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)

Alcohol withdrawal syndrome (AWS) may result in nausea, vomiting, diarrhea, weakness, sweating, tremors, tachycardia, hypertension, agitation, delirium, hallucinations, seizures, and death beginning 6 hours after alcohol cessation in alcoholics. Benzodiazepines are cross-tolerant with ethanol and are considered first-line therapy for treating AWS. Chlordiazepoxide and diazepam are first metabolized by hepatic oxidation, then glucuronidation. Lorazepam and oxazepam undergo only hepatic glucuronidation. Benzodiazepine oxidation is decreased in persons with liver disease and the elderly. Accumulation with resultant excessive sedation and respiratory depression may be significant when administering chlordiazepoxide or diazepam to patients with impaired oxidative metabolism. Lorazepam and oxazepam metabolism is minimally affected by age and liver disease. Chlordiazepoxide and diazepam are erratically absorbed by the intramuscular route. Lorazepam is predictably absorbed by the intramuscular route. Oxazepam is not available in parenteral form. Lorazepam appears to be the safest empiric choice among the various benzodiazepines for treating AWS in the elderly and in patients with liver disease, or those who require therapy by the intramuscular route.
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PMID:Benzodiazepines for alcohol withdrawal in the elderly and in patients with liver disease. 870 Jul 92

The goal of this paper is to draw conclusions about the usefulness of the standard EEG in psychiatry. In general, two thirds of psychiatric referrals for an EEG are expected to provide useful information. The emphasis in schizophrenia is placed on left-sided abnormalities, especially on the left temporal area. In mood disorders the emphasis is on right-sided foci, in addition to the controversial 6/sec spike and wave complexes, small sharp spikes and positive spikes. In the acute stage of alcoholism, a relationship is seen between the degree of intoxication and the amount of slow activity, while in the chronic stage an increase in slow activity is seen, but another change is fast activity on the temporal areas. During withdrawal a low seizure threshold can be seen as irregular bilateral spike and wave complexes. During abstinence 2-4 yr may be required before slow wave sleep is normal in all regards. Among the organic mental syndromes, delirium shows slow activity, except in delirium tremens, which often is associated with a normal record with fast activity. In dementia the prevalence of EEG abnormalities is related to the degree of impairment. After five sessions of ECT diffuse slow waves are often seen. In other conditions, among developmental disorders about one half of autistic children show abnormalities and epileptiform activity is not uncommon. Mild nonspecific abnormalities are seen in about 40% of dyslexics and also in behavior disorders. Anxiety disorders include anorexia nervosa, showing abnormal background activity related to the effect of starvation on cerebral metabolism. In panic attacks paroxysmal activity can be seen. In borderline personality positive spikes have been (again) associated with impulsivity and 6/sec spike and wave complexes with interpersonal problems. Of the drugs of abuse psilocybin and phencyclidine are often associated with generalized epileptiform patterns and with marijuana the alpha shows a decreased frequency with increased amplitude. Typically, an increase in slow activity is seen with psychotropic drugs if there is a change in the level of awareness. Finally, distinctive personality traits are, at times, seen in temporal lobe epilepsy and the phenomenon of "forced normalization" may appear when seizures stop and psychotic symptoms appear.
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PMID:A review of the usefulness of the standard EEG in psychiatry. 871

Hereditary factors play a substantial role in the etiology of alcohol dependence. Alcohol mediates its reinforcing effects by an activation of the mesolimbic dopamine system. These findings suggest that the genes encoding the dopamine receptor (DR) subtypes represent high-ranking candidates for susceptibility genes to addictive disorders. Our present population-based association study investigated whether sequence variants of the dopamine D1, D2 and D3 receptor genes confer susceptibility to alcohol dependence in 278 alcoholics, and clinically more homogeneous subgroups ascertained through positive family history, early age at onset, delirium, withdrawal seizures and antisocial tendencies. No evidence for an allelic association was found for the PCR-based TaqA RFLP fo the DRD2 gene and a Bsp1286I RFLP of the DRD1 gene. Without correction for multiple testing, we found a significantly increased allele frequency of a common DRD3 gene variant expressing a serine at position 9 in the extracellular N-terminal part of the receptor protein in 55 alcohol-dependent individuals with delirium (chi 2 = 4.1, df = 1, p = 0.042). Further studies have to examine whether this amino acid substitution or a nearby mutation confers genetic susceptibility to at least a subgroup of alcohol-dependent individuals with delirium.
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PMID:Dopamine D1, D2 and D3 receptor genes in alcohol dependence. 875 Mar 59

