Types Of Convulsions Research Articles

Convulsions bénignes du nourrisson. Étude collaboratrice française

Benign infantile non febrile seizures are not well known, leading us to study their clinical and EEG characteristics.Between 1981 and 1994, we assembled 34 patients with the following inclusion criteria: non febrile seizures between 1 month and 2 years of age, normal personal history, no abnormality on clinical, biological and radiological investigations, normal developmental outcome with at least 1 year follow-up.These 34 patients were recognized as 14 familial cases (identical seizures affecting parents) and 11 non familial cases. The other nine cases had different or undefined epilepsy in the family. The clinical and EEG characteristics were the same: at the mean age of 6 months, brief partial seizures (often secondarily or apparently generalized) occurring in a cluster of two to 12 episodes a day for a mean duration of 2.5 days, with ictal EEG showing focal discharge, often slow waves or focal spikes on post-ictal tracing and normal interictal EEG.The clinical and EEG characteristics are important in order to recognize this type of infantile convulsions (familial or not familial), which have a good prognosis and need no aggressive treatment.

Infantile spasms: Recognition, treatment and prognosis

156 years ago Dr West wrote to the Lancet describing 'a peculiar type of convulsion' occurring in his 4-month-old son, so documenting the first case of West's syndrome or infantile spasms. Despite the huge advances in medicine since that time, infantile spasms still remain a poorly understood entity. Although with newer imaging techniques we are more often able to elicit the underlying causes of these spasms, still little is known about their pathophysiological basis and treatment remains problematic.

Central action of 9-methyl-7-bromoeudistomin D (MBED), a derivative of eudistomin D isolated from Eudistoma olivaceum.

The behavioral responses of mice following intracerebroventricular (i.c.v.) injection of 9-methyl-7-bromoeudistomin D (MBED) were studied. Head-twitches were produced 20-90 min after the injection of 2, 20 and 200 nmol/mouse but such twitches were not significantly induced by caffeine (1000 nmol/mouse). The locomotor activity, as assessed by the Animex autometer, increased 0-120 min after the injection with doses of 2, 20 and 200 nmol/mouse, whereas a large dose of caffeine (500 nmol/mouse also increased the activity counts. Simultaneous injection of picrotoxin (3 mg/kg, s.c.) and MBED (50, 100 and 200 nmol/mouse) produced clonic and tonic extensive convulsions, but caffeine (1000 nmol/mouse) in combination with picrotoxin did not cause any type of convulsion.

Gelastic epilepsy: video-EEG, MRI and SPECT characteristics

Gelastic epilepsy, or ictal laughter, is a relatively uncommon type of seizure which may occur singly or, more frequently, with other types of convulsions. Gelastic seizures have been observed to be associated with many different conditions, mainly hypothalamic hamartomas. We report on a patient whose ictal laughter was the only neurologic disturbance. Ictal video-EEG demonstrated seizure arising from the left frontal region with subsequent involvement of the contralateral homologous area and secondary generalization. MRI showed an enlarged left frontal horn of the lateral ventricle. Postictal SPECT, performed 6 min after the seizure had ended, showed hypoperfusion in the bilateral frontoparietal region and in both cerebellar hemispheres; the presence of this abnormality may be due to the spreading of the cortical epileptogenic focus and to the complex intercommunication between the frontal cortex and the cerebellar hemispheres. Interictal SPECT, in accordance with MRI features, demonstrated a left frontoparietal hypoperfusion. The neurofunctional features observed in the reported child could suggest that gelastic epilepsy originates in the frontal cortex. However, further studies are undoubtedly needed to define the pathogenetic mechanisms of ictal laughter.

