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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Refractory status epilepticus (RSE) is defined as status epilepticus that continues despite aggressive treatment. A 9.8-year-old boy with a past history of daily left focal motor seizures was transferred to University of California at Los Angeles (UCLA) Hospital in pentobarbital coma after 4 days in RSE. The RSE was treated with very high doses of all appropriate antiepileptic drugs (AEDs), alone and in combination. The pentobarbital was titrated to burst suppression on EEG, but whenever pentobarbital was decreased, the seizures recurred. An ictal positron tomography scan of glucose metabolism demonstrated a right frontal area of hypermetabolism corresponding to an epileptic focus on EEG and magnetic resonance lesion. Eight days after the boy was admitted to UCLA, the right frontal focus was surgically removed, with immediate control of the status epilepticus. Whereas before onset of RSE, he had daily focal seizures, the boy has been seizure-free postoperatively for greater than 1 year. Operative treatment should be considered in patients with RSE in whom a focus of seizure onset can be demonstrated and who are reasonably considered surgical candidates.
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PMID:Neurosurgical treatment of refractory status epilepticus. 159 35

This is a report of an intentionally administered overdose of dimenhydrinate to a 4 month-old infant who subsequently presented with status epilepticus, coma, and life threatening ventricular dysrhythmias. Initial toxicologic analysis of the serum by fluorescence polarization immunoassay was positive for tricyclic antidepressants. Repeat analysis of the serum at 6 hours post ingestion by gas chromatography mass spectrometry analysis defined diphenhydramine 4.8 micrograms/mL. The infant was managed with IV sodium bicarbonate as utilized in tricyclic antidepressant intoxication. The dysrhythmias resolved and the infant recovered without sequelae.
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PMID:Response of life threatening dimenhydrinate intoxication to sodium bicarbonate administration. 166 Sep 38

We retrospectively evaluated the clinical and EEG features of status epilepticus (SE) in 47 comatose adult patients in whom SE was suspected clinically or because the EEG revealed repetitive electrographic seizures or continuous spike-and-wave activity. Three groups of patients were identified. Group-1 patients (n = 33) had SE both clinically and on EEG. They usually had subtle, clonic movements restricted to the eyes, face, and upper extremities, and the EEG most commonly showed repetitive electrographic seizures or continuous spike-and-wave activity. Group-2 patients (n = 9) also had subtle motor manifestations of seizures, but the EEG was not that of SE, consisting of either irregular slowing with frequent spikes and sharp waves, an irregular mixed-frequency background with episodic accentuation, or diffuse slowing; one patient also had an intermittent burst-suppression pattern. The five patients in Group 3 lacked any clinical signs of seizures, but the EEG showed repetitive electrographic seizures or continuous spike-and-wave activity. There were no significant differences between groups in etiology of SE, response to therapy, or outcome, and there was no obvious relationship between the EEG findings and duration of SE. We conclude that recognition of SE in comatose patients may require both clinical and EEG evaluation since either approach by itself may fail to establish the diagnosis. Furthermore, the EEG findings in established SE do not necessarily progress through the series of defined stages suggested by some authors.
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PMID:Clinical and EEG features of status epilepticus in comatose patients. 173 88

Status epilepticus represents one of the most frequent neurological reasons for admission to the intensive care ward. If it resists well-managed treatment, more aggressive measures must be taken. We report 3 such situations in which patients were treated by barbiturate coma under continuous electroencephalographic monitoring. On the basis of this experience we attempt to elaborate guidelines for the use of this technique.
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PMID:[Barbiturate coma in the treatment of refractory status epilepticus in adults. Usefulness of continuous electroencephalography in intensive care]. 185 49

