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PubMed1995

Relationship between structure and convulsant properties of some beta-lactam antibiotics following intracerebroventricular microinjection in rats.

The epileptogenic activities of several beta-lactam antibiotics were compared following their intracerebroventricular administration in rats. Different convulsant potencies were observed among the various beta-lactam antibiotics tested, but the epileptogenic patterns were similar. The patterns consisted of an initial phase characterized by wet-dog shakes followed by head tremor, nodding, and clonic convulsions. After the largest doses of beta-lactam antibiotics injected, clonus of all four limbs and/or the trunk, rearing, jumping, falling down, escape response, transient tonic-clonic seizures, and sometimes generalized seizures were observed, followed by a postictal period with a fatal outcome. At a dose of 0.033 mumol per rat, cefazolin was the most powerful epileptogenic compound among the drugs tested. It was approximately three times more potent than benzylpenicillin in generating a response and much more potent than other cephalosporins, such as ceftriaxone, cefoperazone, and cefamandole. No epileptogenic signs were observed with equimolar doses of cefotaxime, cefonicid, cefixime, and ceftizoxime in this model. The more convulsant compounds (i.e., cefazolin and ceftezole) are both characterized by the presence of a tetrazole nucleus at position 7 and show a marked chemical similarity to pentylenetetrazole. Imipenem and meropenem, the two carbapenems tested, also showed epileptogenic properties, but imipenem was more potent than meropenem, with a convulsant potency similar to those of ceftezole and benzylpenicillin. In addition, the monobactam aztreonam possessed convulsant properties more potent than those of cefoperazone and cefamandole. This suggest that the beta-lactam ring is a possible determinant of production of epileptogenic activity, with likely contributory factors in the substitutions at the 7-aminocephalosporanic or 6-aminopenicillanic acid that may increase or reduce the epileptogenic properties of the beta-lactam antibiotics. While the structure-activity relationship was also investigated, there seem to be no convincing correlations among the rank order of lipophilicities and the convulsant potencies of the compounds studied. The lack of marked convulsant properties of cefixime, cefonicid, cefuroxime, and cephradine suggests that these antibiotics may interact with a binding site which is different from that by which the beta-lactam antibiotics exert their convulsant effects or may demonstrate a reduced affinity for the relevant site(s).

Animals↗
PubMed1997

Retrospective study of concussive convulsions in elite Australian rules and rugby league footballers: phenomenology, aetiology, and outcome.

OBJECTIVES: To study the ictal phenomenology, aetiology, and outcome of convulsions occurring within seconds of impact in violent collision sport. DESIGN: Retrospective identification of convulsions associated with concussive brain injury from case records from medical officers of football clubs over a 15 year period. SUBJECTS: Elite Australian rules and rugby league footballers. MAIN OUTCOME MEASURES: Neuroimaging studies, electroencephalography, neuropsychological test data, and statistics on performance in matches to determine presence of structural or functional brain injury. Clinical follow up and electroencephalography for evidence of epilepsy. RESULTS: Twenty two cases of concussive convulsions were identified with four events documented on television videotape. Convulsions began within 2 seconds of impact and comprised an initial period of tonic stiffening followed by myoclonic jerks of all limbs lasting up to 150 seconds. Some asymmetry in the convulsive manifestations was common, and recovery of consciousness was rapid. No structural or permanent brain injury was present on clinical assessment, neuropsychological testing, or neuroimaging studies. All players returned to elite competition within two weeks of the incident. Epilepsy did not develop in any player over a mean (range) follow up of 3.5 (1-13) years. CONCLUSIONS: These concussive or impact convulsions are probably a non-epileptic phenomenon, somewhat akin to convulsive syncope. The mechanism may be a transient traumatic functional decerebration. In concussive convulsions the outcome is universally good, antiepileptic treatment is not indicated, and prolonged absence from sport is unwarranted.

Adult↗
PubMed1985

The risk of seizure disorders among relatives of children with febrile convulsions.

