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)

Using univariate and multivariate regression analysis, we studied seizure duration, seizure type, age, etiologies, other clinical features, and mortality among 253 adults with status epilepticus (SE) admitted to the Medical College of Virginia. Cerebral vascular disease and discontinuation of antiepileptic drugs (AEDs) were the most prominent causes of SE, each accounting for approximately 22% of all patients in the series. The other principle etiologies were alcohol withdrawal, idiopathic, anoxia, metabolic disorders, hemorrhage, infection, tumor, drug overdose, and trauma. When the patients were divided into two groups, the group with SE lasting < 1 h had a lower mortality as compared with seizure duration > or = 1 h. Low mortality rates were noted in alcohol and AED discontinuation etiologies. Anoxia and increasing age were significantly correlated with higher mortality. The mortality rates of partial and generalized SE were not significantly different. Race and sex did not affect mortality significantly. Our findings represent the first multivariate analysis of predictive indicators of mortality in SE and demonstrate that specific factors influence mortality rate in SE.
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PMID:Determinants of mortality in status epilepticus. 811 54

We report 2 patients with transient abnormalities on magnetic resonance imaging (MRI) associated with partial status epilepticus (SE). A man with a 4-month history of partial seizures had complex partial SE for 9 days, with left temporal maximum on ictal EEG. Left temporal lobe T2 signal was increased on MRI during SE, but cerebral MRI was normal 9 weeks later. A woman with "cryptogenic" temporal lobe epilepsy for 16 years had complex partial SE for 1 week, with right temporal maximum on ictal EEG. T2 Signal was increased over the entire right temporal lobe, extending into the insula, without mass effect, on MRI 1 month after SE ended. Repeat MRI 1 month later showed marked decrease in volume of increased T2 intensity, without gadolinium enhancement, but with mild mass effect over the right anterioinferomesial temporal areas. A gemistocytic astrocytoma was resected. Focal cerebral MRI abnormalities consistent with cerebral edema may be due to partial SE but also may indicate underlying glioma, even in long-standing partial epilepsy. Focal structural imaging changes consistent with neoplasm should be followed to full resolution after partial SE.
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PMID:Focal cerebral magnetic resonance changes associated with partial status epilepticus. 811 55

A 59-year-old female had been treated for epilepsy over 20 years. She had frequent convulsive seizures in spite of medication and was admitted to our hospital in status epilepticus. CT showed low density cyst with calcified wall at right suprasellar region and irregular ring enhancement in the frontal lobe which was continuous with the cyst. Angiography revealed tumor stain in the venous phase. The frontal mass was removed with evacuation of the cyst. Pathological findings were suggestive of squamous cell carcinoma arising from the epithelial component of the pre-existing dermoid cyst. The patient died six months after the operation with severe hyperglycemia, ketoacidosis and hypotension probably due to chemical meningitis and hydrocephalus.
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PMID:A squamous cell carcinoma originated from intracranial dermoid cyst. 844 93

We retrospectively reviewed the clinical course of adult patients treated for generalized status epilepticus (SE) at the San Francisco General Hospital (SFGH) from 1980 to 1989. The review was designed to determine whether the etiologies of SE at our hospital have changed over the last two decades, and to investigate the relationships between etiology, response to anticonvulsant therapy, and short-term clinical outcome. Of 154 patients reviewed, the four leading etiologies for SE were anticonvulsant drug withdrawal (39), alcohol-related (39), drug toxicity (14), and CNS infection (12). This pattern was essentially unchanged from observations made at SFGH in the 1970s. Sixty percent of all patients responded to first-line drug treatment (usually phenytoin +/- diazepam), and the remainder required an additional agent (usually phenobarbital) for control of SE. The best response to anticonvulsants occurred in patients with SE related to tumor, anticonvulsant drug withdrawal, or refractory epilepsy, and the poor responders had anoxia, drug toxicity, CNS infection, or other metabolic abnormalities. Seventy-six percent of the patients had good outcomes. Of the 22 patients who died, SE was a likely cause of death in only two (ie, 1.3% of the entire study group). Metabolic abnormalities, stroke, and anoxia were associated with particularly poor outcomes compared with other etiologies. These observations show that the etiologies of SE have remained similar over two successive decades, and that the etiology of SE may help predict both the initial response to drug therapy and the short-term outcome.
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PMID:Status epilepticus at an urban public hospital in the 1980s. 845 Sep 88

