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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Status epilepticus is a condition in which multiple epileptic seizures occur without complete recovery from the physiological effects of one seizure before another seizure occurs. There are as many types of SE as there are kinds of epileptic seizures. Generalized convulsive status epilepticus initially presents with repeated generalized convulsions without full recovery of consciousness between seizures. If untreated or undertreated, the convulsive activity becomes progressively subtle and is accompanied by a predictable series of progressive EEG changes. Non-convulsive SE refers to complex partial SE or absence SE, both of which exhibit an epileptic twilight state of altered contact with the environment. In simple partial SE there is no impairment of consciousness, and the behavioural changes reflect focal ictal discharges confined to one area of the cortex. There are between 65,000 and 150,000 cases of the SE in the US each year. Both acute and remote cerebral insults can cause SE, as can severe systemic disease that causes SE secondary to a toxic-metabolic encephalopathy. Mortality is high, but is largely a reflection of underlying aetiology when SE is treated appropriately and aggressively. Treatment is focused on terminating ongoing seizure activity as quickly as possible, both because the longer SE persists the more likely permanent neuronal damage will ensure and also because of strong evidence that the longer SE persists the more refractory to treatment it will be. Currently the most commonly accepted treatment protocol involves rapid initiation of therapy with intravenous lorazepam (0.1 mg/kg), followed, if necessary, by 20 mg/kg of phenytoin, followed, if necessary, by 20 mg/kg of phenobarbital. However, some neurologists still use intravenous diazepam (because of its more rapid antistatus effect) followed by phenytoin. New experimental data in the rat suggest that phenytoin followed by diazepam may be more effective, but this order of administration still has to tested in properly designed clinical trials.
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PMID:Status epilepticus. 906 83

The inclusion criteria for afebrile cluster seizures in infancy are defined as follows: (1) frequency of afebrile seizures at least 2 episodes within 72 hours; (2) seizure onset between 2 months and 3 years of age; (3) excluding febrile convulsion, central nervous system infections, status epilepticus, well-known epileptic syndromes in infancy (e.g. early myoclonic encephalopathy, early infantile epileptic encephalopathy, benign myoclonic epilepsy, infantile spasms. Lennox-Gastaut syndrome), electrolyte imbalance, watery diarrhea, head injury and intoxication. From 1986 to 1996, retrospectively and prospectively 22 patients were collected who fulfilled the above criteria. Based on whether or not a strong family history was present and a history of mild diarrhea was associated with seizure onset, they were divided into three groups: Group I, benign infantile familial convulsions (4 patients); Group II, cluster seizures with mild diarrhea in infancy (5 patients); Group III, cluster seizures without diarrhea in infancy (13 patients). Before seizure onset and during follow-up, all of the patients had normal development. The seizure pattern in all was generalized, most tonic type with duration of seizure less than five minutes in the majority. Recurrence rate was 100% in Group I and no recurrence in Group II. In 16 patients who were seizure-free over 12 months, the duration of persistence varied from 1 day to 8 months, and was shortest in Group II (range, 1 to 3 days). It was concluded that the vast majority of afebrile cluster seizures in infancy are benign in nature. Whether anticonvulsant therapy is justified must be individualized.
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PMID:Clinical analysis of 22 infants with afebrile cluster seizures. 923 May 37

Midazolam infusion was tried as the treatment for 48 episodes of refractory status epilepticus or a cluster of seizures in 16 children. The mean age of patients was 3.5 years (range, 1 month to 18 years). Nine children had epilepsy, one purulent meningitis, one encephalitis, one acute cerebral infarction, and the remaining four had acute phase of hypoxic ischemic encephalopathy. The type of the seizure was a generalized tonic clonic seizure (including a partial seizure secondarily generalized) in 41 episodes, a tonic seizure in 3, an atypical absence in 1, and a complex partial seizure in 3, respectively. All patients received intravenous midazolam at 0.15 mg/kg as bolus, followed by a continuous infusion at 0.1-0.15 mg/kg/hr initially. The dose was increased gradually up to 0.3 mg/kg/hr until the complete control of seizures was achieved. Fourty-one of the 48 episodes of seizures were controlled within 30 minutes after the initiation of midazolam therapy. The mean infusion rate of midazolam required was 0.22 mg/kg/hr. The mean duration of the treatment was 4.1 days. None of the patients had serious changes in the blood pressure or respiratory status attributable to the use of midazolam. In conclusion, midazolam infusion is an effective and safe therapeutic approach for the management of childhood status epilepticus.
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PMID:[Efficacy of continuous intravenous infusion of midazolam in the treatment of status epilepticus in children]. 969 22