We studied the risk for seizure disorders among relatives of probands with febrile convulsions. The risk for febrile convulsions was raised in siblings, offspring, and nieces and nephews of probands. Risks to siblings were higher if one or both parents also had febrile convulsions, or the proband had no identified neurologic abnormality before the febrile convulsion, if the proband had recurrent febrile convulsions, or the febrile convulsions were complex. The risk for epilepsy was raised in siblings of probands, but not in other relatives. If the proband had febrile convulsions followed by epilepsy, risk to siblings for febrile convulsions and for epilepsy was significantly higher than when probands had either condition alone.

Adolescent↗
PubMed1998

Hippocampal malformation as a cause of familial febrile convulsions and subsequent hippocampal sclerosis.

OBJECTIVE: One hypothesis proposes that a pre-existing alteration of medial temporal lobe structures contributes to febrile convulsions and subsequent hippocampal sclerosis (HS) in patients with temporal lobe epilepsy (TLE) and antecedent febrile convulsions. It is possible that such a structural alteration does not always lead to convulsions and may also be present in clinically unaffected relatives. METHODS: We tested this hypothesis by MRI investigation of 23 members of two families, of whom 13 had experienced febrile convulsions and 10 had not. One member of each family with febrile convulsions subsequently developed TLE. We compared the right/left ratios of hippocampal volumes (RHV) with 23 age- and sex-matched controls. Additionally, two independent raters assessed hippocampal signal intensity and pattern in T2- and fluid-attenuated inversion recovery images. RESULTS: Both TLE patients showed left HS. All subjects with febrile convulsions who did not develop epilepsy and six clinically unaffected relatives also showed asymmetric RHV (>3 standard deviation) but a normal hippocampal signal intensity. In all of these subjects, the left hippocampus was smaller. Visual inspection of these smaller hippocampi revealed blurred internal pattern or flat hippocampal bodies or both in one family and smaller hippocampal heads in the other. The pattern of HS in TLE patients showed a structural correlation with the abnormalities seen in their relatives. One subject with febrile convulsions had additional subcortical heterotopias. CONCLUSION: These findings suggest a subtle, pre-existing hippocampal malformation that may facilitate febrile convulsions and contribute to the development of subsequent HS.

Adolescent↗
PubMed1992

[Effects of drugs on the convulsions induced by the combination of a new quinolone antimicrobial, enoxacin, and a nonsteroidal anti-inflammatory drug, fenbufen, in mice].

The effects of drugs on the convulsions induced by the combination of a new quinolone antimicrobial, enoxacin, and a nonsteroidal anti-inflammatory drug, fenbufen, were studied in mice. The combination of enoxacin at 30 or 100 mg/kg, p.o. and fenbufen at 100 mg/kg, p.o. induced convulsions; and the mice died as a result of the convulsions. Pretreatment with either phenobarbital, phenytoin, valproic acid intraperitoneally, or morphine intravenously did not influence the convulsions. A high dose of diazepam or clonazepam prolonged the survival time, but could not prevent the mice from dying. After the occurrence of convulsions induced by enoxacin with fenbufen, administration of the excitatory amino acid antagonist MK-801 at 1 mg/kg, i.v. extended the survival time, even though all the mice died as a result of the convulsions. Simultaneous intravenous injections of MK-801 and diazepam suppressed the convulsions. This suppression was stronger than that produced by MK-801 or diazepam, injected separately. However, no mouse survived at the end. From these results, participation of both GABA-ergic and excitatory amino acidergic systems in the convulsions induced by enoxacin and fenbufen was discussed.

Amino Acids↗
PubMed2000

Increase in cerebral blood flow as a predictor of hyperbaric oxygen-induced convulsion in artificially ventilated rats.

In spontaneously breathing rats, a transient increase in cerebral blood flow (CBF) has been shown to be a predictor of hyperbaric oxygen (HBO)-induced convulsion. In the present study, we evaluated whether artificially ventilated animals also show an increase in CBF prior to the onset of HBO-induced convulsion. Rats were ventilated with 100% oxygen in 5 atmospheres. CBF, blood pressure, and an electroencephalogram were monitored continuously. Convulsion was observed at 41 +/- 12 min after the initiation of HBO treatment. A single abrupt increase in CBF, reaching 223 +/- 39% of the control level, was observed at 29 +/- 13 min after the initiation of HBO exposure and lasted until the onset of convulsion 12 +/- 2 min later. The time of the increase in CBF correlated strongly with the onset of convulsion (r = 0.99, P < 0.001). Further, the logistic regression curve demonstrated a close relationship between the duration of increased CBF and percentage of epileptiform electrical-discharge incidence (r = 0.92, P < 0.006). The durations of increased CBF causing convulsion in 10%, 50%, and 90% of the rats were 8.4 min, 11.7 min, and 15.1 min, respectively. These results indicate that an increase in CBF is a predictor of HBO-induced convulsion in artificially ventilated rats. The increase in CBF may be involved in the pathogenesis of HBO-induced convulsion.

