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)

A 3-year-old male developed hemiplegia and aphasia after convulsive status epilepticus. Diffusion-weighted magnetic resonance images demonstrated cytotoxic edema in the white matter 6 days after the seizure episode and subsequently in the gray matter after an additional 7 days. Diffusion-weighted magnetic resonance images demonstrated a subacute evolution of the pathologic process after the status epilepticus.
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PMID:Changes in diffusion-weighted MRI after status epilepticus. 1078 54

Encephalopathy with electrical status epilepticus during sleep or ESES is an age-dependent and self-limited syndrome whose distinctive features include a characteristic age of onset (with a peak around 4-5 years), heterogeneous seizures types (mostly partial motor or unilateral seizures during sleep and absences or falls while awake), a typical EEG pattern (with continuous and diffuse paroxysms occupying at least 85% of slow wave sleep) and a variable neuropsychological regression consisting of IQ decrease, reduction of language (as in acquired aphasia or Landau-Kleffner syndrome), disturbance of behaviour (psychotic states) and motor impairment (in the form of ataxia, dyspraxia, dystonia or unilateral deficit). Despite the long-term favourable outcome of epilepsy and status epilepticus during sleep (SES), the prognosis is guarded because of the persistence of severe neuropsychological and/or motor deficits in approximately half of the patients. No specific treatment has been advocated for this syndrome, but valproate sodium, benzodiazepines and ACTH have been shown to control the seizures and the SES pattern in many cases, although often only temporarily. Subpial transection is proposed in some instances as in non-regressive acquired aphasia. Recent data support the concept that ESES syndrome may include a large subset of developmental or acquired regressive conditions of infancy.
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PMID:Encephalopathy with electrical status epilepticus during slow sleep or ESES syndrome including the acquired aphasia. 1099 61

Alzheimer's disease is a known risk factor for seizures, and age older than 60 years is a recognized risk factor for poor outcome from convulsive and nonconvulsive status epilepticus. The authors suspect that there may be a causal relationship between dementia pathology and the development and maintenance of refractory seizures. They report two selected patients with complex partial status epilepticus whose presentation and clinical course provide partial support for this hypothesis. Their methods include case reports with clinical, EEG, imaging, and pathologic correlations. The patients were 70 and 85 years of age. Both had central and peripheral brain atrophy on imaging studies (with some regions that were affected more than others), left temporal seizure foci corresponding to areas of greatest cortical atrophy, and early presentation with inhibitory epileptic symptoms (aphasia), with evolution to complex partial status epilepticus. Pathologic confirmation of Alzheimer's disease was obtained in one patient who had not been diagnosed previously. It involved maximally the cortex underlying the seizure focus. A diagnosis of probable Alzheimer's disease was established in the other patient. Alzheimer's disease may be causal in some cases of complex partial status epilepticus. Additional observations in support of this hypothesis are needed.
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PMID:Alzheimer's disease underlies some cases of complex partial status epilepticus. 1108 55

Brain CT or MRI occasionally shows transient or permanent changes in the brain after status epilepticus (SE). The mechanism for these changes has not been well elucidated. We performed repeated imaging studies on a patient with febrile SE characterized by right hemiconvulsion. CT showed transient mild edema on both hemispheres immediately after the cessation of SE. The edema improved the next day. But aphasia and right hemiparesis were observed. On day 17, CT revealed edema on left hemisphere and MRI showed a high signal intensity in cortex and subcortical white matter of the left hemisphere on T2-weighted images. Although right hemiparesis and aphasia were improved, severe atrophy of the left hemisphere was noted on CT and MRI. The results suggest that brain edema observed in several days after SE but not edema observed immediately after the cessation of SE is more pathological for the permanent brain damage. Possible mechanisms of the initial brain edema and the second edema preceded severe atrophy in left hemisphere were discussed.
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PMID:Sequential changes of brain CT and MRI after febrile status epilepticus in a 6-year-old girl. 1193 19

We report a 12-year-old child with episodes of migraine-like headaches with visual and motor auras a year after the surgical resection and radiation therapy for medulloblastoma The patient presented with an episode of headache, prolonged aphasia, right hemiparesis, status epilepticus, and salt wasting. There was no evidence of a structural lesion. The neurologic deficits resolved over a period of 6 weeks. Because of the progressive deterioration in neurologic deficits, the patient underwent an extensive battery of laboratory tests and multiple neuroimages, all of which were normal. The unusually prolonged neurologic deficit in this patient without demonstrable structural lesions and his eventual complete recovery were most likely caused by ischemia in the left hemisphere secondary to vasospasm. This presentation mimics migraine headache. Evidence suggesting that this represents a long-term complication of treatment of children with central nervous system neoplasia is presented.
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PMID:Pseudomigraine with prolonged aphasia in a child with cranial irradiation for medulloblastoma. 1195 86

