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PubMed1993

Pharmacological dissociation of the motor and electrical aspects of convulsive status epilepticus induced by the cholinesterase inhibitor soman.

In an effort to validate methods to be used in a screen for drugs effective as anticonvulsants for soman-induced convulsions, scopolamine (0.2 mg/kg) or diazepam (1 mg/kg) were given (i.m.) to male guinea pigs as a pretreatment 30 min before a convulsant dose of soman. Pyridostigmine, atropine and pralidoxime chloride also were given to counteract the lethality of soman. All animals challenged with soman and which did not receive either diazepam or scopolamine exhibited convulsive status epilepticus (SE), identified by continuous electrographic seizure activity (EGSA) and continuous motor convulsions. Despite the presence of continuous motor convulsions in all animals pretreated with diazepam and challenged with soman, EGSA was not observed in five of the seven animals. Continuous motor convulsions developed in four of seven animals pretreated with scopolamine and challenged with soman, but EGSA was not observed in any scopolamine-pretreated guinea pig. Neuronal necrosis was observed in the hippocampus, thalamus, amygdala, and cerebral and pyriform cortices in each animal with EGSA, but not brain damage was found in subjects without EGSA. Thus, although convulsions, EGSA and brain damage normally occur together in animals exposed to soman, the convulsions can be pharmacologically dissociated from the EGSA and brain damage, demonstrating that the clinically manifested convulsions are not dependent on EGSA recorded from the cortex or on abnormal activity which leads to neuronal necrosis in the forebrain.

Analysis of Variance↗

PubMed2004

Ascorbate modulates pentylenetetrazol-induced convulsions biphasically.

Ascorbate is an antioxidant vitamin that is found in high concentrations in the brain which seems to have neuroprotective properties in some experimental models of excitotoxic neurological disorders, including convulsive behavior and reactive species-related damage. In this study we tested whether ascorbate (30, 100 or 300 mg/kg, i.p.) protects against the convulsions, protein carbonylation and inhibition of Na(+),K(+)-ATPase activity induced by pentylenetetrazol (PTZ; 1.8 micromol/striatum), a classical convulsant agent that has been fairly used for the study of epilepsy and screening of new compounds with antiepileptic activity. The intrastriatal injection of PTZ caused convulsive behavior in a dose-dependent manner and an increase in the total protein carbonyl content of the injected striatum. However, duration of PTZ-induced convulsive episodes did not correlate with protein carbonyl content of the injected striatum. Ascorbate, at high doses (300 mg/kg), protected against PTZ-induced convulsions, protein carbonylation and inhibition of Na(+),K(+)-ATPase activity in the rat striatum, further suggesting a anticonvulsant and neuroprotective role for this vitamin. Conversely, intermediate doses of ascorbate (100 mg/kg) potentiated the duration of the convulsive episodes, but had no additive effects on protein carbonylation or Na(+),K(+)-ATPase activity inhibition induced by PTZ. Low doses of ascorbate (30 mg/kg) prevented PTZ-induced increase of total striatal carbonyl protein content, but did not alter PTZ-induced convulsions and Na(+),K(+)-ATPase activity inhibition. Collectively, these data indicate that the anticonvulsant activity of ascorbate is not related to its antioxidant action and support a dual role for this compound as a neuroprotective agent, since while it protects against PTZ-induced cellular oxidative damage, it has a biphasic effect on PTZ-induced convulsions.

Analysis of Variance↗

PubMed1985

History of convulsions and use of pertussis vaccine.

Data on 2062 reports from the Monitoring System for Adverse Events Following Immunization, Centers for Disease Control (CDC), were analyzed to compare the risk of a personal or family history of convulsions in children who had a neurologic adverse event after receipt of diphtheria-tetanus-pertussis (DTP) vaccine with those who had a nonneurologic adverse event. Children with a neurologic event after DTP vaccine had a 7.2 times higher risk for personal history of convulsions (95% confidence limits 4.5 to 11.5) and a 4.5 times higher risk for family history of convulsions (95% confidence limits 3.1 to 6.7) than did children with an adverse event that did not affect the nervous system. Children with either a febrile or nonfebrile convulsion after receipt of DTP were significantly more likely to have a personal history of convulsions than children with a nonneurologic adverse event (P less than 0.0001). Children with a febrile convulsion after receipt of DTP but not children with nonfebrile convulsions were significantly more likely to have a family history of convulsions than those with a nonneurologic adverse event. It is recommended that pertussis vaccination be deferred in children with a personal history of a convulsion until it can be determined that an evolving neurologic disorder is not present. If such disorders are found, these children should be given the combined pediatric diphtheria and tetanus toxoids (DT) vaccine to complete the series.