Animals↗
PubMed1976

Experimental study of the effects of imidazol, papaverine and histamine on convulsive-seizure reactivity.

In experiments on male albino rats and mice a study is made of the effects of imidazol which is a phosphodiesterase stimulator, papaverine which inhibits phosphodiesterase and histamine which stimulates adenylate cyclase, on the convulsive-seizure reactivity. The substances are introduced intraventricularly and intracerebroventricularly, imidazol also intraperitoneally in different doses and at different intervals before the convulsive agent. Electrical, pentylenetetrazol (Cor) and strychnine convulsion models are used. The effect of imidazol on the spontaneous cortical bioelectrical activity is studied throuth its i. v. administration in rabbits. Imidazol markedly increases the convulsive reactivity, and in large doses it alone results in electrographic and motor convulsions. Paperine slightly lowers the convulsive-seizure reactivity only in pentylenetetrazol convulsions. The results obtained and their comparison with the results of previous experiments of ours with other drugs affecting the cyclic adenosinemonophosphate (cAMP) system, such as lithium, haloperidol, caffeine and theophyline, do not permit to assume a considerable significance of the influence of these substances (in the doses tested) on the cAMP system in the mechanisms of their effects on the convulsive-seizure reactivity.

Animals↗
PubMedDate not supplied

Knowledge, attitude and practices of parents of children with febrile convulsion.

CONTEXT: Parental anxiety and apprehension is related to inadequate knowledge of fever and febrile convulsion. AIMS: To study the knowledge, attitude, and practices of the parents of children with febrile convulsions. SETTINGS AND DESIGN: Prospective questionnaire based study in a tertiary care centre carried over a period of one year. SUBJECTS AND METHODS: 140 parents of consecutive children presenting with febrile convulsion were enrolled. STATISTICAL ANALYSIS USED: Chi-square test. RESULTS: 83 parents (59.3%) could not recognise the convulsion; 90.7% (127) did not carry out any intervention prior to getting the child to the hospital. The commonest immediate effect of the convulsion on the parents was fear of death (n= 126, 90%) followed by insomnia (n= 48, 34.3%), anorexia (n= 46, 32.9%), crying (n= 28, 20%) and fear of epilepsy (n= 28, 20%). Fear of brain damage, fear of recurrence and dyspepsia were voiced by the fathers alone (n= 20, cumulative incidence 14.3%). 109 (77.9%) parents did not know the fact that the convulsion can occur due to fever. The long-term concerns included fear of epilepsy (n= 64, 45.7%) and future recurrence (n= 27, 19.3%) in the affected child. For 56 (40%) of the parents every subsequent episode of fever was like a nightmare. Only 21 parents (15%) had thermometer at home and 28 (20%) knew the normal range of body temperature. Correct preventive measures were known only to 41 (29.2%). Awareness of febrile convulsion and the preventive measures was higher in socio-economic grade (P< 0.05). CONCLUSIONS: The parental fear of fever and febrile convulsion is a major problem with serious negative consequences affecting daily familial life.

Adult↗
PubMedDate not supplied

[Febrile convulsions: should some drugs be contraindicated?].

Should certain drugs be contraindicated in children who have had febrile seizures or who present a risk of convulsions? There are no publications dealing specifically with this problem. However, many drugs can induce convulsions and may be dangerous if they are associated with another determining factor (e.g. fever). Camphor known to be toxic and its use must be avoided in young children. Other terpenes given to children with colds may be convulsant if they are used for prolonged treatment or associated with other convulsant drugs (sympathomimetics, piperazine derivatives, antihistamines, etc.). On the basis of a retrospective study of 23 cases of febrile convulsion among 343 cases of infantile convulsion reported to the Poison Control Center and the Pharmacovigilance Center of Marseille between 1973 and 1991, we propose that camphor and sympathomimetics be avoided and that potential convulsant drugs and their association be used with caution. A prospective study is underway to determine responsibility of certain drugs in the occurrence of recurrence of febrile convulsions.