Postictal aphasia has been described in left temporal lobe seizures. It may be of fluent, non-fluent or global type. We present here a patient who displayed signs of mixed transcortical aphasia (MTCA). The patient was a 67 year old man who underwent excision of a left frontal parasagittal meningioma in 1987. Since then he has been treated with phenytoin for generalized tonic-clonic seizures (GTCS). He was admitted in status epilepticus. On awakening, the patient was non-fluent with palilalia and echolalia. His repetition was relatively preserved but all the other language functions were impaired. This picture faded away within a few hours. Brain CT, performed during this postictal state, was normal except for signs related to frontal craniotomy. SPECT, which was performed after language functions returned to normal, displayed left frontal, cingular and insular hypoperfusion. The postictal language dysfunction of the patient corresponded to MTCA. Although our case has frontal, he had no other structural lesion that could explain either diffuse ischemia of the left hemisphere or watershed areas secondary to the generalized seizures. The uniqueness of this case is the combination of postictal MTCA with good prognosis.
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PMID:Postictal mixed transcortical aphasia. 1202 78

We report a 62-year-old man with non-convulsive status epilepticus (NCSE) presenting as a progressive aphasia that developed insidiously over 5 weeks. On video-EEG monitoring, aggravation of the aphasia coincided with occurrence of seizure activities arising from the left fronto-temporal area. Brain MRI was noncontributory but a fluorodeoxyglucose-PET scan revealed a hypometabolism in the left anterior temporal area. Following anticonvulsant treatment, aphasia recovered gradually over several weeks despite prompt resolution of epileptic discharges on EEG. Our patient's findings, gradual onset of isolated aphasia with gradual resolution after initiation of treatment, may differ from previously reported cases with aphasic status epilepticus because their aphasia showed abrupt onset and rapid resolution with anticonvulsant medication.
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PMID:Nonconvulsive status epilepticus presenting as a subacute progressive aphasia. 1223 73

The study aimed at investigating epileptic attack's semiology and other electroclinical characteristics in Landau-Kleffner syndrome as well as therapeutic efficacy. Six patients with Landau--Kleffner syndrome, 5 boys, 1 girl, aged 6-10 years, mean age 7.5 years, have been analyzed. Epileptic attacks were observed only in 3 patients with debut at the age of 2.5-6 years (mean 4 years). In 50% of the cases, the attacks were not detected. The types of epileptic attacks were specified as follows: atypical absences--3 patients; pharyngo-oral--2; secondary generalized--2; atonic falls--1; hemiconvulsive--1. In routine EEG study, regional epileptiform activity was observed in all the patients, being localized in central temporal (3 cases), posterior temporal (1) and fronto-temporal (1) leads. In 3 cases (50%), diffusive epiactivity was also detected. During sleep, emergence of prolonged diffuse epiactivity was revealed for all the patients, with appearance of electrical status epilepticus during slow sleep in 50%. Valproates in dosage 30-60 mg/kg daily were highly effective for stopping epileptic seizures. Significant improvement of speech functions was observed only if antiepileptics sulthiame (ospolot) or clobasam (frizium) were used in addition to basic therapy. Clobasam in dosage 0.5-0.75 mg/kg daily was the most efficient in blockade of EEG diffuse epileptiform activity, reduction of aphasia symptoms and behavior improvement.
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PMID:[Electroclinical characteristics of Landau-Kleffner syndrome]. 1457 70

Non convulsive status epilepticus is a heterogeneous condition consisting of very different electroclinical syndromes. It is difficult to make the diagnosis and identify common factors among patients. We report two cases with an unusual presentation. A 31 years old woman having discoid lupus presented with a prolonged exogenous psychosis that lasted two and half months, associated to echolalia. After the episode the patient remained with a severe frontal syndrome that could be the consequence of a non convulsive status epilepticus. A 60 years old woman with an epilepsy diagnosed at the age of 30, presented with recurrent episodes of aphasia. During one of these crises, the electroencephalogram showed continuous epileptiform activity.
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PMID:[Non convulsive status epilepticus: an heterogeneous disease with a difficult diagnosis. Report of 2 cases with unusual presentation]. 1463 93

Diffusion-weighted imaging (DWI) has demonstrated a focal area of cytotoxic oedema during partial status epilepticus (PSE). However, vasogenic oedema related to the breakdown of the blood-brain-barrier (BBB) and ictal hyperperfusion could be the predominant DWI findings in the epileptogenic area during PSE. We report a case of PSE with ictal aphasia, right hemiparesis, and repetitive focal motor seizure of the right side. T2-weighted image (T2WI) and apparent diffusion coefficient (ADC) maps obtained during PSE showed an increased signal in the left temporo-parietal area, indicative of vasogenic oedema. EEG documented the ictal activities and single photon emission tomography (SPECT) showed asymmetrically increased perfusion in the corresponding area. Follow-up T2WI, DWI, and ADC maps obtained 3 months later showed the disappearance of the previous abnormalities. However, T2WI showed cortical atrophy and newly developed white matter changes in the corresponding area. This case shows that DWI findings may be variable during PSE, dependent on the predominance of cytotoxic and vasogenic oedema.
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PMID:Diffusion changes suggesting predominant vasogenic oedema during partial status epilepticus. 1515 2


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