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)

Legionella is a frequent etiologic agent in the development of both nosocomial and community acquired pneumonias. Involvement of the nervous system is common in Legionella infections. We present a case of Legionnaires' disease which illustrates distinctive neurologic findings including delirium and cerebellar dysfunction. Furthermore, this paper reviews the neurological and psychiatric features of 609 Legionella infected patients with involvement of the nervous system. The most common signs were disorientation (58%), headache (52.4%), and somnolence (39.7%). Less frequent or rare were: cerebellar dysfunction (11.2%), hallucinations (8.4%), agitation or stupor (4.1%), affective disorders (3.1%), peripheral neuropathy (2.8%), pyramidal disturbances (2.1%), memory loss (1.6%), seizures (1.5%), cranial nerve palsies (1.5%), incontinence (0.7%), and extrapyramidal disturbances (0.3%). Cranial CT scans, cerebrospinal fluid findings, and nerve and muscle biopsies were usually unremarkable. Neuropathologic examinations failed to demonstrate specific characteristics. Hyponatremia and serum CPK level elevation were present in up to 89% and 50% of patients, respectively. Prognosis of disturbances of the nervous system was mainly good. We conclude that in the presence of definite neurological findings, pulmonary infection, hyponatremia, and CPK elevation Legionella infection should be considered.
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PMID:[Neurologic and psychiatric symptoms of legionella infection. Case report and overview of the clinical spectrum]. 927 65

The syndrome of water intoxication, resulting from dilutional hyponatremia and characterized by lethalgy, confusion, seizures, and coma was seen in two autistic boys living in the institution for mentally retarded children. Patient 1, a 19 year-old autistic boy showed loss of attention, inactiveness, sleepiness and delirium and then followed by overbreathing, severe vomiting and finally convulsive seizures several times, or coma, since October 1985. In August 1988, he was admitted with generalized tonic clonic convulsion associated with frequent vomiting EEG showed diffuse spike and wave complex with slow background activity. Laboratory data showed inappropriately high serum ADH level (8.5 pg/ml), low sodium concentration (121 mOsm/m/l), serum osmolality (237 mOsm/l) which was lower than urine osmolality (334 mOsm/l), and remarkable body weight gain (8.5 kg). He was diagnosed as water intoxication due to compulsive water drinking and SIADH. Diminished GH secretion to insulin-induced hypoglycemia and exaggerated prolactin response to LHRH stimulation suggested a hypothalamic lesion. Patient 2, a 17-year-old autistic boy, showed essentially the same symptoms and laboratory data as Patient 1, except that he had no epileptic discharge in EEG, and curious GH response to insulin-induced hypoglycemia. A remarkable daily body weight change suggested excessive water drinking and a possible episodic release of ADH. With mild water restriction, this became smaller. Since Patient 1 had epileptic attacks several times without hyponatremia and his EEG showed epileptic discharges, he was diagnosed as having epilepsy. Patient 2 has been seizure-free until now. Abnormality of hypothalamic or pituitary defects and polydipsia and possibility of water intoxication should always be considered when an autistic patients shows recurrent epileptic attacks or episodic strange behaviors with hyponatremia.
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PMID:[Two cases of infantile autism with intermittent water intoxication due to compulsive water drinking and episodic release of antidiuretic hormone (SIADH)]. 929 11

We conducted an observational study of 539 episodes of alcohol withdrawal in a general hospital, to determine the natural history, the incidences of seizures, hallucinations and delirium, and the risk factors for these events. The reaction began soon after arrival, at a median time of 5 h, and resolved at a median time of 22 h. Patients with a blood alcohol level of zero were in withdrawal on arrival, and only four patients had reactions lasting 120 h or longer. Complications were observed in 113 patients (21%) during the admission. Seizures occurred on arrival, hallucinations usually in the first 24 h and delirium in the first 48 h. No mortality was associated with alcohol withdrawal itself, but complications did extend length of stay by a median of 4 days, with delirium contributing most to the increase. Patients over 70 years of age or admitted with seizures had an increased risk of complication, but the greatest risk was associated with a delay in assessment of > 24 h. We conclude that in general hospitals, the alcohol withdrawal reaction becomes established very early, and detection and monitoring of patients within the first 24 h is the most important element in management.
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PMID:The course of alcohol withdrawal in a general hospital. 932 36