A 24-year-old man was admitted to our hospital, because two days before the admission he had abruptly lost consciousness following generalized convulsive seizures. He had a past history of transient amnesia and a favor for peanuts. His grandparents had a record of consanguinity. On admission, he was comatose and flaccid with his four extremities. Laboratory examination revealed the followings; mild degree of abnormal liver function, slight elevation of blood ammonia, irregular theta basic rhythm on EEG, marked brain edema on CT and a normal liver ultrasonography. From the second hospital day, in addition to antiepileptic drugs and adrenocorticosteroids, branched chain amino acid was administered to reactivate damaged brain functions. Thereafter, the concentration of blood ammonia increased to more than 3,000 micrograms/dl, and as a result he fell into status epilepticus. On the fourth hospital day, the levels of citrulline in the plasma and urine taken on the first hospital day were found to have increased by 20 and 100 times, respectively. Although the transfusion of branched chain amino acid was stopped, he died while in coma on the 12th hospital day. Enzymatic analyses of necropsied liver specimens revealed that the quantitative activity of argininosuccinate synthetase had decreased to less than 10% in his urea cycle. In this patient, it was noted that, after transfusion of branched chain amino acid, his brain activities turned worse and blood ammonia was markedly elevated. There is a possibility that intravenous administration of branched chain amino acid may interrupt the urea cycle balance in an adult patient of citrullinemia with dysfunction of the brain, kidney and muscle, especially with brain edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adverse effects of branched chain amino acid transfusion on type-II citrullinemia--report of an adult case]. 191 26

A 48-year-old woman with status epilepticus was admitted to our hospital. On admission, she was comatose with horizontal conjugate deviation of eye balls to the left side. Convulsive seizure of Jacksonian type involved initially the left mouth angle and sequentially the left arm and leg, developing into general convulsion. Routine laboratory examinations revealed no significant abnormality. CT scan was normal but carotid angiogram showed a persistent proatlantal intersegmental artery on the left side. Convulsive seizure lasted five days, followed by left hemiparesis. She recovered completely two weeks later. The origin of her illness remained unclear but the causal relationship between neurological symptoms and the persistent primitive artery was presumed.
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PMID:[A case of persistent proatlantal intersegmental artery with status epilepticus]. 204 12

In a series of 20 EEGs from 15 patients, well-defined brief attenuations occurred interspersed among the background activity. These episodic low-amplitude events (ELAEs) typically lasted 0.5-4 s. They were hemispheric or bisynchronous and occurred in patients with coma of various etiologies, including status epilepticus. The episodes of attenuation were brief and no bursts of activity were present, distinguishing this finding from burst-suppression. Prognosis was poor in the patients with coma due to entities other than status epilepticus. In the setting of status epilepticus, the prognosis depended on the etiology. This pattern may be an ictal phenomenon, or a product of waveform simplification. ELAEs are a manifestation of seriously abnormal EEG activity and correlate with a 50% mortality.
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PMID:Episodic low-amplitude events: an under-recognized phenomenon in clinical electroencephalography. 205 Aug 20

Among patients with a prolonged confusional state after convulsive seizure, we diagnosed 8 cases as generalized nonconvulsive status epilepticus. Six had a history of seizures, and 2 had new onset. The convulsive seizures were generalized in 6 and focal in two. The postictal confusion lasted up to 36 hours in the most prolonged case, and a delayed response to anticonvulsant medications occurred in all cases. The clinical symptoms ranged from mild confusion to coma. Psychiatric manifestations or automatisms were rare. The presumed etiology was due to diverse causes, but a withdrawal state was the most common. EEG demonstrated continuous or nearly continuous generalized ictal discharges of variable morphology. These cases call attention to the fact that some prolonged confusional states following convulsive seizures are in fact due to persistent seizure activity that can be diagnosed by EEG.
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PMID:Prolonged confusion following convulsions due to generalized nonconvulsive status epilepticus. 223 23

Significant neurotoxicity including seizures, encephalopathy and coma may complicate the use of cyclosporin A (CyA). Two patients are described, receiving CyA, who presented with abnormal behaviour, stupor, focal motor activity and were shown to be in complex partial status epilepticus (CPSE). Abnormalities of behaviour and/or stupor in patients receiving CyA may be a manifestation of CPSE. Patients receiving CyA who develop an encephalopathy should have electroencephalography performed at the time of the abnormal behaviour.
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PMID:Complex partial status epilepticus associated with cyclosporin A therapy. 250 48

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


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