Antitussive Agents↗
PubMed2004

[Refractory generalized convulsions in a patient undergoing brain tumor resection during propofol anesthesia].

Propofol has been used to treat convulsions, while the drug is known to induce convulsions. We described a case of generalized convulsions during brain tumor resection under propofol anesthesia. A 24-year-old man was scheduled to undergo brain tumor resection. He had no history of epilepsy. Anesthesia was induced and maintained with propofol and fentanyl. During the craniotomy, the patient developed generalized convulsions. Diazepam, thiamylal, and phenytoin were given intravenously and the seizure activity resolved. Generalized convulsions recurred three times during the operation. Postoperative course was uneventful. On the 16 th postoperative day, the patient underwent ventriculoperitoneal shunt under general anesthesia using sevoflurane, nitrous oxide and oxygen. Convulsions were not noted intra- and postoperatively. Because convulsions did not occur during sevoflurane anesthesia and the patient had no history of epilepsy, propofol may have induced a generalized convulsions on the first operation.

Adult↗
PubMed1976

On certain relationships between gamma-aminobutyric acid (GABA) and adrenergic mechanisms in convulsive-seizure reaction.

In experiments on male albino mice it has been established that upon intracerebroventricular administration in doses of 50, 100 and 300 mug per mouse GABA markedly inhibits the convulsive-seizure reactions in pentylenetetrazol and electroconvulsions and has no substantial effect on strychnine convulsions (the dose of 300 mug is toxic). Diethyldithiocarbamate (DDC) in a dose of 400 mg/kg, introduced i.p. 3 hours in advance, increases the convulsive reactivity in pentylenetetrazol and electroconvulsions. On the background of DDC the inhibitory effect of GABA is expressed only in antagonizing of the DDC effect increasing the convulsive reactivity. Alpha-methyl-paratyrosine (a-MT) in a dose of 250 mg/kg, introduced i.p. 4 hours in advance, has no substantial effect on the convulsive reactivity. On the background of alpha-MT the inhibitory effect of GABA in electroconvulsions does not change essentially, however, in pentylenetetrazol convulsions the GABA effect is practically not manifested. The results obtained show that the changes in the correlations between the catecholamines and GABA in the central nervous system result in substantial changes in the convulsive-seizure reactivity. The lower catecholamines level does not permit the marked manifestation of the GABA inhibitory effect. However, GABA counteracts to a certain extent the rise in the convulsive reactivity as a result of the drop in the brain level of the catecholamines.

Aminobutyrates↗
PubMed1990

Soman- or kainic acid-induced convulsions decrease muscarinic receptors but not benzodiazepine receptors.

[3H]Quinuclidinyl benzilate (QNB) binding to muscarinic receptors decreased in the rat forebrain after convulsions induced by a single dose of either soman, a potent inhibitor of acetylcholinesterase, or kainic acid, an excitotoxin. A Rosenthal plot revealed that the receptors decreased in number rather than affinity. When the soman-induced convulsions were blocked, the decrease in muscarinic receptors at 3 days was less extensive than when convulsions occurred and at 10 days they approached control levels in most of the brain areas. The most prominent decrements in QNB binding were in the piriform cortex where the decline in QNB binding is probably related to the extensive convulsion-associated neuropathology. The decrements in QNB binding after convulsions suggest that the convulsive state leads to a down-regulation of muscarinic receptors in some brain areas. In contrast to the decrease in QNB binding after convulsions, [3H]flunitrazepam binding to benzodiazepine receptors did not change even in the piriform cortex where the loss in muscarinic receptors was most prominent. Thus, it appears that those neuronal processes that bear muscarinic receptors are more vulnerable to convulsion-induced change than those with benzodiazepine receptors.

Animals↗
PubMed1990

The influence of cortical lesions on penicillin induced convulsive activity in the awake rat.