We observed a young patient with slight mental retardation, suffering from drug-resistant tonic-clonic seizures, who presented a status epilepticus (SE), in two separate periods when valproic acid (VPA) was added to the phenobarbital (PB) already being used in the patient's therapy. The VPA-induced SE was characterized by normal plasma levels of antiepileptic drugs (AEDs), normal ammonemia and normal liver function. The case we studied represents the first report on a VPA-induced SE. Furthermore the case confirms that VPA, as well as causing encephalopathy secondary to hyperammonemia, may also provoke a primary involvement of the central nervous system (CNS), specially when used in young epileptic, mentally retarded subjects. In an attempt to explain the paradoxical effect of VPA we hypothesise that the SE could be due to an increase in excitatory activity producing a consequent epileptogenic effect in those subjects with a predisposition for toxic reaction to VPA therapy due to congenital anomalies of neural networks.
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PMID:Valproate-induced epileptic tonic status. 970 Aug 38

Seizures are commonly encountered in patients who do not have epilepsy. Factors that may provoke such seizures include organ failure, electrolyte imbalance, medication and medication withdrawal, and hypersensitive encephalopathy. There is usually one underlying cause, which may be reversible in some patients. A full assessment should be done to rule out primary neurological disease. Treatment of seizures in medically ill patients is aimed at correction of the underlying cause with appropriate short-term anticonvulsant medication. Phenytoin is ineffective in the management of seizures secondary to alcohol withdrawal, and in those due to theophylline or isoniazid toxicity. Control of blood pressure is important in patients with renal failure and seizures. Non-convulsive status epilepticus should be considered in any patient with confusion or coma of unclear cause, and electroencephalography should be done at the earliest opportunity. Most ill patients with secondary seizures do not have epilepsy, and this should be explained to patients and their families. Only those patients with recurrent seizures and uncorrectable predisposing factors need long-term treatment with anticonvulsant medication.
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PMID:Medical causes of seizures. 980 2

Magnetic resonance imaging (MRI), single photon emission computed tomography (SPECT) and magnetic resonance spectroscopy (MRS) were successively recorded in a 3-year-old girl with the acute hemiplegia syndrome. She was admitted to our hospital with complaints of fever, loss of consciousness and right side dominant clonic convulsions evolving into status epilepticus, and then recovered with sequelae of aphasia and right hemiparesis. Electroencephalography showed a generalized slow rhythm at the onset, and very low activities on the left hemisphere in the follow-up records. Brain CT and MRI revealed edema of the left hemisphere initially, followed by left side dominant brain atrophy. No cerebral vascular lesion was detected by magnetic resonance angiography. N-Isopropyl-[123I]-iodoamphetamine SPECT showed marked hypoperfusion of the left hemisphere accompanied by crossed cerebellar diaschisis. MRS at the initial stage detected decreased N-acetyl-aspartic acid and increased lactic acid signals in the bilateral hemisphere, which subsequently normalized only on the right side. These findings suggested brain damage and neural cell death in the left cerebral hemisphere, caused by acute encephalopathy. SPECT and MRS are useful new techniques to study the pathophysiology of the acute hemiplegia syndrome.
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PMID:[MRI, SPECT and MRS findings in a case of acute hemiplegia syndrome with a marked hemispheric brain edema]. 978 Jul 43

