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)

Three patients are described who developed cerebral complications and an EEG abnormality for several days after metrizamide myelography. Clinically, the patients showed a fluctuating confusional state with dysphasia and retrograde amnesia, while their EEGs were dominated by runs of slow wave activity interspersed with frequent spikes. The runs appeared either continuously or in paroxysmal bursts. The clinical symptoms and the EEG are compatible with complex partial status epilepticus and are similar to the symptomatology of ten patients described in the literature. This rare clinical entity should be distinguished from a more common complication of metrizamide--non-specific slow wave abnormality of variable degree in the EEG with or without clinical signs. Clinical manifestations may include transient aphasia and weakness of the limbs with pyramidal signs.
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PMID:Metrizamide and the EEG: three case reports and a review. 407 99

This report concerns a 32-year old man with non-herpetic acute limbic encephalitis. He was admitted to our hospital because of high fever and consciousness disturbance. Cranial MRI revealed abnormal signal intensities in the bilateral mesial temporal lobes. On the second hospitalization day, he developed status epilepticus, which necessitated general anesthesia. Following administration of intravenous (IV) methylprednisolone pulse therapy (1 g/day, 3 days), his consciousness disturbance began to improve. Treatment with high-dose IV methylprednisolone was continued for about 2 weeks, but on the 7th day, he showed severe anterograde amnesia and retrograde amnesia regarding the preceding 5 or 6 years. Subsequently, however, his amnesic disorders improved markedly, and on the 46th day, memory dysfunction had disappeared. Autoantibodies against the glutamate receptor subunits epsilon2 and delta2 were detected in both the CSF and serum, but these antibodies in the CSF became normal during the clinical course. The voltage-gated potassium channel antibody was negative. This case report indicates that high-dose IV methylprednisolone therapy may be an affective treatment for non-herpetic acute limbic encephalitis, possibly associated with autoimmune mechanisms.
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PMID:[Successful use of methylprednisolone therapy in a case of non-herpetic acute encephalitis with antibodies against ionotropic glutamate receptor epsilon2 and delta2]. 1753 79

Generalized convulsive status epilepticus is a life-threatening emergency, because recurrent convulsions can cause death or injury. A common form of generalized convulsive status epilepticus is of focal onset. The neuronal circuits activated during seizure spread from the hippocampus, a frequent site of seizure origin, to the bilateral motor cortex, which mediates convulsive seizures, have not been delineated. Status epilepticus was initiated by electrical stimulation of the hippocampus. Neurons transiently activated during seizures were labelled with tdTomato and then imaged following brain slice clearing. Hippocampus was active throughout the episode of status epilepticus. Neuronal activation was observed in hippocampus parahippocampal structures: subiculum, entorhinal cortex and perirhinal cortex, septum, and olfactory system in the initial phase status epilepticus. The tdTomato-labelled neurons occupied larger volumes of the brain as seizures progressed and at the peak of status epilepticus, motor and somatosensory cortex, retrosplenial cortex, and insular cortex also contained tdTomato-labelled neurons. In addition, motor thalamic nuclei such as anterior and ventromedial, midline, reticular, and posterior thalamic nuclei were also activated. Furthermore, circuits proposed to be crucial for systems consolidation of memory: entorhinal cortex, retrosplenial cortex, cingulate gyrus, midline thalamic nuclei and prefrontal cortex were intensely active during periods of generalized tonic-clonic seizures. As the episode of status epilepticus waned, smaller volume of brain was activated. These studies suggested that seizure spread could have occurred via canonical thalamocortical pathway and many cortical structures involved in memory consolidation. These studies may help explain retrograde amnesia following seizures.
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PMID:Parallel pathways of seizure generalization. 3123 45