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)

We describe an adolescent epileptic patient who presented in nonconvulsive status epilepticus that appeared to be related to treatment with carbamazepine. The absence status, which was resistant to multiple anticonvulsants, produced increased intracranial pressure and transient abnormalities observed on MRI.
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PMID:Prolonged absence status epilepticus associated with carbamazepine therapy, increased intracranial pressure, and transient MRI abnormalities. 143 36

We report two patients who developed focal abnormalities on MRI after partial status epilepticus. Maximum radiological modification occurred in the area of maximal epileptic discharge. Subsequent MRI failed to demonstrate persistent abnormalities. These transient abnormalities on MRI could be an expression of cerebral edema caused by focal epileptic status.
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PMID:Transient abnormalities on magnetic resonance imaging after partial status epilepticus. 162 86

The MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) can be difficult to identify. We report MRI abnormalities that we believe are specific to this disorder in three patients with complete or partial MELAS syndrome. The patients all showed an unusual pattern on T2-weighted MRI with multifocal areas of hyperintense signal confined to the cortex of the cerebrum, cerebellum, and adjacent white matter. Some images suggested selective cortical involvement of deeper layers only. Deep white matter was relatively spared, distinguishing this from usual cerebrovascular disease or the edema after status epilepticus. Specificity of these findings is further suggested by a good correlation of these findings with the previously described unique postmortem brain pathology of MELAS.
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PMID:Magnetic resonance imaging shows specific abnormalities in the MELAS syndrome. 206 32

We present the concept of an 'epileptic syndrome' which is important for prognostic statements and the application of appropriate therapeutic measures. We then discuss the epileptic seizure and the assessment of suspected seizure, indications for admission to a hospital, diagnostic measures (EEG, CT scan, laboratory tests, lumbal puncture, MRI scan, PET scan, angiography), therapy and procedures for imminent status epilepticus. Finally, we try to answer the question whether anticonvulsant medication should be instituted after a first epileptic seizure.
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PMID:[Diagnostic and therapeutic aspects of the initial epileptic seizure]. 223 63

A 35-year-old female patient suffering from epilepsy was examined during status epilepticus with simple partial and complex partial seizures by means of EEG, CT, MRI and ictal SPECT. All these examinations showed focal abnormalities with identical location due to oedema and hypervascularisation; these were, however, absent during examinations carried out before and after status epilepticus.
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PMID:CT, MRI and SPECT neuroimaging in status epilepticus with simple partial and complex partial seizures: case report. 278 9

Status epilepticus is usually a straightforward diagnosis when a patient has two or more seizures without regaining consciousness. However, when status is non-convulsive and, in particular, has a temporal lobe flavour the clinical presentation may be misleading. Presentation with automatic or psychic behaviour is well recorded. We report a patient with nonconvulsive status who presented with progressive dysphasia with widespread CT and MRI changes. The dysphasia and imaging changes led to a diagnosis of a probable neoplastic brain process but reversed with anticonvulsant treatment.
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PMID:Status epilepticus presenting as progressive dysphasia. 747 49

Cerebral cortical dysgenesis (CD) is a heterogeneous disorder of cortical development and organization commonly associated with epilepsy, with a variety of subtypes. We reviewed the clinical, EEG and neuroimaging features in 100 adult patients with CD. There were 39 men and 61 women with a median age of 27 years (range 15-63 years). All patients were referred because of medically refractory epilepsy. Median age at seizure onset was 10 years (range 3 weeks to 39 years); in 30 patients, onset was in adulthood. The epilepsy was classified as generalized in 16 patients and localization-related in 84. Of the latter, the epileptic syndromes in decreasing frequency were frontal (32%), temporal (31%), parietal (14%) and occipital (7%). Only 15% of patients had a history of status epilepticus. Prenatal/perinatal problems were reported in 32 patients but these were severe in only four: exposure to drugs (three) and infection (one) during the first trimester. Delayed developmental milestones were seen in 10%, mental retardation in 9%, additional congenital abnormalities in 4% and neurological deficits in 14% of patients. Diagnosis of CD was based on neuroimaging in 70, pathology in four and both methods in the remaining 26. The following subcategories were identified: agyria/diffuse macrogyria (four patients), focal macrogyria (16), focal polymicrogyria (one), focal macrogyria/polymicrogyria associated with a cleft (11), minor gyral abnormalities (seven), subependymal grey matter heterotopia (20), bilateral subcortical laminar grey matter heterotopia (eight), tuberous sclerosis (five), focal cortical dysplasia/microdysgenesis (seven) and dysembryoplastic neuroepithelial tumours (DNT) (21). Sixty-eight percent of patients had normal CT and 19 out of 36 patients had normal previous conventional MRI. MRI-based hippocampal volume measurements in 47 patients revealed ratios (smaller: larger hippocampus) of < 0.90 in 16, 0.90-0.94 in 14 and > or = 0.95 in 17 patients. EEGs were normal in only five patients. Alpha rhythm was preserved in 78 patients, including one patient with bilateral posterior macrogyria. Localized polymorphic slow activity was present in 43 patients. Five of 68 patients with focal/unilateral CD had only bilateral independent/synchronous spiking and 14 out of 32 with diffuse/bilateral CD only focal/unilateral spiking. In 60 patients with nondiffuse CD or with abnormal gyration or DNT, the epileptiform abnormalities were less extensive than coextensive with the lesion in 28, more extensive than and overlapped the lesion in 18 and remote from the lesion in five; nine patients did not have epileptiform abnormalities. There was poor correlation between the epileptic syndromes and EEG abnormalities and the location/extent of CD as defined by MRI and pathology.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Abnormalities of gyration, heterotopias, tuberous sclerosis, focal cortical dysplasia, microdysgenesis, dysembryoplastic neuroepithelial tumour and dysgenesis of the archicortex in epilepsy. Clinical, EEG and neuroimaging features in 100 adult patients. 760 83

We present a patient with aphasia of several days' duration that was secondary to spontaneous partial status epilepticus arising from the left basal temporal region. Evidence from MRI, EEG, and PET confirmed the origin of the seizures in the basal temporal area. Both the seizure discharges and the aphasia resolved after antiepileptic therapy. This case, to our knowledge, is the first documented example of epileptic aphasia secondary to spontaneous partial status epilepticus originating from the basal temporal area.
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PMID:Aphasia secondary to partial status epilepticus of the basal temporal language area. 764 64

We report on a 10-year-old girl with systemic lupus erythematosus who presented in status epilepticus as the only manifestation of central nervous system involvement. MRI of the brain showed diffuse gray and white matter lesions which almost completely resolved after treatment with methylprednisolone. MRI findings in this child are similar to those in adults with diffuse clinical manifestations. The study is essential in the initial evaluation of patients suspected of central nervous system lupus.
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PMID:MRI changes in the central nervous system in a child with lupus erythematosus. 764 97

We report bilateral temporal lobe MRI findings in a patient following an episode of prolonged hypoglycemia uncomplicated by coexisting anoxia, hypotension, acidosis, drug intoxication, infection, or status epilepticus. The MRI findings are discussed in relation to the experimental and human data on hypoglycemic neuronal injury.
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PMID:Bilateral temporal lobe MRI changes in uncomplicated hypoglycemic coma. 775 77


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