Child↗

PubMed1989

Family history of convulsions and use of pertussis vaccine.

To evaluate the risk of neurologic events after vaccination with diphtheria-tetanus-pertussis (DTP) vaccine, we used data from the Centers for Disease Control Monitoring System for Adverse Events Following Immunization to compare the family history of convulsions in persons reporting neurologic events with that in persons reporting nonneurologic events; these events have an onset within 3 days of immunization with DTP vaccine, given either alone or with oral poliovirus vaccine. Persons reporting neurologic events were 6.4 times more likely to report a prior personal history of convulsions than those reporting nonneurologic events (95% confidence interval 4.7 to 8.8), and were 2.4 times more likely to report a history of convulsions in first-degree family members, that is, siblings or parents (95% confidence interval 1.7 to 3.4). Similar risks were noted for subgroup analyses controlling for type of event (febrile vs nonfebrile convulsion), age at immunization, source of report, number of previous doses of DTP vaccine, and day of onset. Because the Centers for Disease Control monitoring system receives reports on a nonrandom sample of all adverse events after immunization, selection bias could not be ruled out. On the basis of these data, we conclude that children with a family history of seizures are at increased risk of neurologic events, primarily febrile convulsions, after DTP vaccination. However, this increase in risk may reflect a nonspecific familial tendency for convulsions rather than a specific vaccine effect. Considering the rare occurrence of neurologic events after DTP vaccination, the generally benign outcome of febrile convulsions (which make up the majority of these neurologic events), and the possible increased risk of pertussis in the general population if the estimated 5% to 7% of persons with a first-degree family history of convulsions were exempted from pertussis vaccination, we further conclude that a history of convulsions in siblings or parents should not be a contraindication to pertussis vaccination. Special care in the prevention of postvaccination fever may be warranted in children with a family history of seizures.

Centers for Disease Control and Prevention, U.S.↗

PubMed2002

Intracerebroventricular injection of the antibiotic cefoselis produces convulsion in mice via inhibition of GABA receptors.

A majority of beta-lactam antibiotics (e.g., cephalosporins and penicillins) have convulsive activity to a greater or lesser extent. (6R,7R)-3-[[3-Amino-2-(2-hydroxyethyl)-2H-pyrazol-1-ium-1-yl]methyl]-7-[(Z)-2-(2-aminothiazol-4-yl)-2-methoxyiminoacetylamino]-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylate monosulfate (cefoselis), a newly developed injectable beta-lactam antibiotic with activity against methicillin-resistant Staphylococcus aureus (MRSA), might induce convulsions if cerebral concentrations become highly elevated. In the present study, we examined whether or not cefoselis had convulsive activity after direct brain administration, and we attempted to clarify the pharmacological mechanism of action. When cefoselis was injected into the lateral ventricle of the mouse brain at doses higher than 20 microg/animal, it produced convulsions dose-dependently. Cefoselis (50 microg/animal)-induced convulsions were prevented by pretreatment with 5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801), diazepam and phenobarbital (ED(50) values (mg/kg) of 0.78, 1.59 and 33.0, respectively), but not by carbamazepine or phenytoin. When the effects of these anticonvulsants on the convulsions induced by intracerebral injection of bicuculline methiodide (BMI) or N-methyl-D-aspartate (NMDA) were investigated, the inhibitory profile of anticonvulsants on cefoselis-induced convulsions was similar to those induced by BMI (125 ng/animal) but differed markedly in their inhibitory activity on NMDA (100 ng/animal)-induced convulsions, which were not inhibited by diazepam. These results suggest that cefoselis may be convulsive at higher concentrations through a mechanism involving inhibition of gamma-aminobutyric acid (GABA)(A) receptors.

