Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 3700 and 3900 children are admitted annually to this children's hospital. During the past four years a total of 455 children with convulsions were admitted for investigation. 255 of these cases were calcified as epilepsy, 202 as febrile convulsions and 28 as neonatal convulsions. A quarter of the epileptic children showed fits of the petit mal type. There were only 5 cases of infantile propulsive petit mal. High frequency of fits and, in particular, status epilepticus, were very rarely seen in the present study. A case of self-induced photosensitive epilepsy, later combined with psychomotor epilepsy, is referred to in detail. Of 149 children with grand mal epilepsy, 36 were classed as idiopathic, and 88 as symptomatic cases. 37 of the symptomatic cases showed focal epilepsy with generalisation. It was concluded from the clinical course and the EEG that the combined effects of familial predisposition towards fits and exogenous cerebral lesions were operative factors in 14 patients. Children with febrile, convulsions possessed an EEG suggestive of a familial predisposition towards fits in slightly more than 50% of the cases. No cause could be found for the seizures in 5 infants with neonatal convulsions, but the mother of one of these infants was an epileptic herself, undergoing treatment with anticonvulsive drugs in high dosage and a withdrawal syndrome was suspected in this particular case. 17 infants with neonatal convulsions were symptomless on leaving hospital and remained so during the first year of life. Of the remaining cases, 10 showed neurological disturbances and one died. There was only one case in which neonatal convulsions progressed directly to epilepsy. The peak incidence of the first appearance of fits occurred during the first year of life (136 children), with 18% of the entire case material presenting within the first 6 months. 108 children presented with fits for the first time during the second year of life. Thereafter, the tendency towards the development of fits for the first time in life declined with increasing age.
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PMID:[Aspects of epilepsy in childhood (author's transl)]. 81 19

The GABA withdrawal syndrome (GWS) is a new model of focal epilepsy in which paroxysmal activity is induced through the interruption of a chronic, intracortical infusion of GABA. Preliminary studies have shown extraordinary resistance of this epileptogenic activity to classic anticonvulsants including diazepam, the most effective agent for treating status epilepticus. However, GWS can be inhibited by GABA itself. The rat with petit mal-like seizures is a genetic model of generalized non-convulsive epilepsy (GNCE), with behavioral characteristics and electrical (spike-and-wave discharges) signs resembling absences. Moreover, GABAmimetics aggravate this type of seizure. Rats with GWS induced by cessation of a localized GABA infusion (50 micrograms/microliters/h for 24 h), and the rat model of GNCE, were treated with HEPP, a new anticonvulsant agent. In the case of GWS, the drug produced a significant decrease of focal spike activity in animals which started discharging at low frequencies while in rats with higher frequency discharge, HEPP was without effect. HEPP administered on the second day of the GWS in naive rats had no effect. In rats with GNCE, doses of 50 and 100 mg/kg i.p. blocked the spike-and-wave discharges. The higher dose produced sedation in this absence seizures model. Although the mechanism of action of HEPP is still unknown, its unique antiepileptic profile deserves further studies.
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PMID:Effects of 3-hydroxy,3-ethyl,3-phenylpropionamide (HEPP) on rat models of generalized and focal epilepsy. 139 31

Benzodiazepines given intravenously abort status epilepticus, and abolish paroxysmal EEG discharges. The study reported concerns the effect of small doses (about 1 mg) of lorazepam on these EEG changes, assessed visually, in the resting record, as well as during overbreathing and photic stimulation. Thirty patients were examined, approximately half had primary generalised and the remainder focal epilepsy. All showed rapid reduction of paroxysms in the first few minutes following injection. This occurred faster and was much more persistent for the generalised than for the focal group. The effect of chronic oral administration of lorazepam in these patients is under investigation.
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PMID:Lorazepam: its effect on the EEG paroxysmal activity in patients with epilepsy. 612 58

