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)

Phencyclidine hydrochloride abuse has become increasingly common and should be considered in patients with unexplained acute psychosis, dystonic reactions, status epilepticus, or coma. Two phencyclidine-intoxicated patients had bizarre combinations or disorientation, hallucination, agitation, and dyskinetic motor activity. Supportive care and reduction of sensory stimulation are the basis for management of the symptoms.
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PMID:Phencyclidine poisoning. 124 70

A 61-year-old male had a recurrent fever (approx. 38 degrees C) and one month later, disorientation and forgetfullness became gradually apparent. His mental and somatic status deteriorated progressively with the recurrence of fever; 3 years later he was in a persistent vegetative state accompanied by status epilepticus, and died after 5 years. Mononuclear cytosis (8-20/microliters) and increased protein (20-70 mg/100 ml) were observed in the cerebro-spinal fluid (CSF) at each examination. There was no increase of antibody titers against various viruses, chlamydia, mycoplasma and toxoplasma in the serum and CSF. Neuropathologically, the prominent microscopic finding was patchy scarred foci consisting of neuronal loss replaced by glial tissue throughout the gray matter. A few gliomesenchymal nodules were found. In addition, rod-shaped macrophages were found to varying degrees in all areas of the brain and spinal cord. No viral inclusion bodies were identified. Electron microscopic examination revealed no viral particles in the affected areas. Suspensions of the frozen brain and CSF were inoculated into primary neuron cultures derived from fetal mice and into mouse brains, but the results were negative. There had been five reported cases of chronic nodular encephalitis up until 1971; this case seems to differ from the others by the presence of persistent inflammation and by neuropathologic findings.
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PMID:Chronic persistent nodular polioencephalomyelitis presenting with brain atrophy. 236 92

A prospective study of non-convulsive status epilepticus was undertaken in order to evaluate the occurrence and characteristics of this condition in adults. The diagnosis was established in 22 of 113 patients (19 per cent) presenting with status epilepticus over a 23-month period. Non-convulsive status was most prevalent in the over 60 age group. Its two subgroups, absence status (18 cases) and complex partial status (four cases) were both manifest clinically by a prolonged alteration of consciousness of variable extent. Absence status presented de novo (six cases) or against a background of epilepsy (12 cases), often with a long seizure-free interval before presentation. Precipitating factors included infection, inadequate anticonvulsant medication and benzodiazepine withdrawal. The clouding of consciousness was usually characterised by confusion, disorientation and partial responsiveness. Myoclonic or clonic movements of the eyes, face or jaw were evident in all but two patients. Automatisms, including ambulatory behaviour (three cases) were less common. Serious psychiatric disorders preceded the status in seven cases, and contributed to the difficulty in diagnosis. Complex partial status was associated with underlying cerebrovascular disease in three of four cases, and is characterised by a more severe and variable clouding of consciousness, less frequent facial clonic movements, episodic adversive head and eye movements, and a more gradual recovery after treatment.
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PMID:Non-convulsive status epilepticus: a prospective study in an adult general hospital. 365 54

A 78-year-old woman was admitted to our hospital because of disorientation and fever on January 21, 1992. Two days before admission she experienced vomiting, anorexia and general malaise. Laboratory examinations on admission disclosed a hemoglobin level of 11.1 g/dl and a platelet count of 8,000/microliters. The peripheral blood smear revealed anisocytosis with numerous schistocytes and poikilocytes. Polychromatophilic and nucleated red blood cells were also seen, and the reticulocyte count was 38/1000. Her serum lactate dehydrogenase (LDH) value was 2,977 WU and the total serum bilirubin level was 3.5 mg/dl with 2.7 mg/dl indirect reacting fraction. Serum creatinine was 4.7 mg/dl. Her consciousness became semicomatose after a systemic seizure which lasted approximately 15 seconds and her hemoglobin level decreased to 8.5 g/dl on hospital day 2. Therefore, we diagnosed her as having thrombotic thrombocytopenic purpura (TTP) because of the presence of all 5 features, that is, thrombocytopenia, microangiopathic hemolytic anemia, fluctuating neurologic abnormalities, renal dysfunction and fever. A plasmapheresis with fresh frozen plasma (FFP) replacement was begun on that day. She was also treated with anti-platelet agents, 80 mg/day aspirin, and 300 mg/day dipyridamole. Moreover, packed red blood cells (PRC) were infused. While also receiving diphenylhydantoin and phenobarbital to prevent convulsions, status epilepticus developed on day 3. Because of inhibited spontaneous respiration which was an adverse effect derived from diazepam and sodium thiamylal administered intravenously to treat the status epilepticus, an artificial respiration was initiated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An elderly case of thrombotic thrombocytopenic purpura]. 848 87

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
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PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

The clinical course of a 9-year-old diagnosed with attention-deficit hyperactivity disorder, obsessive-compulsive disorder, and Tourette's disorder and treated with a combination of methylphenidate, clonidine, and fluoxetine is described. The patient experienced over a 10-month period, signs and symptoms suggestive of metabolic toxicity marked by bouts of gastrointestinal distress, low-grade fever, incoordination, and disorientation. Generalized seizures were observed, and the patient lapsed into status epilepticus followed by cardiac arrest and subsequently expired. At autopsy, blood, brain, and other tissue concentrations of fluoxetine and norfluoxetine were several-fold higher than expected based on literature reports for overdose situations. The medical examiner's report indicated death caused by fluoxetine toxicity. As the child's adoptive parents controlled medication access, they were investigated by social welfare agencies. Further genetic testing of autopsy tissue revealed the presence of a gene defect at the cytochrome P450 CYP2D locus, which results in poor metabolism of fluoxetine. As a result of this and other evidence, the investigation of the adoptive parents was terminated. This is the first report of a fluoxetine-related death in a child with a confirmed genetic polymorphism of the CYP2D6 gene that results in impaired drug metabolism. Issues relevant to child and adolescent psychopharmacology arising from this case are discussed.
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PMID:Fluoxetine-related death in a child with cytochrome P-450 2D6 genetic deficiency. 1075 79

