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PubMedDate not supplied

[Neonatal convulsions caused by incontinentia pigmenti with left opercular dysgenesia].

AIMS: In this paper we review the main publications on incontinentia pigmenti (IP) and the current knowledge of the etiopathogenesis of the disease and of the convulsions in the neonatal period, by considering a clear case of neonatal IP, with skin, eye, brain and bone lesions. CASE REPORT: Our patient, a female, started with clonic seizures in the right half of the body at the age of three days. Method. IP, or Bloch Sulzberger syndrome, is a genetic multisystemic neuroectodermic disorder. It is a disease of low incidence (1% of all neuroectodermic disorders) which is transmitted by means of a pattern of dominant inheritance linked to X, and is lethal in males, except in rare cases of somatic mosaicism and Klinefelter. In the family forms the gene is located in the p11 (IP 1) and q28 (IP 2) regions of the X chromosome. It has recently been discovered that the cause lies in a mutation of a gene called NEMO (IKK gamma). Together with Bourneville s tuberous sclerosis it is the only neurocutaneous syndrome that can begin with neonatal convulsions. The convulsions start on the second or third day of life and are often limited to a single side of the body, although it can also appear as encephalitis. The origin of the convulsions has been linked with recurring encephalomyelitis, or with an alteration of the neuronal migration. CONCLUSIONS: The cause of the early convulsions in our patient, which we put down to a left perisylvian focal dysgenesia (unilateral opercular syndrome) observed in the computerised axial tomography (CAT scan), has not been reported up to the present associated with IP.

Humans↗
PubMed1992

A comparative study on the convulsant activity of carbapenems and beta-lactams.

Beta-lactams are well known to have potent convulsant activity. Imipenem, the first carbapenem antibiotic introduced in the clinical field, has been reported to induce convulsions. The neurochemical mechanism of the convulsions induced by carbapenems and cephalosporins were studied. Intraventricular injection of cefazolin, cephaloridine and imipenem, and of panipenem (a new carbapenem), induced convulsions in a dose-dependent manner in mice. They inhibited the receptor binding of gamma-aminobutyric acid (GABA), an inhibitory transmitter in the mammalian central nervous system. These in-vitro and in-vivo results suggest that carbapenems and cephalosporins might induce convulsions through the inhibition of GABA receptor binding when they are accumulated in the central nervous system.

Animals↗
PubMed1992

Convulsions in senescence-accelerated mice (SAM-R/1/Eis).

Senescence-accelerated mice (SAM) are one of the animal models used for studying senescence, which consist of several substrains such as SAM-R/1, R/2, P/1, P/2. SAM-R/1/Eis maintained in Eisai Tsukuba Research Laboratories, Ibaraki, Japan, was originally introduced as a substrain of a normal control SAM-R/1 from Kyoto University, Japan. We have noted signs of convulsions in SAM-R/1/Eis mice during routine animal care, particularly while changing cages. We identified the clinical signs and determined the concentrations of glucose and immunoreactive insulin in plasma of SAM-R/1/Eis mice. There were no differences in the male:female ratios of mice showing prodrome only, grand mal, or no-signs. The ages at which prodrome and grand mal were first noted peaked between 20 and 25 weeks. Concentrations of glucose and immunoreactive insulin in plasma did not indicate the mice were in insulin hypoglycemia, which is one cause of convulsions. AKR strain mice, some of which originated with the SAM strain are known to become convulsive by repeated "throwing" stimulations. Conversely, in SAM-R/1/Eis, throwing stimuli are not needed to cause convulsive signs. Thus it is likely that in SAM-R/1/Eis mice the signs are triggered by repeating mild environmental changes, such as changing cages. The results of this study show that SAM-R/1/Eis is neither a normal control strain, nor an original SAM-R/1 strain. But it is possible that SAM-R/1/Eis is another useful animal model for studying spontaneous convulsion.

Aging↗
PubMed2003

Effect of 7-nitroindazole alone and in combination with phenobarbitone and diazepam on picrotoxin-induced convulsions in rats.

