A Study of the Association between Psychotropic Drugs and Cognitive Dysfunction in Patients with Schizophrenia

Background: Cognitive deficits among patients with schizophrenia are now recognized as being widelyprevalent and one of the most disabling aspects of the illness, as they are associated with poor functionaloutcomes. Psychotropic medications and benzodiazepines, which are often used in these patients couldimpact cognition as could the extrapyramidal side-effects. Yet, here are hardly any Indian studies on thesubject. The aim of this study was to determine whether cognitive dysfunction among patients withschizophrenia is associated with extrapyramidal symptoms, anticholinergic burden of psychotropic drugsand benzodiazepine dosageMethodology: 40 clinically stable, out-patients suffering from schizophrenia, without any pre-existingneurological disorders between the ages of 18 to 60 years, who had been compliant with medications wereselected. Extrapyramidal symptoms (EPS) were assessed using the modified Simpson-Angus scale,anticholinergic burden (ACB) was evaluated using the Anticholinergic burden scale. The benzodiazepinedosage was noted. Cognition was assessed using the Stroop Color and Word Test and the Wisconsin Cardsorting test. The correlations between scores on EPS and ACB and neuropsychological tests were carriedout using partial correlations controlling for positive and negative symptoms.Results: There were no significant associations noted between extrapyramidal symptoms, anticholinergicburden, benzodiazepine dosage and performance on the neurocognitive tests used.Conclusion: Methodological differences make it difficult to construct comparisons across studies but thereis some evidence to support our findings

Update on Medications in Schizophrenia

Antipsychotics are a pharmacologically heterogeneous group of compounds, but all act as D2 dopamine receptor antagonists, an action linked to their antipsychotic effect. Today, sixty years on since 1952, we have the FGAs and the SGAs. These medications continue to be useful, and continue to have some troubling adverse effects. As a class, the FGAs are more likely to be associated with EPS but this is primarily true of medications that bind tightly with D2 neuroreceptors, such as haloperidol, and less true of medications that bind weakly, such as chlorpromazine. Anticholinergic effects are especially prominent with weaker-binding FGAs, as well as with the SGA clozapine. As a class, the SGAs, especially clozapine and olanzapine generally tend to cause more problems relating to the metabolic syndrome, such as obesity and type 2 diabetes mellitus. All antipsychotic medications are associated with an increased likelihood of sedation, sexual dysfunction, postural hypotension, prolonged QT interval and sudden death. Primary care physicians need to be familiar with the individual adverse effect profiles of these medications.

Síntomas de discontinuación luego de suspensión abrupta de olanzapina / Discontinuation symptoms following olanzapine abrupt withdrawal

Extended use of atypical neuroleptics in clinical practice, may be explained by their effectiveness as antipsychotics and also with recent approvals for therapeutic benefits of this drugs beyond psychotic disorders. Receptor adaptation mechanisms rises critical issues about treatment discontinuation strategies. Clinical data of two patients who have required the use of atypical antipsychotics are discussed. In both cases, abrupt discontinuation of the drug occurred followed by the emergence of extrapyramidal symptoms. Adaptation mechanisms in synaptic structures would be responsible for this phenomena and the subsequent amelioration of this extrapyramidal symptoms when initial treatment is replaced. The authors concluded that atypical antipsychotics, as other psychotropic agents shouldn't be abruptly discontinued even when they are replaced by other drugs from the same family.

El uso de los antipsicóticos atípicos ha ido aumentando con el tiempo entre otras cosas, por el hecho de que se están usando no sólo para los cuadros psicóticos sino que también para otras patologías. Como con otros fármacos que actúan a nivel de receptores deben considerarse los mecanismos de adaptación receptorial que se producen con su uso. Lo anterior es de suma importancia cuando pensamos en la discontinuación del tratamiento y en sus formas de hacerlo. En este trabajo presentamos dos casos clínicos de pacientes que han requerido el uso de antipsicóticos atípicos. En ambos casos se ha realizado una suspensión brusca del fármaco lo que ha generado la aparición de síntomas extrapiramidales, que en nuestra opinión, son explicados por mecanismos de adaptación a nivel sináptico y que han disminuido con el reinicio del tratamiento inicial. Debemos tener presente que estos fármacos no deben ser discontinuados en forma súbita aun cuando sean remplazados por otros de la misma familia.

Comparison of Intramuscular Olanzapine and Intramuscular Haloperidol in Treatment of Acute Agitation in Patients of Schizophrenia.

Objectives: To determine the antipsychotic efficacy and extra pyramidal safety of intramuscular olanzapine and intramuscular haloperidol during the first 24 hours of treatment of acute agitation in schizophrenia. Methods: Patients (n = 29) with schizophrenia were randomly allocated to receive one to three injections of intramuscular olanzapine (10 mg, n =14), intramuscular haloperidol (10 mg, n = 14) over a 24-hour period. Agitation was measured with the excited component of the positive and negative symptom scale (PANSS) and agitation behavior scale (ABS). Results: After the first injection, IM olanzapine was comparable to IM haloperidol for reducing mean changes in scores from baseline on excited component of PANSS at 2 hours to ( -13.08 olanzapine, -8.07 haloperidol ) and at 24 hours (-9.86 olanzapine, -8.07 haloperidol ). Mean changes in the scores of ABS scale from baseline was at 2 hours (-9.78 olanzapine, -8.54 haloperidol) and at 24 hours (-6.14 olanzapine, -6.6 haloperidol). Patients treated with IM olanzapine had significantly fewer incidence of treatment emergent Parkinsonism (0% olanzapine versus 6.66% haloperidol, p = 4.55), no patient had akathisia with olanzapine as compared to 13.33% of patients with haloperidol, p = 2.03. No patient developed acute dystonia compared to 6.66% of patients with haloperidol, p = 2.59. Conclusion: IM olanzapine was comparable to IM haloperidol in reduction of symptoms of acute agitation in schizophrenia during first 24 hours of treatment, the efficacy of both being evident within 2 hours after first injection. More Extra pyramidal symptoms were observed during treatment with IM haloperidol than with IM olanzapine.