Cases reported "Status Epilepticus"

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1/554. An unusual case of Lafora body disease.

    A case is described in which non-convulsive status epilepticus (NCSE) prompted further investigation leading to the diagnosis of Lafora body disease (LBD). The onset of NCSE was temporally related to the withdrawal of sodium valproate and introduction of carbamazepine, which may have been precipitating factors. NCSE has not previously been reported in LBD. Implications for its drug management are discussed.
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2/554. Nonconvulsive status epilepticus in theophylline toxicity.

    CASE REPORT: A 53-year-old cocaine user was on chronic therapy with theophylline, albuterol, and ipratropium for asthma and nifedipine for hypertension. Acute asthma treatment that increased the serum theophylline to 35 micrograms/mL was associated with tonic clonic seizures followed by bizarre, lateralized posturing. Electroencephalogram seizure activity lasting 10 days was consistent with nonconvulsive status epilepticus, Complex Partial, type II. theophylline was considered the probable instigator of this underdiagnosed neurologic disorder.
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3/554. MRI abnormalities associated with partial status epilepticus.

    OBJECTIVE: To report neuroimaging findings in patients with complex partial status epilepticus. BACKGROUND: During status epilepticus, neuroimaging may be used to exclude other neurologic conditions. Therefore, it is important to identify the neuroimaging features that are associated with status epilepticus. In addition, MRI characteristics may provide insight into the pathophysiologic changes during status epilepticus. methods: The history and neuroimaging examination results of three patients with complex partial status epilepticus were reviewed. Studies obtained during status epilepticus included diffusion-weighted MRI (DWI), MR angiography (MRA), postcontrast T1-weighted MRI, T2-weighted MRI, and CT. Follow-up MRI was obtained in two patients, and autopsy results were available for the third. RESULTS: Some of the MRI and CT findings during partial status epilepticus mimicked those of acute ischemic stroke: DWI and T2-weighted MRI showed cortical hyperintensity with a corresponding low apparent diffusion coefficient, and CT showed an area of decreased attenuation with effacement of sulci and loss of gray-white differentiation. However, the lesions did not respect vascular territories, there was increased signal of the ipsilateral middle cerebral artery on MRA, and leptomeningeal enhancement appeared on postcontrast MRI. On follow-up imaging, the abnormalities had resolved, but some cerebral atrophy was present. CONCLUSIONS: The radiologic characteristics of status epilepticus resemble those of ischemic stroke but can be differentiated based on lesion location and findings on MRA and postcontrast MRI. The MRI abnormalities indicated the presence of cytotoxic and vasogenic edema, hyperperfusion of the epileptic region, and alteration of the leptomeningeal blood-brain barrier. These changes reversed, but they resulted in some regional brain atrophy.
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4/554. Truly a team effort.

    Jane was a healthy 16 year old girl who attended a high school dance and subsequently had a grand mal seizure--her first! She was taken home, developed a decreasing level of consciousness and was admitted to the local hospital, where it progressed to status epilepticus. We will describe the classifications of seizures including status epilepticus, which demands the highest level of clinical expertise and attention to preventative medicine, for a desirable outcome. During the eleven months of care a massive multi disciplinary team approach was instituted which extended across borders. Jane's story demonstrates a truly Neuroscience team effort from acute care to a rehabilitation center to home.
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5/554. camphor toxicity.

    camphor ingestion led to status epilepticus in a 20-month-old girl who required intubation and ventilation. She was treated with intravenous valium and phenobarbitone, and nasogastric activated charcoal. She made a complete neurological recovery. A number of products containing a high concentration of camphor were found to be available in the local community.
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6/554. Clinical experience of three pediatric and one adult case of spike-and-wave status epilepticus treated with injectable valproic acid.

    Subclinical or nonconvulsive status epilepticus may cause severe postmorbid neurologic dysfunction. It is, therefore, critical to rapidly identify and treat these cases. The recent availability of injectable valproic acid (Depacon) provides an additional method for treatment of status epilepticus, although studies concerning its effectiveness are not widely available in the literature. We report four cases (three pediatric, one adult) of patients who presented to us in status epilepticus. All had previously failed more than one other common method of treatment for this condition. Treatment with injectable valproic acid resulted in the elimination of all clinical indications of status epilepticus as well as a return to the baseline EEG condition in all four cases. Seizure types included focal, multifocal, and generalized spike and wave forms, suggesting potential benefit from injectable valproic acid treatment in a wide range of status epilepticus patients. We present these cases for review.
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7/554. Persistent occipital electrographic status epilepticus.

    A 13-year-old girl of normal intellect had clinically silent occipital electrographic status epilepticus that persisted for more than 3 years. neurologic examination and cranial magnetic resonance imaging were entirely normal. [18F]Fluorodeoxyglucose positron emission tomography demonstrated a hypermetabolic focus in the right occipital lobe. Electrographic status lasting years can be seen in epilepsia partialis continua. However, the absence of focal clinical seizures, nonprogressive course, and normal magnetic resonance imaging study seen in this patient are not features characteristic of epilepsia partialis continua.
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8/554. 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.
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9/554. 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.
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10/554. 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.
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