1. Experiments were performed to investigate the effects of cortical lesions on convulsive behaviour. Rats were lesioned in the left motor or sensory cortex by aspirating cortical tissue 2 to 3 months prior to the elicitation of convulsions. Convulsions were induced in the awake rats by the GABA antagonist Na-penicillin (Na-PCN) which was applied into the superficial layer of the foreleg field of their right motor cortex. Convulsive activity was recorded by means of the EEG. 2. The time courses of convulsive cortical activity were similar in the animals without or with a cortical lesion. Generalized seizures belonged to the tonic-clonic type in both intact and lesioned rats. 3. The early period of convulsive activity was described by the time to the onset (latency) of the first convulsive potential, jerk and seizure, and by the mean repetition rate of jerks during the first ten minutes, and the duration of the first generalized seizure. None of these parameters was significantly affected by a cortical lesion. 4. The median duration of the convulsive activity in intact animals was 162 min. In rats with a lesion in the sensory cortex it raised to more than 540 min while a lesion of the motor cortex increased the median duration to more than 273 min. The differences between intact and lesioned rats were significant (p less than 0.01 and p = 0.05, respectively). 5. The median time to the onset of the last generalized seizure in intact rats corresponded to 92 min with respect to the time of Na-PCN application. In rats with a lesion of the sensory cortex the last seizure was generated 433 min and in animals with a lesion of the motor cortex 167 min after Na-PCN treatment of the motor cortex of one side. This increase of latency of the last seizure was significant for the rats with a lesioned sensory area (p less than 0.02) or motor area (p = 0.05) compared to that of the intact rats. Additionally, the number of generalized seizures was significantly (p less than 0.01) increased by both groups of rats with a lesion of the motor or sensory cortex. 6. It is suggested that a substantial lesion of the cortex decreases predominantly the intrinsic cortical inhibition thus destabilizing brain function. This destabilizing effect becomes pronounced under the condition of superimposed suppression of the GABAergic cortical component. It is concluded that the intrinsic cortical inhibitory mechanism which in the intact brain acts against hyperexcitation and prevents the development of neuronal synchronization, i.e. the formation of seizures, becomes less effective in performing this task once an abnormal brain activation has developed.

Animals↗
PubMed1990

[Clinical evaluation of the patients with epilepsy following febrile convulsions].

We studied clinical, EEG and developmental features of 46 epileptic children following febrile convulsions. Incidence of developing epilepsy was 9.9 percent. Eleven patients (group G) out of 46 had generalized epileptic seizures, and 34 patients (group P) had partial seizures. Febrile convulsions of early onset, partial seizures and postictal neurological symptoms were more striking in group P (p less than 0.05), whereas febrile convulsions of late onset and prolonged seizures were slightly dominant in group G. And EEG abnormalities were more frequent in group P (p less than 0.05). Group P patients had significant number of risk factors (complex features of febrile convulsions) than group G patients (p less than 0.01). The interval between the last febrile convulsion and subsequent epileptic seizures was shorter in group G (p less than 0.01). Although subsequent epileptic seizures were well controlled in the both groups (91% in group G and 82% in group P), intractable seizures were recognized in 9% of group P patients. The patients who had risk factors of prolonged seizures, postictal neurological symptoms and early onset manifested poor controlled epileptic seizures (p less than 0.01). Motor or mental deficits were more frequently associated with group P: in some patients they had been observed before the onset of febrile convulsions. These results suggest that pathogenesis of epilepsy following febrile convulsions may be different among various seizure types of subsequent epilepsy. And the risk factors during febrile convulsions may be related to the prognosis of subsequent epileptic seizures as well as the incidence of developing epilepsy.

Child, Preschool↗
PubMedDate not supplied

Catecholamines in the rat brain during hypoglycemic convulsions and coma.

The purpose of the study was to investigate the relation between the catecholamines: noradrenaline and dopamine in the rat brain on one hand and hypoglycemic convulsions and coma on the other. Concentrations of noradrenaline in the hypothalamus, brain stem and cerebral cortex were decreased during hypoglycemic convulsions and were lower during coma than those during convulsions. Dopamine concentration in the striatum was decreased during convulsions and coma. It was shown that the decrease in concentration of catecholamines was a result of hypoglycemia but not of insulin action itself. Clonidine- alpha 2 agonist accelerated occurrence and prolonged duration of hypoglycemic convulsions. Haloperidol-dopamine receptor blocker had no effect on the time of occurrence or duration of convulsions and coma. The results indicate that noradrenaline may exert an inhibitory influence on hypoglycemic convulsions. No evidence has been provided to support involvement of dopamine in the control of hypoglycemic convulsions and coma.

