Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A child had complex partial status epilepticus after resection of a craniopharyngioma. The status epilepticus was manifested by confusion and documented electroencephalographically by continuous focal seizure patterns in the right temporal region. Complex partial status epilepticus is an electroclinical syndrome of prolonged or repetitive complex partial seizures (with continuous interictal confusion) accompanied by electroencephalographic seizure patterns, which are either focal (usually temporal lobe) or secondarily generalized from a focal pacemaker.
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PMID:Complex partial status epilepticus: case report and proposal for diagnostic criteria. 9 91

Complex partial status epilepticus (CPSE) has rarely been reported in children. We experienced a 5-year-old girl having had an abrupt onset of complex partial seizure with a fluctuating state of consciousness and aphasia. Electroencephalogram revealed repetitive epileptiform discharges originating from bilateral temporal and parieto-occipital regions over the background of diffuse continuous slow activity. Computerized tomography of the brain showed mild atrophy without focal lesions. All the other studies including bacteriology, virology, toxicology and metabolic screening were unremarkable. Intravenous administration of diazepam was ineffective for recovery of consciousness level and cease of seizure activity. A lasting control of the status was not achieved until intravenous phenytoin and oral carbamazepine were added for one more weeks. Paroxysmal attacks of periodic apnea with subsequent hyperpneic movements occurred the fourth month after the onset of illness. She regained language on rehabilitation program. Unfortunately, the patient had recurrence four months later despite medication. Finally, she died of aspiration pneumonia and status epilepticus eleven months after the onset of the disease. Compared with the other previously documented cases of prolonged complex partial status epilepticus, this case is notable for its unusual, complicated and severe symptomatology and long duration (three more months) with poor prognosis.
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PMID:Complex partial status epilepticus: report of one case. 263 6

Complex partial status epilepticus with aphasia as the sole manifestation has been reported only twice before. We studied a 60-year-old diabetic who was aphasic for 12 days. The diagnosis of aphasic status was supported by electroencephalographic seizure patterns in the left hemisphere.
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PMID:Aphasic status epilepticus: a case report. 616 33

Complex partial status epilepticus (CPSE) has rarely been described in children. We have recently studied four girls, aged 1 to 4 years, who presented with CPSE. Their seizures were characterized by decreased level of consciousness, lack of response to familiar persons, diminished response to pain, starting, slow visual tracking, eye deviation, picking at nearby objects, and lip smacking. Three patients developed focal clonic activity during their seizures and one progressed to a generalized motor seizure after 4 hours of CPSE. Two patients had ictal electroencephalograms demonstrating temporooccipital polyspikes and slow waves.
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PMID:Complex partial status epilepticus in young children. 725 14

Complex partial status epilepticus developed in two patients following myelography with metrizamide. The status epilepticus was manifested by confusion and complex motor symptoms, and electroencephalograms (EEGs) showed ictal activity alternating independently over both hemisphere. Immediate clinical improvement occurred with antiepileptic treatment, and to date no sequelae have been observed. Neither patient had a previous history of epileptic seizures, but both had preexisting EEG abnormalities.
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PMID:Complex partial status epilepticus following myelography with metrizamide. 743 76

Complex partial status epilepticus (SE) has been reported rarely in children. We describe the clinical case of a 14 year-old girl with complex partial seizures (CPS) since age 10 who developed a complex partial SE probably because she was not adherent to treatment. The neurologic examination and computed tomography scan were normal. During the SE she received diazepam and phenytoin and became free of the seizures after 5 minutes. The ictal EEG showed spikes and slow waves over the right temporal region.
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PMID:Complex partial status epilepticus in a child. 748 37

Determining the prognosis in nonconvulsive status epilepticus (NCSE) is complicated by several factors: under-recognition of NCSE with its spontaneous resolution (thus decreasing the "denominator" of total cases that will have a poor outcome); incorrect diagnosis of NCSE based on misinterpretation of EEG "epileptiform" activity; mis-classification of certain EEG patterns as NCSE (e.g. PLEDs; triphasic waves); and grouping of different populations that have markedly different co-morbidities (ambulatory patients with NCSE together with comatose patients with electrographic seizure activity on EEG). There are almost no prospective studies with premorbid neuropsychometric studies, and retrospective studies typically include isolated cases, or case series that include conditions in which the cause of NCSE itself causes cognitive morbidity. To summarize available data, absence status (ambulatory generalized non-convulsive status epilepticus) would appear to carry no lasting morbidity. Complex partial status epilepticus in ambulatory patients rarely results in measurable permanent neurologic deficit, although rarely, short or long-standing deficits may clearly occur. Because intensive treatment with intravenous anticonvulsants (e.g. benzodiazepines or phenytoin) can confer morbidity, the equation has not yet been made as to whether the morbidity of such intensive treatment for all cases of NCSE exceeds the morbidity of the disease itself. Larger, prospective studies will be needed to truly determine the prognosis in the different types of NCSE, stratified according to associated degrees of impairment (minimally impaired, moderately obtunded, comatose).
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PMID:Prognosis in nonconvulsive status epilepticus. 1117 48

In this second paper the clinical features and electrophysiological underpinnings of more complex psychotic states associated with epilepsy are reviewed. (a) Complex partial status epilepticus, in particular of temporal lobe origin, may result in mental states remarkably similar to those seen in the primary psychoses. This non-convulsive state is associated with prolonged epileptic discharges on intracranial stereoelectroencephalography (SEEG) in hippocampal and other mesial temporal structures, sometimes without abnormalities on the scalp EEG. Where hallucinatory or psychotic symptomatology does occurs, it can be considered an examples of an ictal psychosis. The phenomenology and electrophysiological features of this condition are reviewed. (b) Postictal psychosis is noted for its similarity to schizophrenia-like/paranoid and affective psychoses and there is convincing SEEG evidence that, for some cases at least, the psychosis is not in fact postictal but rather an ictal psychosis due to ongoing limbic seizure activity and a form of non-convulsive status epilepticus. It has been suggested that postictal psychosis should be divided into two sub-groups: the classical 'nuclear' postictal type and an atypical periictal type. (c) Interictal hallucinosis in epilepsy has been poorly studied, but is probably commoner than appreciated. To what extent it represents subclinical epileptic discharges (i.e. auras) is not known. It may interestingly also be associated with abnormal affective states in epilepsy. (d) The interictal psychosis of epilepsy is often indistinguishable from primary schizophrenia. It occurs more commonly in temporal lobe (limbic) epilepsy, in those with frequent seizures and only in patients with a long history of epilepsy (usually over 10 years). There is convincing SEEG evidence of frequent, semi-continuous and sometimes continuous epileptic activity in limbic structures at the time of psychotic and hallucinatory ideation and behaviour, suggesting that in some cases at least, the epileptic activity is the cause of the symptoms. Whether the psychosis is directly 'driven' by subclinical electrographic activity or is indirectly a consequence of function change induced by such activity is not clear. An intriguing question also arises as to whether similar electrophysiological changes could underpin psychosis in patients without epilepsy but evidence on this point is sparse. The effects of temporal lobe surgery on the psychoses of epilepsy are described and these might throw light on the mechanisms of epileptic psychosis. The principles of pharmacological therapy of epileptic hallucinosis and psychosis are outlined.
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PMID:Delusions, illusions and hallucinations in epilepsy: 2. Complex phenomena and psychosis. 1944 90