Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Naive rats were electrically stimulated in the amygdala with biphasic square wave pulses at 3 Hz in a model of partial status epilepticus (SE). This treatment led to the rapid kindling of seizures in all rats, and the subsequent induction of SE in 100% of rats stimulated for approximately 30-60 min. Extensive gliosis and degeneration was seen in the basal forebrain of the SE brains. This method of inducing SE is simpler, more rapid, and more reliable than similar methods reported previously.
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PMID:Rapid and reliable induction of partial status epilepticus in naive rats by low-frequency (3-Hz) stimulation of the amygdala. 152 29

Transient elevation of serum prolactin frequently follows generalised tonic-clonic and complex partial seizures. However, the levels of prolactin during status epilepticus are not increased above the normal range. Exhaustion of central prolactin supplies has been proposed as a possible mechanism for the absence of prolactin increase during status epilepticus. To test this hypothesis we injected intravenous metoclopramide (10 mg) in eight consecutive patients with status epilepticus. One patient had generalised tonic-clonic status epilepticus. Seven patients had EEG-verified non-convulsive status epilepticus, consisting of one typical absence status, one atypical absence status and five complex partial status epilepticus. Metoclopramide raised the mean (SD) prolactin levels at least five-fold in all patients, from 5.8 (8.0) micrograms/l to 87.0 (39.0) micrograms/l, within 60 minutes after the injection. Thus the mechanism for low prolactin values in status epilepticus is not cellular depletion of stored prolactin, but more likely an altered regulation, presumably induced by prolonged seizure activity.
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PMID:Serum prolactin response to metoclopramide during status epilepticus. 152 38

A new model of status epilepticus (SE), which was induced by intermittent electrical stimulation (20 Hz for 20 sec every min for 180 min) of the deep prepyriform cortex, has been developed in the conscious rat. SE was induced in 9 of 16 rats in the drug-free group. The number of stimulation trains required to induce SE in this status subgroup was 125.6 +/- 12.7 (mean +/- SEM) and the mean duration of self-sustained seizure activity (SSSA) occurring after cessation of the stimulation session was 295.4 +/- 111.4 min. Some animals showed secondary generalized seizures. Significant cell loss was observed in the hippocampal CA3 pyramidal cell layer ipsilateral to the stimulation site and bilateral CA1 areas in the status subgroup compared with the group subjected to sham operation. In addition, there was a significant negative correlation between the duration of SSSA subsequent to the stimulation session and the total number of intact pyramidal neurons observed in the bilateral CA1 and ipsilateral CA3 subfields of the status subgroup. There were significant differences between the status and non-status subgroups with respect to the number of afterdischarges (ADs) and the total AD duration during the stimulation session. Pretreatment with phenobarbital (30 mg/kg) prevented the development of SE and hippocampal cell loss completely. Pretreatment with MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist (0.25 or 1 mg/kg), also prevented hippocampal cell loss, although it did not block SE generation completely, which suggests dissociation of the mechanisms underlying the development of SE and hippocampal damage. These results indicate that prolonged SSSA actually causes hippocampal damage and it is critically dependent upon NMDA receptor participation.
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PMID:Mechanisms in the development of limbic status epilepticus and hippocampal neuron loss: an experimental study in a model of status epilepticus induced by kindling-like electrical stimulation of the deep prepyriform cortex in rats. 153 85

Sudden unexplained death syndrome (SUDS) accounts for about 10% of deaths in patients with epilepsy. It is associated with subtherapeutic postmortem serum antiepileptic drug (AED) levels but no anatomic cause of death on autopsy. The mechanisms of death are not known. We investigated 44 cases of SUDS for details of seizure history, treatment, medical and psychological history, events at the time of death, and postmortem findings. Cases of status epilepticus, drowning or other identifiable causes of death were excluded. Two groups emerged: five children with uncontrolled seizures receiving multiple AEDs and good compliance with medications, and 39 adults with less frequent seizures, often receiving monotherapy, but noncompliant with medications. Four children (80%) but only one adult (3%) had fully therapeutic postmortem AED levels. Sixty-three percent of adults recently had experienced an unusually stressful life event. Investigation of the circumstances at the time of death suggested two possible modes of death: (a) a seizure with an immediately fatal arrhythmia, or, (b) a seizure, recovery, then delayed secondary respiratory arrest or arrhythmia. Even though the mechanisms of death are unknown, the risk of SUDS may be reduced by encouraging patients to be compliant with medications, especially in times of unusual life stress.
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PMID:The sudden unexplained death syndrome in epilepsy: demographic, clinical, and postmortem features. 154 60

Intrarectally (i.r.) administered diazepam (DZP) solution at doses of 20 and 30 mg in the treatment of serial seizures was studied in 39 adult patients with refractory partial epilepsy. Patients were randomly distributed into two groups (20 mg, n = 21; 30 mg, n = 18). Plasma levels of DZP were assessed over 24 h following i.r. injection. The efficacy of i.r. DZP in the treatment of serial seizures in adults was confirmed; onset of effect was noted approximately 10 min after the injection, and the effective dose was 0.50 mg/kg. Tolerance and acceptability were good. Intrarectal injection of DZP can be performed even by unskilled personnel and may be recommended in patients with serial seizures in the hope of preventing development of status epilepticus.
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PMID:Intrarectal diazepam in epileptic adults. 154 66

