Cases reported "Status Epilepticus"

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11/649. Use of intravenous valproate in three pediatric patients with nonconvulsive or convulsive status epilepticus.

    OBJECTIVE: To report the pharmacokinetics of intravenous valproate (VPA) in children with generalized convulsive status epilepticus (GCSE) or nonconvulsive status epilepticus (NCSE). To provide loading and maintenance dosing for patients with hepatic induction secondary to concurrent anticonvulsants. CASE SUMMARY: Two patients (10 y, 34 mo) with GCSE refractory to benzodiazepines, phenobarbital, phenytoin, and pentobarbital received intravenous VPA. Apparent volume of distribution (Vd) following a 20 mg/kg loading dose was 0.29 L/kg. maintenance infusions of 4-6 mg/kg/h produced steady-state total concentrations of 66 mg/L and 92.4 mg/L (unbound concentration 44.6 mg/L). Clearance ranged from 63-66 mL/h/kg. An eight-year-old with NCSE received intravenous VPA (13.4 mg/kg load followed by 9 mg/kg every 8 h). Total and unbound steady-state VPA concentrations were 32.9 mg/L and 21.2 mg/L, respectively. Elimination half-life was eight hours. DISCUSSION: We constructed a pharmacokinetic simulation using VPA parameters from children receiving mono- or polyanticonvulsants. Our Vd and elimination half-life rates were comparable with published pediatric values. patients on hepatic inducers had clearance rates 2.5 times those of children receiving oral anticonvulsant polytherapy. Unbound fractions (48.3% and 66%) were significantly higher than normal. CONCLUSIONS: A 20 mg/kg loading dose should produce a concentration after the bolus dose of approximately 75 mg/L. Initial infusion should consider hepatic induction (noninduced = 1 mg/kg/h, polyanticonvulsant therapy = 2 mg/kg/h, and high-dose pentobarbital = 4 mg/kg/h). Adjustments should be based on response and serum concentrations. ( info)

12/649. status epilepticus-induced brain damage and opercular syndrome in childhood.

    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. ( info)

13/649. Nonconvulsive status epilepticus in childhood localization-related epilepsy.

    PURPOSE: To report on three children with localization-related epilepsy who exhibited minor seizures (atypical absences, brief atonic, and myoclonic) and nonconvulsive status epilepticus (NCSE) consisting of these minor seizures, and to elucidate their significance. methods: We studied the electroclinical characteristics of these children. Ictal electroencephalograms (EEGs) of NCSE were evaluated by using simultaneous video-EEG-electromyogram (EMG) polygraphic recordings. RESULTS: All patients began to have partial seizures between the ages of 6 months and 2 years 7 months, with minor seizures appearing later, between the ages of 1 year 11 months and 6 years 6 months. These minor seizures evolved into NCSE. Complex partial seizures remained after suppression of the minor seizures. Interictal EEGs taken when the minor seizures appeared showed excessive diffuse epileptic discharges in addition to multifocal spike-waves. Before and after suppression of the minor seizures, focal epileptic discharges predominated on the EEGs. On ictal EEGs of brief atonic and myoclonic seizures, diffuse spike-wave and polyspike-wave bursts were detected. Ictal EEGs of the atypical absences revealed diffuse spike-wave bursts mixed with irregular high-voltage slow waves, often interspersed with brief atonic and myoclonic seizures. When atypical absences lasted for a long time, patients manifested NCSE. Polytherapy might be related to the occurrence of minor seizures and NCSE, because all patients were treated with polytherapy at their appearance, and simplification of antiepileptic drug (AED) therapy seemed to be effective. CONCLUSIONS: We concluded that this NCSE is a type of atypical absence status which is an age-dependent, transient, electroclinical condition. The mechanism of occurrence of these minor seizures might be related to secondary bilateral synchrony. ( info)

14/649. Development of focal chronic epilepsy following focal status epilepticus in adult patients.

    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. ( info)

15/649. Two cases of nonconvulsive status epilepticus in association with tiagabine therapy.

    We report two patients with intractable partial seizures who developed generalized nonconvulsive status epilepticus (NCSE) after receiving tiagabine (TGB). Neither had a history of absence seizures or generalized epileptic discharges on prior EEG monitoring. Clinicians need to be aware of a possible association between TGB and NCSE. ( info)

16/649. Folinic acid-responsive neonatal seizures.