There are no reports on the effect of 7-nitroindazole (7-NI) on chemically-induced convulsions. Hence, in the present study, its (100 and 200 mg/kg) action was tested alone and in combination with phenobarbitone (20 mg/kg) and diazepam (0.25 mg/kg) on picrotoxin (PCT)-induced convulsions in rats. The changes produced by 7-NI on nitric oxide synthase (NOS) activity and nitric oxide (NO) concentration were determined in the brain. The effect of 7-NI was tested in L-arginine (1000 mg/kg) pretreated (30 min) animals. The smaller dose (100 mg/kg) of 7-NI did not alter NOS activity and NO concentration, but inhibited PCT-induced convulsions indicating that its anticonvulsant action was devoid of an involvement of NO. But, an inhibition of NOS activity, by a larger (200 mg/kg) dose of it, resulted in a promotion of the convulsant action of PCT and in an impairment of the anticonvulsant effect of both phenobarbitone and diazepam. The proconvulsant action of 7-NI was reverted by L-arginine. These results suggest that 100 and 200 mg/kg of 7-NI produce distinguishable action on PCT-induced convulsions because NOS activity is inhibited by 200 mg/kg and not by 100 mg/kg of it. The results further suggest that NO acts as anticonvulsant and that the NOS inhibitors, like 7-NI, cannot be used as an anticonvulsant either alone or in combination with other anticonvulsants.

Animals↗
PubMed2006

Effect of cyclooxygenase-2 (COX-2) inhibitors in various animal models (bicuculline, picrotoxin, maximal electroshock-induced convulsions) of epilepsy with possible mechanism of action.

Enzyme cyclooxygenase (COX) is reported to play a significant role in neurodegeneration and may play a significant role in the pathogenesis of epilepsy. Bicuculline (4 mg/kg; ip), picrotoxin (8 mg/kg; ip) and electroshock (60 mA for 0.2 sec) significantly induced convulsions in male Laka mice. COX-inhibitors viz. nimesulide (2.5 mg/kg; ip) and rofecoxib (2 mg/kg, ip) administered 45 minutes prior to an epileptic challenge prolonged mean onset time of convulsions, decreased duration of clonus and decreased % mortality rate against bicuculline- and picrotoxin-induced convulsions in mice. COX-2 inhibitors were ineffective towards maximal electroshock-induced convulsions. Nimesulide (1 mg/kg) and rofecoxib (1 mg/kg) also enhanced the effect of subprotective dose of muscimol against picrotoxin-induced convulsions. The result of the present study strongly suggests for a possible role of cyclooxygenase isoenzymes particularly, COX-2 in the pathophysiology of epilepsy and its GABAergic modulation.

Animals↗
PubMed2006

[Clinical observation on acupuncture combined with medicine for treatment of infantile febrile convulsion].

OBJECTIVE: To explore an effective therapy for treatment of infantile febrile convulsion. METHODS: Seventy infants of febrile convulsion were randomly divided into two groups, a combined acupuncture and drug group (n = 36) were treated with Xingnao Kaiqiao needling method with Shuigou (GV 26) selected as main combined with intramuscular injection of luminal and intravenous perfusion of diazepam; and a drug group (n = 34) treated with simple intramuscular injection of luminal and intravenous perfusion of diazepam. Their therapeutic effects, the time of inducing the stopping convulsion, and the recurrence rate were investigated. RESULTS: The total effective rate was 86.1% in the combined acupuncture and drug group, better than 79.4% in the drug group (P<0.05), and the time of inducing the stopping convulsion in the combined acupuncture and drug group was shorter than that in the drug group (P<0.01), and the recurrence rate in the combined group was lower than that in the drug group (P<0.05). CONCLUSION: Acupuncture combined with intramuscular injection of luminal and intravenous perfusion of diazepam is an effective and safe method for febrile convulsion.

Acupuncture Points↗
PubMed1975

[The pathogenesis of the convulsion syndrome in children].

The report contains some results of clinical, biochemical and EEG studies convened in 24 children with convulsive attacks and in 34 children with organic lesions of the CNS and epileptiform syndromes. The authors point out to the important role of the diencephalic area in the pathogenesis of convulsive syndromes. Changes in the glucocortical functions of the adrenal system during the period of convulsive attacks are related to a disturbed regulation in the hypothalamo-hypophysar structure. The processes of readaptation are more disturbed in patients with organic lesions of the CNS in frequent attacks. The results of such studies speak of certain indications to hormone therapy in repeated convulsions in children, especially if the convulsions have an epileptiform character and occur in patients with organic lesions of the CNS.