Lidocaine (lignocaine) was given in 42 episodes of status epilepticus (SE) in 36 patients either because of limited pulmonary reserve (22 patients) or because of lack of response to diazepam (14 patients). Lidocaine (1.5-2 mg/kg) was given intravenously in two minutes. A further identical bolus was infused if no response had occurred or if seizures recurred. With the first bolus 11 episodes of SE did not stop, but 31 responded, always in less than one minute. In 19 episodes, however, this response lasted less than 30 minutes. Twelve episodes did not recur, but 30 needed a second bolus because of recurrence. Of these, 19 episodes responded at once but SE reappeared in seven. In these seven episodes the mean control time with the second dose was 102 minutes. Five of these subsequently responded to a continuous infusion of lidocaine. Eleven patients, who had not responded to the first bolus, had no response to the second. Lidocaine is a drug that may be epileptogenic at high doses. At the doses used here, however, lidocaine seems to be a rapid acting anticonvulsant, useful in the short term management of SE and may be indicated in patients in whom respiratory or consciousness depression is undesirable and in those with no response to diazepam. The absence of response to lidocaine indicates SE resistant to treatment and poor prognosis. These data show that prompt lidocaine administration may be worthwhile when management of respiratory depression is not possible.
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PMID:Role of lidocaine (lignocaine) in managing status epilepticus. 154 99

A term infant, observed at birth to be microcephalic, developed status epilepticus and died 36 hours later. At autopsy a markedly atrophic brain was found which, by microscopic examination, demonstrated changes consistent with neuronal ceroid-lipofuscinosis. Cerebral lipidosis with microcephaly presenting at birth is extremely rare. Congenital neuronal ceroid-lipofuscinosis is an atypical form of ceroid-lipofuscinosis and should be considered in the differential diagnosis of the microcephalic neonate with seizures.
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PMID:Congenital ceroid-lipofuscinosis. 138 26

In this retrospective study, experience in status epilepticus (SE) over an 18-month period at the Port-of-Spain General Hospital is reported. Sixty-three episodes in 41 patients were studied. Fifty-one per cent of patients were under 10 years of age. Fifty-one per cent of patients were classified as remote symptomatic, 29% idiopathic, 15% acute symptomatic and 5% febrile. Bolus doses of diazepam were used in 62 of 63 episodes, phenytoin in 18, diazepam infusion in 9, paraldehyde in 12 and phenobarbitone in 9. Seizures were controlled within half-hour of starting treatment in 55 episodes (87%). In 3 episodes in 2 patients (5%), control was poor and exceeded 18 hours. No deaths were recorded. Two neurological deficits and 8 other morbid events were recorded. Mean hospital stay was 2.9 days. No patient was ventilated or admitted to the Intensive Care Unit. Current drug therapy is highly effective in SE even in institutions where modern intensive care technology is limited. Prognosis is excellent in patients in whom the underlying aetiology is benign.
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PMID:Status epilepticus. Recent experience at the Port-of-Spain General Hospital, Trinidad. 156 89

Acute and chronic effects of seizures induced by intraperitoneal (i.p.) injection of kainic acid (KA) were studied in developing rats (postnatal days (P) 5, 10, 20, 30, and adult 60). For 3 months following KA-induced status epilepticus, spontaneous recurrent seizure (SRS) occurrence was quantified using intermittent video monitoring. Latency to generalized seizures was then tested using flurothyl, and brains were histologically analyzed for CA3 lesions. In P5-10 rats, KA caused generalized tonic-clonic ('swimming') seizures. SRS did not develop, and there was no significant difference between control and KA-treated rats in latency to flurothyl-induced seizures. In contrast, rats P20 and older exhibited limbic automatisms followed by limbic motor seizures which secondarily generalized. Incidence and frequency of SRS increased with age. P20-30 rats with SRS had shorter latencies to flurothyl seizures than did KA-treated P20-30 rats without SRS or controls. KA-treated P60 rats (with or without SRS) had shorter latencies than controls to flurothyl seizure onset. SRS in P60 rats occurred sooner after KA than in P20-30 rats. CA3 lesions were seen in P20-60 rats with and without SRS, but not in P5-10 rats. These data suggest that there are developmental differences in both acute and chronic responses to KA, with immature animals relatively protected from the long-term deleterious effects of this convulsant.
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PMID:Kainic acid seizures in the developing brain: status epilepticus and spontaneous recurrent seizures. 157 66

Status epilepticus may be resistant to intravenous anticonvulsive drugs. In these cases treatment with the inhalation anaesthetic agent isoflurane may be helpful in the further management. We describe a 35-year-old female patient who suffered from status epilepticus with partial seizures. In spite of therapy with benzodiazepine and phenytoin the status evolved into tonic clonic seizures. Treatment with thiopentone sodium did not stop seizure activity. Anaesthesia with isoflurane (dosage up to 1.5 vol.%) carried out twice within 72 h finally led to a termination of status epilepticus. From our own experience and reports in the literature we conclude that general anaesthesia with isoflurane can and should be used in the treatment of severe status epilepticus that does not respond to intravenous anticonvulsive agents.
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PMID:Isoflurane anaesthesia in the treatment of convulsive status epilepticus. Case report. 157 16


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