Animals↗

PubMed1999

Low convulsive activity of a new carbapenem antibiotic, DK-35C, as compared with existing congeners.

Since carbapenems and cephalosporins have been suggested to induce convulsive side effects through an inhibitory action on the central gamma-aminobutyric acid (GABA)-mediated inhibitory transmission, the present study evaluated the convulsive activity of a new carbapenem antibiotic (1R,5S,6S)-6[(R)-1-hydroxyethyl]-2-[(3S,5S)-5(S-methyl-4thiomorpholin ylcarbonyl)pyrrolidin-3-thio]-l-methylcarbapen-2-em-3- carboxylic acid (DK-35C) in in vitro and in vivo experiments, in comparison with cefazolin, imipenem and meropenem. In in vitro experiments, their abilities to inhibit [3H]muscimol (5 nM) binding to GABA(A) receptors were measured using crude synaptic membranes prepared from the rat cerebral cortex. The concentrations (mM) of the antibiotics which inhibit 50% of the specific binding, were 0.6 for imipenem, 1.8 for cefazolin, 15.4 for DK-35C and 27.6 for meropenem. In in vivo experiments, intracerebroventricular (i.c.v.) injections of cefazolin, imipenem and DK-35C induced convulsions in a dose-dependent manner in rats. The doses (nmol/rat) of the antibiotics which induce convulsions in 50% of rats, were 57 for imipenem, 96 for cefazolin, 377 for DK-35C and >3000 for meropenem. In the mouse pentylenetetrazole (PTZ) convulsive model, intravenous pretreatment with cefazolin (800 mg/kg) or imipenem (200 mg/kg) shifted the dose-response curve of PTZ (i.p.) to the left, indicating enhancement of the convulsive activity of PTZ. However, pretreatment with cefazolin, meropenem or DK-35C at a dose of 400 mg/kg did not produce any marked effects on the convulsive activity of PTZ compared with the saline vehicle-pretreated control. The results clearly demonstrate a good correlation between in vitro GABA(A) receptor binding assay and in vivo i.c.v. convulsive model using rats, and suggest that DK-35C may possess a relatively weak convulsive activity mediated through an interaction with GABA(A) receptors.

Animals↗

PubMed1981

[Convulsions in neonates. Clinical, electrographic, etiopathogenic and prognostic aspects].

121 cases of neonatal convulsions, including 79 cases of status epilepticus and 42 cases of isolated convulsions are studied. The great number of premature infants (40/121 newborns born before a gestational age of 37 weeks) must be pointed out. The clinical symptoms and EEG activity occurring during the first 24 hours following the onset of convulsions are analysed. Their descriptions confirm previous ones. Comparison of the populations of preterm and term infants demonstrates that the pre- and post-ictal neurological states are equally severe in both groups and that there is no difference between groups in the more or less precocious onset of convulsions. The value of the interictal EEG already described in status epilepticus of terms infants as predicting a poor prognosis, is confirmed. In addition, the very poor prognosis of an abnormal EEG pattern of the premature newborn, i.e. an EEG lacking any pattern corresponding to any gestational age, is demonstrated. Such EEGs of very poor prognosis have been detected in 46 cases. They reveal the degree of severity of the cerebral lesions, EEG abnormalities and cerebral lesions varying with gestational age. This study confirms the relatively mild severity of isolated convulsions as compared to status epilepticus. It demonstrates the severity of convulsions in premature newborns and of the electrographical discharges without simultaneous clinical event. The prognostic value of the absence or presence of a sleep cycle as early as the 24 hours following the onset of convulsions must be noted. Most of the neonatal convulsions are secondary to birth hypoxia or asphyxia and to meningo-encephalitis. In this study the small number of seizures due to metabolic factors is striking and contrasts with their great frequency in other series. The cause of the seizures is unknown in 12% of the cases; some of these cases of unknown origin correspond to the description of the 'convulsions of the 5th day'. The prognosis in full-term newborns has been improved greatly in recent years, probably due to improvement in obstetrical and neonatal intensive care.