Low sodium levels in serum are associated with subsequent febrile seizures

Fever plays an important role in causing disturbances in fluid and electrolyte balance. Hyponatraemia has been thought to enhance the susceptibility to seizures associated with febrile illnesses in childhood. We have studied serum electrolyte levels in children with simple and complicated febrile convulsions. Sodium levels were lower in those children with complicated convulsions in comparison with those having simple convulsions (136.07 +/- 3.06 mmoll-1, mean +/- SD, n = 42, and 137.62 +/- 2.63 mmoll-1, n = 71, respectively; p < 0.01, Student's t-test). The sodium concentrations were lowest in children with repeated seizures (134.20 +/- 2.30 mmoll-1, n = 15) compared with children having simple (p < 0.01, ANOVA, Duncan's test) or other complicated types of febrile convulsions: focal seizures (137.08 +/- 3.82 mmoll-1, n = 12, p < 0.01), seizures lasting longer than 15 minutes (138.00 +/- 2.45 mmoll-1, n = 5, p < 0.05) and children over 5 years (136.70 +/- 2.06 mmoll-1, n = 10, p < 0.05). Serum potassium levels showed no statistically significant differences between the patient groups. Our results show that hyponatraemia may increase the risk for multiple convulsions during the same febrile illness.

Value of brain CT scan in children with febrile convulsions

Studies specifically dealing with the value of brain CT scans in different types of febrile convulsion are lacking when compared to the large amount of studies on other favorable convulsive disorders. This study is a correlation study between children who presented with febrile convulsions ( n = 38) and the results of their brain CT scans. Twenty four patients had risk factors for subsequent epilepsy (group A), 3 of them had abnormal CT scans in the form of mild diffuse brain atrophy, and all 3 patients were found to have prior neurodevelopmental deficits. The other 14 patients did not have such risk factors (group B) and had normal brain CT scans. Despite the small size of the study, the results are unequivocal, and it can be concluded that brain CT scan is not indicated in the management of simple or complex febrile convulsions. Brain CT may be justifiable, but may not be clinically useful in the management of febrile convulsion patients with prior neurodevelopmental deficits.

Corticosteroids enhance convulsion susceptibility via central mineralocorticoid receptors.

Recently, interest in the roles of central nervous system mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) has increased. In vitro results have implicated MR in the enhancing effects of corticosteroids and GR in the suppressing effects of corticosteroids on hippocampal excitability. Although indirect evidence exists suggesting that opposing actions of central MR and GR occur in vivo, direct evidence from studies employing receptor agonists and antagonists is only beginning to emerge. Work in our laboratory suggests that increased corticosterone levels are associated with increased severity of ethanol, pentobarbital, and diazepam withdrawal. Further work with chemical convulsants suggests that MR mediate excitatory effects of corticosteroids on convulsion susceptibility. The circadian rhythm in convulsion susceptibility varies with the circadian rhythm of plasma corticosterone levels and MR binding. The types of convulsions affected by manipulations of MR activity are believed to be of limbic origin, suggesting that limbic convulsions may be alleviated by the use of specific MR antagonists. In addition, because MR are substantially bound at rest and maximally occupied during the circadian peak in corticosteroid levels and during stressor exposure, these receptors are implicated in the maintenance of and in changes in the arousal state of animals.

A case of meningioangiomatosis without von Recklinghausen's disease

Meningioangiomatosis is rare disease and is classified as hamartoma in central neurofibromatosis. Unlike most cases of meningioangiomatosis, the very rare case reported here was not associated with von Recklinghausen's disease. We could find only 12 previous cases reported in the literature. A review was carried out of the clinical features, imaging characteristics, and histopathological findings in those 12 plus ours for a total 13 cases. Several types of convulsion were identified as clinical symptoms in 11 of the 13 cases. They were treated surgically. Prognosis was satisfactory in most cases. Proliferation of small blood vessels accompanied by endothelial cells with glial tissue as background and proliferation of fibroblasts or meningothelial cells in the perivascular space were observed to be the most frequent histopathological features.

Benign partial epilepsy with secondarily generalized seizures in infancy.

Seven infants with benign idiopathic partial epilepsy presented with apparently generalized tonic-clonic seizures (GTCs) which proved to be partial seizures evolving to secondarily generalized seizures. All were easily controlled with phenobarbital (PB) or carbamazepine (CBZ), and remained seizure-free > 3 years even after discontinuation of medication, and had a normal developmental outcome. The initial seizure manifestation consisting of motion arrest, staring or blank eyes, or crying associated with focal paroxysmal discharges was followed by GTCs in accordance with generalization of paroxysmal discharges. Four infants had a family history of benign type of childhood convulsions. The term "benign partial epilepsy in infancy" is proposed to combine this syndrome with the previously described benign infantile epilepsy with complex partial seizures.

