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

Growing, mongrel dogs were fed high fat (22%), low calcium (.1%) semipurified and purified diets with and without 77 ppm lead as lead acetate to experimentally induce the seizures and lead encephalopathy historically associated with accidental canine lead toxicity. Seizures were observed in 44% of the lead toxic dogs and microscopic encephalopathy was observed in 89% of the lead toxic dogs. The encephalopathy was characterized by bilaterally symmetrical areas of vacuole formation involving the neuropile especially in a laminar pattern at the tips of the gyri of the cerebral cortex. The spongy state was accompanied by capillary activation and gliosis. These lesions are similar to those reported in accidental lead toxicoses in other species but previous efforts to experimentally induce these lesions in young dogs fed low-calcium, normal-fat (16%) purified diets have been unsuccessful.
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PMID:Lead-induced encephalopathy in dogs fed high fat, low calcium diets. 46 67

The cases presented with psychic troubles and repeated somnolence episodes accompanied by dysarthria in 5 cases, myoclonic jerks in 4 cases and epileptic seizures in 1 case. In all cases the EEG was disturbed. It showed symetrical, paroxystic, bilateral, monomorph slow activity with more or less frequent paroxysms. The average serum aluminium level was at 407 microgram/l in the acute phase, at 161 microgram/l in the remission phase and at 123 microgram/l three months later. After interruption of oral and dialytic aluminium intake the remission is maintained. However in 2 cases the transitory readministration of aluminium gel was followed by reversible recurrency. The role of both aluminium gel and dialysate aluminium as the origin of encephalopathy is discussed.
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PMID:[Reversible dialytic encephalopathy after interruption of aluminium intake. 6 cases (author's transl)]. 49 78

The record of 67 cases under 15 years of age who were hospitalized during status convulsivus from 1975 to 1978, the 348 cases who visited the hospital for the first time with epilepsy (Oct. 1977 to Sept. 1978) and the 32 cases who were hospitalized during status epilepticus from 1969 to 1974 and who are being followed up as outpatients were studied. The frequency of status epilepticus was 8% among epileptic children. There was no difference in the frequency of incidence between male and female. Patients with mental retardation, however, were revealed to have status epilepticus twice to three times more frequently as compared to cases without mental retardation. The major seizure types of status epilepticus in childhood were generalized tonic clonic convulsion and unilateral clonic convulsion. In 25% of the cases, status epilepticus was the first ictal manifestation. The major cause of status convulsivus was epilepsy, followed by encephalitis and encephalopathy, but cases due to brain tumor were rare. The drug of first choice for status convulsivus is diazepam. If there is any difficulty in controlling status convulsivus with diazepam, it may be worthwhile to consider what the problem is, causes of status convulsivus, seizure type, or basic disease of the patient. The effective dose of diazepam was within the range of 0.3--0.5 mg/kg. When the effect is not sufficient, the dose of diazepam should be increased to 1 mg/kg while watching the general condition of the patient. Factors affecting the prognosis of status convulsivus were its cause, duration, onset age and effectiveness of therapy during the acute stage. The frequency of cases who suffered disability after status epilepticus was 56%. (transient disability 43%, permanent disability 13%) The most frequent type of transient disability was hemiplegia. Most epileptic children who had repetitive status convulsivus revealed psychomotor retardation before first status. Factors which cause repetitive status seem to be hemispheric brain damage or diffuse corticocentrencephalic damage.
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PMID:Therapy and prognosis of status convulsivus in childhood. 52 Sep 66

An ultrastructural study of cerebral cortex was performed in rats during the preictal period following the administration of the convulsant methionine sulfoximine (MSO). The morphologic changes were restricted to astrocytes and consisted of cytoplasmic enlargement, mitochondrial and rough endoplasmic reticulum proliferation, accumulation of glycogen, development of cisternal and saccular smooth endoplasmic reticulum, nuclear chromatin clumping, and hydropic degenerative changes. These findings resemble those seen in experimental ammonia encephalopathy, suggesting an important role of ammonia in the evolution of these morphologic changes. The findings, moreover, suggest that the primary effect of MSO is on astrocytes and that abnormalities in astrocytes may play a role in the development of MSO-induced seizures.
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PMID:Ultrastructural study of methionine sulfoximine-induced Alzheimer type II astrocytosis. 55 86