Brain↗

PubMed1994

Lignocaine-induced convulsion does not induce c-fos protein (c-Fos) in rat hippocampus.

Recent studies have shown that proto-oncogene c-fos mRNA is induced in the central nervous system by a variety of stimuli including generalised convulsions. In this study, the expression of c-fos protein (c-Fos) following lignocaine-induced convulsions was examined and compared with that following convulsions induced by non-anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain. Administration of 120 mg.kg-1 lignocaine by the intraperitoneal route induced generalised convulsions in all rats examined within 10 min. C-Fos was markedly induced in the piriform cortex and amygdala, and slightly induced in the neocortex and thalamus, while no c-Fos expression was observed in the hippocampus. In contrast, c-Fos expression following generalised convulsions induced by non-anaesthetic convulsants was very marked in the hippocampal region, piriform cortex and amygdala, and extended to the thalamus and neocortex. These results contradict those of previously reported local cerebral metabolic studies using 2-deoxyglucose as a metabolic marker, and suggest that lignocaine-induced convulsions, unlike those induced by non-anaesthetic convulsants, may not cause severe sequelae (plastic changes) in the hippocampus.

Animals↗

PubMed2004

Studies on cerebrospinal fluid ionized calcium and magnesium concentrations in convulsive children.

BACKGROUND: The concentrations of ionized calcium (iCa) and ionized magnesium (iMg) were measured in the cerebrospinal fluid (CSF) of convulsive and non-convulsive children, to investigate the relationship between seizure manifestation and CSF iCa and iMg concentrations. Standard concentrations of CSF iCa and iMg were also established. METHODS: CSF samples from 23 patients, ages 0-15 years, with various forms of seizures and 26 age-matched non-convulsive children were collected by lumbar puncture. CSF was obtained anaerobically and the concentrations of CSF iCa and iMg were measured with an electolyte analyzer (Stat Profile Ultra M1, NOVA, USA) immediately after the lumbar puncture. RESULTS: The concentrations of CSF iCa were significantly higher in non-convulsive children younger than 11 months old compared with children older than 12 months. The concentrations of CSF iMg in non-convulsive children did not differ significantly with aging. The concentrations of CSF iCa in convulsive children did not differ significantly from the concentrations of non-convulsive children. The concentrations of CSF iMg in convulsive children were significantly lower than in non-convulsive children. CONCLUSION: These results suggest that seizure manifestation is related to age-dependent changes in iCa and decreased iMg in the developing brain.

Adolescent↗

PubMed1993

Involvement of inhibitory and excitatory neurotransmitters in levofloxacin- and ciprofloxacin-induced convulsions in mice.

We studied the effects of gamma-aminobutyric acid (GABA)-benzodiazepine receptor agonists and glutamate receptor antagonists on levofloxacin (LVFX)- and ciprofloxacin (CPFX)-induced convulsions using intrathecal (i.t.) injections in mice. We also studied the effects of these agonists and antagonists on exacerbated convulsions induced by coadministration of the quinolone with 4-biphenylacetic acid (BPAA). The agonists or antagonists were injected i.t. 5 min and BPAA was administered orally 30 min before a single i.t. injection of the quinolone (10 microliters per animal). The animals were observed for clonic convulsion and death, and latency times to the appearance of convulsion were determined. Among the agonists, baclofen showed marked inhibition of both LVFX- and CPFX-induced convulsions, while other compounds such as GABA, muscimol, diazepam, and 3-aminopropylphosphonic acid had slight effects. Among the antagonists, kynurenic acid showed the strongest inhibition of convulsions caused by all doses of LVFX and CPFX and prolonged latency times; gamma-glutamyl-aminomethylsulfonic acid (GAMS) also markedly inhibited convulsions. The antagonists D-AP-5, AP-7, and 6,7-dinitroquinoxaline-2,3-dione (DNQX) had slight effects. Additionally, GAMS, DNQX, and MK-801 significantly lowered the incidence of death in the groups treated with CPFX. The enhanced convulsive activities of LVFX or CPFX by pretreatment with BPAA were clearly blocked by baclofen, kynurenic acid, GAMS, and DNQX. D-AP-5 and AP-7 also showed clear effects on the activity of LVFX. These results suggest that LVFX has fewer effects on the brains than CPFX and that convulsions induced by these quinolones alone and by these quinolones administered with BPAA may be mediated largely through glutamate and GABA(B) rather than GABA(A) receptors in mice.