Animals↗
PubMed1979

Convulsions following oral polio immunisation.

Since the introduction of oral polio vaccine in 1962, 30 cases of convulsions were registered within 30 days after the immunisation in Hamburg. 29 further cases from the surroundings came also to our attention. The majority of these cases occurred within 8 days after the vaccination (44 cases), afterwards only single cases were recorded. 33 patients were males, 24 females (2 cases sex unknown). The majority of the patients had the postvaccinal convulsions between 7 to 36 months of age, a characteristic period for febrile convulsions. 28 patients showed a course typical for febrile convulsions. In some cases intercurrent infections (pneumonia, otitis media purulenta) could also explain the nerval reactions. In 11 cases encephalopathy or encephalitis (1 case due to mumps) had been diagnoses. 8 patients suffered later from a convulsive disorder. Between 1964 and 1974 165,000 children born in Hamburg, were immunised thrice with OPV. In this period 19 convulsions and 3 permanent convulsive disorders were observed (1 case per 8,600 vaccinees; 1 convulsive disorder per 55,000 vaccinees).

Age Factors↗
PubMed1980

Ketamine suppression of chemically induced convulsions in the two-day-old white leghorn cockerel.

Ketamine has been evaluated for convulsant properties in animals and humans with contradictory results. The present investigation evaluated the convulsant properties of ketamine in a previously unreported animal model. Two-day-old chicks were selected as test animals because they have incomplete blood-brain barriers and thus greater penetrance of xenobiotics affecting the central nervous system. Control and experimental animals were given a central nervous system stimulant, pentylenetetrazol (Medtrazol) at a dosage level (100 mg/kg) causing convulsions in 90% of animals. The effect of ketamine pretreatment was then observed for the: (1) number of animals convulsing; (2) time of onset of convulsions; and (3) mortality. Ketamine (100 mg/kg) significantly decreased the number of animals that convulsed and decreased mortality; 10 mg/kg of ketamine significantly prolonged the time of onset of convulsions. This study does not support the conclusion that ketamine is a convulsant. Ketamine has significant anticonvulsant properties in the young chick model.

Animals↗
PubMed1995

Clinical signs of ivermectin toxicity and the efficacy of antigabaergic convulsants as antidotes for ivermectin poisoning in epileptic chickens.

The clinical signs of ivermectin toxicity were determined in 6 groups of 10 epileptic and 8 non-epileptic chickens for 72 h after dosing with sc injections of 5.0, 7.5, 10.0, 12.5 or 15.0 mg ivermectin/kg bw. At the 5.0 mg/kg dose, mild diarrhea developed 4 h post-dosing and lasted until the end of the 72-h monitoring period. With higher doses of ivermectin body weight, egg production and feed and water consumption were markedly reduced. Severe diarrhea, mydriasis, bradypnea, ataxia, sedation, coma and death occurred with the highest dose of ivermectin. No differences in the signs of ivermectin toxicity were observed between epileptic and non-epileptic chickens. To assess the efficacy of the antiGABAergic convulsants, methyl-beta carboline-carboxylate (beta-CCM), picrotoxin and pentylenetetrazol (PTZ), as antidotes for ivermectin toxicity, 8 epileptic and 6 non-epileptic chickens/treatment group were given dosages of each convulsant which previously induced convulsions in 50% (ED50) and again in 100% (ED100) of treated chickens. These convulsants were given 6 h after dosing with 15.0 mg ivermectin/kg. The ED100 dosages of picrotoxin and PTZ alleviated mydriasis and sedation, but did not reduce the diarrhea. The ED50 dose convulsants were not effective in reducing or alleviating ivermectin toxicity, nor was alleviation of any sign of ivermectin toxicity obtained with any dosage of beta-CCM. Although the dosages of these antiGABAergic convulsants used normally produced convulsions in epileptic and non-epileptic chickens, no convulsions were observed in chickens with ivermectin toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