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

The dynamics of ultrastructural changes in axonal endings were studied after experimental epileptic seizures. Mice and rats from strains with genetically--determined audiogenic epilepsy were used as a model of epilepsy. The animals were divided into 3 groups: in group 1 only one seizure was evoked, in group 2 eight seizures within 4 hours, group 3 served as control. The animals were killed immediately after the last seizure, 30 min. after it or 1 hour after the seizure. Hippocampal gyrus cortex was impregnated with zinc-iodide-osmium tetroxide and synapses were examined under electron microscope. The number of synaptic vesicles showing positive reaction with zinc iodide was calculated in 20 synaptic boutons in each group. A significant correlation was demonstrated between the frequency of seizures and the survival time after the seizure on the one hand, and synaptic changes, on the other. In the control group 97% of synaptic vesicles were filled with neurotransmitter substance giving positive reaction with zinc iodide. Immediately after the single seizure 46% of synaptic vesicles were found emptied, 30 min. later the neurotransmitter substance was demonstrated in 79% of vesicles, 1 hour later 82% of vesicles had normal appearance. Immediately after serial seizures 91% of vesicles were found empty, 30 min. later the neurotransmitter was present in 50% of vesicles, 1 hour later in 78%. In another group of animals seizures were evoked once daily for 40 days (chronic epilepsy model). Synaptic changes were different: the synaptic boutons were swollen, the number of vesicles was reduced, greatly enlarged vesicles and clear membrane-bound vacuoles appeared. They evidenced degenerative character of changes. It is suggested that degenerative synaptic changes may be a substrate of epileptic dementia.
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PMID:[Dynamics of synaptic changes in experimental audiogenic epilepsy]. 1 11

A 40 year old man developed seizures, intermittent fever, and progressive dementia ending in coma and death after four years. The cerebrospinal fluid showed variable pleocytosis and occasional elevation of protein. The necropsy revealed many lesions characteristic of Whipple's disease confined to the grey matter of the brain. The pathological changes were studied with the light and electron microscope. The findings permitted an understanding of the temporal sequence of changes in the lesions. Involvement of the brain in this condition is rare, but the disease is treatable and the diagnosis can be made by brain biopsy.
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PMID:Whipple's disease confined to the brain: a case studied clinically and pathologically. 7 5

We present a family with infantile onset of progressive choreoathetosis. The movements affected the legs predominantly and also impaired gait. No dementia, seizures, or rigidity was noted. Inheritance was autosomal dominant. This new familial movement disorder can be differentiated easily from other hereditary choreas.
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PMID:Familial inverted choreoathetosis. 15 19

The responsibility of the folate deficiency in some neuropsychiatric disorders is recent knowledge. The role of the folate on the nervous system is not yet well definite, but the action on the metabolism of the amino-acids, on the purine and the pyrimidine synthesis and on the metabolism of the catecholamins are certainly essential. The neuropsychiatric diseases secondary to the folate deficiency are numerous: dementia, schizophrenia like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, pueperal psychosis, peripheral neuropathy, myelopathy (spinal cord syndrome and/or pyramidal tract damage), restless legs syndrome. Clinically the diagnosis may be difficult with sub acute combined degenration secondary to the pernicious anaemia, and the dosage of the folate (in serum, in red-cells and in cerebrospinal fluid) is necessary. The congenital defects in the uptake or utilization of the folate are associated with neuropsychiatric disturbances. The treatment is easy and safe if the vitamin B12 deficiency is eliminated and if employed with caution in epileptic patients because folate can induced seizures.
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PMID:[Folate and the nervous system (author's transl)]. 22 16

208 patients with epilepsy were investigated by computertomography (Emi Scanner CT 1010 and CT 5005). In 173 patients with generalised epilepsy 87 had a normal scan, 51 revealed a definitive diagnosis and 37 showed generalised atrophy. Of the 35 patients with partial seizures a definitive diagnosis was possible in 22; representing a higher proportion than the group with generalised seizures. A definitive diagnosis from the CT Scan was significantly more common in both patients with generalised and partial seizures when pathological neurological findings were also present. Symptomatic epilepsy was only significantly commoner in Dementia patients with generalised seizures. A significantly higher proportion of patients over 30 years old demonstrated a symptomatic epilepsy than those under 30 years of age.
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PMID:[The importance of computer tomography in the diagnosis of epilepsy (author's transl)]. 25 54