Acetamides↗

PubMed2000

Clinical characteristics of febrile convulsions during primary HHV-6 infection.

OBJECTIVE: To clarify clinical characteristics of children with febrile convulsions during primary human herpesvirus 6 (HHV-6) infection. SUBJECTS AND METHODS: The clinical characteristics of first febrile convulsion were compared between those with and without primary HHV-6 infection in 105 children. HHV-6 infection was verified by culture or acute/convalescent anti-HHV-6 antibody titres. RESULTS: Primary infection with HHV-6 was seen in 21 of 105 patients with febrile convulsions (3 upper respiratory infection, 1 lower respiratory infection, and 17 exanthem subitum). 13 of 23 patients < 1 year, 19 of 79 patients with first febrile convulsion, and 2 of 15 with second convulsion were infected with HHV-6. The median age of patients with first febrile convulsion and HHV-6 was significantly lower than those without infection. The frequency of clustering seizures, long lasting seizures, partial seizures, and postictal paralysis was significantly higher among those with primary HHV-6 infection than among those without. The frequency of atypical seizures in 19 patients with first febrile convulsion associated with primary infection was significantly higher than in 60 patients without primary infection. The frequency in infants younger than 1 year of age was also significantly higher than that in 10 age matched infants without primary infection. CONCLUSIONS: These findings suggest that primary infection with HHV-6 is frequently associated with febrile convulsions in infants and young children and that it often results in the development of a more severe form of convulsions, such as partial seizures, prolonged seizures, and repeated seizures, and might be a risk factor for subsequent development of epilepsy.

Age Distribution↗

PubMed1989

Some correlations between procaine-induced convulsions and monoamines in the spinal cord of rats.

The relationships between the convulsions induced by the local anesthetic procaine and monoamines in the spinal cord were investigated in rats. The levels of dopamine (DA) and serotonin (5-HT) in the spinal cord were time-dependently increased after procaine (170 mg/kg, i.p.), which induced clonic convulsions, but the level of norepinephrine (NE) was unchanged. The rats that died during convulsions had a marked increase in DA. Phenobarbital (25 mg/kg, s.c.) produced both depletion of DA and elevation of 5-HT in the spinal cord and completely protected rats against convulsions. A 5-HT precursor, 5-hydroxytryptophan (5-HTP; 20-80 mg/kg, i.p.), suppressed the convulsions in a dose-dependent manner as shown by a decrease in the incidence and a prolongation of the latency, but a DA precursor, 3,4-dihydroxyphenylalanine (L-DOPA; 20-80 mg/kg, i.p.), markedly shortened the latency. Furthermore, the effect of L-DOPA on the convulsions was inhibited by the combination of 5-HTP. alpha-Methyl-p-tyrosine (20-80 mg/kg, i.p.) or DL-p-chlorophenylalanine (20-80 mg/kg, i.p.), an inhibitor of NE and DA or 5-HT biosynthesis, had a slight effect on the convulsions. These results suggest that procaine causes significant elevations of rat spinal DA and 5-HT in the convulsive process and suggest that dopaminergic and serotonergic neurons may be associated with procaine-induced convulsions.

Animals↗

PubMed1991

Some correlations between local anesthetic-induced convulsions and gamma-aminobutyric acid in rat spinal cord.

