quadrigeminal plate and discuss the literature of midbrain hemorrhage. A 13-year-old boy developed severe headache and vertigo on April 1st, 1983. On admission, he was comatose and tetraplegic with bilateral facial palsy and total ophthalmoplegia. CT scan revealed a hemorrhage in the midbrain and ambient cistern, but vertebral angiogram no abnormal vessels. Seven hours after admission, continuous ventricular drainage was performed. Disturbance of consciousness, ophthalmoplegia and speech disturbance were gradually improved. CT scan with contrast medium 3 weeks after admission showed a small high density spot in the right quadrigeminal plate. It might be suggested that this spot was the bleeding point and was probably a cryptic microvascular malformation. At the discharge only a minimal limitation of eye ball movement was left.
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PMID:[Hemorrhage in the quadrigeminal plate--a case report]. 332 Aug 3


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