The present study tested the hypothesis that the short, low activity variant of a biallelic polymorphism in the 5' regulatory region of the human serotonin transporter (5-HTT) gene confers susceptibility to severe alcohol dependence marked by severe withdrawal symptoms. Applying a phenotype-genotype strategy, our population-based association analysis included 216 German controls and an extreme sample of 103 severely affected alcoholics who were selected from 315 German alcohol-dependent subjects by a history of alcohol withdrawal seizure or delirium. The frequency of the short allele (S) was significantly increased in the severely affected alcoholics, compared with that in the controls (X2 = 3.87, df = 1, nominal p = 0.049). The post-hoc exploration indicated that this allelic association resulted exclusively from a significant excess of the S/S genotype in the severely affected alcoholics (p = 0.035), suggesting a recessively acting effect. Consistently, we found a weak but significant correlation (p = 0.013) between the frequency of the S/S genotype and severity of withdrawal symptoms (WDS): no WDS [18.3%, odds ratio (OR) = 1.16], vegetative WDS only (21.8%, OR = 1.44), and severe WDS with either withdrawal seizure only or delirium only (25.0%, OR = 1.69), and both withdrawal seizure and delirium (30.8%, OR = 2.30). Further studies are required to test whether the tentative genotype-phenotype relationship occurred by chance or reflects a real genotypic association between a recessively modifying effect of the short variant of the functional 5-HTT promoter polymorphism and alcohol withdrawal vulnerability.
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PMID:Association analysis of a regulatory variation of the serotonin transporter gene with severe alcohol dependence. 939 4

Subacute encephalopathy with seizures in alcoholics (SESA syndrome) is a rare disease entity following chronic alcohol ingestion. It is quite distinct from alcohol withdrawal syndromes, such as delirium, withdrawal seizures or CNS complications of alcohol, such as Wernicke-Korsakow syndrome, central pontine myelinolysis or Marchiafava-Bignami disease, and was proposed in 1981 by Niedermeyer and coworkers. This syndrome consists of multiple neurological deficits, such as hemiparesis or hemianopia, and of recurrent focal and generalized seizures associated with prominent EEG features (periodic lateralized discharges, PLEDs). A 72-year-old Caucasian male with chronic alcoholism and an otherwise unremarkable past medical history was admitted to our hospital because of several secondary generalized simple partial seizures. Laboratory investigations revealed elevated levels of gamma-glutamyltranspeptidase and of mean corpuscular volume. Other laboratory investigations and the CSF examinations on three occasions revealed normal values. Cranial computed and magnetic resonance tomography showed cerebral microangiopathy and generalized atrophy. Despite triple anticonvulsive therapy and an intravenous treatment with acyclovir and thiamine, the epileptic seizures persisted. Several EEGs revealed left parietooccipital periodic lateralized epileptiform discharges (PLEDs). The patient died of an intercurrent pulmonary infection about 3 months after the onset of symptoms. The described clinical picture resembles the symptoms of SESA syndrome.
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PMID:[Subacute encephalopathy with epileptic seizures in a patient with chronic alcoholism (SESA syndrome)]. 955 62

