Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most effective method to maintain clinical improvement in the course of schizophrenia is the continuation of neuroleptic therapy. Sometimes we face the dilemma whether neuroleptic administration could be discontinued. There are some unconditional indications for treatment cessation (signs of intolerance, complications, general medical conditions); all other situations can be considered as relative indications. The risk and benefit of treatment discontinuation should be carefully evaluated. Neuroleptic withdrawal seems to be safer among older patients, with single episode of the psychosis of mild severity, with no family history of schizophrenia. It is necessary to achieve a stable clinical improvement before neuroleptic withdrawal. Worsening of the clinical status creates the most important risk of treatment discontinuation. Other risk factors include unacceptable threatening behavior, increase of family burden. The appearance of withdrawal symptoms such as nausea, vomiting, dyskinesia, insomnia, anxiety, etc. are to be considered. These symptoms are rare, and the risk of relapse is smaller when patients were treated with depot neuroleptics before treatment discontinuation than in the case of treatment with oral neuroleptics. Neuroleptic discontinuation and introduction of placebo cause more risk of relapse than continuation of active treatment.
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PMID:[The risk of neuroleptic discontinuation in schizophrenia]. 1078 16

The annexins are water soluble proteins possessing a hydrophilic surface, which belong to a family of proteins which (a) bind ('annex') both calcium and phospholipids, and (b) form voltage-dependent calcium channels within planar lipid bilayers. Annexins types are diverse (94 annexins in 45 species) and they belong to an enormous multigene family that ranges throughout all eukaryotic kingdoms. Although the structure of these proteins is now well known their functional and physiological roles remain largely unknown and circumstantial. Various experimental approaches provided evidence that annexins function as Ca(2+) channels that could act as regulators of membrane fusion. The identity of annexins is derived from the conserved 34 kDa C-terminal domain which comprises four repeats - except for annexin VI, with eight repeats - of a sequence of approximately seventy amino acids, which holds the area known as the 'endonexin fold', with its identifying GXGTDE. Annexins have been placed into three subgroups of (1) tetrad core and short amino terminal, (2) tetrad core and long amino terminal, and (3) octad core and short amino terminal. The repeats are highly conserved, each forming a compact alpha-helical domain comprising five alpha-helices wound in a right-handed superhelix. Four domains are formed, arranged in a nearly flat and cyclical array, with domains I and IV, and II and III respectively forming two tightly organised modules with almost twofold symmetry. A hydrophilic pore lies at the centre of the molecule, forming a prominent ion channel coated with charged and highly conserved residues. The annexin molecule is slightly curved, with both a convex and a concave face. The cation/anion permeability ratios and the selectivity sequence of the ion channels formed by several annexins confirm the selectivity of the annexins for Ca(2+) over other divalent cations, and reveals the importance of structural sites, e.g. amino acid positions 17, 78, 95 and 112 for the identification of the ion channel's position, function and regulation. Some are sensitive to low doses of the phenothiazine drugs, trifluoperazine (an anti-schizophrenia drug) and promethazine (anti nausea drug) La(3+) and Cd(2+), (blockers of voltage-gated Ca(2+) channels) nifedipine (an inhibitor of non-activating Ca(2+) channels). There are two main competing models used to explain in vitro ion channel activity of annexins: one involves changes in the conductance of ion via electrostatic disturbance of the membrane surface; the other involves a much more extensive alteration in protein structure and a correspondingly deeper penetration into the membrane.
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PMID:Biophysical and molecular properties of annexin-formed channels. 1095 28

We report the use of naltrexone for treatment of alcohol use disorder in patients with major psychiatric illness. We reviewed the records of 72 mentally ill outpatients treated with naltrexone for alcohol use disorders at a community mental health center. The psychiatric diagnoses included major depression (n = 37), schizophrenia (n = 17), bipolar illness (n = 11), schizoaffective disorder (n = 7), and gender identity disorder (n = 4). Sixty-one patients (85%) had histories of psychiatric hospitalization. Total retention in naltrexone treatment for at least eight weeks was 81.9%: 5 (6.9%) were lost to follow-up, and 8 (11.1%) discontinued the medication because of side effects, primarily nausea. Patients showed good clinical response to naltrexone, with 82% reducing their drinking by at least 75%, and only 17% relapsing at eight weeks. We conclude that naltrexone is useful in the treatment of dually-disordered patients. The hypothesis that clinical response to naltrexone is facilitated by active alcohol drinking during treatment is discussed.
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PMID:Use of naltrexone in the treatment of alcohol use disorders in patients with concomitant major mental illness. 1107 20