11-Hydroxycorticosteroids↗
PubMed1991

Dizocilpine, ketamine and ethanol reverse NMDA-induced EEG changes and convulsions in rats and mice.

Electroencephalographic (EEG) activity in neocortex of rats following intracerebroventricular (icv) administration of NMDA (0.25-2 nmol/10 microliters) and its modification by noncompetitive NMDA-receptor antagonists, dizocilpine (MK-801) (0.025-0.1 mg/kg, ip) and ketamine (10-50 mg/kg, ip) was recorded at 0, 0.5, 4, 8 and 24 hr with chronically implanted electrodes. NMDA (0.25 and 1 nmol) showed longer lasting decrease in frequency in cortical neurons while 2 nmol produced convulsions and death. Administration of MK 801 (0.05 mg/kg) and ketamine (50 mg/kg) prior to NMDA offered protection in 40% of animals against NMDA-induced convulsions and blocked NMDA-induced long term influence. However, ketamine and MK 801 showed an increase in percent amplitude and also had long lasting effects per se. In conscious mice, NMDA (0.5-10 nmol/microliters icv) induced dose dependent convulsions. Both MK 801 and ketamine showed potent anticonvulsant effect. Ethanol (0.5-2 g/kg, ip) also offered significant protection against NMDA-induced convulsions. MK 801 (0.1 mg/kg) when administered concurrently with ethanol (0.5 g/kg) exhibited synergistic anticonvulsant effect. The EEG study in rats and effect of NMDA in conscious mice provide a direct evidence for the role of NMDA-receptor system in convulsions and in anticonvulsant action of ethanol.

Animals↗
PubMedDate not supplied

Antagonism of caffeine-induced convulsions by ethanol and dizocilpine (MK-801) in mice.

Ethanol (1 and 2 g/kg, i.p.) and MK-801 (1 mg/kg, i.p.), N-methyl-D-aspartate (NMDA) receptor antagonist, offered protection against caffeine-induced convulsions in mice. Subeffective doses of ethanol (0.5-g/kg, i.p.) and MK-801 (0.5 mg/kg, i.p.) when administered concurrently, did not provide a facilitatory anticonvulsant action against caffeine-induced convulsions. Ethanol (0.5 g/kg, i.p.) when administered concurrently with adenosine (100 mg/kg, i.p.) or dipyridamole (5 mg/kg, i.p.) elicited a facilitatory anticonvulsant action. However, concurrent administration of subeffective doses of MK-801 (0.5 mg/kg i.p.) with adenosine (100 mg/kg, i.p.) did not offer a facilitatory anticonvulsant action against caffeine-induced convulsions. The protective effect of ethanol (1 g/kg, i.p.) against caffeine-induced convulsions was reversed by an imidazobenzodiazepine, Ro 15-4513 (4 mg/kg, i.p.). Ro 15-4513 did not produce any proconvulsant effect with caffeine. It is suggested that ethanol and MK-801 elicit their anticonvulsant actions against caffeine-induced convulsions through different receptor mechanisms and that the anticonvulsant action of ethanol may be partly attributed to its ability to act via central adenosinergic mechanisms.

Animals↗
PubMed1990

Effect of MK-801 and its interaction with adenosinergic agents and carbamazepine against hypoxic stress-induced convulsions and death in mice.

Effects of MK-801, adenosinergic agents and carbamazepine were investigated against hypoxic stress-induced convulsions and death in mice. MK-801, a N-methyl D-aspartate antagonist, offered a significant protective effect against hypoxic convulsions. Adenosinergic agents such as adenosine, 2-chloroadenosine, N6-cyclohexyladenosine and dipyridamole produced theophylline-sensitive protective effect as they dose-dependently prolonged the latencies for onset of convulsions and death. Pretreatment with adenosinergic agents and MK-801 markedly enhanced the protective effect of the stable analogs of adenosine namely, 2-chloroadenosine and N6-cyclohexyladenosine. However, pretreatment with combination of MK-801 and adenosine or dipyridamole did not show enhanced protective effect. Carbamazepine also exhibited dose-dependent theophylline-sensitive protective effect. The pretreatment with combination of carbamazepine and MK-801 showed significantly enhanced protective effect. The observed enhanced protective effect of MK-801 and adenosinergic agents was reversed by pretreatment with theophylline. These results indicate the possible involvement of adenosinergic mechanisms in preventing hypoxic stress-induced convulsions and the role of NMDA receptors in hypoxia-induced convulsions and death as MK-801 not only showed effect per se but also potentiated the response due to adenosinergic agents.