We examined 199 consecutive patients who underwent 220 liver transplantations, to define the type, frequency and aetiology of posttransplant neurological complications and their prognostic value. We found neurological complications in 63 patients (32%), mostly involving the central nervous system. The most frequent complications were mental status changes ranging from delirium to coma and seizures. The aetiology was multifactorial, cyclosporin A neurotoxicity being the main cause. Patients with neurological complications had a higher mortality rate than those without. In our series, neurological complications represented a major medical problem with increased morbidity and mortality.
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PMID:Neurological complications of liver transplantation. 875 May 50

We reviewed the records and radiologic studies of eight patients who developed new focal neurologic abnormalities while receiving interleukin-2 (IL2)-based immunotherapy for malignancy or HIV infection. Initial confusion and delirium in the patients evolved into coma, ataxia, hemiparesis, seizures, and cortical syndromes including aphasia, apraxia, and cortical blindness. Imaging studies showed multiple white and gray matter lesions with a predilection for the occipital poles, centrum semiovale, and cerebellum. After cessation of IL2 treatment, seven patients improved to normal or near-normal neurologic function paralleled by resolution of the lesions on scans. One patient improved only minimally. Possible etiologies for the lesions include an IL2-induced cerebral vasculopathy, a direct toxic effect of IL2, or immunologically mediated damage.
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PMID:Multiple cerebral lesions complicating therapy with interleukin-2. 875 14

In a retrospective study of 15.326 EEGs performed from 1983 to 1992 in a psychiatric institute, 83 EEGs (62 patients-13 men and 49 women ranging in age from 59 to 90 years, with a mean age of 74 years) had triphasic waves (TWs). All 62 patients were awake, though they were often confused. Most (n = 56) had dementia, usually severe; 15 also had delirium. There were six nondemented patients (age range, 59-79 years, with a mean age of 67 years). Infrequent etiologies included neuroleptic malignant syndrome (n = 1) and hepatic encephalopathy (n = 1); in four, the cause was uncertain, although all were receiving lithium. EEG features analyzed included frequency of background rhythms, distribution of the TWs, periodicity, and epileptiform abnormalities. Background rhythms were slow in all but seven patients (mean, 6.2 +/- 1.7 [SD] Hz). TWs were maximal posteriorly in 47 patients and anteriorly in six and were diffuse in nine. Neuroimaging studies showed prominent posterior abnormalities in only one case. Periodicity was prominent in four patients; in two the TWs were maximal anteriorly. Interictal epileptiform activity was present in six, a history of seizures in eight, and myoclonus in four. TWs are uncommon in a psychiatric population; they occur primarily in elderly, severely demented patients. They are usually associated with background slowing, are often maximal posteriorly, and occasionally are periodic.
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PMID:Triphasic waves in a psychiatric population: a retrospective study. 885 94

Hereditary factors confer susceptibility to alcohol dependence. Alcohol mediates its reinforcing effects by enhancing dopamine activity in the mesolimbic dopamine system. The role of the dopamine transporter in terminating dopaminergic activity in synaptic neurotransmission suggests that variants of the dopamine transporter gene (DAT1) might contribute to individual differences in vulnerability to addictive behavior. Our population-based association study investigated whether variants of DAT1 confer susceptibility to alcohol dependence in 293 alcoholics and clinically more homogeneous subgroups formed by: positive family history, early age-at-onset, delirium, withdrawal seizures, antisocial tendencies, type 1 and 2 alcoholics. Analyzing a VNTR polymorphism in the 3' untranslated region of DAT1, we found a significantly increased prevalence of the nine-repeat allele in 93 alcoholics displaying withdrawal seizures or delirium, compared with 93 ethnically matched nonalcoholic controls (p = 0.003; OR = 2.44; 95% confidence interval: 1.35-4.43). Our data provide evidence that a major genetic determinant of DAT1 influences vulnerability to severe alcohol withdrawal symptoms.
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PMID:Allelic association of a dopamine transporter gene polymorphism in alcohol dependence with withdrawal seizures or delirium. 902 52