Antagonism of various tonic convulsions in mice by dextrorphan and dizocilpine

To define their efficacy and mechanism of action, the possible antagonistic effects of intravenously administered dextrorphan and dizocilpine, non-competitive N-methyl-D-aspartic acid (NMDA) receptor antagonists, on tonic convulsions and death in a variety of experimental mice models were compared. Dextrorphan not only produced dose-dependent protection against the tonic convulsions caused by an intracerebroventricular injection of NMDA, but also showed a broad spectrum of anticonvulsant activities against tonic convulsions caused by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainic acid (KA), bicuculline, pentylenetetrazole or electroconvulsive shock. The anticonvulsant action of dizocilpine was found to be more efficacious for any type of tonic convulsions and was 20- to 70-fold more potent than that of dextrorphan. Dizocilpine, unlike dextrorphan, impaired motor function at doses showing its anticonvulsant activity. Bay k-8644 (a Ca2+ channel agonist)-induced seizures were not antagonized by dextrorphan. Dextrorphan and dizocilpine were characteristically selective for protective functions against death, especially with three subtypes of glutamate receptors, as death caused by NMDA but not by AMPA and KA was selectively and markedly inhibited by both dextrorphan and dizocilpine. In view of these results, the efficacy of dextrorphan and dizocilpine as antagonists of convulsant effects appears to be consistent with the interpretation that a variety of convulsants cause tonic convulsions via direct or indirect interaction with the NMDA receptor complex. Furthermore, it is suggested that influx of Ca(2+) and intracellular Ca(2+) activity, such as the Bay k-8644-modulated activation of Ca(2+) binding proteins, are not directly modified by the administration of dextrorphan, itself.

Immunohistochemistry of c-fos in Mouse Brain During Postnatal Development: Basal Levels and Changing Response to Metrazol and Kainate Injection.

Levels and cellular distribution of FOS, the product of c-fos (onco)gene, were studied by immunohistochemistry during the development of mouse brain at rest and after the administration of convulsants. Basal FOS immunoreactivity became detectable only after postnatal day 20 (P20). Metrazol and kainate at the appropriate doses induced convulsions at all ages but, in both cases, FOS accumulated in limbic areas (particularly in the dentate gyrus) only after a certain age: P20 for kainate and P30 for Metrazol. Surprisingly, considering the different molecular targets of Metrazol and kainate, respectively, and the different type of convulsions elicited, the cell groups in the limbic areas in which FOS increased were the same in the two cases. These results suggest that both drugs produced FOS increase by finally activating the same circuit. During ontogeny, the ability to accumulate FOS, which appears after P20, could be the sign of the attained maturity of signal transduction mechanisms in the cells of the hippocampal formation; endogenous signals originating from the activity of the nervous system increase the basal FOS levels and exogenous signals (i.e. like those given, probably locally, by kainate) further increase these levels. Metrazol manifests its capability to induce FOS accumulation only at later ages. We suggest that this occurs because the Metrazol target is probably distant from the hippocampal region and thus the maturity of a nerve pathway(s) is also required for c-fos induction.

Improved anticonvulsant activity of phenytoin by a redox brain delivery system. III: Brain uptake and pharmacological effects.

Phenytoin (DPH) was delivered to the brain by a dihydropyridine in equilibrium pyridinium salt redox system, which was evaluated for anticonvulsant activity. Following iv injection of the lipophilic delivery system of DPH (2) to rats, concentrations of DPH were lower but sustained and, after 30 min, essentially the same as the levels after equimolar administration of DPH. While 2 delivered the same levels of DPH to the brain as DPH did, it was twice as potent as DPH in rats (ED50 was 7.5 mumol/kg for 2 and 14.2 mumol/kg for DPH) and mice (2: 10.5; DPH: 23.9) against maximal electroshock seizures (MES), and seven times more potent in mice (2: 10.0, DPH: 70.6) against maximal pentylenetetrazole seizures (MPS). Moreover, 2 was active against pentylenetetrazole threshold seizures (PTS) in mice and rats (ED50 = 44.1 and 40.5 mumol/kg, respectively), while DPH was ineffective (up to a dose of 79.2 mumol/kg). After evaluation of acute neurological toxicity in rats, 2 was found to possess 1.5 times higher a protective index (for MES) than DPH. It appeared also that while DPH was 2.9 times less sensitive to MPS than to MES, 2 was equally potent to both types of convulsions. Thus, the data indicate that 2 delivered DPH more efficiently to the brain. The better anticonvulsant activity (quantitatively as well as qualitatively) of 2 can be explained on the basis of an improved distribution in the brain due to its higher lipophilicity, and by favorable regional differences in the rates of conversion of 2 to DPH at the convulsing foci.

