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)

Thirty-four children (20 boys, 14 girls) with congenital and acquired cortical blindness were analyzed for visual outcome in relation to etiology, visual evoked potentials, electroencephalography, and cranial computed tomography. All 7 children with congenital cortical blindness remained blind on subsequent examination. Of the 27 children with acquired blindness, 16 (59%) had poor visual outcome. Poor visual outcome occurred in those with cardiac arrest, hypoxia, status epilepticus, intracranial hemorrhage, cerebral thrombosis, and head trauma. Good visual outcome occurred in children with hypotensive episodes after cardiac surgery. Of the 12 children with recovery of vision, the interval from acute loss of vision to partial or total recovery was 2 weeks to 5 months. Seven children had complete recovery of vision with no residual visual field defect. The majority of children (87%) had focal or multifocal spike-and-waves and slow sharp-wave discharges on electroencephalography. None had photic recruitment response or occipital spike-and-wave discharges. Flash visual evoked potential studies performed during acute episodes of cortical blindness documented 11 with absent response, 10 with bilateral increases in latency, and 6 with normal responses. There was no correlation between normal visual evoked potentials and a good visual outcome. Only 2 of 6 children with normal responses had normal vision. Abnormal or absent responses are more predictive of a poor recovery of vision because only 3 of 21 (14%) had normal vision on subsequent examination. Abnormal electroencephalographic findings with focal or multifocal spike-and-wave discharges or cerebral atrophy on cranial computed tomography are also poor prognostic signs.
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PMID:Cortical blindness in children: a study of etiology and prognosis. 187 97

We reviewed retrospectively a series of 100 inpatients with onset of epileptic seizure after the age of 60. All of them were investigated by EEG and 96 by CT scan. The most frequent cause of seizure was previous stroke, with 25 cerebral infarcts and 5 hemorrhages. Neoplastic lesions were present in 18 cases, with glioma (high grade), meningioma and metastases in the same proportion. Other etiologies included toxico-metabolic (18 cases), post-traumatic (9 cases), cerebral atrophy (4 cases) and miscellaneous (14 cases). The causes of seizure remained unknown in 7 patients, of whom 6 had focal signs in either clinical examination or EEG. Focal seizures (with or without secondary generalization) accounted for 65% of all cases and generalized seizures for 35%. The EEG was normal in 12 patients and abnormal in 88, with diffuse slowing in 55 patients and focal signs in 70 (some patients had both diffuse slowing and focal signs). Fourteen patients presented status epilepticus. Ten died during hospitalization. We conclude that epileptic seizure with onset after age 60 is nearly always symptomatic, and neuroradiologic investigations are necessary in the search for cerebral lesions. In our study, the prevalence of "idiopathic epilepsy" is lower than previously described.
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PMID:[Initial epileptic crisis after the age of 60: etiology, clinical aspects and EEG]. 234 61

Between 1982 and 1985, 14 infants aged 3-26 weeks presented with severe hypoxic episodes as a result of the 'near miss' sudden infant death syndrome (SIDS). They all had metabolic acidosis, cardiovascular instability, acute renal failure, ischaemic colitis, or acute neurological dysfunction. Investigation of the cause excluded infection and trauma, or a primary metabolic, pulmonary, cardiac, or seizure disorder. Seven infants were deeply comatose on admission, never regained consciousness, and died within 60 hours. A characteristic evolution of hypoxic-ischaemic encephalopathy not previously clearly described after near miss SIDS was seen in the seven who lived. Five of the seven were conscious within one hour of resuscitation and showed a striking interval of near normality before neurological deterioration that was characterised by status epilepticus, deep coma, and brain stem dysfunction from 36-96 hours after the event. A biphasic course was not apparent in the remaining two, each of whom was comatose on admission, though refractory seizures did develop. Computed tomograms of the brain more than a week after the event showed cortical infarction or cerebral atrophy. Six of the survivors, followed up from 16-55 months, have serious residual deficits including spastic quadriplegia, delayed development, cortical blindness, or infantile spasms.
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PMID:Hypoxic-ischaemic encephalopathy after near miss sudden infant death syndrome. 273 Jan 24

A case of status epilepticus with transient motor deficit is reported in a 66 year old male treated with fluvoxamine. Fluvoxamine is supposed to induce few epileptic seizures. The patient had no previous history of epilepsy. Two factors seem to have favoured the occurrence of epilepsy: presence of an incipient arteriopathic impairment, cortical and subcortical brain atrophy and perhaps drug overdosage causing a tremor in the days before the epileptic fit.
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PMID:[Epileptogenic action of fluvoxamine. Apropos of a case]. 311 16