The effects of local anesthetics (procaine and lidocaine) on the gamma-aminobutyric acid (GABA) and L-glutamic acid (Glu) levels in rat spinal cord were studied during the convulsive process. The present study also investigated the influence of central GABA manipulations on the local anesthetic-induced convulsions. An increase in spinal GABA levels was observed at the preconvulsive and convulsive states after administration of procaine (170 mg/kg, i.p.) or lidocaine (120 mg/kg, i.p.), which induced clonic convulsions; in the depressive state, GABA levels returned to normal; in all states, Glu levels were unchanged. Semicarbazide (25-100 mg/kg, i.p.), a glutamic acid decarboxylase inhibitor, produced a decrease in spinal GABA content and strongly enhanced both local anesthetic-induced convulsions as shown by a shortening of the latency and an increase in the mortality. Aminooxyacetic acid (AOAA; 10-40 mg-kg, i.p.), a GABA transaminase inhibitor, dose-dependently increased spinal GABA content and markedly suppressed procaine-induced convulsions. However, lidocaine-induced convulsions were enhanced by AOAA. These results suggest that the spinal GABA neuron may respond to the convulsions induced by local anesthetics. Furthermore, there is a clear relationship between spinal GABA content and procaine-induced, but not lidocaine-induced, convulsions.

Aminooxyacetic Acid↗

PubMed1977

Convulsions in the first three years of life.

A prospective study of convulsions in 5803 consecutive newborn infants from an Australian city is described; 535 children were lost to study, leaving 90.9% of the original sample. Of the remaining 5268, 325 had at least one convulsive episode during the first three years of life--an incidence of 61.7 per thousand. Convulsions following breath-holding attacks were experienced by 8.1 per thousand, while a further 4.0 per thousand had simple breath-holding attacks associated with transient loss of consciousness, but no convulsion. Convulsions associated with fever were experienced by 39.9 per thousand. In addition, 8.2 per thousand had idiopathic convulsions, 2.8 per thousand had neonatal convulsions and 2.7 per thousand had convulsions of mixed aetiology. Factors relating to the convulsion are described in detail. Pregnancy and birth data are compared with those of a control group taken from the study.

Australia↗

PubMed2006

Cyclooxygenase system contributes to the maintenance of post convulsive period of epileptic phenomena in the genetically epileptic El mice.

Recent studies have shown that cytokines and cyclooxygenase (COX)-2 are up-regulated in the brain of human epilepsy patients and animal models of epilepsy. We investigated the effect of inflammatory responses induced by intramuscular injection of turpentine on the epileptic phenomenon in genetically epileptic El mice. As parameters of epileptic seizure, seizure threshold (number of toss-ups to induce convulsion), duration of actual convulsion and duration of post actual convulsive period (period from the offset of convulsion to full recovery) were evaluated. The post actual convulsive period was prolonged without any change of seizure threshold or duration of actual convulsion 24 h after turpentine injection. Although pretreatment with indomethacin for one week did not change the seizure parameters, indomethacin suppressed the prolongation of the post actual convulsive period induced by turpentine. The mRNA expression of IL-1beta, IL-6 and COX-2 in the cerebral cortex was detected by RT-PCR. There was no difference in the mRNA expression in the cerebral cortex before and 24 h after seizure. The mRNA levels of IL-1beta, IL-6 and COX-2 in the cerebral cortex were up-regulated 24 h after turpentine injection. On the other hand, the up-regulated mRNA levels of IL-1beta, IL-6 and COX-2 in the cerebral cortex after turpentine treatment were not suppressed by indomethacin. These results suggest that prostaglandins induced with COX-2 in the cerebral cortex seem to play an important role in the maintenance of the post convulsive period, but not in induction and maintenance of the actual convulsive state.

Animals↗

PubMed2002

Febrile convulsion--an overview.

Febrile convulsion is the most frequently occurring epilepsy syndrome, experienced in infants/children between 6 months and 5 years of age associated with fever >38 degrees C. Children having first or second degree relative with history of febrile convulsion, neonatal nursery stay of more than 30 days, developmental delay or attendance at day care centre are at increased risk of developing febrile convulsion. Single febrile convulsion does not increase the risk of epilepsy and there is no causal relationship between febrile convulsion and subsequent epilepsy. It has been recognised that there is significant genetic component for susceptibility to febrile seizures. To make the diagnosis of febrile convulsion, meningitis, encephalitis, serious electrolyte imbalance and other acute neurologic illnesses are to be excluded. While managing acute attack the steps to be taken are--airway management, a semi-prone position to avoid aspiration, monitoring vital signs and other supportive care. Diazepam or lorazepam is the drug to be used. There is no reason to expect phenobarbitone administered at the time of fever to be effective in prevention of febrile convulsion. The parents should be counselled about the benign nature of the convulsion. Although the febrile convulsion a frightening event, still it is a benign condition.

