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 report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
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PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

A 69-year-old woman presented with an ictal Anton-Babinski syndrome (asomatognosia with hemiparesis). Except for head and eye deviation to the side of the paralyzed limb, epileptic nystagmus, brief episodes of impaired consciousness, and automatisms, clinical symptomatology was identical to Anton-Babinski syndrome of vascular origin. Results of MRI imaging were normal. EEG showed a simple partial nonconvulsive status epilepticus of right parieto-temporal origin. Anton-Babinski syndrome may thus be a functional expression of focal status epilepticus.
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PMID:Ictal asomatognosia with hemiparesis. 967 22

The non-convulsive status epilepticus (NCSE) is a complication of petit mal epilepsy or epilepsy with temporal lobe seizures. Very rarely it is the primary manifestation of a symptomatic epilepsy. This report is on a 30-year old female inpatient with NCSE as the primary manifestation of symptomatic epilepsy, occurring four years after HIV infection (stage B3 according to the CDC classification) through heterosexual contact. After an initial tonic-clonic seizure, the patient suffered from NCSE for four weeks with diminished consciousness and major cognitive deficits. During this whole time period the EEG showed bilateral synchrone 1-2 Hz spike-wave complexes. After several failed treatment attempts, the NCSE was successfully and permanently treated with a combination of valproic acid and ethosuximide. The cerebrospinal fluid, cranial CT and cranial MRI were completely uneventful with regard to a CNS infection by the HI-virus or other infectious agents. 20 days after the initial symptoms, MRI showed bilateral cortical-subcortical and bilateral hippocampal lesions which stood out as focal edema zones, gradually disappeared completely and occurred in combination with the development of a discrete brain and right sided hippocampal atrophy. The EEG continued to show signs of right-temporal epileptic discharges with tendencies to generalise after 3 months but normalised after 6 months. Epileptic seizures are rarely an initial clinical sign of an infection with the HI-Virus even if no signs of encephalitis is detectable in the cerebrospinal fluid or in the cerebral MRI.
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PMID:[Prolonged non-convulsive status epilepticus as an early clinical manifestation of epilepsy in connection with HIV infection--case report with EEG and MRI follow-up]. 969 7

We demonstrate clinical data and findings of MRI, transcranial Doppler (TCD), single photon emission computed tomography (SPECT) and electroencephalography (EEG) in an 8 month follow-up study of a 15 year old girl who developed focal status epilepticus with sensory and visual illusions. EEG showed right temporal and occipital seizure activity and attenuation of the alpha activity with right predominance. MRI showed a right temporo-parietal hyper signal on the T2 weighted images involving the cortex with sulcal effacement. MRI-angiography suggested insufficient flow in the right transverse sinus. TCD detected an elevated flow velocity in the ipsilateral middle cerebral artery during status epilepticus, corresponding to an increased perfusion of the epileptic area revealed by SPECT. After normalization of the TCD finding, the MRI detected persistent cortical abnormality beyond the 70th day after admission. MRI normalized on the 103rd day of follow-up. Serial EEG frequency analysis demonstrated the recovery of alpha peak frequency on the left side, but the attenuation of rhythmic signals remained persistent on the right. In our case, the restitution of postictal EEG lag behind the consolidation of MRI signal abnormality.
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PMID:Reversible focal MRI abnormalities due to status epilepticus. An EEG, single photon emission computed tomography, transcranial Doppler follow-up study. 992 85

This study reports on a girl with a permanent cerebral lesion and opercular syndrome after status epilepticus (SE). She had previously been healthy and had her first focal motor seizure at 5 years of age, which was controlled with intravenous phenytoin and rectal diazepam. Twenty-four hours later, she developed partial SE consisting of right facial twitching and right-hand clonic movements. These uncontrollable seizures lasted for 5 days, after which the partial SE changed to generalized SE, and the seizures continued for another 5 days. CT performed the day before onset of SE revealed no brain abnormality. Another CT performed a year later disclosed bilateral brain lesions, more severe in the left hemisphere. Follow up at 16 years of age revealed moderate motor sequelae of the right-hand side of the body, anarthria, difficulty chewing, dysphagia, bilateral facial weakness, and drooling, all of which clinically characterize opercular syndrome. An MRI study performed at 14 years of age showed a cerebral parenchymatous lesion which extended between the parietal cortices of both hemispheres, more severe on the left side, and which crossed the corpus callosum, destroying the posterior-middle zone. Evidence from the CT indicates that the lesion was not present before onset of SE. It seems likely that the focal SE caused the focal brain damage, but the possibility that the subsequent generalized SE played a role cannot be excluded.
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PMID:Status epilepticus-induced brain damage and opercular syndrome in childhood. 1087 32

