Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CONVULSIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1987

Immunogenetic aspects of febrile convulsions.

Thirty-nine mentally normal unrelated children diagnosed as having febrile convulsions were included in this study. The following have been carried out: (a) detailed anamnesis and clinical examination; (b) cerebrospinal fluid investigation; (c) EEG examination between attacks; (d) HLA-antigen determination; (e) estimation of serum IgA, IgG, IgM; and (f) counting of percent spontaneous E-rosette formation. The results were statistically compared to normal Egyptian controls. The results could be summarised as follows. (1) Only HLA-B5 antigen frequency is high among patients (chi 2c = 19.1, P less than 0.0001). Relative risk is 4.4 which shows significant association (WY2 = 29.145, P less than 0.0001) and etiologic fraction equals 0.377. (2) The means of IgA and E-rosette in the patients were significantly low (t = 3.46, P less than 0.01 and t = 3.92, P less than 0.001, respectively), (3) HLA-B5 is the only antigen with high frequency among the two groups of patients with low IgA and E-rosette (chi 2c = 11.9 and 18.2, respectively). (4) There is a significant association between B5 and low IgA (P less than 0.05) but not with low E-rosette (P greater than 0.05). The suggestion is that the genetic control of febrile convulsions is in linkage disequilibrium with HLA-B5, low IgA and low total T-cells. This altered immune function in otherwise normal children with febrile convulsions may predispose them to acute infections and high fever which precipitate convulsions.

Child↗
PubMed1986

A clinical study of convulsive syncope.

An analysis of the clinical features of patients having evidence of a syncopal onset to convulsive episodes is reported. The range of convulsive phenomena was quite wide and did not appear to differentiate the syndrome from primary epilepsy in terms of seizure morphology, occurrence of incontinence or pattern of post-ictal recovery. It is therefore suggested that the premonitory and precipitating features are more specific in the diagnosis of convulsive syncope. Skin pallor was often reported during attacks. Although EEG abnormalities were seen in some cases, the follow-up results indicate a low incidence of unprovoked convulsions in patients with this condition without anticonvulsant treatment.

Adolescent↗
PubMed1978

Comparative effects of centrophenoxine on the picrotoxin convulsive-seizure threshold in non-irradiated and irradiated mice.

A comparative study is made of the effect of centrophenoxine (CP) on the picrotoxin convulsive-seizure threshold (PCST) in non-irradiated and irradiated 3 and 7 days previously male mice. It is found that the CP appliked intracerebroventricularly in doses of 200 and 400 micrograms/mouse (weight 18-22 g), increases PCST. In non-irradiated mice the PCST-increasing effect of CP occurs rapidly (5 min) and it is brief (it can be observed until the 15th min). When the irradiation is performed three days previously, the PCST-increasing effect of CP is prolonged (it is observed until the 6th hour after its application). When the irradiation is performed seven days previously the characteristic features of the PCST-increasing effect of CP are similar to those in the early stage (3 days), the only difference being that the duration of the effect is prolonged to 120 min. Generally, these specificities of the CP effect are valid for all three phases of the convulsive seizure (general excitation, clonic convulsive seizure and tonic convulsive seizure.

Animals↗
PubMed1986

Convulsive effects and pharmacokinetics of laudanosine in the rat.

Laudanosine, which is a degradation product of atracurium, is a convulsant drug in the rat. Laudanosine plasma concentrations were measured by high performance liquid chromatography after administration of both laudanosine and atracurium; protein binding and renal excretion of laudanosine were also determined. A continuous laudanosine infusion of 25 mg kg-1h-1, or less, did not cause convulsions. Eight times ED90 for twitch depression of atracurium gave rise to a laudanosine plasma concentration of less than 8 micrograms ml-1. The convulsive plasma-concentration level for laudanosine was over 17 micrograms ml-1 in the rat. The protein binding of laudanosine was 80%. The kidney excreted 15-20% laudanosine. We conclude that convulsive levels of laudanosine will be very unlikely in any species provided that normal atracurium doses are used no matter how long the procedure.

Animals↗
PubMed1985

Cerebrospinal fluid leucine-enkephalin-like levels in febrile convulsions.