Clinical studies of epilepsy in 137 patients of old age demonstrated that epileptical dementia preserves its nozological specificity. In genuine epilepsy it was not possible to detect symptoms of cerebral atherosclerosis, while in symptomatical epilepsy there were definite signs of arteriosclerotic dementia. Convulsive seizeures in old age become less frequent and are substituted by abortive and psychomotor elementary seizures or are arrested altogether. Epileptic equivalents lose their specifity.
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PMID:[Course of epilepsy in persons of middle and old age with the disease beginning in childhood]. 40 13

A 39-year-old female died 25 years after the onset of epileptic seizure. In the clinical course, she suffered epileptic seizures, left hemiparesis and muscular atrophy of the left upper extremity, psychological character change, dementia, forced laughter and hallucinatory and delusional states. Pathologically, severe changes were found in the right hemisphere consisting of lesions of white matter with myelin loss, especially in the frontal, temporal and occipital lobes. Gliosis was diffusely observed in the white matter excepting areas with severe changes. In some parts of the cortex, the cytoarchitecture was destroyed and in this area, blood vessels numerously increased. In the left occipital white matter, perivascular infiltration mainly consisting of lymphocytes was observed with numerous fat granule cells and gemystocytic astrocytes around them. The present case may belong to the category of multiple leucoencephalitis, however, it had many characteristic features, such as a long clinical course (25 years) and pathologically revealed hemiatrophy of the brain.
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PMID:An autopsy case of multiple leucoencephalitis showing hemiatrophy of the brain. 45 58

The author has operated on 40 patients with giant intracranial aneurysms, using various surgical approaches. Giant aneurysms predominated in females (3:1) and were most common in the age group 30 to 60 years. Patients presented with subarachnoid hemorrhage (17), visual disturbance (18), chronic headache (14), transient or progressive hemispheric deficit (6), seizure (2), dementia (2), and cerebrospinal fluid rhinorrhea (1). Giant aneurysms were located at the carotid artery (25), the basovertebral artery (8), the anterior communicating artery (5), and the middle cerebral artery (2). Eight of 40 patients had one or more other aneurysms and/or associated arteriovenous malformations. Aneurysms were treated with intramural thrombosis (21), neck occlusion (7), trapping (10), proximal parent artery ligation (1), and aneurysmorrhaphy (1). After as much as 8 years of follow-up, 32 patients (80%) showed complete or marked improvement in signs and symptoms; two patients (5%) had a poor recovery. There were six surgical mortalities (15%). Giant aneurysms can be treated with respectable results if the surgeon selects the technique best suited to the particular aneurysm. In general, neck occlusion, trapping, and aneurysmorrhaphy are best for giant aneurysms of the anterior circulation, and intramural thrombosis is best for those of the posterior circulation. Extra- and intracranial vascular anastomotic techniques are also of value. For success, a flexible approach is essential.
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PMID:Direct surgical treatment of giant intracranial aneurysms. 50 18

A boy with mild hand tremor since age 2 1/2 was found at 4 to have cherry-red spots and mild trucal ataxia without seizures or dementia. Biochemically, he had striking hexosaminidase deficiency (serum: 4.6 percent of normal, 88.9 percent heat-labile; leukocyte: 2.2 percent of normal, 84.6 percent heat-labile; fibroblast 12.8 percent normal, 93.1 percent heat-labile). The residual hexosaminidase activity migrated electrophoretically in two bands. The major band comigrated with hexosaminidase A, the minor with hexosaminidase S. Hexosaminidase B was totally absent. The parents had partially reduced hexosaminidase with a decreased heat-stabile fraction. This disorder may result from a new mutation closely related to that causing Sandhoff-Jatzkewitz disease.
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PMID:A new juvenile hexosaminidase deficiency disease presenting as cerebellar ataxia. Clinical and biochemical studies. 56 95

The problem of differential diagnosis of childhood schizophrenia versus gross brain pathology is a difficult one. The clinical picture, for instance, of dementia infantalis (Heller's Disease) is indistinguishable from that of schizophrenia (Shaw & Lucas, 1970). The same is true of some major metabolic disorders (Bray,1970). Coexisting neurological and EEG findings for seizures are not helpful since these are often seen in schizophrenia (Bender, 1947; Fish, 1977). Mental retardation may coexist with schizophrenia or any of the other disorders. The following is an unusual case illustration of a child presenting symptoms of schizophrenia, seizures, and retardation without neurological abnormalities. Until his gross anatomical brain pathology was found by neurologic evaluation, he was subjected to the inappropriate treatment of psychotherapy.
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PMID:Davidoff-Dyke-Masson syndrome presenting as childhood schizophrenia. 57 29


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