Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029089 (ophthalmoplegia)
 3,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four term infants were found by computerized cerebral tomography (CT) to have intraventricular hemorrhage. All were male infants who had experienced substantial intrapartum complications. One infant had subtle clinical signs at 2 days of age; the others had major neurologic findings including seizures and ophthalmoplegia that occurred at 1, 4, and 6 weeks of age, respectively. Three infants in whom the hemorrhages were indistinguishable by CT from those described in preterm infants now have arrested hydrocephalus and normal development. The fourth infant was found to have a large glioblastoma at the site of origin of his initial hemorrhage. These cases emphasize the need to consider this diagnosis in neonates born at term who have abnormal neurologic signs.
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PMID:Intraventricular hemorrhage in the neonate born at term. 47 46

A 68-year-old man had ventriculoperitoneal shunt placement for normal-pressure hydrocephalus. Three and a half years later, he had repeated episodes of seizures and ophthalmoplegia. He eventually died of recurrent acute bacterial meningitis. At autopsy the distal segment of the shunt catheter was found inside the stomach, a condition believed to be responsible for the repeated attacks of bacterial meningitis.
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PMID:Recurrent meningitis associated with intragastric migration of a ventriculoperitoneal shunt catheter in a patient with normal-pressure hydrocephalus. 821 46

We present a patient whose only physical manifestation of a partial sensory seizure was bilateral pupillary constriction and internal ophthalmoplegia. The onset and offset of each attack corresponded distinctly with an electroencephalographic discharge of the left temporo-occipital region. We propose involvement of a cortical pupillary constrictive center in the temporal-occipital area.
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PMID:Miosis and internal ophthalmoplegia as a manifestation of partial seizures. 190 18

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

Meningoencephalitic syndrome can be caused by many infective agents. Over a period of 13 years, 15 of 170 cases of neurocysticercosis (NCC) presented as meningoencephalitis. The basis of diagnosis of NCC was positive subcutaneous nodule histopathology (4), CT scan (9) and autopsy (3) findings. The age of the patients ranged from 7-68 years (mean 32). Fever was encountered in 12, altered sensorium in 7, seizures in 10 and abnormal behaviour in 3 cases. All cases had papilloedema. Focal neurological signs included optic atrophy, lateral rectus palsy, hemiplegia, internuclear ophthalmoplegia and cerebellar ataxia. Cerebrospinal fluid was abnormal in 8 of 13 cases, leading to a suspicion of tuberculous meningitis. Twelve patients improved with therapy. Three cases ended fatally and autopsy confirmed the diagnosis.
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PMID:Cysticercal meningoencephalitis. 193 70

The neurologic evaluation of an individual cardiac transplant recipient often does not lead to a succinct bedside diagnosis. There are few consistent clinical observations. The onset of seizures in the early postoperative period is associated with embolic cerebral infarction. Seizures occur most commonly, however, as a neurotoxic manifestation of cyclosporine. The onset of an acute delirium or psychosis in the first week after cardiac transplantation usually has multiple causative factors and is reversible. A postoperative brachial plexopathy or mononeuropathy can be identified with a neurologic examination, confirmed by appropriate electrophysiologic testing and is usually reversible. The onset of periorbital inflammation, ophthalmoplegia, and nasal turbinate or sinus invasion and necrosis is consistent with phycomycosis. Most patients, however, present with nonspecific findings of impaired mentation with or without focal neurologic signs. These patients require a fairly systematic search for potentially treatable neurologic complications (see Table 3). In a medically stable patient an aggressive diagnostic approach, at times including stereotaxic brain aspirate or biopsy, is indicated. In the severely ill patient with multiple organ failure, empirical therapy for the most probable treatable disorder is justified.
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PMID:Neurologic complications of cardiac transplantation. 304 45

