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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Similar movement disorders developed in two 8-year-old retarded children while they were receiving phenytoin. Seizures subsequent to a diphtheria-pertussis-tetanus immunization had developed in each child at 1 to 2 months of age. A static encephalopathy ensued, characterized by mental retardation, ataxia, spasticity, and a mixed seizure disorder. Intermittent dystonia and choreoathetosis developed insidiously while serum phenytoin concentrations were in the therapeutic range. Sustained dystonia and choreoatheosis developed 2 hours after an oral provocation with phenytoin. The baseline abnormalities on the electroencephalogram remained unchanged during the choreoathetosis. Recognizable metabolic abnormalities known to be associated with similar movement disorders were excluded. It was concluded from these studies that the movement disorder is secondary to phenytoin and can occur at therapeutic serum concentrations. Phenytoin is a central anticholinergic agent and a central stimulant of serotonin, and may induce movement disorders as a result of altering these neurotransmitters in the brain. The variable expression of these movement disorders may relate to the nature of the preexisting striatal insult.
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PMID:Phenytoin-induced dystonia and choreoathetosis in two retarded epileptic children. 94 1

Twenty-one neonates of over 36 weeks' gestation suffered perinatal asphyxia but not chronic hypoxia. Three clinical stages of postanoxic encephalopathy were distinguished. Stage 1 lasted less than 24 hours and was characterized by hyperalertness, uninhibited Moro and stretch reflexes, sympathetic effects, and a normal electroencephalogram. Stage 2 was marked by obtundation, hypotonia, strong distal flexion, and multifocal seizures. The EEG showed a periodic pattern sometimes preceded by continuous delta activity. Infants in stage 3 were stuporous, flaccid, and brain stem and autonomic functions were suppressed. The EEG was isopotential or had infrequent periodic discharges. Infants who did not enter stage 3 and who had signs of stage 2 for less than five days appeared normal in later infancy. Persistence of stage 2 for more than seven days or failure of the EEG to revert to normal was associated with later neurologic impairment or death.
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PMID:Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study. 98 69

The author reports an analysis of 83 cases of salaam seizures in children from the standpoint of their aetiopathogenesis. In accordance with Jeavons she separates a group with congenital nervous system damage and a group of children who developed initially normally but in whom an acquired factor, most often of allergic character, caused nervous system changes manifesting themselves with salaam seizures. The comparison of both groups demonstrated a number of significant differences. The author believes that it would be wrong to consider all children with salaam seizures as a homogenous group because the only common factor in them is the occurrence of seizures. The author regards that it is insufficient to explain the type of EEG changes and the type of seizures as determined by the degree of nervous system development. Additional factors must exist, and fetal injury is this factor in the group of congenital seizures while in the group of acquired seizures the allergic factor is probably responsible. The isolation of both groups is important mainly from the standpoint of prognosis and treatment since in the group with acquired disease an acute cerebral process is the cause, in contrast to the group congenital damage, and the process is amenable to successful treatment if this treatment is applied sufficiently early. In the congenital group the prognosis is usually unfavourable in view of the underlying cause which is congenital encephalopathy acquired in the first place in pregnancy.
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PMID:[Etiopathogenesis of salaam seizures]. 98 86

Reye-Johnson syndrome was found in 17 patients in a retrospective study of 235 children with acute encephalopathy seen at the Mayo Clinic in the period 1955 through 1971. Eight of the nine patients under 4 years of age developed the syndrome prior to 1968; eight children 10 to 15 years of age acquired the disorder from 1968 through 1971. Seven patients were admitted during the month of February. Prodromal symptoms preceded the encephalopathy in 13 patients. Eight patients had seizures. Progressive deterioration with brainstem signs led to death in 15 patients. Electroencephalographic findings correlated well with the clinical course and eventual outcome. However, no correlation was found between seizure activity and the electroencephalogram. Autopsy findings in 14 cases included cerebral edema, tonsillar herniation, hypoxic neuronal degeneration, and fatty inflitration of the liver and kidneys.
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PMID:Encephalopathy and fatty infiltration of the viscera (Reye-Johnson syndrome): a 17-year experience. 109 86