Eleven of 89 dogs (12 per cent) developed neurological signs within six days of surgical attenuation of a congenital extrahepatic portosystemic shunt. Neurological signs were not associated with hepatic encephalopathy or hypoglycaemia. Signs varied in severity from non-progressive ataxia (three dogs) to generalised motor seizures (four dogs), progressing to status epilepticus (three dogs). In a further four cases, ataxia and disorientation were treated vigorously with anticonvulsant medication, presumably preventing the development of seizures. Two dogs that developed status epilepticus died or were eventually euthanased. All other animals survived, although some had persistent neurological deficits. Postligation neurological complications were not prevented by gradual shunt attenuation. Prophylactic treatment with phenobarbitone (5 to 10 mg/kg preoperatively, followed by 3 to 5 mg/kg every 12 hours for three weeks) did not significantly reduce the incidence of neurological sequelae (2/31 [6 per cent] dogs with phenobarbitone vs 9/58 [16 per cent] without phenobarbitone; P = 0.2). However, no animal receiving phenobarbitone experienced generalised motor seizures or status epilepticus. In conclusion, these observations suggest that postligation neurological syndrome comprises a spectrum of neurological signs of variable severity. Perioperative treatment with phenobarbitone may not reduce the risk of neurological sequelae, but may reduce their severity.
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PMID:Neurological dysfunction in dogs following attenuation of congenital extrahepatic portosystemic shunts. 1113 52

Fever is one of the most frequent causes of hospital admission in patients with end-stage renal disease. Lack of an identified source of infection and/or lack of clinical response to the first empirical antibiotic treatment favour the use of broader spectrum antibiotics. The availability of fourth-generation cephalosporins (e.g. cefepime) and the increasing incidence of bacterial resistances to classical antibiotics has increased their use in the clinical practice. We present two cases of non-convulsive status epilepticus in patients with advanced chronic renal failure who received cefepime at doses corrected for the degree of renal function according to the manufacturer's instrument as. The clinical symptoms included shouthough, processes, disorientation, loss of attention, and the later appearance of myoclonus. In both cases the electroencephalogram (EEG) was compatible with non-convulsive epileptic status. After cefepime withdrawal there was a clinical remission of symptoms and normalization of the EEG. It is concluded that cefepime treatment can induce a non-convulsive epileptic status in patients with advanced chronic renal failure. Pharmacokinetic studies are urgently needed to clearly define the appropriate dose of cefepime in patients with advanced chronic renal failure.
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PMID:[Non-convulsive status epilepticus secondary to adjusted cefepime doses in patients with chronic renal failure]. 1121 51

There is a growing number of publications in the recent literature reporting the incidence of non-convulsive status epilepticus in the elderly, including both absence epilepsy and partial epileptic seizures. Absence status epilepticus creates a diagnostic problem because of its clinical features: confusion ranging from slight disorientation to stupor. Duration of such states may vary from one hour to a few weeks, with fluctuations and epileptic features in EEG recording (a typical pattern of spikes-slow waves, 3 Hz frequency, symmetrical and synchronical) that disappear after an intravenous injection of benzodiazepines. Absence status epilepticus can be evoked by toxic, metabolic or pharmacological factors as well as by convulsive epileptic seizures. Besides absence epileptic states of middle-cerebral origin there is a rising concern about absence status resulting from simple or complex partial seizures. Generalized non-convulsive status epilepticus following either simple partial or simple complex seizures is characterized by the presence of various focal signs associated with confusion, stupor or coma. The latter may be masking the clinical picture of an underlying cerebral pathology (e.g. brain tumor, hemorrhage, etc.), and epileptic changes can be seen in EEG recording only. Absence status epilepticus can occur in various forms of brain pathology, including stroke, brain tumors, traumatic lesions and other conditions, as well as in systemic diseases affecting the central nervous system function. Therefore, the authors emphasize the importance of electroencephalography in severely ill and unconscious patients, as well as the role of proper anti-epileptic treatment, as this may improve the outcome.
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PMID:["De novo" non-convulsive status epilepticus in adults and in the elderly]. 1459 57

The purpose of this study is to report the case of a patient with normal lithium serum levels who developed non-convulsive status epilepticus (NCSE). A 52-year-old woman with bipolar disorder type I (DSM-IV) treated with lithium experienced bradypsychism and episodes of confusion and spatial disorientation without signs or symptoms of lithium intoxication. Lithium serum levels were in the normal range. A brain MR scan was negative; the electroencephalogram (EEG) revealed a background 3-4 Hz delta rhythm and diffuse spike discharges. Prompt EEG and clinical response to intravenous diazepam therapy was observed. Based on these findings, a diagnosis of NCSE was made and lithium therapy was withdrawn, resulting in symptom remission and EEG normalization. The treatment was resumed after two months to test the correlation between NCSE and lithium therapy. Resumption of therapeutic range lithium induced the same clinical symptoms and EEG patterns; the therapy was thus definitively discontinued. The present data-signalling the temporal correlation of clinical and EEG changes with drug administration and withdrawal-suggest that even in the therapeutic range lithium treatment may trigger NCSE onset in predisposed subjects.
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PMID:Non-convulsive status epilepticus during lithium treatment at therapeutic doses. 1660 39


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