A study of nine patients, aged 23 to 67 years, showed a remarkable sequence of EEG findings in progressive uremic encephalopathy. The initial characteristics suggested a disorder of subcortical gray matter, followed by involvement of cortical gray matter and finally white matter. The same EEG findings tended to persist in the early stages of the disease and were present throughout the night and during dialysis. During dialysis, the EEG background and clinical picture between paroxysms sometimes showed deterioration. Seizures indicated a grave prognosis. Five of six patients with seizures died. In some patients, progressive uremic encephalopathy may develop without hemodialysis. Routine EEGs in dialysis units or in patients prior to admission can help uncover progressive uremic encephalopathy before the clinical emergence of this disorder.
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PMID:Clinical and electroencephalographic changes in progressive uremic encephalopathy. 56 66

The subcortical arteriosclerotic encephalopathy of Binswanger is characterized clinically by hypertension, dementia, spasticity, syncope, and seizures. It is usually diagnosed pathologically by the finding in white matter of diffuse demyelination or foci of necrosis plus arteriosclerotic and hypertensive vasculopathy. We present a case in which the diagnosis was made on the basis of the clinical course and a computerized tomogram which demonstrated extensive white matter degeneration. Postmortem examination confirmed both the diagnosis and the extent of the degeneration as shown by CT scan.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger): computerized tomography. 57 97

Large doses of phenytoin were administered on 159 occasions to 139 adult patients. Most patients had had more than three seizures or were in status epilepticus. Based on response to treatment, patients could be divided into two groups. Those with excellent response (recurrent seizures, 10%; mortality, 1%) included known epileptics with exacerbation of seizures (n = 75), atypical alcohol withdrawal (6), or miscellaneous conditions (17). Those with poor results (recurrent seizures, 57% mortality, 38%) included patients with anoxic or metabolic encephalopathy (14), stroke or other vascular disease (14), brain tumor (5), or trauma (5).
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PMID:Intravenous phenytoin in acute treatment of seizures. 57

4 cases of nonketotic hyperglycinemia (glycine encephalopathy), one with autopsy, are presented and the literature on 61 cases is reviewed. Major clinical signs include early hypotonia, lethargy and erratic and massive myoclonias with respiratory distrubances, starting during the first days of life after a symptom-free interval. Early death is common. Survivors are severely retarded and exhibit various types of seizures including infantile spasms. The EEG pattern consists initially of periodical paroxysmal bursts on an almost flat tracing, evolving later into a hypsarrhythmic pattern. Spongiosis of the myelinated pathways is the main pathological finding. Elevated CSF glycine seems to be the essential determinant of the neurological disturbances and it is, therefore, suggested that the term glycine encephalopathy be used instead of non-ketotic hyperglycinemia. A classification of disorders associated with hyperglycinemia is proposed.
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PMID:Glycine encephalopathy. 58 64

The observation in 14 dialysis patients of an encephalopathy associating myoclonia, dysarthria, generalised seizures in some cases, worsening over a few months, led to an aetiological inquiry based upon comparative study of patients with or without encephalopathy treated in the same centre or at home, and controls. Higher levels of aluminium were found in the frontal cortex grey matter of encephalopathy patients as compared to the control group. The same applies to manganese in the white matter. Copper, zinc and iron contents were not different. Aluminium levels in blood, dialysis bath and tap water supply were higher in center dialysis than in home dialysis. Blood aluminium levels at the end of hemodialysis were correlated with bath aluminium levels. The ingestion of alumine gels was not greater in the encephalopathy patients than in other hemodialysis patients; its estimation, in each case, was not related to the blood aluminium levels at the begining of hemodialysis. These finding indicate the need of a routine measure of metal content - mainly aluminium and manganese - in tap water used for dialysis, in order to treat this water if necessary.
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PMID:[Progressive myoclonic encephalopathy in dialysis patients. The role of the water used for haemodialysis (author's transl)]. 65 14

Neuropathological considerations were performed on a case, who went into Lennox syndrome after an acute encephalopathy at the infantile period, and moreover who fell into an akinetic-mute state derived from brain damage by herniation caused by a head injury and subsequent status epilepticus. Neuropahtological background in the present case of Lennox syndrome is thought to be based on the widespread unilateral cerebral lesions and the basal ganglional, especially thalamic, degenerations derived secondarily from the diffuse cerebral damage. The patient revealed akinetic mutism with the disappearance of the epileptic seizures and the desynchronization of the EEG's, when the brain lesions formed at the adult period spread over the opposite hemispheric limbic system and the brain stem tectum.
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PMID:Neuropathology of secondary generalized epilepsy--(Lennox-Gastaut syndrome)--a case report. 65 45


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