Enkephalin levels were measured in the cerebrospinal fluid (CSF) of 17 patients with febrile convulsions and 11 control patients without a history of pain or convulsive disorders. Enkephalins were extracted from CSF by adsorption with synthetic resin XAD-2 eluted with methanol, and assayed using the radioreceptor assay (RRA). Results were expressed as Leucine-Enkephalin (Leu-E) equivalents. Enkephalin levels in CSF were 2.27 +/- 0.42 pmol/ml (mean +/- SE) in the convulsion group and the 4.8 +/- 0.8 pmol/ml (mean +/- SE) in the control group. Statistical comparison in both groups shows significant differences (p less than 0.001). These results suggest a correlation between convulsions and enkephalin levels in CSF.

Adolescent↗
PubMed1984

[Association of schizophrenic and convulsive manifestations in children].

The authors studied 25 preschool children with schizophrenia and schizophreniform states associated with residual-organic damage to the brain who also presented various convulsive manifestations. Patients with this combination were far less numerous than patients with convulsive manifestations without schizophreniform symptoms and with schizophrenia without convulsive manifestations. With regard to paroxysmal phenomena per se, no significant differences were discovered in patients with the schizophreniform symptomatology versus patients with convulsive manifestations without symptoms of schizophrenia. The study showed that in the majority of cases, the patients had infantile schizophrenia against an organically altered background. In schizophreniform conditions that resulted from residual symptoms of the organic damage to the brain, the epileptiform syndrome was more stable. The schizophreniform symptomatology in some cases was associated with temporal lobe epilepsy. Differentiation of "schizoepilepsy" as a separate nosological entity was found to be unsubstantiated. Administration of neuroleptics induced enhancement of paroxysmal manifestations in some patients.

Antipsychotic Agents↗
PubMed1984

Shigellosis: incidence of convulsions and resistance to antibiotics.

One hundred and ninety-three children with bacillary dysentery were admitted to the "Assaf Harofeh Hospital" during the years 1975-1980. Generalized convulsions were observed in 37 (19.2%) children. The incidence of seizures was significantly higher in children whose age ranged between 1 and 6 years when compared to those below or above this age range. Convulsions were not observed when fever was below 38 degrees C, however, higher fever was not associated with a parallel increase in their incidence. Temperature above 38 degrees C was less common in infants compared to older children. These findings suggest that convulsions in shigellosis do not differ from simple febrile convulsions in respect to age, sex, presence and degree of fever. The incidence of resistance to either ampicillin or trimethoprim-sulfamethoxazole was similar in all the various shigella strains isolated in our population.

Age Factors↗
PubMed1981

Change in sensitivity to insulin hypoglycemic convulsions after gold thioglucose treatment: time course of development.

The sensitivity to insulin hypoglycemic convulsions has been shown to decrease at early times (16 and 24 hr) and increase at later times (1 week) after gold thioglucose (GTG) treatment. Systemically administered GTG is well known to produce hyperphagia, resulting in obesity, and cytological damage focused relatively selectively in the ventromedial hypothalamic area (VMH). Both of these effects on insulin hypoglycemic convulsions occur before the weight gain, but at a time when histological damage visible with cresyl violet stain has already appeared. Both of these changes reflect a difference in the convulsive response to hypoglycemia, rather than a differences in the degree of hypoglycemia in response to insulin. No functional change in the convulsive sensitivity was found at still earlier times during the latency in establishing the histological damage visible with cresyl violet. These results suggest that GTG lesions a relatively discrete brain region involved in adjusting the functional response of the brain to hypoglycemia, including a composite of two opposite regulatory components. The significance of such a control center in relation to energy metabolism in brain is discussed. Moreover, it has been postulated that the glucose moiety of GTG binds to glucoreceptors in the VMH to focus the cytoxicity of the gold thioportion at that site. These results are also discussed in relation to this proposed mechanism for concentration and hence localization of GTG toxicity in the VMH.

Animals↗
PubMed1983

Tofizopam enhances the action of diazepam against tremor and convulsions.