Late febrile convulsions: A clinical follow-up

A joint study was performed on patients from the Pediatric Clinics of Catania and Modena. Two hundred and twenty-two children who presented with febrile convulsions (FC) after the age of six years (LFC) were followed up in order to evaluate the risk of recurrence and type of convulsions. The overall results showed that 94 patients out of 222 (42.3%) had subsequent fits, both febrile and afebrile. The present study suggests that the risk of subsequent afebrile crises in LFC is higher (15.8%) than observed after "simple" FC (2-3%) and similar to that reported after "complex" FC (13-17%).

Clinical findings in children with occipital paroxysmal discharges.

Occipital paroxysmal discharges (OPDs) have been related to a variety of clinical problems. To evaluate associated symptoms and patient outcome, we studied 293 children with OPDs. Follow-up of more than 6 months was available in 141 children. Mental retardation, neurological symptoms, behavior problems, ocular symptoms, and convulsions of various types were present. Eight patients had ictal visual phenomena consistent with the diagnosis of benign epilepsy with occipital spike and wave (BEOSW). In the 141 children with at least 6 months follow-up, 58 had other types of convulsions. Clinical and EEG normalization was observed in 25 and clinical normalization only in 17. The use of antiepileptic drugs did not seem to influence the outcome although seizure control was obtained in 26 patients. In all the cases where follow-up was 9 or more years, clinical normalization was observed. Clinical symptoms in these patients were quite heterogeneous and frequently not ictal. The disappearance of OPDs with increasing age points to their being "not lesional" in origin.

Anticonvulsant profile of the dihydropyridine calcium channel antagonists, nitredipine and nimodipine

The effects of the dihydropyridine calcium channel antagonists, nitredipine and nimodipine, on convulsions produced by different mechanisms have been studied in rats. Nitrendine and nimodipine significantly raised the thresholds to pentyleneterazzol for up to six hours after their injection. The calcium channel agonist, BAY K 8644, lowered the convulsion threshold to pentylenetetrazol and antagonised the effects of nitrendipine. In contrast, the severity of seizures produced by N-methyl-dl-aspartate (NMA) was increased by nitrendipine. BAY K 8644 also slightly increased the effects of NMA. Nimodipine and nitredipine caused small, but significant, increases in the threshold pressures for the convulsions caused by raising the atmospheric pressure with helium gas. The compounds had no effect on strychnine convulsions. The conclusion is that the calcium channel antagonists are anticonvulsant against only certain types of convulsions, such as pentylenetetrazol and high pressure (and ethanol withdrawal, reported previously). Others may be increased, such as NMA seizures, or unaffected, such as strychnine-induced convulsions.

Benign complex partial epilepsies in infancy

Nine infants with benign complex partial seizures, diagnosed by simultaneous electroencephalogram and video recordings, are described. At mostly 3–10 months of age, these infants demonstrated clusters of seizures which consisted of motion arrest, decreased responsiveness, staring or blank eyes mostly with simple automatisms, and mild convulsive movements associated with focal paroxysmal discharges. The seizures were controlled easily with carbamazepine or phenobarbital and all patients remained seizure-free for more than 3 years. Four patients had family histories of benign types of infantile convulsions. Interictal electroencephalogram and psychomotor development were normal in all patients.

Modification of electroshock and pentylenetetrazol seizure patterns in rats affer precollicular transections

Rats with precollicular transections leaving the brain stem intact were subjected to electroshock or pentylenetetrazol-induced convulsions. Animals with transections failed to display the face and forelimb clonus (with or without rearing) typically seen in sham-operated rats subjected to pentylenetetrazol- or minimal electroshock-induced convulsions elicited with corneal electrodes. Moreover, rats with transections exhibited all other components of pentylenetetrazol- and electroshock-induced seizures. These findings support the hypothesis that tonic and some types of clonic convulsions can occur independently of seizure discharge in forebrain structures, whereas clonus restricted to the face and forelimbs depends on seizure discharge emanating from structures within the forebrain for expression.