We asked whether acute symptomatic status epilepticus (SE) increases the risk for subsequent unprovoked seizure compared with less prolonged acute symptomatic seizure. We also explored whether the risk of unprovoked seizure differs by cause. We ascertained all first episodes of acute symptomatic seizure among residents of Rochester, Minnesota, through the Rochester Project's records-linkage system. Information was collected on seizure duration, age, sex, cause, and subsequent unprovoked seizure. At 10 years of follow-up, the risk of unprovoked seizure was 41% for those with acute symptomatic seizure with SE and 13% for those without SE. Controlling for age, sex, and cause, SE increased the risk for subsequent unprovoked seizure 3.3-fold (95% confidence interval, 1.8-6.1) compared with brief acute symptomatic seizures. Among patients with SE, the risk of unprovoked seizure was increased 18.8-fold for patients with anoxic encephalopathy, 7.1-fold for patients with a structural cause, 3.6-fold for patients with a metabolic cause. The increased risk for unprovoked seizure after SE compared with shorter seizures may be due to SE being a marker for severity of injury, damage caused by SE, or a biological substrate associated with the tendency to experience SE.
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PMID:Risk of unprovoked seizure after acute symptomatic seizure: effect of status epilepticus. 985 35

Trichothiodystrophy was diagnosed in a 3-year-old male presenting with speech delay, brittle hair, chronic neutropenia, and a history of febrile convulsions. Cranial magnetic resonance imaging revealed a focal subcortical and periventricular gray matter heterotopia. An acute encephalopathy with status epilepticus and coma occurred when he was 4 years of age during an upper respiratory tract infection. Magnetic resonance imaging revealed multifocal T2-weighted hypersignal lesions involving mainly the thalami, hippocampi, midbrain, and pons. Analysis of cerebrospinal fluid revealed hyperproteinorachia without pleocytosis. Results of an extensive metabolic evaluation of this acute brain injury, resembling the syndrome of acute necrotizing encephalopathy of childhood described in Japan, were negative. Focal neuronal migration disorder and acute encephalopathy with symmetric thalamic involvement are newly described neurologic manifestations of syndromes with trichothiodystrophy, which suggests that these conditions may have a common genetic background.
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PMID:Gray matter heterotopia and acute necrotizing encephalopathy in trichothiodystrophy. 988 Jan 48

Status epilepticus from cat-scratch encephalopathy is often recalcitrant to usual therapies, causing treatment to focus on critical care management of the patient that may require aggressive interventions, such as continuous pentobarbital administration. We describe two children whose initial clinical presentation of cat-scratch disease was status epilepticus with normal cerebrospinal fluid studies. A history of cat exposure (specifically, kitten and/or fleas), regional lymphadenopathy, and a papule or inoculation site should be sought, but are not essential for diagnosis. The presumptive diagnosis of cat-scratch disease can be made by serology alone even in the absence of classic diagnostic criteria. Our two cases and other reports in the literature show a favorable prognosis in most cases, despite the occurrence of status epilepticus. The diagnosis of cat-scratch disease should be strongly considered in all children with unexplained status epilepticus or encephalopathy and serologic testing for Bartonella henselae should be done.
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PMID:Cat-scratch disease causing status epilepticus in children. 993 33

Selective amygdalo-subicular degeneration was observed in a 25-year-old woman with encephalopathy of unknown etiology. Following flu-like symptoms, the patient presented with confusion and generalized seizures. Subsequently, she developed persistent stupor with absence of the brainstem reflexes, refractory status epilepticus accompanied by hyperthermia, and exhibited choreoathetoid movements. Despite therapies her condition showed no improvement, and she died four months after the onset of disease. Postmortem examinations revealed no evidence suggestive of viral encephalitis, and instead distinctive bilateral lesions were seen in the subiculum (the subiculum proper and the prosubiculum) and the basolateral nuclear group of the amygdala. The hippocampus proper from CA1 to dentate fascia was unremarkable. The selective amygdalo-subicular degeneration, for which pathogenesis remained unknown, was inconsistent with her serious clinical condition. To our knowledge, similar pathology has not been described so far.
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PMID:Amygdalo-subicular degeneration in a young adult with status epilepticus and choreoathetoid movements of acute onset. 998 39


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