Prolonged or repeated seizures--or status epilepticus (SE)--presents diagnostic and therapeutic problems and is one of the most common neurologic emergencies. SE is defined as seizure lasting longer then 30 minutes or the repetition of at least two seizures within a short period of time, independently of the patient's state of consciousness or the type of seizure. At least 10% of epileptic patients suffer an SE during the course of their disease. Fifty percent of SEs appear in patients with no known history of epilepsy. SE is more frequent in symptomatic epilepsies, particularly those arising from trauma, tumor or infection. Most are found in epilepsies involving the frontal lobe. SE is present in nearly all epileptic syndromes, even idiopathic ones, although it is more frequent in cryptogenic and symptomatic forms. Tonic-clonic SE is the best known type and its diagnosis is simple. Partial SE, above complex partial SE, presents a diagnostic challenge. Particularly difficult is the differential diagnosis of complex partial SE and absence SE, above all the form termed late-onset de novo absence SE, which presents as confusional syndrome in the elderly. The treatment of SE, which is always a medical emergency, is based on intravenous benzodiazepines along with phenytoin, barbiturates or both. We discuss the utility of other drugs, such as lidocaine and valproic acid i.v., as well as the possibility of drugs like phosphenytoin becoming available in the near future.
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PMID:[Status epilepticus]. 905 51

Sixty-three children with new-onset temporal lobe epilepsy (TLE) underwent extensive clinical, EEG, and neuroimaging investigation as part of a prospective, community-based cohort study of the natural history of TLE in childhood. Complex partial seizures occurred in 94% of the children, and tonic-clonic seizures occurred in 14%. Developmental, behavioral, or learning problems were present in 38%. Eighteen children (29%) had a significant illness/event prior to the onset of TLE, including febrile status epilepticus in seven, meningitis in four, respiratory arrest in two, and head injury in one. Magnetic resonance imaging or computed tomography revealed structural abnormalities of the temporal lobe in 24 children (38%), including hippocampal sclerosis (HS) in 13 and tumor in eight. There was a strong association between HS and a history of significant illness/event prior to the onset of TLE (p < 0.001). Analysis of past history and neuroimaging findings led us to propose three etiologically defined subgroups of TLE; developmental TLE (10 children with long-standing, nonprogressive temporal lobe tumors and malformations), TLE with HS/significant antecedents (18 children with HS or a history of a significant illness/event), and cryptogenic TLE (34 children with normal neuroimaging findings and no significant past history). Etiologic differences between children with new-onset TLE may confer prognostic information that will be useful for counselling families and planning treatment.
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PMID:Temporal lobe epilepsy in childhood: clinical, EEG, and neuroimaging findings and syndrome classification in a cohort with new-onset seizures. 933 74

Bilateral motor seizures with retained consciousness are rare and often mistaken for pseudoseizures. In the few reported cases, the seizures were brief and the underlying lesion usually was a tumor. Here the authors describe a patient with bilateral focal motor status epilepticus with retained consciousness after a stroke. A seizure should be considered as the possible cause of continuous bilateral limb movements with retained consciousness.
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PMID:Bilateral focal motor status epilepticus with retained consciousness after stroke. 1069 Sep 97