The neurological manifestations of six cases of acquired central nervous system toxoplasmosis are compared with the 39 well-documented cases from the literature. Half of the patients had underlying systemic diseases (18 malignant neoplasms, two renal transplants, three collagen vascular diseases) treated with intensive immunosuppressive therapy. The remainder had primary toxoplasmosis. Three major neurological patterns were seen: (1) diffuse encephalopathy with or without seizures, (2) meningoencephalitis, and (3) singular or multiple progressive mass lesions. Routine neurological diagnostic studies were not helpful. The Sabin-Feldman dye test or IgM indirect fluorescent antibody test or both were effective in confirming the diagnosis. Twenty-seven patients died without a clinical diagnosis of toxoplasmosis. The diagnosis was made terminally in four additional patients. Thirteen of fourteen patients who received a full course of sulfadiazine or pyrimethamine or both did well. Toxoplasmosis should be considered in the immunosuppressed patient who appears with neurological involvement.
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PMID:Acquired toxoplasmosis. A neglected cause of treatable nervous system disease. 109 93

A patient with a traumatic arteriovenous fistula of the kidney developed encephalopathy with seizures and was unconscious for 48 hours before undergoing a left nephrectomy, excision of a false aneurysm of the left renal artery, and colostomy closure. He has remained in good health for two years following the final operative intervention.
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PMID:Traumatic arteriovenous fistula of the kidney; an unusual cause of hypertensive encephalopathy. 112 64

From 1950 to 1970 in Hamburg, 9240 patients under 15 years of age were treated as inpatients for pertussis. 1674 patients had pneumonia due to pertussis, 114 had pertussis encephalopathies, and 41 seizures. The fatality from pneumonia went from 2,26% (1950-1960) to 0,4% (1961-1970). Fatality from encephalopathy was less influenced (24% respectively, 17,9%). The mild clinical course of pertussis is also reflected in the reduced number of hospitalizations due to pertussis (1956, 3,7%; 1970, 0,8%). Permanent damage from complications due to pertussis was seen in 0,7% of survivors from pertussis pneumonia and in 3,4% after pertussis encephalopathy.
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PMID:[Pertussis and it complications-analysis of hospitalized patients in Hamburg 1950-1970 (author's transl)]. 120 1

Five patients with an unusual encephalopathy, possible secondary to measles virus infection, are described. Features common to these patients are: an existing chronic disease, neurologic deterioration 2 1/2 to 6 months after a measles infection, and death several weeks later. These events occurred when the chronic disease (e.g. leukemia or neuroblastoma) was in remission. That the measles virus was the causative agent is suggested only by finding in brain and extracranial tissues intracytoplasmic and intranuclear inclusions which contained measleslike particles. Additional clinical features seen in each of the five patients were: seizures, hypertension, and the inappropriate secretion of antidiuretic hormone.
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PMID:Encephalopathy following measles infection in children with chronic illness. 127 Nov 91

A patient with progressive spastic paraparesis originally ascribed to multiple sclerosis developed recurrent encephalopathy and seizures. A diagnosis of HTLV-I-associated myelopathy/tropical spastic paraparesis was established prior to death. Autopsy confirmed chronic inflammatory myelopathy and active inflammation in the white matter of the temporal lobes.
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PMID:Recurrent encephalopathy and seizures in a US native with HTLV-I-associated myelopathy/tropical spastic paraparesis: a clinicopathologic study. 143 55

This paper reviews the neurological complications of malaria. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red blood cells causing blood sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes a nonspecific, immune-mediated, inflammatory response with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations in malaria remains unexplored, but offers excellent perspectives for research at clinical as well as experimental level.
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PMID:Neurological complications of malaria. 129 73


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