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)

Propofol is a new anaesthetic agent commonly used because of its rapid pharmacokinetic. Lately, anecdotal reports suggest its utility in the treatment of convulsive status epilepticus. We describe four cases of convulsive status due to severe encephalopathy of various etiology. They were resistant to diazepam and other drugs and remitted only after treatment with propofol. The infusion, even protracted to 8 days, did not cause any toxic or proconvulsive side-effects. The very short duration of its central depressant action permitted monitoring of the underlying neurological status whenever needed.
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PMID:Propofol in the treatment of convulsive status epilepticus: a report of four cases. 180 75

The EEG is a useful and, at times, an essential test in the evaluation of delirium. In most patients with delirium, the EEG will show diffuse slowing and thus is helpful in differentiating organic etiologies from functional, psychiatric disorders. The degree of the EEG changes correlates with the severity of the encephalopathy so that the EEG may be used to help monitor therapy. In some delirious patients, the EEG may indicate whether the patient is suffering from focal, rather than global, impairment. Furthermore, the EEG is the only test that can identify an ongoing epileptic state (e.g., nonconvulsive status epilepticus) as being responsible for the clinical picture of confusion. Other electrophysiological tests that may prove helpful in the evaluation of delirium, such as computerized EEG spectral analysis, topographic brain mapping, and sleep studies, are briefly reviewed.
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PMID:Utility of EEG in delirium: past views and current practice. 181 75

The MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) can be difficult to identify. We report MRI abnormalities that we believe are specific to this disorder in three patients with complete or partial MELAS syndrome. The patients all showed an unusual pattern on T2-weighted MRI with multifocal areas of hyperintense signal confined to the cortex of the cerebrum, cerebellum, and adjacent white matter. Some images suggested selective cortical involvement of deeper layers only. Deep white matter was relatively spared, distinguishing this from usual cerebrovascular disease or the edema after status epilepticus. Specificity of these findings is further suggested by a good correlation of these findings with the previously described unique postmortem brain pathology of MELAS.
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PMID:Magnetic resonance imaging shows specific abnormalities in the MELAS syndrome. 206 32

A retrospective study was performed to determine the clinical and pathologic features, etiology, and outcome of children with the reversal sign. The reversal sign, a striking CT finding, probably represents a diffuse, anoxic/ischemic cerebral injury. CT features of the reversal sign are diffusely decreased density of cerebral cortical gray and white matter with a decreased or lost gray/white matter interface, or reversal of the gray/white matter densities and relatively increased density of the thalami, brainstem, and cerebellum. Twenty children with the reversal sign were retrospectively analyzed. We divided the patients into three groups: (1) acute reversal, (2) intermediate group, and (3) chronic reversal. There were nine cases of trauma (seven of child abuse); nine hypoxia/anoxia incidents (birth asphyxia, drowning, status epilepticus); one bacterial meningitis; and one degenerative encephalitis. All acute- and intermediate-group patients had respiratory problems requiring ventilator support and intensive care. In five of seven patients who died, autopsy findings were consistent with anoxic/ischemic encephalopathy. Surviving patients have profound neurologic deficits with severe developmental delay. The CT reversal sign carries a poor prognosis and indicates irreversible brain damage.
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PMID:Reversal sign on CT: effect of anoxic/ischemic cerebral injury in children. 210 31

We reviewed the clinical features and ictal EEGs in 23 adults with myoclonic status epilepticus (MSE). Anoxic encephalopathy was the most common cause of MSE, occurring in 15 patients; 8 developed MSE within 14 hours following the anoxic insult. Metabolic encephalopathies were present in 4 patients, while 2 had degenerative CNS disorders. In 2 patients with generalized epilepsy, MSE developed during a medication change. Five types of EEG patterns were associated with MSE. Generalized periodic complexes (usually spikes, polyspikes, or sharp waves), often with attenuation of background activity between complexes (11 patients) or a burst-suppression pattern (4 patients), were the most common types. Outcome was poor: 20 patients died without regaining consciousness, while 1 remains in a vegetative state. The 2 patients with generalized epilepsy, both of whom were conscious during MSE, survived without sequelae.
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PMID:Myoclonic status epilepticus: a clinical and electroencephalographic study. 211 5

