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

Twenty cases of cysticerosis involving the central nervous system were seen during a 6-year period. Twelve patients presented with symptom and signs of raised intracranial pressure, 6 with seizures and 1 each with subacute meningitis and psychosis. The diagnosis of cerebral cysticercosis was established by brain biopsy in 8 patients, at autopsy in 3, and by biopsy of a subcutaneous nodule in 7. It was presumed on the basis of typical intracranial calcification in 1 case and soft tissue calcification in another. The protean clinical manifestations of this condition and the diagnostic difficulties it raises are discussed.
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PMID:Cerebral cysticercosis. 63 39

Modification of cocaine's stimulant and local anesthetic behavioral effects as a function of chronic treatment was evaluated in seven female cats. Video tape of behavior pre- and post-cocaine (iv) on days 1, 4, 7, 10, and 13 in seven cats, and in addition, on days 21, 28, and 35 for s subset of four cats, was rated for several scales of the Behavioral Rating Inventory for Drug-Generated Effects (BRIDGE), developed to quantify stimulant-induced behaviors. Preseizure events were measured using scales for Tremor Intensity and Preseizure-Seizure Intensity (PSI), developed to quantify local anesthetic-induced behaviors. Behaviors associated with cocaine's local anesthetic effects, i.e., Tremor Intensity and PSI levels, showed tolerance over the treatment period, while behaviors associated with cocaine's psychomotor stimulant effects, i.e., the BRIDGE measures, showed augmentation, or reverse tolerance. These data are discussed in terms of catecholamine supersensitivity, kindling mechanisms, and stimulant models of psychosis.
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PMID:Behavioral analysis of chronic cocaine intoxication in the cat. 66 28

In a controlled investigation the clinical findings in 96 patients with paranoid/hallucinatory psychosis and partial epileptic seizures with complex symptoms, were compared with the findings in 96 control patients with the same type of epilepsy without psychosis of median 24 years' duration. The median age at onset of psychosis was 34 years, after epilepsy of median 21 years' duration. The seizure frequency of complex, partial seizures was significantly lower in the psychotic group, while the frequency of generalized seizures did not differ. A significant preponderance in the psychotic group of left-handed patients, etiological factors and neurological signs reflecting organic damage, and seizures of automatic behaviour indicates that epileptic psychoses are caused by structural lesions affecting the deep parts of the temporal lobe.
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PMID:Psychomotor epilepsy and psychosis. I. Physical aspects. 67 63

The EEG findings in waking, sleep, and sphenoidal electrode recordings in 96 patients with partial epileptic seizures with complex symptoms, who, after a median interval of 18 years developed paranoid/hallucinatory psychosis, were compared with the findings from a group of patients without psychosis, who had had the same type of epilepsy in median 24 years. There were no significant differences between the two groups with regard to median age at onset of epilepsy or complex partial seizures, age, or duration of epilepsy at time of examination. The psychotic patients had a significant preponderance of temporal medio-basal spike foci, recorded on the sphenoidal electrode, indicating deep temporal lobe dysfunction as an important factor in the pathogenesis of psychosis. A significant higher frequency of bilateral and multiple spike foci, together with a significant frequency of slow-wave admixture to the waking background EEG activity, indicated more extensive and severe epileptogenic lesions in the psychotic patients. There was no correlation between psychosis and unilateral EEG-foci in either temporal lobe.
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PMID:Psychomotor epilepsy and psychosis. II. Electroencephalographic findings (sphenoidal electrode recordings). 67 64

Fifty chronic alcoholics (37 men and 13 women, ages 26--55, mean age 39.9 years) with different clinical syndromes (alcoholic psychosis, alcoholic encephalopathies) were studied by computerized cranial tomography. Cerebral atrophy was detected in 96% of all cases. Combined cortical and subcortical signs were encountered in almost all cases. Cortical atrophy seemed to be detectable more easily by CT than by pneumencephalography. The computerized tomographic findings were studied in their relations to age, sex, duration of abuse, clinical syndromes, frequency of relapse (and seizures, too), etc. Cerebral atrophy was correlated primarily with the subjects' age and the duration, and less with the intensity of alcoholism. The most distinct changes were found in delirium syndromes and, in cases with relapse of psychosis, especially in combination with seizures. Wernicke-Korsakow encephalopathies showed the widest third ventricles when combined with repeated syndromes of withdrawal in their case histories. Computerized tomographic examinations of ten patients during acute psychosis as well as 4 weeks later showed identical findings; transitory changes, e.g., cerebral edema, were not detected. Computerized cranial tomography appears to be extremely useful to study the numerous open questions concerning the pathogenetic role of age, duration, and severity of abuse with cerebral atrophy.
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PMID:[Brain atrophy in chronic alcoholism. Clinical and computer tomographic study]. 73 66