Current trends and controversies in the antiepileptic drug therapy are reviewed from a clinical view. The usefulness of prophylactic therapy of febrile seizures and posttraumatic seizures or posttraumatic epilepsy is compromised by difficulties in the management of the patients especially by noncompliance. Previously untreated epilepsies can be treated successfully in 70--80% of the patients. Phenytoin or carbamazepine are equally effective for generalized tonic-clonic seizures of focal seizures, while absence seizures are controlled by ethosuximide or valproic acid. Only when the epilepsy is uncontrolled despite high plasma concentrations which cannot be raised because of side effects, a second drug should be given. A second drug is successful in about one out of six patients with focal epilepsy. Phenytoin, carbamazepine, phenobarbital and primidone seem to be equally effective for these drug-resistant cases. Status epilepticus can be treated with intravenous diazepam or phenytoin and, if necessary, with an infusion of phenytoin. Rectal diazepam is useful for acute pediatric therapy. Drugs of second choice are clonazepam, phenobarbital, lidocaine, and clomethiazole. In the pregnant epileptic patient a drop in the plasma concentration of antiepileptic drugs mainly through non-compliance and seizure provocation through sleep deprivation are major sources for the deterioration of epilepsies during pregnancy. The "fetal antiepileptic drug syndrome", malformations and an increased risk for epilepsy in the child are discussed as an interaction of parental epilepsy and drug-exposure during pregnancy. Finally, the interpretation of abnormal clinical chemistry data is reviewed. Disorders of the liver, bone, thyroid gland and blood are rarely seen in treated epileptic patients usually when specific risk factors are present. The over-interpretation of laboratory abnormalities e.g. an isolated increase of gamma-GT may lead to iatrogenic deterioration of epilepsy when the effective dose of the drug is reduced for unfounded fear of hepatic toxicity.
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PMID:[Pharmacotherapy of epilepsy--current problems and controversies]. 641 28

Successful drug therapy for symptomatic focal epilepsy is often difficult to achieve. The aim of our study was to determine predictors of seizure-free versus therapy-resistant courses of epilepsy. To accomplish this, we evaluated clinical data obtained early in the course of focal symptomatic epilepsy to determine which factors best determine the probability of therapeutic success. This retrospective study included 70 patients who were treated at the Neurology Clinic, University of Greifswald, between 1984 and 1992. Inclusion criteria were: Clear clinical diagnosis, a minimum of 3 years follow up in our epilepsy outpatient clinic, therapy with standard anticonvulsant drugs, and good compliance. We distinguished between patients who were seizure-free for at least two years and those who were not. 22 patients (31.4%) were seizure-free, whereas 48 patients (68.6%) remained resistant to pharmacotherapy. Prognostic factors for seizure-free outcome were: Focal grand mal seizures as the only seizure type ever experienced by the patient, the occurrence of only one type of seizures during the course of the illness, the occurrence of only nocturnal seizures, few grand mal seizures before starting an effective anticonvulsant therapy, no previous status epilepticus, and the remission of focal epileptic EEG patterns during effective drug therapy.
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PMID:[Prognostic factors and clinical outcome in symptomatic focal epilepsies]. 905 91

Benign occipital epilepsy of childhood is an idiopathic partial epilepsy syndrome with elementary visual symptomatology, frequently associated with other ictal phenomena. Seizures are usually followed by postictal headache and are often associated with interictal occipital rhythmic paroxysmal EEG activity that appears only after eye closure. In some children the ictal visual symptoms or the interictal EEG abnormalities may not be demonstrated. The clinical and/or EEG manifestations of other forms of idiopathic partial or generalized epilepsy may be found in association. Occipital spikes in non-epileptic children with defective vision, occipital slow spike-and-wave found in some patients with the Lennox-Gastaut syndrome, focal epilepsy due to occipital lesions, seizures originating in the temporal lobe secondary to an occipital abnormality, and complicated or basilar migraine must be considered in the differential diagnosis. Early-onset benign occipital epilepsy or seizure susceptibility syndrome deserves to be considered separately. It has been defined by Panayiotopoulos as consisting of brief, infrequent attacks or prolonged status epilepticus and characterized by ictal deviation of the eyes and/or head and vomiting, occurring in children usually between the ages of 3 and 7 years. Advances in molecular genetics will help decide whether these two disorders are indeed distinct. Benign occipital and benign rolandic epilepsy are commonly associated with migraine. The selective involvement of the occipital lobe in migraine has not been fully explained. The association between benign occipital epilepsy and migraine is likely related to this underlying mechanism as well. The "fixation off" phenomenon or blocking of occipital epileptic discharges by eye opening is not specific to benign occipital epilepsy of childhood and may be found in symptomatic epilepsies as well. Migraine and epilepsy are distinct disorders, both as far as their pathophysiologic mechanisms and clinical symptomatology are concerned. There is however an overlap in some patients and a causal relationship may exist in some, leading to clinically distinct migraine epilepsy syndromes. Here too, clarification of the molecular basis of migraine and of epilepsy will throw light on the nature of the relationship between the two conditions.
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PMID:The benign occipital epilepsies of childhood: an overview of the idiopathic syndromes and of the relationship to migraine. 1048