Both antidepressants and neuroleptics are widely used in psychopharmacological treatment. In view of the often equal efficacy of substances belonging to the same class of drugs, potential side effects have become the most important criteria for the selection of a specific drug. The therapeutic effect of antidepressants is mediated by their inhibition of the reuptake of the neurotransmitters noradrenaline and of serotonin. Significant adverse effects may occur through the interaction of the antidepressants with other receptors believed not to be related to the therapeutic action, most importantly the muscarinic acetylcholine receptor (M), the histamine-1 (H1) receptor and the alpha-1 (alpha 1) adrenergic receptor. In contrast to the classical tricyclic antidepressants, the newly available selective serotonin reuptake inhibitors neither block the M1-, H1- nor the alpha 1 receptors. Although the rate of side effects is considerably lower compared to tricyclic antidepressants, adverse effects may, however, occur through the stimulation of different serotonin receptor subtypes (5-HT2A, 5-HT2B, and 5-HT3), leading to anxiety, sleep disturbances and nausea. Neuroleptics are often administered for years or even decades in the treatment of schizophrenia or schizoaffective disorder. The main adverse effects are extrapyramidal symptoms, including parkinsonism, akathisia, dystonic reactions, and tardive dyskinesias. With the introduction of the atypical neuroleptics (e.g. clozapine, risperidone, olanzapine) it became apparent that the antipsychotic effect and the extrapyramidal unwanted effect are not always and inextricably linked. The evidence for the hypotheses of the pathogenetic mechanisms leading to extrapyramidal side effects is reviewed. Both the dopamine receptor hypersensitivity hypothesis and the hypothesis of mitochondrial respiratory chain inhibition are as yet based on indirect evidence. However, if, as suggested by the analyses of mitochondrial energy metabolism, the antipsychotic effect and the adverse effects are unrelated properties of neuroleptics, new principles should be applied in the development of novel neuroleptics. Neuroleptics might then be developed that are effectively antipsychotic but are less likely to produce limiting extrapyramidal side effects.
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PMID:Cell-mediated side effects of psychopharmacological treatment. 1171 30

Ziprasidone is a new antipsychotic with combined dopamine and serotonin receptor antagonist activity. The initial evidence suggests an effective dosage range of 80-160 mg/day. Clinical trials suggest that the drug is an effective antipsychotic in schizophrenia and schizoaffective disorder with a beneficial effect on negative symptoms and symptoms of depression. The main adverse effects appear to be somnolence (14%) and nausea (10%). Ziprasidone has relatively fewer side-effects and yet has at least equivalent efficacy for florid 'positive' symptoms compared with conventional antipsychotics. The additional serotonergic actions deliver further efficacy against 'negative' and affective symptoms of schizophrenia. Reduced effects on cognitive abilities compared to conventional antipsychotics make ziprasidone more attractive still. Barring any unforeseen complications, it appears to a most valuable addition to the antipsychotic agents.
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PMID:Focus on ziprasidone. 1175 85

Well-known adverse effects of amisulpride include nausea, insomnia or tiredness, gastrointestinal, extrapyramidal and endocrine symptoms. Cardiac disorders, however, appear to be an extremely rare complication of the drug. Only a few case reports on this complication have been published so far, which deal with QT prolongation, hypotension, hypertension and palpitations. Bradycardia has not yet been mentioned. Here, we will report on a case of asymptomatic bradycardia that developed subsequent to therapeutic doses of amisulpride in a 25-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient had been rehospitalized for an acute exacerbation of the psychosis. When the patient failed to respond at the beginning of hospitalization, the treatment was changed from clozapine to amisulpride. After a complete switchover to amisulpride, the patient's ECG showed sinus bradycardia and QT prolongation. When the daily dose of amisulpride was reduced from 800 mg/d to 600 mg/d, the patient's ECG quickly normalized (including blood pressure and pulse rate) within a few days. The patient did not report any cardiovascular-related complaints. Since the cardiovascular-specific diagnostics did not yield any indicative results, bradycardia may be a rare complication of amisulpride treatment.
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PMID:Asymptomatic bradycardia associated with amisulpride. 1177 48