CEREBROSPINAL FLUID MYELIN BASIC PROTEIN IMMUNOREACTIVITY AS AN INDICATOR OF BRAIN DAMAGE IN CHILDREN

Cerebrospinal fluid (CSF) myelin basic protein (MBP) was measured blind by double antibody competitive inhibition radioimmunoassay (RIA) in 20 children who had seizures and 17 children with hydrocephalus. MBP values correlated with clinical outcome and mean maximum intracranial pressure (ICP) in the hydrocephalic group, and with type of convulsion in the epileptic group. A value of 20ng/ml or more was regarded as significantly raised. A significant rise in MBP levels could be demonstrated in those with ICP alone and in patients with additional problems, whose levels tended to be even higher. Hydrocephalic children with normal ICP and children with seizures had similar normal MBP levels, and in the latter group clinical outcome was not related to MBP levels. For individual patients CSF MBP is of little value as a prognostic indicator, or as a method of quantifying cerebral damage.

Benign post-traumatic encephalopathy syndrome in young people. Critical review of the literature

A trivial head injury can transiently render a child lethargic or even comatose. There have been several isolated reports concerning such conditions. Critical analysis disclosed that all these reports had certain factors in common: 1) they occurred in young people, 2) after head injury, 3) with several minutes to hours of lucid period; 4) neurological signs and symptoms were transient, and 5) complete recovery was usual. On closer checking, however, these syndromes could be categorized into three groups, i.e., nonconvulsive, convulsive, and brain swelling types. A typical non-convulsive type was the juvenile head trauma syndrome (Haas et al.). Injuries were usually trivial. After a short time, nausea, vomiting, lethargy, headache, cortical blindness, hemiparesis, and/or brain stem signs occurred. Not only a similarity of the manifestations with the periodic syndrome and migraine attacks but also the presence of migraine diathesis was frequently reported. Altogether 50 cases of the convulsive type were collected from the literature. Most of them were young children with minor head injury. Some became stunned, or received skull fractures. Convulsions were mostly focal motor. The third type consisted of 23 cases of diffuse brain swelling in children with a lucid period reported by Bruce et al. Vomiting, headache, disturbed consciousness from lethargy to coma, pupillary changes, apnea, and/or convulsive seizure were noted. CT scans disclosed small ventricles and effacement of the perimesencephalic cistern. All recovered without deficits except one who died from delayed brain swelling. In the first and second types of patients, no brain swelling was documented. Two patients who, after a minor head injury, convulsed and died of severe brain swelling have been separately reported. Three cases of the first type and one case of the second type recently experienced by the authors showed normal CT scans in the acute stage. All these three types might have a common underlying mechanism and they might be collectively termed as ‘benign post-traumatic encephalopathies in young people’, modified from Guthkelch. Children and young adults must have low thresholds against external force or more specifically either to increased extracellular potassium or to cerebral vasospasm. The relationship with migraine diathesis was noted only in the first type, which probably indicates a lower threshold in such predisposed youngsters.

Potentiation of phenobarbital-induced anticonvulsant activity by pipecolic acid

Pipecolic acid (PA) is an intermediate of lysine metabolism in the mammalian brain. Recent findings suggest a functional connection of PA as neuromodulator in GABAergic transmission. Since many drugs are postulated to produce their effects by interaction with the central GABA system, the influence of PA on the anticonvulsant activity of phenobarbital was examined. Pretreatment of mice with 50 mg . kg-1 of PA potentiated the suppressing effects of the barbiturate on electrically and chemically induced convulsions. However, there was no potentiation of the behavioral effects and hypothermia induced by phenobarbital. PA itself had no or only little effect on the convulsions, motor function and rectal temperature when given in i.p. doses up to 500 mg . kg-1. Intraventricular administration of 500 microgram of PA also did not suppress either type of convulsion, although it produced ptosis, hypotonia, sedation and hypothermia. The results are discussed in relation to GABA system.