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)

Seventy-eight patients with post-stroke seizures were studied retrospectively to determine the clinical, EEG and CT features of these seizures and their prognosis. There were 57 cerebral infarctions and 21 hemorrhages. Twenty-eight (36%) initial seizures occurred within one month after the stroke (0-24 hours in 19 cases) and were classified as early-onset seizures. Fifty (64%) initial seizures occurred more than 3 months after the stroke (3-12 months in 33 cases) and were classified as late-onset seizures. Compared with a population of 1938 strokes admitted during the same period, the proportion of patients with alcohol abuse, infarction in the anterior cerebral artery territory, watershed infarcts and lobar haemorrhages was significantly greater in our series. The proportion did not vary with the nature of the stroke (infarction or hemorrhage), except for early onset seizures in which the proportion of hemorrhages was significantly greater. Nor did it vary with the cause of hemispheric infarctions (cardioembolism or atherothrombosis or others). Ninety-five percent of the lesions affected the cerebral cortex or the subcortical white matter or both. Of all 78 initial seizures, 64% were partial motor (simple or secondarily generalized); 32% were primarily generalized, and 4% were partial not motor; status epilepticus was seen in 14% of the cases. An initial EEG, performed in 76 patients was normal in 7. Among the remaining 69 patients EEG showed focal or diffuse slowing down in 63% and epileptic features in 37% (including 10 cases of PLEDs). Early post-seizure EEG and repeated recordings significantly increased the specificity of EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Epileptic crisis during and after cerebrovascular diseases. A clinical analysis of 78 cases]. 130 71

A pilot case-control quantitative study of the hippocampus in patients with severe status epilepticus was performed to identify specific patterns of pyramidal cell loss. Pyramidal cell densities from five patients who died following status epilepticus were compared with five normal controls and five controls matched for age, hypoxia/ischemia, previous epilepsy, and alcohol abuse. Neuronal densities were greatest in the normal control group and least in patients with status epilepticus. Significant reductions were identified in Sommer's sector (prosubiculum and CA1) as well as in CA3 when compared to normal controls.
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PMID:Hippocampal pyramidal cell loss in human status epilepticus. 173 57

The authors studied 286 patients with epilepsy with disease onset past the age of 20 years (176 males, 110 females) from the urban and rural populations. In 57% of cases the aetiology of epilepsy was undetermined. Among the known aetiological factors head trauma accounted for 15.5% of cases, inflammatory processes in the central nervous system for 4.5%, alcoholism for 7%, vascular lesions for 6%, tumours for 5.2%, degenerative and atrophic changes for 1.5%. Over 40% of patients had had attacks for up to 15 years and over 18% for over 20 years. In 80% of cases grand mal seizures occurred, and in 33% of these cases more than 12 attacks occurred annually. Six cases of status epilepticus were observed with 2 deaths. The attacks were precipitated by menstruation, alcohol abuse, infection, stressed, television watching. Among the signs accompanying or following the seizures tongue biting and urination prevailed. Neurological signs were demonstrated in 21% of cases, encephalopathy in 65%, other psychic disturbances in 9.5%. Systematic treatment was received by 75% of the patients (over 80% in urban population), and therapy with multiple drugs was most frequent. Drug-resistant epilepsy was found in 34% of cases. The patients from the rural population had a lower educational level and had more children. About 70% of the patients were in employment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Analysis of clinico-social features of epilepsy]. 404 96

In 1979-80, 82 cases of grand mal status epilepticus (71 patients, 39 male and 32 female) were admitted to the Casualty Department of Meilahti University Hospital in Helsinki, Finland. The cause of the underlying epilepsy was symptomatic in 43 cases (52.4%) and idiopathic in 19 cases (23.2%). In 6 cases (7.3%), there was a history of alcohol withdrawal seizures, and in 14 cases (17.1%) there was no earlier history of convulsions. Status epilepticus was associated with an acute or progressive cerebral disorder in 14 episodes. These comprised 6 bouts of status with brain tumour, 4 with acute stroke and 4 with brain injury. Alcohol abuse preceded the status in 29 episodes (35.4%), 23 of which occurred in men (53.5% of the male cases). Excessive use of alcohol was the only obvious precipitating factor for status in 16 cases, and in 6 cases the status presented as a prolonged alcohol withdrawal seizure. A change or irregularity of anticonvulsive drug therapy could be documented in 14 cases and an acute infection outside the central nervous system in 7 cases. Intravenous diazepam, used as the only therapy for status epilepticus, was effective in 58 of 78 episodes. In 7 cases of prolonged status, a thiopental sodium anaesthesia proved effective. The total mortality was 4.2%, including 2 deaths from concomitant extracerebral disorders and one late death from brain metastasis.
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PMID:Status epilepticus and alcohol abuse: an analysis of 82 status epilepticus admissions. 651 94

We reviewed the case records of 249 adult patients with generalized convulsive status epilepticus (SE) examined in San Francisco General Hospital between 1977 and 1989 and identified 27 patients (10.8%) in whom alcohol abuse was the only identifiable precipitating cause of SE. In 12 patients (44% of the study group), SE was the first presentation of alcohol-related seizures. Seizures with focal features were observed in 11 patients (40.1%), but there was little correlation with localized computed tomography (CT) or EEG abnormalities. SE was controlled with phenytoin (PHT), with or without a benzodiazepine (BZD), in 18 patients (66.7%). Twenty-two patients (81.5%) were discharged with no new neurologic deficits, but time to recovery of baseline mental status was prolonged (> 12 h) in 24 patients. With regard to alcohol abuse history, study patients did not differ from a comparison group with isolated alcohol withdrawal seizures. The results indicate that alcohol abuse is a common cause of SE and that SE may be the first presentation of alcohol-related seizures. Furthermore, the outcome of patients with alcohol-related SE compares favorably with that of patients with SE due to other causes, but recovery of these patients may be complicated by a prolonged postictal state.
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PMID:Status epilepticus related to alcohol abuse. 824 53

