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 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results are reported of our operative experience with 22 cases of external congenital ophthalmoplegia. The familiality, the muscular enzymes and isoenzymes, and often the skeletal electromyography have been studied, with the latter three being significantly altered in most cases. The main indication for surgery is the need to improve the anomalous position of the hyperextended neck. In the presence of inherent ptosis, this is achieved by suspending the upper eyelid from the frontalis muscle by using an autogenous fascia lata. A review of the previously published reports on eyebrow suspension leads one to conclude that autogenous fascia lata is the best material for this purpose.
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PMID:Ptosis correction in the context of the treatment of external congenital ophthalmoplegia. 248 17

A 63-year-old white male with a 25-year history of hypertension experienced the onset of intermittent diplopia and gait disturbance 24 hours after a change in antihypertensive medication from atenolol 50 mg/d to enalapril 5 mg bid. Three weeks later, the patient was admitted with a worsening of symptoms. Cerebral arteriography revealed significant bilateral vertebral artery stenosis. Symptoms continued to progress in the hospital, and at the time of posterior circulation revascularization the patient had a persistent bilateral internuclear ophthalmoplegia and right ptosis. The need for a neurovascular workup and adjustment of therapy in patients with antihypertensive-associated cerebral ischemia is discussed.
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PMID:Hemodynamic vertebrobasilar insufficiency as an adverse effect of antihypertensive therapy. 254 68

Two patients (a 50-year-old and a 35-year-old men) with focal cytochrome c oxidase deficiency, manifesting ptosis and external ophthalmoplegia of 13 and 6 years' duration, respectively, were reported. Patient 1 (a 50-year-old male) had also slight muscular weakness of the proximal limb and neck flexor muscles. Diagnosis of myasthenia gravis had been made on the clinical findings including ptosis and external ophthalmoplegia, diurnal fluctuation of symptoms, and equivocal positive Tensilon test. However, waning phenomenon on repetitive nerve stimulation or elevation of titer of the anti-acetylcholine receptor antibody was not detected on both patients. Needle EMG showed mild myopathic changes. Finally, pathological and biochemical analyses of the biopsied muscles confirmed the diagnosis of mitochondrial myopathy (focal cytochrome c oxidase deficiency).
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PMID:[Two cases of mitochondrial myopathy (focal cytochrome c oxidase deficiency), long-term follow-up on a diagnosis of ocular type myasthenia gravis]. 255 82

Many reports of diabetic ophthalmoplegia have been published from the clinical points of view. However, there have been only three autopsied cases in which the ocular nerves were investigated histopathologically. A 72-year-old housewife was diagnosed to have glycosuria at the age of 67, but no medical treatment was done. She admitted to the hospital, because of acute onset of right eyelid drooping and diplopia for previous four days. She showed complete eyelid ptosis, moderate dilatation of right pupil, loss of light reaction, and extraocular muscle palsy except abduction on the right. Blood pressure was normal. A glucose tolerance test was diabetic and HbA1c was moderately increased. Her diabetes was fairly well-controlled with a diet therapy and injection of lente insulin. Two and a half months after admission, the course of illness became regressive. Seven months later, external ophthalmoplegia was disappeared and only slight anisocoria was seen. She readmitted to the hospital one year and eleven months later, because of anorexia and emaciation. She died of adenocarcinoma of the stomach without chemotherapy. The duration from onset of ocular symptoms to death was two years and one month. At postmortem examination, stomach cancer infiltrated extensively to the abdominal and pelvic viscera, but no metastasis to the nervous system or intraorbital tissues was found. There were mild to moderate atherosclerotic changes in the small-and middle-sized arteries of the kidneys, pancreas and adrenal glands corresponding to her age. Moderate atherosclerosis was found in all of the major arteries including Willis ring, siphon of the right internal carotid artery and Vertebro-basilar one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic ophthalmoplegia--a clinico-pathological study of the first case in Japan]. 269 31

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

Six cases of internal ophthalmoplegia due to direct head injury are presented. All six patients had a dilated, nonreactive pupil. Four had no extraocular palsies or ptosis and two had partial extraocular palsies or ptosis. Disturbance of consciousness was absent or very mild, and all patients fully recovered within 1 to 7 days after the traumatic event. No patient had a history that suggested a cause for oculomotor nerve palsy, and emergency CTscans showed no mass lesions. The internal ophthalmoplegia was recognized immediately after trauma. Although minimal oculomotor nerve palsies due to unruptured intracranial aneurysms have been described, none of our patients complained of periorbital or retroorbital pain either before or after the trauma, which rules out intracranial aneurysms as the cause of the internal ophthalmoplegia. Therefore, we concluded that the internal ophthalmoplegia was due to direct head injury. The pathophysiological mechanism of the internal ophthalmoplegia appeared to be slight injury of the pupillomotor fibres on the ventromedial surface of the third nerve at the posterior petroclinoid ligament, which acted as the fulcrum due to the downward displacement of the brainstem at the time of impact.
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PMID:Primary internal ophthalmoplegia due to head injury. 271 3

A clinicopathological report is presented of a British male, aged 59 years, who died after an illness of 10 years, manifested by progressive respiratory failure, ptosis, and dysphagia. At no time was there evidence of ophthalmoplegia, Parkinsonism or dementia. At necropsy the main finding was of neurofibrillary tangles in the neurons of the pontine and medullary reticular formation, with particularly severe involvement of the nucleus ambiguus, dorsal motor nucleus of the vagus and nucleus tractus solitarius. Morphologically, by light and electron microscopy and immunostaining, the tangles were similar to those of other neurofibrillary degenerative diseases. Although similar in some respects to progressive supranuclear palsy and amyotrophic lateral sclerosis of the Guam type, the combination of clinical and neuropathological features suggest that this is a distinct disease entity.
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PMID:Progressive medullary failure associated with neurofibrillary degeneration. 273 35

Descending ocular myopathy is a rare progressive disease characterized by bilateral ptosis, external ophthalmoplegia and progressive dystrophy of the proximal skeletal muscles. A case of descending ocular myopathy with post-operative corneal ulceration is reported. Mitochondrial abnormalities are found on skeletal muscle biopsy. Nosologic classification of this case is discussed.
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PMID:[Descending ocular myopathy--apropos of a case]. 280 12

A patient with actinomycosis, involving the meninges and right cavernous sinus, presented with diplopia due to a total right external ophthalmoplegia and left abduction weakness. These was partial right ptosis but the pupils were spared. The diagnosis was made by biopsy of a neck mass. A complete recovery was made in response to intravenous penicillin.
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PMID:Ophthalmoplegia due to actinomycosis. 294 22

We report a case of chronic progressive inflammatory polyradiculoneuropathy with a subacute exacerbation that included ataxia, tendon areflexia, ptosis, and ophthalmoplegia. Spinal fluid protein was elevated and electrophysiological studies revealed a demyelinating neuropathy. This case suggests a continuum between chronic inflammatory polyradiculoneuropathy and the Miller Fisher variant of acute inflammatory polyneuropathy.
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PMID:Chronic inflammatory polyradiculoneuropathy with ophthalmoplegia. 294 24


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