2-Chloroadenosine↗
PubMed1990

Anticonvulsant effects of clonazepam on chemically induced convulsions.

The anticonvulsant effects of two doses of clonazepam (CZP, Rivotril Roche, 0.1 and 1 mg/kg i.p.) were studied on model motor seizures induced by strychnine, bicuculline, 3-mercaptopropionic acid and metrazol in male laboratory rats (Wistar strain). In the first part the effects of different doses of the convulsants were investigated and for interaction with CZP doses were chosen after which more than 70% of the animals displayed generalized tonic-clonic convulsions (a grand mal seizure). Strychnine induced this type of seizure only: two doses (2 and 3 mg/kg s.c.) were used. CZP reduced the incidence of convulsions only after the larger dose, but plain solvent (propylene glycol, ethanol, water) was equally effective. The other substances first induced a seizure of minimal (mainly clonic) convulsions and only later a grand mal seizure. CZP was highly effective against bicuculline (3 mg/kg s.c.) and metrazol (100 mg/kg s.c.), but was less so against 3-mercaptopropionic acid. The effect on grand mal seizures was more pronounced in every case than on minimal seizures. The decisive role in the anticonvulsant effect of CZP is played by the mechanisms by which the convulsants induce epileptic manifestations. CZP is most effective against substances acting on the supramolecular complex GABA receptor (benzodiazepine receptor) chloride ionophore (bicuculline and probably metrazol).

3-Mercaptopropionic Acid↗
PubMedDate not supplied

Intravenous injection of flunarizine elicits epileptiform convulsions. Preliminary evaluation of anti-epileptic drugs.

The possibility to elicit convulsions in rabbits after flunarizine, iv was investigated. A flunarizine solution, 3.3 mg/ml, was given iv at a rate of 1.5 ml/min in three fractional doses every 30 min. Action of anti-epileptic drugs in seizures induced by flunarizine was additionally examined. Convulsive seizures occurred 2-10 min after the last successive dose of flunarizine as alternating clonic and tonic seizures. A treatment with anti-epileptic drugs showed that both phenobarbital at doses 6, 7 and 7.5 mg/kg iv and pentobarbital at doses of 15, 20 and 25 mg/kg, iv did not entirely suppress convulsive seizures, although convulsive episodes were rare. Diazepam at doses of 1-1.5 mg/kg, iv suppressed convulsive seizures.

Animals↗
PubMedDate not supplied

The impact of socio-cultural factors on febrile convulsions in Nigeria.

Certain socio-cultural factors such as the beliefs of parents regarding febrile convulsions, and the actions they took when their children began to convulse, were examined among Nigerian parents. It was discovered that an overwhelming majority of parents had gross misconceptions about febrile convulsions, and took inappropriate or even harmful actions in an attempt to control the convulsions. It is thought that these social attitudes and behaviours contribute immensely to the high prevalence rate, high morbidity and unfavourable prognosis of febrile convulsions in this part of the world.

Adolescent↗
PubMed1989

[Factors influencing the effectiveness of preventive treatment of febrile convulsions].

The influence of risk factors predisposing to recurrences was assessed in 103 children with febrile convulsions who were given prophylactic treatment with phenobarbitone, primidone or sodium valproate at adequate doses and whose compliance with treatment was monitored. There was a greater risk of recurrence among girls. Increasing risk was observed with decreasing age at which children suffered the first febrile convulsion. Neither a family history of epilepsy, failure of previous treatment, history of perinatal incidents, focal or prolonged febrile convulsions, recognition of neurological disease nor the number of previous febrile convulsions led to any significantly greater risk in these children. There was an increased tendency for recurrence with increasing interval between the first febrile convulsion and the start of prophylactic treatment.