Ziprasidone is a new antipsychotic with combined dopamine and serotonin receptor antagonist activity. The initial evidence suggests an effective dosage range of 80-160 mg/day. Clinical trials suggest that the drug is an effective antipsychotic in schizophrenia and schizo-affective disorder with a beneficial effect on negative symptoms and symptoms of depression. The main adverse effects appear to be somnolence (14%) and nausea (10%). Ziprasidone has relatively fewer side effects and yet has at least equivalent efficacy for florid 'positive' symptoms compared to conventional anti psychotics. The additional serotonergic actions deliver further efficacy against 'negative' and affective symptoms of schizophrenia. Reduced effects on cognitive abilities compared to conventional anti psychotics make Ziprasidone more attractive.
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PMID:Brief report on Ziprasidone. 1239 87

A 30-year-old white man with schizophrenia developed anorexia and nausea, and was admitted to hospital for confusion and delirium. He was on olanzapine, 10 days prior to admission. On admission, typical neuroleptic malignant syndrome (NMS) developed with elevated body temperature (39.7 degrees C), obtundation, tremor, rigidity, diaphoresis, fluctuating pupillary diameter, tachycardia, labile hypertension, elevated serum creatine kinase and severe hypernatremia (190 meq/l). Olanzepine was stopped few days after admission to the hospital and the NMS manifestations resolved by hospital day 12. The patient had all of the major manifestations of NMS. There was no other likely explanation for his illness. This is the first case reported in which NMS was associated with olanzapine and extremely elevated levels of serum sodium. Copyright 2001 John Wiley & Sons, Ltd.
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PMID:Neuroleptic malignant syndrome with olanzapine associated with severe hypernatremia. 1240 81

DMSO is an amphipathic molecule with a highly polar domain and two apolar methyl groups, making it soluble in both aqueous and organic media. It is one of the most common solvents for the in vivo administration of several water-insoluble substances. Despite being frequently used as a solvent in biological studies and as a vehicle for drug therapy, the side-effects of DMSO (undesirable for these purposes) are apparent from its utilization in the laboratory (both in vivo and in vitro) and in clinical settings. DMSO is a hydrogen-bound disrupter, cell-differentiating agent, hydroxyl radical scavenger, intercellular electrical uncoupler, intracellular low-density lipoprotein-derived cholesterol mobilizing agent, cryoprotectant, solubilizing agent used in sample preparation for electron microscopy, antidote to the extravasation of vesicant anticancer agents, and topical analgesic. Additionally, it is used in the treatment of brain edema, amyloidosis, interstitial cystitis, and schizophrenia. Several systemic side-effects from the use of DMSO have been reported, namely nausea, vomiting, diarrhea, hemolysis, rashes, renal failure, hypertension, bradycardia, heart block, pulmonary edema, cardiac arrest, and bronchospasm. Looking at the multitude of effects of DMSO brought to light by these studies, it is easily understood how many researchers working with DMSO (or studying one of its specific effects) might not be fully aware of the experiences of other groups who are working with it but in a different context.
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PMID:Multidisciplinary utilization of dimethyl sulfoxide: pharmacological, cellular, and molecular aspects. 1266 39

As the prevalence of tobacco use has decreased, it has become clear that individuals with mental illness comprise a substantial portion of the remaining smokers. Seventy to eighty percent of patients with schizophrenia smoke and their smoking is established before their first psychotic episodes or the initiation of treatment. Many patients with schizophrenia, and approximately 50% of their first degree relatives have abnormalities in auditory sensory gating and/or smooth pursuit eye movements. These abnormalities are corrected by nicotine, and they appear to be transmitted as autosomal dominant traits. Evidence is accumulating that these abnormalities reflect genetic variations in nicotine receptor number and function, that may increase susceptibility for schizophrenia. Recent studies suggest that bupropion, added to treatment with an atypical antipsychotic, can enhance the likelihood of smoking cessation or reduction in patients with schizophrenia. The prevalence of smoking is also substantially increased among patients with bipolar disorder, perhaps especially so among those with psychotic features. Nicotine delivered by gum or transdermal patch can provide short term relief for exacerbations of Tourette's Syndrome, but its use is limited by frequent toxicity, primarily nausea.
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PMID:The importance of nicotinic acetylcholine receptors in schizophrenia, bipolar disorder and Tourette's syndrome. 1276 15


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