In several experimental models, status epilepticus (SE) leads to secondary brain hyperexcitability and epileptogenesis. In humans, such phenomena have been rarely demonstrated, particularly in cases of SE involving the neocortical structures. We report a 36 year old woman that presented partial SE in May 1991 involving the right cerebral hemisphere. The patient was then treated in the intensive care unit with artificial ventilation and anesthesia by pentobarbital and clometiazole. MRI showed transient right parietal and temporal posterior cortical hyperintensity. The cause of SE was not determined. Three months later, the patient developed partial complex seizures with aura characterized by vertigo, nausea and auditory hallucination. Ictal video/EEG recording showed a clear right temporal posterior onset of the discharges. We speculate that status epilepticus created the lesions which subsequently caused the focal chronic epilepsy.
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PMID:Development of focal chronic epilepsy following focal status epilepticus in adult patients. 1043 Dec 92

Seizures, particularly multiple episodes and/or status epilepticus (SE) are prevalent in pediatric patients. Pediatric SE is associated with brain changes that have been hypothesized to contribute to the onset of temporal lobe epilepsy (TLE). In order to gain insight into the effects of seizures on the immature brain and the risk for later TLE, we have developed a model of limbic SE in the pigtailed macaque monkey. In separate studies, bicuculline methiodide or a bicuculline 'cocktail' was infused into three regions of the brain (area tempestas, hippocampus, entorhinal cortex) to induce seizures. Measures included MRI, electrophysiology, behavior and morphology. Our results suggest that monkey models of SE may provide useful tools for understanding the effects of prolonged seizures during infancy and the origins of TLE in humans.
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PMID:Development of a model of status epilepticus in pigtailed macaque infant monkeys. 1057 59

Two patients with status epilepticus due to specific conditions were examined using MRI and stable Xe/CT CBF. [Case 1] A 30-year-old woman developed a grand mal seizure during delivery. She was comatose, and MRI revealed abnormal high intensity areas bilateral basal ganglia, compatible with eclampsia. Regional CBF was decreased in bilateral occipital lobes and right basal ganglia. Six days after onset. Regional gray matter flow was increased, especially in the thalami and basal ganglia. [Case 2] The patient is a 31-year-old male diagnosed with temporal lobe epilepsy since 10 years. At the onset, he had a prolonged right hemiconvulsion followed by generalized tonic-clonic convulsion. MRI 13 days after onset showed left hemispheric edematous swelling of gray matter. Stable Xe/CT 3 weeks after onset demonstrated increased cortical CBF corresponding to edematous area. The results suggested that regional CBF decreased immediately after status epilepticus and then increased for 1-3 weeks in the interictal period. We speculate that the energy debt incurred during prolonged seizure causes relative ischemic condition in the neurons, with the increase in CBF resulting from accelerated energy production for a long period.
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PMID:Regional cerebral blood flow after status epilepticus. 1075 Mar 44

We report a case of Jarisch-Herxheimer reaction in a patient with neurosyphilis, which was complicated by nonconvulsive status epilepticus. The EEG features suggested a focal seizure onset, although the patient's MRI was normal. JHR is common in the treatment of neurosyphilis, but usually produces only transient systemic constitutional symptoms. Neurologic deterioration is rare, but can be dramatic, as in our patient. NCSE should be considered as an explanation for persistent obtundation and transient focal neurologic findings in this setting.
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PMID:Nonconvulsive status epilepticus resulting from Jarisch-Herxheimer reaction in a patient with neurosyphilis. 1092

In two patients eclampsia started 9 days postpartum. Headache and visual disturbances preceded seizures but none of the classic pre-eclamptic signs oedema, proteinuria, and hypertension were present until shortly before seizure onset. Brain herniation (patient 1) and status epilepticus (patient 2) necessitated neurointensive care management. Brain MRI initially showed only frontal sulcal effacement in one patient but later showed white matter hyperintensities on T2 weighted images and a previously undescribed pattern of cortical-subcortical postgadolinium enhancement on T1 weighted images in both. Neurological deficits and MRI findings were reversed with therapy in both patients. It is concluded that late postpartum eclampsia can manifest without classic prodromi and that characteristic MRI findings may lag behind clinical manifestation.
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PMID:Late onset postpartum eclampsia without pre-eclamptic prodromi: clinical and neuroradiological presentation in two patients. 1108 Feb 41


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