Cases reported "Status Epilepticus"

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1/199. Unusual presentation and course of hiv-1 progressive encephalopathy.

    The present report concerns a vertically human immunodeficiency virus type 1 (hiv-1)-infected 7-year-old child, in whom a neurodegenerative disease occurred after an acute neurologic disorder that was in all likelihood symptomatic of hiv-1 encephalitis. At the steady state the neurologic disease fulfilled the accepted criteria of HIV-related progressive encephalopathy of childhood and was characterized by involvement of multiple neural systems and subcortical dementia. The neurologic disease displayed, however, atypical presentation and course, and its acute focal onset led the authors to postulate an acute and direct involvement of the brain in hiv-1 infection. The correlation between the cliniconeuroradiologic data and levels of HIV-rna in the cerebrospinal fluid and the response to different antiretroviral treatments are also discussed.
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ranking = 1
keywords = childhood
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2/199. 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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ranking = 6.219132759823
keywords = lobe
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3/199. 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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ranking = 4
keywords = childhood
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4/199. 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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ranking = 13344.605750203
keywords = epilepsy, childhood
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5/199. 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.
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ranking = 13340.605750203
keywords = epilepsy
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6/199. 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.
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ranking = 80.952356031989
keywords = frontal, lobe
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7/199. 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.
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ranking = 2668.1211500406
keywords = epilepsy
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8/199. Tiagabine-induced absence status in idiopathic generalized epilepsy.

    Several medications such as baclofen, amitriptyline and even antiepileptic drugs such as carbamazepine or vigabatrin are known to induce absence status epilepticus in patients with generalized epilepsies. Tiagabine (TGB) is effective in patients with focal epilepsies. However, TGB has also been reported to induce non-convulsive status epilepticus in several patients with focal epilepsies and in one patient with juvenile myoclonic epilepsy. In animal models of generalized epilepsy, TGB induces absence status with 3-5 Hz spike-wave complexes. We describe a 32-year-old patient with absence epilepsy and primary generalized tonic-clonic seizures since 11 years of age, who developed her first absence status epilepticus while treated with 45 mg of TGB daily. Administration of lorazepam and immediate reduction in TGB dosage was followed by complete clinical and electroencephalographic remission. This case demonstrates that TGB can induce typical absence status epilepticus in a patient with primary generalized epilepsy.
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ranking = 21344.969200325
keywords = epilepsy
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9/199. Focal status epilepticus: clinical features and significance of different EEG patterns.

    PURPOSE: Focal status epilepticus is typically diagnosed by the observation of continuous jerking motor activity, but many other manifestations have been described. EEG evidence of focal status may take several forms, and their interpretation is controversial. We detailed the clinical spectrum of focal status in patients diagnosed by both clinical deficit and EEG criteria and contrasted clinical manifestations in patients with different EEG patterns. methods: patients were diagnosed with a neurologic deficit and discrete recurrent focal electrographic seizures or rapid, continuous focal epileptiform discharges on EEG. Clinical findings were determined by chart review. RESULTS: Of 41 patients with focal status, acute vascular disease was the cause in 21; 10 of 41 had exacerbations of prior epilepsy. A variety of clinical seizure types occurred, both before and after the EEG diagnosis, but the diagnosis was not expected in 28 patients before the EEG. Three had no obvious clinical seizures. Focal motor seizures and an abnormal mental status were the most common manifestations at the time of the EEG. With antiepileptic drugs, almost all had control of clinical seizures, and most improved in mental status. patients with rapid continuous focal epileptiform discharges were nearly identical in presentation, likelihood of diagnosis, subsequent seizures, response to medication, and outcome to those with discrete seizures on EEG. CONCLUSIONS: Focal status epilepticus may be seen with a wide variety of clinical seizure types or without obvious clinical seizures. The diagnosis is often delayed or missed and should be considered after strokes or clinical seizures when patients do not stabilize or improve as expected. The diagnosis should be made equally whether patients have discrete electrographic seizures or continuous rapid focal epileptiform discharges on the EEG, and the same response to medications and outcome should be anticipated for the two groups.
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ranking = 2668.1211500406
keywords = epilepsy
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10/199. Postoperative pseudostatus: not everything that shakes is epilepsy.

    Postoperative epileptic seizures are recognised but rare. Psychogenic seizures and pseudostatus epilepticus are relatively common, particularly in the peri-operative period. Our series of five cases of postoperative pseudostatus epilepticus demonstrates that the failure to recognise the psychogenic nature of this condition may cause anaesthetists to give inappropriate and potentially harmful treatment. Psychogenic 'status' is easy to diagnose once it has been considered. Convulsive episodes lasting longer than 90 s, closed eyes during a 'tonic-clonic' attack, retained pupillary response and resistance to eye opening are useful signs. Often there is a history of multiple admissions with 'status epilepticus' and of previous postoperative 'status'.
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ranking = 10672.484600162
keywords = epilepsy
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