A 67-year-old man was admitted for status epilepticus, right hemiparesis, repeating vertigo and vomiting. Computed tomography showed no abnormality except for slight brain atrophy. Angiogram demonstrated bilateral vertebral artery stenosis at the origin, especially on the left side, and bilateral cervical internal carotid artery stenosis associated with ulceration. Intracranially, bilateral anterior cerebral artery was filled only by right internal carotid artery. Internal carotid artery on both sides did not fill the posterior cerebral artery. From these findings, we thought that both bilateral internal carotid artery and left vertebral artery should be surgically reconstructed. On June 4, 1986, left vertebral transposition to the common carotid artery and left carotid endarterectomy using double-balloon shunt were performed. Waiting for recovery of the general condition, right carotid endarterectomy was carried out on June 27, 1986. Postoperative angiogram demonstrated disappearance of bilateral internal carotid artery stenosis, and good filling of left vertebral artery through left common carotid artery. Postoperative course was uneventful and right hemiparesis gradually improved. Vertigo and vomiting completely subsided. The method and indication of combined reconstruction for extracranial vertebral and carotid artery were discussed.
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PMID:[A case of combined reconstruction of extracranial vertebral and carotid artery stenosis]. 337 49

We report the case of a 49 year-old man who presented a partial status epilepticus with left-sided clonic seizures after the occurrence of a left cerebral hematoma. The patient had left-side hemiplegia that progressively recovered in 3 months. Neuroimaging studies revealed a moderate cerebral atrophy on the right side and crossed cerebellar atrophy. Six years later, he had a partial status epilepticus with left hamiconvulsions leading to permanent left hemiplegia. The right cerebral and the left cerebellar atrophy observed one year later were significantly increased. Cerebral hemiatrophy associated with epilepsy in adulthood is exceptional. Our case suggests that the occurrence of partial status epilepticus, even during adulthood, may aggravate cerebral hemiatrophy formally silent.
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PMID:[Hemicerebral atrophy and epilepsy in an adult]. 977 25

Magnetic resonance imaging (MRI), single photon emission computed tomography (SPECT) and magnetic resonance spectroscopy (MRS) were successively recorded in a 3-year-old girl with the acute hemiplegia syndrome. She was admitted to our hospital with complaints of fever, loss of consciousness and right side dominant clonic convulsions evolving into status epilepticus, and then recovered with sequelae of aphasia and right hemiparesis. Electroencephalography showed a generalized slow rhythm at the onset, and very low activities on the left hemisphere in the follow-up records. Brain CT and MRI revealed edema of the left hemisphere initially, followed by left side dominant brain atrophy. No cerebral vascular lesion was detected by magnetic resonance angiography. N-Isopropyl-[123I]-iodoamphetamine SPECT showed marked hypoperfusion of the left hemisphere accompanied by crossed cerebellar diaschisis. MRS at the initial stage detected decreased N-acetyl-aspartic acid and increased lactic acid signals in the bilateral hemisphere, which subsequently normalized only on the right side. These findings suggested brain damage and neural cell death in the left cerebral hemisphere, caused by acute encephalopathy. SPECT and MRS are useful new techniques to study the pathophysiology of the acute hemiplegia syndrome.
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PMID:[MRI, SPECT and MRS findings in a case of acute hemiplegia syndrome with a marked hemispheric brain edema]. 978 Jul 43

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

A 44-year-old man with treated neurosyphilis presented with subclinical status epilepticus (SE) refractory to intravenous high-dose lorazepam, phenytoin, and valproic acid over 4 days. Ketamine infusion was instituted after low-dose propofol sedation with gradual control of electrographic seizures over 72h. Reevaluation 3 months later revealed diffuse cerebellar and worsened cerebral atrophy, consistent with animal models of N-methyl-D-aspartate antagonist-mediated neurotoxicity. Animal studies of prolonged ketamine therapy are required before widespread human use in SE.
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PMID:Ketamine for refractory status epilepticus: a case of possible ketamine-induced neurotoxicity. 1260 30

Clinical course and serial neuroimaging findings are not fully described in children who have had neurological sequelae following status epilepticus. We found four patients who had neurological sequelae out of 42 children with status epilepticus in 2004. MRI studies were reviewed with specific attention to diffusion-weighted images (DWI) and the apparent diffusion coefficient (ADC). Proinflammatory cytokines, including tumor necrosis factor-alpha and interleukin-6, were measured in the cerebrospinal fluid (CSF) (3 patients). The clinical course showed biphasic; initial status epilepticus and neurological exacerbation along with seizure recurrence four to five days after onset. Within three days after initial status epilepticus, CT (all patients) and MRI (2 patients) did not show any abnormalities. From four to ten days after onset, MRI demonstrated diffuse hyperintensity in the cerebral white matter on DWI and hypointensity on ADC maps in all patients. Diffuse brain atrophy progressed thereafter. Tumor necrosis factor-alpha or interleukin-6 was elevated in all patients. A biphasic clinical course may be a specific feature for neurological sequelae. The preferential white matter involvement on MRI and elevated CSF cytokines indicate that glial dysfunction may play an important role in the pathophysiology of status epilepticus-associated cerebral damage.
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PMID:Biphasic clinical course and early white matter abnormalities may be indicators of neurological sequelae after status epilepticus in children. 1654 66


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