We report 2 brothers with progressive ataxia, seizures, myoclonus, supranuclear ophthalmoplegia, progressive visual loss and embolic strokes. The epilepsy and myoclonus came on many years after the onset of the ataxia. In the more severely affected brother the myoclonus was often unilateral and focal but ultimately involved both sides of the body. His sibling had only unilateral myoclonus after a contralateral middle cerebral artery stroke. When focal, persistent and unilateral, the myoclonus in both brothers was clinically similar to epilepsia partialis continua except that muscles of the trunk and proximal limbs were the most affected. It was exacerbated by movement of the affected part but was otherwise not stimulus sensitive. The more severely affected brother had a pigmentary retinopathy and a cardiac fibromyxoid valvulopathy. In his sibling, visual loss was not fully investigated and the heart was not examined at autopsy though he had a longstanding heart murmur. Neuropathological studies showed pancerebellar cortical atrophy, cell loss in the inferior olivary nuclei and old right middle cerebral artery infarctions in both brothers. Biochemical assays for known metabolic diseases were negative. We suggest that this syndrome represents a unique autosomal recessive form of progressive myoclonus epilepsy of unclear aetiology. It is distinguished from other familial myoclonus epilepsies by the presence of early onset cerebellar ataxia, supranuclear ophthalmoplegia, pigmentary retinopathy and possibly cardiac valvulopathy with subsequent cerebral emboli.
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PMID:Myoclonus epilepsy in two brothers. Clinical features and neuropathology of a unique syndrome. 308 70

Prior to the antibiotic (AB) era, cavernous sinus thrombosis (CST) was almost uniformly fatal. AB therapy has significantly reduced mortality, but additional treatment with anticoagulants (AC) has remained controversial. We reviewed our experience with seven cases, as well as the literature since Lyons' 1941 introduction of AC treatment, to determine effectiveness, complications, and morbidity among survivors. We divided the cases into (1) those treated with AB alone, and (2) those treated with a combination of AB and AC. We found no conclusive evidence for reduction of mortality when AC was used in combination with AB. However, early AC therapy reduced morbidity (blindness, stroke, ophthalmoplegia, hypopituitarism, focal seizures, and vascular steal syndrome), whereas delayed or inadequate use provided no apparent benefit above AB therapy alone. Complications of AC therapy were rare; cerebral venous thrombosis occurred frequently, but in association with dural sinus thrombosis as a direct result of the disease. We conclude that AC therapy is indicated early in the treatment of CST to reduce morbidity among survivors.
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PMID:The role of anticoagulation in cavernous sinus thrombosis. 328 Oct 56

Progressive supranuclear palsy (PSP) was first recognized as a distinct morbid entity by Richardson, Steele and Olszewski a quarter century ago. Subsequent experience has confirmed and extended their original observations. PSP has become familiar as a chronic progressive disorder with extrapyramidal rigidity, bradykinesia, gait impairment, bulbar palsy, dementia and a characteristic supranuclear ophthalmoplegia. It is an important cause of parkinsonism. Its etiology remains obscure. Familial concentrations have not been observed. Some cases exhibit no oculomotor dysfunction. Dementia is usually mild. Recent neuropsychological studies have defined features consistent with frontal lobe cortical dysfunction. Seizures and paroxysmal EEG activity may occur. CT and MRI scans show midbrain atrophy early and later atrophy of the pontine and midbrain tegmentum and the frontal and temporal lobes. PET scans have shown frontal hypometabolism and loss of striatal D-2 dopamine receptors. Postmortem studies have documented involvement of both dopaminergic and cholinergic systems. Treatment remains palliative and unsatisfactory.
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PMID:Progressive supranuclear palsy. 331 57

The clinical features of 66 patients with histologically defined mitochondrial myopathy are described. The age of onset of symptoms ranged from birth to 68 years, but was before 20 years in 61%. Nineteen patients had similarly affected relatives. Three groups of cases could be identified clinically: a combination of progressive external ophthalmoplegia and weakness of the limbs induced or increased by exertion (55%); such limb weakness alone (18%); and those with clinical features, such as ataxia, dementia, deafness, involuntary movements and seizures, predominantly or exclusively arising from the CNS (27%). There was considerable overlap between these groups, and pigmentary retinopathy, present in 36% of patients, occurred in all three. At a mean disease duration of twenty years, 9 patients (all from Group 3) were severely disabled but 42 were still able to work. In vitro studies of mitochondrial metabolism, performed in 33 cases, most commonly showed deficiencies of the mitochondrial respiratory chain localized to complex I (18 patients) or complex III (9). No typical clinical picture emerged for any of the identifiable biochemical defects.
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PMID:The clinical features of mitochondrial myopathy. 377 73


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