Of 19 adolescents with diagnosed psychogenic seizures, 13 had hysterical convulsions and 4 had amnesiac fugues. Sixteen of the patients were given a diagnosis of hysterical neurosis; 2, process schizophrenia; and 1, borderline psychosis. Thirteen of the patients were initially diagnosed incorrectly as having epilepsy and were treated for an average of 15 months with anticonvulsant medication. The therapist should always consider the possibility of psychogenic factors in children and adolescents who suffer from seizures.
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PMID:Pseudoepilepsy: a study in adolescent hysteria. 76 May 52

The authors report the case of a psychotic preschool child who manifested a seizure disorder while on imipramine treatment. They note that according to his history and physical exam, the child fell within a group which seems predisposed to this side effect. Although tricyclic antidepressant compounds can be used judiciously with seizure-prone individuals, the authors recommend that alternative modalities be given first consideration.
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PMID:Imipramine and seizures. 80 59

Subluxation of the cervical spine either with or without neurologic involvement as a result of epileptic seizure is a rare occurrence. Most of the literature reviewed deals with compression fractures of the spine effected by metrazol-induced convulsions or electroshock therapy for major psychosis. Of further interest in this case is the presumptive diagnosis of a cerebral lesion due to schistosomiasis as the cause of the seizure which produced the cervical subluxation with neurologic changes. The subluxation was reduced and stabilized by inter-body fusion.
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PMID:Subluxation of cervical spine in major epileptic seizure due to cerebral schistosomiasis. 82 9

Chronic administration of the same dose of cocaine to rhesus monkeys for up to 6 months was associated with progressive alterations in pathological behavior and increased susceptibility to seizures. Monkeys initially displaying prominent hyperactive stereotypic responses for up to 2 months began to demonstrate increasing amounts of inhibitory behavior, consisting of catalepsy, motor inhibition, and abnormal visual tracking and staring. Four of 13 animals developed increasing intensities of lingual-buccal dyskinesias after 10 weeks of chronic cocaine. Animals initially showing no convulsions to a given dose of cocaine eventually developed convulsions to the same dose, and then displayed an increased frequency of convulsions following subsequent injections. Levels of the dopamine metabolite, homovanillic acid (HVA), in the cisternal cerebrospinal fluid were significantly elevated during both excitatory stereotypic and inhibitory syndromes; a similar trend was observed for HVA after probenecid administration. Only the probenecid-induced accumulations of the serotonin metabolite 5-hydroxyindoleacetic acid, following acute cocaine administration, were significantly elevated. The progressive increases in convulsions, dyskinesias, and the inhibitory syndrome did not appear related to alterations in peak levels of cocaine in plasma or CSF, and a pharmacological kindling model is suggested as an alternate explanation of the data. The study extends the current models of stimulant-induced psychoses by highlighting the progressive alterations in behavior and neurological sequelae and in suggesting that this progressive mechanism may also be important in the development of psychosis in man.
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PMID:Progressive effects of cocaine on behavior and central amine metabolism in rhesus monkeys: relationship to kindling and psychosis. 82 87

This study is an attempt to investigate cases of temporal lobe epilepsy, the starting point being a large number of psychiatric patients. The data presented in this study suggest that a certain number of schizophrenic-like psychoses are produced by temporal seizural activity. There is some evidence that if there is a centrencephalic seizure at the beginning of such a psychotic state, the patient's behavior will have confusional characteristics (perhaps a postictal centrencephalic state). Some findings suggest that the side localization of the temporal lobe focus affects the feature of the psychotic state. None of the nine patients with periodic psychoses had schizoid or paranoid premorbid personality. As to the interictal behavioral disorders of epileptics, we have noticed that two patients with hysteroepilepsy and two with compensation neurosis had dominant temporal lobe focus. Of 10 cases with behavior disorders, all had grand mal or petit mal epilepsy, and none had a temporal lobe focus. Although this study is not based on sufficient data, it may provide working hypotheses for further research.
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PMID:Psychiatric aspects of temporal lobe epilepsy. 82 4


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