Clozapine has been found to be superior to traditional neuroleptics in the treatment of refractory schizophrenia and is increasingly being used to treat schizophrenia, affective disorders, some neurological disorders, and aggression. For many patients, clozapine offers new hope for the successful pharmacological management of a disabling mental disorder. However, up to 17 percent of patients must discontinue treatment with clozapine because of adverse effects, which also limit the rate at which the dose can be increased and the maximum dose that can be tolerated. This article reviews strategies for minimizing and managing the adverse effects of clozapine, including agranulocytosis, seizures, sedation, delirium, obsessive-compulsive symptoms, hypotension, tachycardia, weight gain, sialorrhea, elevated liver enzymes, constipation, nausea, enuresis, fever, and neuromuscular effects. Incidence and morbidity are presented first. Then, the known or hypothesized pathophysiology of the adverse effects are described. Finally, nonpharmacological and pharmacological interventions are reviewed. Under-standing the incidence, pathophysiology, and treatments of adverse effects is essential for a positive therapeutic outcome when prescribing clozapine.
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PMID:Management of the adverse effects of clozapine. 971 30

Reye syndrome (RS) is an acute encephalopathy in childhood, and is very rare in adulthood. Here we report a 21-year-old woman with RS. Because of her dysmenorrhea, she took 3 tablets of diclofenac sodium (25 mg) per day in 3 divided doses for two days. Two days after the last intake of the medicine, she developed high fever, nausea, vomiting, and disturbance of consciousness with delirium, i.e., acute encephalopathy. She did not have seizure, hemiplegia, or other focal neurological manifestations. The serum GOT level was normal at onset, but in 12 hours dramatically increased up to 8,632 IU/L. The serum bilirubin level was normal. The cerebrospinal fluid revealed normal cell count, and protein. Although the liver biopsy was not performed because of thrombocytopenia, we diagnosed her as an adult case of RS according to the clinical criteria of the Center for Disease Control. In addition to treatment for the brain edema, plasma exchange was performed once treat the encephalopathy at the onset. The next day, her consciousness level and serum GOT level markedly improved. She completely recovered from acute encephalopathy in a week after her admission. In conclusion, diclofenac sodium, as well as aspirin, should be considered as a possible causal agent for RS, and early plasma exchange may be beneficial.
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PMID:[An adult case of Reye syndrome induced by diclofenac sodium, and recovered by plasma exchange]. 974 77

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.
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PMID:[Severe and complicated malaria. Report of six cases]. 977 80

Although outcomes from coronary artery bypass grafting (CABG) surgery have improved in general, there has been little or no improvement in the incidence of postoperative stroke or neurologic dysfunction. Several studies have identified factors that increase the CABG patient's risk for developing a stroke and neurologic complications. It is important to identify those patients at increased risk and differentiate among stroke, delirium, and seizures. Post-CABG patients need to be monitored for neurological dysfunction with appropriate assessments. Neurologic complications must be appropriately managed to optimize patient recovery.
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PMID:Neurologic complications after coronary artery bypass grafting. 978 3

Mu-Opioid receptor-mediated neurotransmission is involved in the reward, tolerance, and withdrawal effects of alcohol. The present association study tested the hypothesis that the common Asn40Asp substitution polymorphism in the N-terminal domain of the human mu-opioid receptor (OPRM) confers vulnerability to subtypes of alcohol dependence. The genotypes of the Asn40Asp substitution polymorphism were assessed in 327 German alcohol-dependent subjects (according to ICD-10) and in 340 control subjects of German descent, using an assay based on allele-specific polymerase chain reaction. To select alcoholics with a presumed high genetic load, three subgroups were delineated, marked by (1) a family history of parental alcoholism (n = 114); (2) the inability to abstain from alcohol before the age of 26 years (n = 73); and (3) a history of alcohol withdrawal seizure or delirium (n = 107). The frequency of the Asp40 allele did not differ significantly between the controls [f(Asp40) = 0.078] and either the entire group of alcoholics [f(Asp40) = 0.107; p = 0.066], or the alcoholics with parental alcoholism [f(Asp40) = 0.114; p = 0.094], or the early-onset alcoholics [f(Asp40) = 0.096; p = 0.471,[ or the alcoholics with severe withdrawal symptoms [f(Asp40) = 0.098; p = 0.350]. Our results do not provide evidence that the common Asn40Asp substitution polymorphism of the OPRM gene contributes a major effect to the pathogenesis of alcohol dependence.
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PMID:Human mu-opioid receptor variation and alcohol dependence. 988 58


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