During seizure-like events (SLEs), intracellular Ca2+ concentration ([Ca2+]i) increases causing depolarization of the mitochondrial membrane and subsequent intramitochondrial accumulation of Ca2+. Mitochondrial depolarization results in an interruption of oxidative phosphorylation and increase in reactive oxygen species. Calcium activates enzymes of the citrate cycle. A characteristic feature of the low-Mg2+-induced SLEs is that they are transformed to a late activity refractory to anticonvulsant drugs, which may be regarded as a model system of difficult to treat status epilepticus. In contrast, 4-aminopyridine (4-AP)-induced activity rarely evolves to such late activity. The autofluorescence of NAD(P)H was used to monitor changes in cellular energy metabolism in the entorhinal cortex in two in vitro models of focal epilepsy. During repetitive 4-AP-induced SLEs there was a short decrease followed by a long-lasting overshoot of the NAD(P)H signal. This sequence remained unaltered during recurring SLEs. In contrast, during recurrent low-Mg2+-induced SLEs, the brief initial NADH signal reduction was unchanged but the following overshoot of NADH displayed a continuous decrease. This indicates a relative energy failure, which may contribute to the transformation to late activity in the low-Mg2+ model.
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PMID:A relative energy failure is associated with low-Mg2+ but not with 4-aminopyridine induced seizure-like events in entorhinal cortex. 991

Spontaneous seizures are the hallmark of human epilepsy but they do not occur in most of the epilepsy models that are used to investigate the mechanisms of epilepsy or to test new antiepileptic compounds. This study was designed to develop a new focal epilepsy model that mimics different aspects of human temporal lobe epilepsy (TLE), including the occurrence of spontaneous seizures. Self-sustained status epilepticus (SSSE) lasting for 6-20 h was induced by a 20-30 min stimulation of the lateral nucleus of the amygdala (100 ms train of 1 ms, 60 Hz bipolar pulses, 400 microA, every 0.5 s). Stimulated rats (n = 16) were monitored with a video-EEG recording system every other day (24 h/day) for 6 months, and every other video-EEG recording was analyzed. Spontaneous epileptic seizures (total number 3698) were detected in 13 of the 15 animals (88%) after a latency period of 6 to 85 days (median 33 days). Four animals (31%) had frequent (697-1317) seizures and 9 animals (69%) had occasional seizures (1-107) during the 6-months follow-up period. Fifty-seven percent of the seizures occurred during daytime (lights on 07:00-19:00 h). At the end of the follow-up period, epileptic animals demonstrated impaired spatial memory in the Morris water-maze. Histologic analysis indicated neuronal loss in the amygdala, hippocampus, and surrounding cortical areas, and mossy fiber sprouting in the dentate gyrus. The present data indicate that focal stimulation of the amygdala initiates a cascade of events that lead to the development of spontaneous seizures in rats. This model provides a new tool to better mimic different aspects of human TLE for investigation of the pathogenesis of TLE or the effects of new antiepileptic compounds on status epilepticus, epileptogenesis, and spontaneous seizures.
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PMID:A new model of chronic temporal lobe epilepsy induced by electrical stimulation of the amygdala in rat. 1064 46

In patients with focal epilepsy, focal neurological dysfunction can occur due to status epilepticus and also as a post-ictal phenomenon. Bulbar dysfunction as evident by drooling, dysarthria, swallowing difficulties, and palatal-glossalpharyngeal weakness has been reported in conjunction with epilepsy. This is non-progressive and is correlated in its severity with the frequency of seizures. Accompanying EEG discharges are often localized to rolandic areas that cortically represent oral movements and salivation. We report a 6-year-old male and a 6 1/2-year-old female with progressive bulbar dysfunction resulting from epilepsy. Ictal EEGs in patient 1 did not confirm a diagnosis of epilepsy. With no evidence of a cortical or brainstem focus from EEG or MRI, it is very difficult to explain the mechanism of bulbar dysfunction. The complete restoration of bulbar function after treatment with antiepileptic drugs demonstrates the need to consider epilepsy in similar clinical situations.
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PMID:Epilepsy with reversible bulbar dysfunction. 1241 18

There is an extremely intimate relationship between sleep and epilepsy. In this manuscript I will review the influence that sleep has on epilepsy. Sleep is a potent activator of interictal epileptiform discharges. Sharp waves are infrequent during wakefulness in benign focal epilepsy of childhood, but may occur in runs of several discharges per page in sleep. The interictal discharges become almost continuous in non-REM sleep in the syndrome of encephalopathy with electrical status epilepticus during slow wave sleep. In some patients with West syndrome a hypsarrhythmia pattern may only appear in sleep whereas in others there may be an increase in discharges in a semiperiodic fashion resulting in a burst-suppression like pattern. Seizures appear to have a very close relationship with sleep in certain epilepsy syndromes. In benign focal epilepsy of childhood the seizures occur almost exclusively in sleep, while supplementary sensorimototor area seizures tend to occur in clusters during sleep. Juvenile myoclonic epilepsy has a close relationship with the sleep-wake cycle with seizures tending to occur predominantly on awakening. I also discuss the role of sleep and sleep deprivation in the EEG evaluation of epilepsy.
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PMID:Effect of sleep on epilepsy. 1248 81


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