Anticonvulsants↗
PubMed1989

Convulsions induced by canatoxin in rats are probably a consequence of hypoxia.

Canatoxin, a convulsant neurotoxin from the seeds of Canavalia ensiformis, induces lipoxygenase-dependent hypoxia and sex-related alterations of carbohydrate metabolism in rats which are blocked by glucose, diazepam and hexamethonium. The present study analyzes the possible casual relationship between the convulsant action of canatoxin and its effects on carbohydrate metabolism. The incidence of canatoxin-induced convulsions was greater in male than in female rats. Pretreatment of male rats with drugs that block hypoxia, such as glucose (2.5 g/kg, iv, 15 min), diazepam (5 mg/kg, ip, at 48 h, 24 h and 15 min), hexamethonium (4 mg/kg, ip, 15 min) and NDGA (125 mg/kg, ip, 1 h), also protected the animals against convulsions, respiratory distress and death. These results suggest that canatoxin-induced convulsions are probably the consequence of hypoxia and both effects are mediated by lipoxygenase activation.

Animals↗
PubMed1989

[Effect of glutamic acid palmitamide or linoleamide on convulsions induced by pentetrazole].

Female Balb-C mice received glutamic acid palmitamide (PGt) or linoleamide (LGt) at doses included between 10 and 135 mg.kg-1 (i.p.) and, 90 min after these injections, pentetrazol (PTZ) at 90 mg.kg-1, i.p. PGt (10 or 100 mg.kg-1, i.p.) reduced significantly latencies of first convulsions and lethality and increased the intensity of convulsions after PTZ. This effect disappeared at 135 mg.kg-1, i.p. and, at high doses (up to 150 mg.kg-1, i.p.) PGt antagonized the PTZ convulsions. LGt (10 mg.kg-1, i.p.) had not any significant effect on the PTZ convulsions and antagonized them when administered at a dose of 100 mg.kg-1, i.p. These results, as well as them obtained with PGt and LGt on the haloperidol or reserpine catalepsy, could be the reflection of the preferential impact of LGt in the striatum and of PGt in the limbic structures and in the substantia nigra. At high doses these compounds could reach brain regions with low density of glutamatergic receptors (thalamus, reticular formation) and develop an activating effect able to antagonize the propagation of the PTZ convulsions. These preferential impacts could augur an antiepileptic action for LGT and a promnesient effect for PGt and LGt.

Animals↗
PubMed1989

Febrile convulsion--a clinical survey and a review of its current concept of management.

Between February 1986 to November 1986, 335 cases of febrile convulsion were admitted to the paediatric ward, Tan Tock Seng Hospital. The study revealed 87 cases (26%) were complex febrile convulsion and 73 cases (21.8%) were recurrent febrile convulsion. 51 patients with complex febrile convulsion and 32 patients with recurrent febrile seizures were put on long term phenobarbitone. The number of patients with recurrent and complex convulsion was big. The role of anticonvulsant prophylaxis is reviewed and its efficacy discussed.

Child↗
PubMed1989

Interactions of angiotensin II with piracetam in exploratory behavior and convulsive-seizure threshold.

The interactions between angiotensin II (AT II) and piracetam in exploratory behavior of rats in open field and in pentylenetetrazol (PTZ) convulsive-seizure threshold in mice were studied. AT II at a dose of 0.5 microgram injected intracerebroventricularly (i.c.v.) increased exploratory behavior. Piracetam at a dose of 600 mg.kg-1 administered orally twice daily for 7 days increased the frequency of the exploratory behavior components. AT II decreased this effect of piracetam. AT II (0.5 microgram i.c.v.) tended to increase the PTZ convulsive-seizure threshold. On single administration piracetam had no effect on the convulsive-seizure threshold but on multiple administration it increased the threshold. The two drugs applied together increased the PTZ convulsive-seizure threshold to a larger extent as compared to the effect they exerted when administered alone. The changes in exploratory behavior and in convulsive-seizure threshold, increased by the combination of AT II and piracetam, are explained by the interactions between the two drugs at the level of AT II and GABA binding sites in brain.

Angiotensin II↗