Risperidone versus haloperidol on secondary memory: can newer medications aid learning?
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The introduction of the new generation of antipsychotic medications for the treatment of schizophrenia has been accompanied by a growing interest in the neurocognitive effects of these drugs. The present study compared the effects of risperidone and haloperidol on secondary memory in a group of treatment-resistant schizophrenia patients. The study design included a baseline phase and two double-blind phases in which patients were randomly assigned to medication under two different dose conditions (fixed dose and flexible dose). Secondary memory was assessed at baseline, fixed-dose, and flexible-dose phases, using the California Verbal Learning Test (CVLT). Six measures were selected, which formed three factors (general verbal learning ability, retention, and learning strategy). Risperidone-treated patients showed greater improvement than haloperidol-treated patients in general verbal learning ability, a finding characterized by significant treatment effects on CVLT measures of learning acquisition, recall consistency, and recognition memory. After controlling for benztropine status, differences on the measures of learning acquisition and recall consistency remained significant, and differences in recognition memory weakened slightly (p = 0.07). No significant treatment effects were noted on retention or learning strategy. These findings suggest that risperidone may exert a facilitating effect on the acquisition of new verbal information, an effect that does not appear to be due to the activation of semantic encoding strategies. (+info)
The effects of clozapine, risperidone, and olanzapine on cognitive function in schizophrenia.
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Cognitive function is markedly impaired in most patients with schizophrenia. Antecedents of this impairment are evident in childhood. The cognitive disability is nearly fully developed at the first episode of psychosis in most patients. The contribution of cognitive impairment to outcome in schizophrenia, especially work function, has been established. Preliminary results indicate that cognitive function, along with disorganization symptoms, discriminate schizophrenia patients who are able to work full-time from those who are not. Typical neuroleptic drugs lack the ability to improve the various domains of cognitive function impaired in schizophrenia. Atypical antipsychotic drugs pharmacologically related to clozapine-quetiapine, olanzapine, risperidone, sertindole, and ziprasidone--share the ability to produce fewer extrapyramidal symptoms than typical neuroleptic drugs and more potent antagonism of serotonin2a relative to dopamine2 receptors. However, they have a number of different clinical effects. We have identified all the studies of clozapine, olanzapine, and risperidone that provide data on their effects on cognition in schizophrenia. Data for each drug are reviewed separately in order to identify differences among them in their effects on cognition. Twelve studies that report cognitive effects of clozapine are reviewed. These studies provide (1) strong evidence that clozapine improves attention and verbal fluency and (2) moderate evidence that clozapine improves some types of executive function. However, results of the effects of clozapine on working memory and secondary verbal and spatial memory were inconclusive. Risperidone has relatively consistent positive effects on working memory, executive functioning, and attention, whereas improvement in verbal learning and memory was inconsistent. Preliminary evidence presented here suggests that olanzapine improves verbal learning and memory, verbal fluency, and executive function, but not attention, working memory, or visual learning and memory. Thus, atypical antipsychotic drugs as a group appear to be superior to typical neuroleptics with regard to cognitive function. However, available data suggest that these drugs produce significant differences in specific cognitive functions. These differences may be valuable adjunctive guides for their use in clinical practice if cognitive improvements reach clinical significance. The effects of the atypical antipsychotic drugs on cholinergic and 5-HT2a-mediated neurotransmission as the possible basis for their ability to improve cognition are discussed. It is suggested that the development of drugs for schizophrenia should focus on improving the key cognitive deficits in schizophrenia: executive function, verbal fluency, working memory, verbal and visual learning and memory, and attention. (+info)
Cognitive rehabilitation for schizophrenia: problems, prospects, and strategies.
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Increasing awareness of the importance of neurocognitive impairments in schizophrenia has fostered considerable interest in the prospects for cognitive rehabilitation. Nevertheless, optimism has outpaced progress. We first review recent literature on the central assumptions that underlie cognitive rehabilitation, including the hypothesis that cognitive deficits play a central role in social disability and other problems schizophrenia patients experience in daily living, and that these impairments must be rectified if we are to achieve effective rehabilitation. We next discuss developments in knowledge about the neurobiology of schizophrenia that bear on the potential for cognitive rehabilitation and the selection of appropriate targets for intervention. Third, we propose a new research strategy for investigating cognitive functioning in schizophrenia and for examining the relationship of cognitive deficits to role functioning in the community: examining patients who have good vocational outcomes in order to identify strengths or compensatory factors that compensate for core deficits. We present new data that lend support to our proposed approach. We next discuss putative limits to cognitive rehabilitation based on data documenting cognitive deficits in healthy siblings and parents. Finally, we briefly describe an interim rehabilitation strategy that minimizes the load on cognitive processes rather than attempting to improve cognitive functioning. (+info)
Cognitive functioning in schizophrenia: implications for psychiatric rehabilitation.