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 relationship between alcohol and seizures is complex and multifaceted. The prevalence of epilepsy in alcohol-dependent patients of western industrialised countries may be at least triple that in the general population, whereas the prevalence of alcoholism is only slightly higher in patients with epilepsy than in the general population. The seizure threshold is raised by alcohol drinking and declines on cessation of drinking. As a result, during withdrawal from alcohol, usually 6-48 hours after the cessation of drinking, seizures may occur. Alcohol acts on the brain through several mechanisms that influence seizure threshold. These include effects on calcium and chloride flux through the ion-gated glutamate NMDA and GABA receptors. During prolonged intoxication, the CNS adapts to the effects of alcohol, resulting in tolerance; however, these adaptive effects seem to be transient, disappearing after alcohol intake is stopped. Although the relationship of seizures to alcohol use is likely to be dose dependent and causal, the available clinical data do not suggest that alcohol use results in seizure genesis. However, a genetic predisposition to alcohol withdrawal seizures is possible. Other seizures in alcohol-dependent individuals may be due to concurrent metabolic, toxic, infectious, traumatic, neoplastic and cerebrovascular diseases and are frequently partial-onset seizures. Alcohol abuse is a major precipitant of status epilepticus (9-25% of cases), which may even be the first-ever seizure type. Prompt treatment of alcohol withdrawal seizures is recommended to prevent status epilepticus. During the detoxification process, primary and secondary preventative measures can be taken. A meta-analysis of controlled trials for the primary prevention of alcohol withdrawal seizures demonstrated a highly significant risk reduction for seizures with benzodiazepines and antiepileptic drugs and an increased risk with antipsychotics. A meta-analysis of randomised, placebo-controlled trials for the secondary prevention of seizures after alcohol withdrawal showed lorazepam to be effective, whereas phenytoin was ineffective. Because withdrawal seizures do not recur if the patient remains abstinent, long-term administration of antiepileptic drugs is unnecessary in abstinent patients. The first seizure not related to alcohol withdrawal should not result in permanent drug treatment in an alcohol-dependent patient, because of poor compliance and the high likelihood of remission. The treatment of alcohol dependence is more important and should be prioritised before the prevention of further seizures.
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PMID:Seizures in alcohol-dependent patients: epidemiology, pathophysiology and management. 1459 42

We conducted a systematic review of all studies of status epilepticus (SE) with more than 30 patients published between January 1, 1990, and December 31, 2008, to determine the frequencies of the common underlying causes and the extent to which the underlying causes affect the prognosis of an episode of SE. The frequencies of underlying causes vary among studies and show marked geographic differences, but in most studies, the most common underlying causes were cerebrovascular disease and low antiepileptic drug levels. A relatively good prognosis of SE is found when the underlying cause is associated with low antiepileptic drug levels or alcohol abuse, and a relatively poor outcome occurs when the underlying cause is cerebrovascular disease, particularly in the case of SE due to acute cerebral anoxia, but in most conditions, the reported prognosis is variable. Also, when SE occurs in the context of an acute cerebral insult, such as cerebral infection or cerebrovascular disease, the prognosis of the acute cerebral event is worsened.
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PMID:Frequency and prognosis of convulsive status epilepticus of different causes: a systematic review. 2069 43

A 60-year-old man with a history of alcohol abuse was admitted to the intensive care unit (ICU) for status epilepticus. At first, laboratory and imagery findings were almost normal, and the symptoms were attributed to severe alcohol withdrawal due to a history of gastroenteritis reported by his family. But, during the following days, haemolytic anaemia, thrombocytopenia, acute renal failure, and ischaemic and haemorrhagic lesions seen on a cerebral CT scan led to the diagnosis of haemolytic-uraemic syndrome (HUS). Despite these severe complications, the patient made a good recovery following ICU and plasma exchange with fresh frozen plasma (FFP), but cognitive deficit still existed after 1 month. It is important to know that neurological manifestations can precede typical biological and radiological signs in HUS, and to not be misled in the diagnosis process, especially when a more common differential diagnosis is possible.
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PMID:A diagnosis of haemolytic-uraemic syndrome blurred by alcohol abuse. 2554 Feb 9

Seizures are defined as a transient occurrence of signs and symptoms due to the abnormal, excessive, or synchronous neuronal activity in the brain characterized by abrupt and involuntary skeletal muscle activity. An early diagnosis, treatment, and specific medical support must be performed to prevent Status Epilepticus (SE). Seizure onset, especially in the child population, is related to specific risk factors like positive family history, fever, infections, neurological comorbidity, premature birth, mother's alcohol abuse, and smoking in pregnancy. Early death risk in children without neurological comorbidity is similar to the general population. Diagnosis is generally based on the identification of continuous or recurrent seizures but Electroencephalogram (EEG) evaluation could be useful if SE condition is suspected. The main goal of therapy is to counteract the pathological mechanism which occurs in SE before neural cells are irreversibly damaged. According to the latest International Guidelines and Recommendations of seizure related diseases, a schematic and multi-stage pharmacological and diagnostic approach is proposed especially in the management of SE and its related causes in children. First measures should focus on early and appropriate drugs administration at adequate dosage, airway management, monitoring vital signs, Pediatric Intensive Care Unit (PICU) admission, and management of parent anxiety.
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PMID:Epilepsy in Children: From Diagnosis to Treatment with Focus on Emergency. 3060 70


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