Tofizopam, an anxiolytic 3,4-benzodiazepine, increases the affinity of benzodiazepine receptors for 1,4-benzodiazepines. In this study we investigated whether this increased affinity of the receptors alters the sensitivity of mice to tremor and to convulsions. Convulsions induced by harmane were not affected by tofizopam (50-300 mg/kg), but diazepam (15 mg/kg) increased the ED50 of harmane from 9.9 to 25.1 mg/kg. Tofizopam did not alter the threshold for electroshock-induced convulsions, while a dose of 10 mg/kg diazepam protected mice from convulsions. Low doses of tofizopam (12.5-25 mg/kg) sensitized mice to the tremorogenic effect of harmaline. Diazepam inhibited tremor: the ED50 of harmaline increased by 153% after 50 mg/kg of diazepam. In contrast to 1,4-benzodiazepines, tofizopam has no anticonvulsive effect. It sensitises mice to the tremor induced by harmaline. In combination with diazepam, however, tofizopam enhanced the anticonvulsive and antitremorogenic actions of this 1,4-benzodiazepine by 12-65%. This effect probably results from a tofizopam-induced increase in the occupation of benzodiazepine receptors.

Animals↗
PubMedDate not supplied

[Influence of catecholaminergic agents on the convulsant effect of corasol in rats].

It has been shown in experiments on rats that preinjection into the animals of amphetamine, isoprenaline hydrochloride, clonidine and phentolamine activating adrenergic transmission increases the resistance to the convulsant action of corasole. Disulfiram and guanethidine that decrease the content of noradrenaline in the body facilitate the development of corasole convulsions. The agents that change functional activity of the dopaminergic synapses (L-DOPA, alpha-methyldopa, apomorphine, perphenazine hydrochloride) exert no substantial effect on the convulsant effect of corasole. It is suggested that alpha- and beta-adrenergic structures participate in the mechanisms of catecholaminergic regulation of convulsant activity.

Animals↗
PubMed1980

Withdrawal convulsions in mice following nitrous oxide.

Mice may be induced to convulse after (but not prior to) breathing nitrous oxide. We found that the incidence of this withdrawal phenomenon is related to the partial pressure of nitrous oxide. A minimum (threshold) value of about 0.5 atm is necessary and the majority of mice convulse following exposure to 0.9 atm or greater. Exposures of longer than 15 to 30 minutes do not significantly increase the incidence of convulsions at any given partial pressure. The mice remain susceptible to the induction of convulsions for only a brief period after removal from nitrous oxide. Although the duration of susceptibility is slightly increased after exposure to higher partial pressures, susceptibility in almost all cases is lost by 90 minutes. In mice, exposure to nitrous oxide is associated with evidence of physical dependence as evidenced by withdrawal symptoms, symptoms that be related to the appearance of excitement which sometimes follows nitrous oxide anesthesia.

Animals↗
PubMed1980

[Diagnosis and course of convulsive states in children].

In 129 children convulsive states were examined with the use of a set of additional examination methods. The age structure of the convulsions and their course in young children are described. Different origin of the convulsive states is shown. The role of pre- and perinatal factors, mineral metabolism disturbances, infectious and other diseases, as well as of aggravated heredity is demonstrated. The importance of the premorbid background for the formation of the character and the course of the convulsive seizures in children, and for the formation of epileptiform syndrome is stressed.

Acute Disease↗
PubMed1980

Febrile convulsions.

Febrile convulsions occur in 3.4 percent of children but are rarely a harbinger of epilepsy. However, children who have two or more uncomplicated, noncomplex or "simple" febrile convulsions should receive anticonvulsant therapy. Phenobarbital is recommended for children who have a single febrile convulsion that is unilateral or focal and lasts more than 15 minutes. It is also recommended for cases involving multiple convulsions in one day, a physical or neurologic abnormality or a subnormal or suboptimal developmental history.

Child, Preschool↗
PubMed1980

Regional brain 3H-digitoxigenin and monoamine content during the development of convulsions produced by system digitoxigenin.

