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 previously healthy 8-month-old girl developed exanthem subitum and acute encephalopathy with status epilepticus, quadriplegia and bilateral abducens nerve palsies. Human herpesvirus-6 DNA was found in the cerebrospinal fluid by the polymerase chain reaction at the acute stage. Cranial computed tomography showed low density areas in the thalami and in the cerebellar and abducens nuclei. The distribution of the lesions was consistent with acute necrotizing encephalopathy. As for the thalamic lesions, a T2 weighted magnetic resonance image on the 24th day of the illness demonstrated low signal intensity surrounded by high intensity; 99mTc-ECD SPECT showed hypoperfusion, which suggested irreversible tissue damage. The patient is now 1 year 6 months old and has spastic quadriparesis with mental retardation and abducens nerve palsies.
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PMID:Serial neuroimages of acute necrotizing encephalopathy associated with human herpesvirus 6 infection. 857 24

A 32-year-old man with hemiconvulsions, hemiplegia, epilepsy (HHE) syndrome is described. He was well developed with a normal pregnancy and delivery, but at age 10 months, he had status epilepticus during a febrile illness. Thereafter, he was noted to have left hemiparesis and mental retardation with recurrent hemiconvulsions. Magnetic resonance (MR) images showed atrophy and degeneration of the right cerebral cortex and white matter, homolateral thalamus, caudate nucleus, and hippocampus, with hyperintensities in both T2-weighted (TR/2200, TE/90) and proton (TR/2200, TE/30) images. There were also slight bilateral cerebellar atrophies. Quantitative single photon emission computed tomographic (SPECT) images using technetium-99m-ethyl cysteinate dimer (99mTc-ECD) revealed markedly reduced cerebral blood flow (CBF) in the right cerebral hemisphere, homolateral thalamus, caudate nucleus and bilateral cerebellum. Bilateral putamen and the medial occipital lobe showed normal findings on MR images and normal regional CBF in SPECT images. We suppose these selective neuronal injures in this case of HHE syndrome will be mainly due to histotoxic factors in epileptic brain damage.
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PMID:[Neuroimaging findings of hemiconvulsions, hemiplegia, epilepsy (HHE) syndrome]. 1039 81

Postictal psychoses are brief psychotic episodes that usually occur after poorly controlled partial complex seizure clusters. The psychosis commonly appears following a lucid interval, ranging from a few hours to days after seizure termination. An underlying structural brain abnormality is common and usually involves the temporal lobe. Postictal psychosis, while well known in adults, has not been described previously in children. We describe a 9-year-old boy with right hemiparesis due to a neonatal stroke, who developed a postictal schizophrenia-like psychosis following status epilepticus. Electroencephalography showed left-sided slowing. A brain computed tomographic scan and magnetic resonance imaging revealed left hemisphere hypoplasia. A 99mTc-ECD single photon emission computed tomographic scan of the brain revealed decreased left-hemisphere perfusion, most pronounced to the medial temporal lobe. The psychosis resolved gradually over 7 days without antipsychotic therapy. To the best of our knowledge, this is the first description of postictal psychosis in a child.
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PMID:Postictal psychosis in a child. 1061 70

Magnetic resonance imaging and single-photon emission computed tomography provide useful information in the evaluation of the pathophysiology of epileptic foci. Ictal magnetic resonance imaging in a 7-year-old male with occipital lobe epilepsy revealed mild swelling of the left temporo-occipital region, with hyperintensity on T(2)-weighted and fluid attenuated inversion recovery images. This lesion, however, was not detected on diffusion-weighted imaging. An ictal single-photon emission computed tomography study using 99mTc-ECD demonstrated left temporo-occipital hyperperfusion. T(2)-weighted and fluid attenuated inversion recovery images revealed hyperintensity without atrophy 4 months after control of his seizures. The focus in nonconvulsive status epilepticus has been reported as showing hyperintensity on T(2)-weighted, fluid attenuated inversion recovery and diffusion-weighted images. Since hyperintensity on diffusion-weighted imaging reflects cytotoxic intracellular edema due to excitotoxicity, and his ictal diffusion-weighted image exhibited no remarkable change, the lesions in the left temporo-occipital region resulted from vasogenic edema. Cytotoxic edema resulting from excitotoxicity leads to neuronal death, causing cortical atrophy. Thus, diffusion-weighted imaging is a useful tool to predict the prognosis of frequent seizures.
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PMID:Magnetic resonance imaging in occipital lobe epilepsy with frequent seizures. 1277 Jun 76

We describe a 62-year-old woman suffering from visual hallucination due to focal status epilepticus investigated by means of Magnetic Resonance Imaging (MRI), Magnetic Resonance Angiography (MRA), Electroencephalography (EEG), and 99m Technetium ethylcysteinate dimer Single Photon Emission Computed Tomography (Tc-99m ECD SPECT). EEG showed spikes in the right parietooccipital area. MRI demonstrated gyral swelling and signal hyperintensity in the right parietooccipital cortex with effacement of adjacent cortical sulci on T2- weighted and Fluid Attenuation Inversion Recovery (FLAIR) images. MRA indicated localized dilation of the right posterior cerebral artery (PCA) and parietal branch of the right middle cerebral artery (MCA), corresponding to the epileptic area shown on EEG. Hyperperfusion in the right parietooccipital lobe was observed by Tc-99m ECD SPECT. All these findings completely resolved on the follow-up studies 2 months later. We present the case showing the transient radiological alterations on MRA corresponding to the epileptic area.
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PMID:Reversible focal radiological changes due to non-convulsive status epilepticus of the right parietooccipital lobe. 2354 19