    We report three cases of folinic acid-responsive intractable neonatal seizures. All patients were born at term following normal gestation and delivery. In the first infant, seizures began on the 5th day of life and were unresponsive to phenobarbital, pyridoxine, and valproate, but stopped within 24 hours of initiation of folinic acid treatment at the age of 6 months. Her sibling had died at age 6 months with intractable seizures. In the second infant, seizures began in the 2nd hour of life. These were initially controlled with phenobarbital; however, at 3 months of age she developed status epilepticus refractory to anticonvulsants, steroids, and pyridoxine and she required repeated induction of pentobarbital coma. seizures stopped within 24 hours of starting folinic acid. seizures and encephalopathy were noted in the third infant on the 2nd day of life. These were controlled with phenobarbital, but at 8 weeks of age seizures recurred and were difficult to control despite the addition of phenytoin. Immediately after folinic acid was initiated the seizures stopped. Breakthrough seizures in all patients have responded to increases in folinic acid; two of the three remain on standard anticonvulsants. All patients have global developmental delay. Cranial magnetic resonance imaging in the second patient shows diffuse atrophy, and in the third patient shows increased signal on T2 images in the white matter of the frontal and parietal lobes. Analysis of cerebrospinal fluid from these patients using high-performance liquid chromatography with electrochemical detection has consistently revealed an as-yet unidentified compound, which can be used as a marker for this condition. We suggest that cerebrospinal fluid be analyzed for the presence of this compound and a trial of folinic acid be considered in neonates with unexplained early onset intractable seizures. ( info)

17/649. Nonconvulsive status epilepticus in a child with congenital bilateral perisylvian syndrome.

    A 9-year-old male with congenital bilateral perisylvian syndrome is described. He had pseudobulbar palsy, mental retardation, and intractable epilepsy. Computed tomography and magnetic resonance images of the brain demonstrated bilateral perisylvian malformations and a diffuse pachygyric appearance. At 8 years of age, he had episodes of excessive drooling, fluctuating impairment of consciousness, unsteady sitting, and frequent head drop that lasted several days. The electroencephalogram demonstrated continuous diffuse slow spike and waves. These findings suggested atypical absence status epilepticus. Intravenous administration of diazepam resulted in transient improvement of clinical and electroencephalographic findings. status epilepticus recurred within several minutes after diazepam administration. Although no patient has been reported to have a history of status epilepticus among those affected by this syndrome, it seems that atypical absence status can occur more frequently than expected, as seen in Lennox-Gastaut syndrome. After recognition and confirmation of nonconvulsive status epilepticus, immediate treatment must be attempted. ( info)

18/649. Fatal status epilepticus associated with olanzapine therapy.

    OBJECTIVE: To report a case of fatal status epilepticus in a patient using olanzapine with no known underlying cause or predisposing factor for seizure. CASE SUMMARY: A 41-year-old white woman developed witnessed seizures at home that progressed to status epilepticus. She subsequently died from secondary rhabdomyolysis and disseminated intravascular coagulation. She had been taking olanzapine for five months prior to the event. No other toxic, metabolic, or anatomic abnormalities were identified pre- or postmortem to explain the seizures. Her seizures were a probable adverse drug reaction based on the Naranjo scale. DISCUSSION: This is the first case of fatal status epilepticus described that has been associated with the use of olanzapine. The pharmacodynamics of olanzapine are similar to those of clozapine, which has been described to induce seizures in 1-4% of patients. It is possible that this patient may have suffered seizures due to a similar effect. Alternate explanations include neuroleptic malignant syndrome and alcohol or benzodiazepine withdrawal seizures, although her clinical history does not suggest these etiologies. CONCLUSIONS: Although olanzapine has infrequently been associated with seizures in premarketing studies, its potential to induce them exists. Postmarketing surveillance should continue to determine how significant this effect may be. ( info)

19/649. hiv infection and seizures.

    New-onset seizures are frequent manifestations of central nervous system disorders in patients infected with human immunodeficiency virus (hiv). seizures are more common in advanced stages of the disease, although they may occur early in the course of illness. In the majority of patients, seizures are of the generalised type. status epilepticus is also frequent. Associated metabolic abnormalities increase the risk for status epilepticus. Cerebral mass lesions, cryptococcal meningitis, and hiv-encephalopathy are common causes of seizures. phenytoin is the most commonly prescribed anticonvulsant in this situation, although several patients may experience hypersensitivity reactions. The prognosis of seizure disorders in hiv-infected patients depends upon the underlying cause. ( info)

20/649. Nonconvulsive status epilepticus in acute brain injury.

    Whether or not nonconvulsive status epilepticus produces permanent brain damage is a source of controversy. Contributing to the controversy is the lack of clarity for classifying the clinical and electrographic phenomena that constitute nonconvulsive status epilepticus. Nonconvulsive status epilepticus commonly occurs in the context of an acute brain injury. For example, it commonly persists in generalized convulsive status epilepticus after convulsive activity has stopped, and it is not uncommonly associated with acute cerebral ischemia. Its clinical characteristics are ambiguous, subtle, and nonspecific making the diagnosis difficult. In the absence of EEG testing, it is likely to be missed or delayed. When acute brain injury and nonconvulsive status epilepticus occur concurrently, the severity of acute brain injury has traditionally been accepted as determining patient outcome. However, increasing evidence suggests that the two conditions are synergistically detrimental and increase brain injury. Guidelines remain to be established for the intensity and duration of anticonvulsant therapy in these patients. Evidence suggests that, in the absence of extreme and irreversible acute brain injury, early intensive intervention is necessary to improve the otherwise poor outcome of these patients. ( info)
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