The uptake of 3H-digitoxigenin (3H-DIGT), administered by intravenous infusion to conscious, unrestrained rats, increased with time in the medulla-pons, cerebellum, cerebral cortex, corpus striatum, hippocampus, hypothalamus, and midbrain coincident with the development of behavioral and motor disruption. At four minutes of infusion, during clonic convulsions, uptake appeared to follow reported differences in regional blood flow, ranging from 0.48 microgram/gm (hypothalamus) to 0.67 microgram/gm (cerebellum). After 5 1/2 minutes of infusion, rats still in clonic convulsions had no further increase in uptake; rats entering tonic convulsions had two- to three-fold increases in 3H-DIGT uptake, ranging from 1.00 microgram/gm (hypothalamus) to 1.65 microgram/gm (cerebellum). Electroshock-induced tonic convusions at 2 minutes of infusion increased 3H-DIGT uptake two- to three-fold in all regions, suggesting that the increased neuronal activity associated with the tonic convulsion enhanced the uptake of 3H-DIGT into all regions. The only significant monamine alteration was a slightly decreased medulla-pons serotonin level after 5 1/2 minutes of infusion.

Animals↗
PubMed1980

[Convulsive seizures in chronic alcoholism].

The observation that convulsive seizures occur as a complication of alcoholism is not new. Several authors have described convulsive seizures as a symptom of withdrawal in alcoholics. Clinical observations have been made in a group of 121 alcoholic patients with convulsive seizures. Only 61 patients of the group presented seizures during a period of abstinence, whereas in 48 cases seizures occurred during chronic intoxication and in 12 cases even during acute intoxication. Pathophysiological aspects of convulsive seizures in alcoholics seem to be different according to the situation in which they occur.

Adolescent↗
PubMed1995

[Convulsive seizure after craniotomy--comparison of isoflurane anesthesia and sevoflurane anesthesia].

The incidence of postoperative convulsive seizure was compared retrospectively during either isoflurane or sevoflurane anesthesia in patients after craniotomy. Overall, 5 of a total of 125 patients suffered convulsive seizures after craniotomy: 2 (4%) of 45 patients with isoflurane anesthesia and 3 (4%) of 80 patients with sevoflurane anesthesia. No significant differences were observed between these two groups. The duration of anesthesia and duration of the MAC.h were similar between these two groups. The occurrence of postoperative convulsive seizure was not related with the inhalational anesthetic agents, the underlying disorders and patient characteristics. It is suggested that either isoflurane or sevoflurane anesthesia in neurosurgical patients may have no specific relationship with the postoperative convulsive seizures.

Adult↗
PubMed1994

[A case of generalized convulsion during induction with Diprivan].

The case report concerns a male patient presenting oligophrenia and epilepsy of long duration, adequately prepared for anesthesia with anticonvulsants, sustaining generalized convulsion during anesthesia induction with Diprivan. On deepening Diprivan anesthesia, the convulsion subsides. The patient runs an uneventful postoperative course, free of convulsions. The issue of small doses Diprivan giving rise to convulsions is comprehensively discussed.

Adult↗
PubMed1994

Anticonvulsant activity of calmodulin antagonist W-7 in convulsions induced by lindane and BayK-8644: effects in c-fos expression.

The anticonvulsant activity of calmodulin antagonist W-7, was investigated on convulsions induced in mice by the insecticide lindane and by the calcium channel agonist BayK-8644. We also studied the inhibitory effect of W-7 on on c-fos mRNA expression induced by both convulsants. We observed a good correlation between doses and the acute convulsive effects of lindane and BayK-8644. The incidence rate and time to onset were clearly dose-dependent. W-7 antagonized the convulsive effects of lindane and BayK-8644 in all the parameters studied. A significant decrease in the incidence rate and time to onset were observed when they are compared with the values obtained with the ED100 of lindane- and BayK-8644 induced seizures. Both were able to activate the mRNA expression of the proto-oncogene. The pattern of this expression displayed by in situ hybridization was very similar. A dramatic increase was found in dentate gyrus and high levels of mRNA expression also occurring in hippocampal fields and cortical regions. In accordance with the behavioural results, W-7 antagonized also the c-fos expression induced by lindane and BayK-8644. Our results suggest that lindane as BayK-8644 may activate voltage-dependent calcium channels leading to calmodulin activation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