We presented the experience at the Emergency Unit of the National Institute of Pediatrics with children with Status Epilepticus (SE). This series studied 70 patients, the greatest frequency was seen among infants (55%), followed by preschool children (17%). The most frequent type of SE was generalized tonic clonic (54%) also being the most critical. The simple partial status or epilepsia partialis continua was found to be another frequent variety. In newborns babies the most common type of SE was generalized tonic. Sixty percent originated as acute process, their main causes were central nervous infections, ischemic-hypoxic encephalopathy, intracranial hemorrhages and intoxications. The remaining 40% were due to chronic processes, the most important was secondary epilepsy. Among these children the main cause was the irregular use of antiepileptic drugs. Other factors were intercurrent infections with fever, head trauma and hyponatremia. Only 12.8% of the cases were idiopathic. Fifteen percent of the SE were successfully treated with diazepam; 44% with phenytoin plus phenobarbital, in 34.2% we used generalized anesthesia with thiopental. In 33% of the acute cases os SE there were sequelae, there were nine deaths (12.8%) all of them with serious illness of the central nervous system.
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PMID:[Status epilepticus in children. Study of 70 cases]. 225 95

A five-year-old male was admitted to the hospital with generalized seizures. Enlarged lymph nodes raised the suspicion of cat-scratch disease. The diagnosis was confirmed by a positive history of a cat bite, typical histopathologic findings in the biopsy of the lymph nodes, and a positive skin test. Brain CT scan and LP were repeatedly normal. The clinical course was remarkable for recurrent episodes of status epilepticus refractory to usual anticonvulsant therapy and prolonged encephalopathy consisting of mental confusion, hemiparesis, tremor, chorea, and vomiting. All neurologic symptoms gradually resolved within nine months, without sequelae. Cat-scratch encephalopathy should be suspected in a child presenting with status epilepticus and enlarged lymph nodes. Aggressive and prolonged anticonvulsant therapy is strongly recommended.
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PMID:Cat-scratch encephalopathy presenting as status epilepticus and lymphadenitis. 232 Apr 87

Eleven patients (6 males, 5 females; ages 7.5 to 40 years, mean 27.8) had prolonged postictal confusion lasting from 4 to 10 days. During that time, the EEG showed a typical encephalopathic pattern. Comprehensive evaluation ruled out the possibility of metabolic, toxic, drug-related, or ongoing nonconvulsive status epilepticus. We have designated this syndrome as prolonged postictal encephalopathy (PPIE). Nine of 11 patients were mildly to borderline mentally retarded. Ten had previous episodes of status epilepticus. Nine of 11 had minimal structural abnormalities (mainly diffuse cortical atrophy). Nine patients had multiple recurrent episodes of PPIE. All episodes occurred following a cluster of seizures: in 8 patients after a cluster of generalized tonic-clonic seizures, in 2 after complex partial seizures, and in 1 patient after a cluster of atypical absence seizures. This series suggests that vulnerability to develop PPIE exists in patients with diffuse structural abnormalities, mild to borderline mental retardation, a history of status epilepticus, and a tendency of seizures to cluster.
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PMID:Prolonged postictal encephalopathy. 234 18

A recent outbreak of human food poisoning, characterized by severe gastrointestinal and neurologic abnormalities, with a fatal outcome in 3 patients, was attributed to the consumption of poisonous mussels containing domoic acid at an abnormally high concentration. The purpose of the present study was to determine if domoic acid, a glutamate analogue extracted from poisonous mussel, was neurotoxic to rats. Groups of female Sprague-Dawley rats were dosed once intraperitoneally with 0, 1, 2, 4, or 7.5 mg domoic acid/kg of body weight and observed for a maximum period of 24 hr. Clinically, control rats and rats in the 1 mg/kg group were unremarkable. Seventy-five percent of the animals in the 2 mg/kg group had equivocal transient behavioral signs. One that was given 2 mg/kg and all rats given in excess of 4 mg/kg of body weight developed unequivocal behavioral and neurologic signs culminating in partial seizures and status epilepticus. Histopathologically, severely affected rats developed selective encephalopathy characterized by neuronal degeneration and vacuolation of the neuropil in the limbic and the olfactory systems, and retinopathy characterized by neuronal hydropic degeneration of the inner nuclear layer and vacuolation of the external plexiform layer. The results of this study suggest that domoic acid is excitotoxic and causes a characteristic syndrome with clinical signs and histopathologic lesions similar to those reported for kainic acid.
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PMID:Acute neurotoxicity of domoic acid in the rat. 236 84

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


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