Clozapine is an atypical antipsychotic medication with proven efficacy in the management of refractory schizophrenia. It is also recommended for patients who do not tolerate the extrapyramidal adverse effects of traditional antipsychotic medications. However, the therapeutic promise of clozapine has been limited by a higher incidence of agranulocytosis. Currently, plasma clozapine concentrations are not routinely used in clinical management. Therapeutic effects are monitored empirically during a 6 to 8 week titration period in which the dosage is raised to 300 to 450 mg/day. Clozapine nevertheless fulfils a number of criteria which make it a candidate for therapeutic monitoring. These include an identifiable therapeutic range, an unpredictable dose-concentration relationship between patients, a potential for clinically relevant pharmacokinetic interaction with other drugs and a high probability of patient noncompliance. The therapeutic threshold plasma concentration appears to be about 400 micrograms/L. Concentrations above 1000 micrograms/L increase the risk of adverse effects on the central nervous system (confusion, delirium and generalised seizures). There is no evidence to link increased concentrations of clozapine or its metabolite to the development of agranulocytosis. We conclude that therapeutic drug monitoring can play a useful role in the clinical management of patients treated with clozapine. The clinician is advised to primarily use clinical judgement during dosage escalation, but intermittent monitoring is recommended to quickly optimise a therapeutic dosage for each patient. At steady state, occasional measurements could be made when clinical signs indicate possible toxicity or lack of effect (possibly caused by a lack of compliance or drug interaction). Long term monitoring would, in our view, not be necessary.
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PMID:Will routine therapeutic drug monitoring have a place in clozapine therapy? 906 25

A case of severe opioid toxicity is described in a 52-year-old cancer patient. The patient presented with classical clinical features of central hyperexcitability associated with opioid toxicity: delirium, myoclonus, hallucinations, hyperalgesia, and a possible seizure. This patient had a background of severe psychosocial distress and somatization in addition to a history of benzodiazepine dependence and alcohol abuse. The occurrence of opioid toxicity in this patient highlights the risks of a unidimensional approach to cancer pain, which ignores the non-organic components of pain, such as psychosocial distress, which will not respond to escalating doses of opioid medication.
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PMID:Severe opioid toxicity and somatization of psychosocial distress in a cancer patient with a background of chemical dependence. 920 57

The clbC form of methylmalonic acidaemia is a rare and poorly understood condition which results from impaired biosynthesis of methylcobalamin and adenosylcobalamin. The consequent functional deficiencies of methylmalonyl-CoA mutase and methionine synthase produce both methylmalonic aciduria and homocystinuria. Systemic symptoms and neurological decompensation comprise the clinical phenotype. In an effort to clarify the phenotype and prognosis, we obtained clinical information on 50 patients with methylmalonic acidaemia whose cells had been assigned to the cblC complementation group. We identified two distinct phenotypes; they differed in age of onset, presence of systemic symptoms, type of neurological symptoms, and outcome after diagnosis and treatment. Forty-four patients presented in the first year of life. Feeding difficulties, neurological dysfunction (hypotonia, seizures, developmental delay), and ophthalmological and haematological abnormalities characterized their clinical picture. About one-quarter of those patients died. Survival was associated with neurological impairment; only one infant was neurologically intact at follow-up. Onset in childhood, in contrast, was associated with less severe haematological abnormalities, largely involving the red cell series. Extrapyramidal signs, dementia, delirium or psychosis characterized the neurological findings. Survival, with mild to moderate disability in some, was typical in patients with later onset. Treatment in both groups included hydroxycobalamin, betaine and carnitine; complete normalization of biochemical parameters was rare.
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PMID:Clinical heterogeneity and prognosis in combined methylmalonic aciduria and homocystinuria (cblC). 926 89


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