Anticonvulsants↗

PubMedDate not supplied

[Neonatal convulsions: influence of the electroencephalographic pattern and the response to treatment on the outcome].

INTRODUCTION: Neonatal convulsions continues being motive for multiple controversies: the diagnosis only by clinical approaches, the necessity to confirm with EEG record and their treatment and control. OBJECTIVE: To establish the incidence of type of clinical neonatal seizures and the correspondence of these to the EEG trace background and the EEG epileptic activity, the underlying etiology, the response to antiepileptic treatment, and their prognosis. PATIENTS AND METHODS: Retrospective study of admitted newborns with the diagnosis of neonatal seizures in our hospital, during the period included between January 1993 and October 2001. Some of variables collected were: birth and gestational age, Apgar, clinical pattern, duration of the convulsions, critical and intercritical EEG traced, EEG background, etiological diagnosis, treatment used and response of the same, evolution and neurological state at hospital discharge and at one year of age (corrected age in preterm infants). RESULTS: 74 children were admitted with neonatal convulsion diagnosis, of these only 56 EEG convulsions were confirmed (42% presented subtle seizures, 33.9% tonic, 64.3% clonic multifocal, 10.7% clonic focal, and 16.1% myoclonic multifocal). 55.4% of the infants had 2 or more types of clinical convulsions, 25% of all had an epileptic state, and 42.9% had at some time of the EEG record, electroclinical dissociation. The more frequent critical EEGs abnormalities was multifocal discharges (64.3%), and together with the focal discharges of low frequency had significant (p<0.01) worse pharmacological control, and also unfavourable outcome. The infants having had EEGs background moderately and markedly abnormal showed unfavourable outcome in 72.2% and 100% respectively, while it was only in 15.4% of the infants who had EEGs background normal or lightly abnormal. With the antiepileptic treatment the clinical control of the convulsions was obtained in more than 80% of the cases, while control of the electrical convulsions was only in 62.5%. There was a higher significant association between favourable response to treatment and normal neurological examination at hospital discharge and at 1 year of age. CONCLUSIONS: The necessity to confirm by means of EEG record the neonatal clinical convulsions, before and after having established the anticonvulsant treatment, due to the control of electrical convulsions improves their neurological outcome.

Anticonvulsants↗

PubMed1991

[Emergency management of convulsions and prevention of status epilepticus with rectal diazepam administered by parents].

The parents of 17 children with a history of convulsions, were shown how to administer liquid diazepam through the rectum using a 1 mL insulin syringe, in order to alleviate a convulsion at home or any where ever this may occur. Eight of the children had suffered from repetitive and/or prolonged non-temperature related convulsions, four had epileptic status and five had suffered from simple fever related convulsions, complicated in four and in a convulsive status in 1; the number of fever-related convulsions ranged between 1 and 6 per child and those non temperature related ranged from one daily to once a month. The observation of the children was done in an 88 month period (between 1 and nine months per child, averaging 5.2 months). In seven of the children, it was required of the parents to administer rectal diazepam a total of 90 times (fluctuating between 2 and 25 doses per child), with no complications, a dose of 0.5 mg/kg was administered in those patients whose convulsions lasted over 5 minutes or more. In 75 occasions, the convulsion stopped within a period of 2 to 5 minutes, in 12 other times there was a need for repeated dosages and in 2 occasions, a third doses was needed. Only in one occasion was hospital management needed. Therefore, we conclude that the administration of rectal diazepam by parents--at home--is a useful and secure method to prevent prolonged convulsions and the epileptic status; it gives parents security and tranquility using an instrument which can be used in any circumstance therefore reducing anguish and the cost of hospital care.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Rectal↗