The United Kingdom National General Practice Study of Epilepsy is a prospective, population-based study of newly diagnosed epilepsy. A cohort of 792 patients has now been followed for up to 14 years (median follow-up [25th, 75th percentiles] 11.8 years, range 10.6-11.7 years), a total of 11,400 person-years. These data are sufficient for a detailed analysis of mortality in this early phase of epilepsy. Over 70% of patients in this cohort have developed lasting remission from seizures, although the mortality rate in the long term was still twice that of the general population. The standardized mortality ratio (SMR), the number of observed deaths per number of expected deaths, was 2.1 (95% confidence interval [CI] = 1.8, 2.4). Patients with acute symptomatic epilepsy (SMR 3.0; 95% CI = 2.0, 4.3), remote symptomatic epilepsy (SMR 3.7; 95% CI = 2.9, 4.6), and epilepsy due to congenital neurological deficits (SMR 25; 95% CI = 5.1, 73.1) had significantly increased long-term mortality rates, whereas patients with idiopathic epilepsy did not (SMR 1.3; 95% CI = 0.9, 1.9). This increase in mortality rate was noted particularly in the first few years after diagnosis. Multivariate Cox regression and time-dependent co-variate analyses were utilized for the first time in a prospective study of mortality in epilepsy. The former showed that patients with generalized tonic-clonic seizures had an increased risk of mortality. The hazard ratio (HR), or risk of mortality in a particular group with a particular risk factor compared to another group without that particular risk factor, was 6.2 (95% CI = 1.4, 27.7; p = 0.049). Cerebrovascular disease (HR 2.4; 95% CI = 1.7, 3.4; p < 0.0001), central nervous system tumor (HR 12.0; 95% CI = 7.9, 18.2; p < 0.0001), alcohol (HR 2.9; 95% CI = 1.5, 5.7; p = 0.004), and congenital neurological deficits (HR 10.9; 95% CI = 3.2, 36.1; p = 0.003) as causes for epilepsy and older age at index seizure (HR 1.9; 95% CI = 1.7,2.0; p < 0.0001) were also associated with significantly increased mortality rates. These hazard ratios suggest that epilepsy due to congenital neurological deficits may carry almost the same risk of mortality as epilepsy due to central nervous system tumors and that epileptic seizures subsequent to alcohol abuse may carry almost the same risk of mortality as epilepsy due to cerebrovascular disease. The occurrence of one or more seizures before the index seizure (the seizure that led to the diagnosis of epilepsy and enrolment in the study) was associated with a significantly reduced mortality rate (HR 0.57; 95% CI = 0.42, 0.76; p = 0.00001). Time-dependent co-variate analysis was used to examine the influence of ongoing factors, such as seizure recurrence, remission, and antiepileptic drug use, on mortality rates in the cohort. Seizure recurrence (HR 1.30; 95% CI = 0.84, 2.01) and antiepileptic drug treatment (HR 0.97; 95% CI = 0.67, 1.38) did not influence mortality rate. There were only 5 epilepsy-related deaths (1 each of sudden unexpected death in epilepsy, status epilepticus, burns, drowning, and cervical fracture), suggesting that death directly due to epileptic seizures is uncommon in a population-based cohort with epilepsy.
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PMID:Mortality in epilepsy in the first 11 to 14 years after diagnosis: multivariate analysis of a long-term, prospective, population-based cohort. 1126 8

The authors report a case of an unusual progression of glioblastoma multiforme in the temporal lobe associated with the first onset of nonconvulsive simple partial status epilepticus (SPSE), a rare form of status epilepticus. The patient underwent a left temporal craniotomy and the tumor was removed. Concurrently, the hippocampus was removed as well. The pathological diagnosis of the tumor and the hippocampus were glioblastoma multiforme and hippocampal sclerosis. The patient's postoperative course was uneventful.
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PMID:Radiologically confirmed de novo glioblastoma multiforme and hippocampal sclerosis associated with the first onset of nonconvulsive simple partial status epilepticus. 1146 Sep 18

Activation of the tumor suppressor gene, p53, has been strongly implicated in selective neuronal cell death. This study investigated p53 expression in the immature and adult rat brain following status epilepticus induced by the administration of lithium-pilocarpine (LPSE). Both p53 mRNA and protein were examined in relation to neuronal degeneration using in situ hybridization and immunohistochemistry, respectively. Injured cells with eosinophilic cytoplasm with increased p53 mRNA were observed in hippocampal subfields, piriform cortex, amygdala and thalamus. p53 mRNA levels reached a peak by 8 h and returned to baseline by 24 h after the onset of LPSE. The magnitude of p53 mRNA induction was greatest in 21-day-old rats. In contrast to the cellular expression pattern of p53 mRNA, immunohistochemistry demonstrated that p53 protein was increased in all of the eosinophilic cells. Further, double-labeling studies revealed that p53 protein was elevated in neurons that were degenerating. This was supported by colocalization of activated caspase 3 in some cells with damaged DNA. These results provide additional evidence for a critical role for the p53 pathway in excitotoxic neuronal cell death due to status epilepticus.
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PMID:Differential induction of p53 in immature and adult rat brain following lithium-pilocarpine status epilepticus. 1184 86


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