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Research in psychopathology and the cognitive neurosciences suggests new applications in psychiatric rehabilitation. Analysis of performance deficits on laboratory tasks can contribute to treatment planning, individual and family counseling, and staff consultation, much like it does in cases of brain injury and other types of central nervous system neuropathology. Recognition of the nature of cognitive impairments in schizophrenia can inform design of psychosocial techniques such as social and living skills training. Cognitive impairments are increasingly seen as potential targets for pharmacological and psychosocial treatment and rehabilitation. In this article, three key issues for application of cognitive technology in psychiatric rehabilitation of schizophrenia and related disorders are formulated as straightforward, clinically relevant questions: (1) What is the prognostic significance of cognitive impairment in acute psychosis? (2) Can cognitive functioning improve in the chronic, residual course? (3) How does cognitive improvement benefit other aspects of recovery and rehabilitation? These questions are addressed through review of previous findings and new multivariate analyses of cognitive functioning in the acute, post-acute, and chronic residual phases of schizophrenia. (+info)
The effects of neurocognitive remediation on executive processing in patients with schizophrenia.
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Approaches to cognitive remediation have differed across studies. Most of the larger studies have concentrated on group treatments designed without the benefit of recent laboratory-based studies. The current study describes a randomized trial of an intensive cognitive remediation program involving individual daily sessions of 1 hour for up to 3 months. It targets executive functioning deficits (cognitive flexibility, working memory, and planning) that are known to be problematic in people with schizophrenia. Procedural learning, as well as the principles of errorless learning, targeted reinforcement, and massed practice, was the basis of the intervention. The program was compared with an alternative therapy (intensive occupational therapy) to control for some of the effects of therapeutic contact. Some improvements in cognition followed both therapies. A differential effect in favor of cognitive remediation therapy was found for tests in the cognitive flexibility and the memory subgroups. There was a trend for those receiving atypical antipsychotic medication to benefit more from cognitive remediation for tests of cognitive flexibility. Although there were no consistent changes in symptoms or social functioning between groups, if improvement in cognitive flexibility tasks reached a threshold then there is some evidence that social functioning improved, even over the short duration of the trial. In addition, cognitive remediation differentially improved self-esteem. This study supports the view that cognitive remediation can reduce cognitive deficits and that this reduction may affect social outcome, at least in the short term. (+info)
Should schizophrenia be treated as a neurocognitive disorder?
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The search is on for meaningful psychopharmacological and cognitive/behavioral interventions for neurocognitive deficits in schizophrenia. Findings in this area are emerging rapidly, and in the absence of integrating frameworks, they are destined to emerge chaotically. Clear guidelines for testing neurocognitive interventions and interpreting results are critical at this early stage. In this article, we present three models of increasing complexity that attempt to elucidate the role of neurocognitive deficits in schizophrenia in relation to treatment and outcome. Through discussion of the models, we will consider methodological issues and interpretive challenges facing this line of investigation, including direct versus indirect neurocognitive effects of antipsychotic medications, selection of particular neurocognitive constructs for intervention, the importance of construct validity in interpreting cognitive/behavioral studies, and the expected durability of treatment effects. With a growing confidence that some neurocognitive deficits in schizophrenia can be modified, questions that seemed irrelevant only a few years ago are now fundamental. The field will need to reconsider what constitutes a successful intervention, what the relevant outcomes are, and how to define treatment efficacy. (+info)
Glucose-induced increase in memory performance in patients with schizophrenia.
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Previous investigations have found that increasing circulating glucose availability can increase memory performance in rodents, healthy humans, and individuals with dementia of the Alzheimer's type. In this study, patients with schizophrenia, healthy control subjects, and controls with bipolar affective disorder were tested using double-blind treatment with either 50 g anhydrous dextrose plus 4 mg sodium saccharin (for "taste") or 23.7 mg saccharin alone, followed by cognitive testing on a complex battery. At this glucose dose, verbal memory performance on a paragraph recall task was increased during the glucose condition relative to the saccharin condition in the patients with schizophrenia; this effect was not detected in either the psychiatric or normal controls. The results provide preliminary support for the hypothesis that memory performance can be improved in patients with schizophrenia by increasing circulating glucose availability and suggest the importance of further evaluation of therapeutic manipulations of glucose availability. (+info)
Cognitive asymmetry patterns in schizophrenia: active and withdrawn syndromes and sex differences as moderators.
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Recognition memory for words and faces was examined in male and female schizophrenia patients for evidence of associations between putative left-right hemisphere asymmetry patterns and active (positive) versus withdrawn (negative) syndromes. Ninety-five normal controls and 104 schizophrenia patients with active, withdrawn, and mixed syndromes or in symptom remission were examined, including an unmedicated subgroup. Memory was poorer in patients than controls, while the remitted group had superior memory to psychotic patients. Active and withdrawn patients showed the hypothesized syndrome-dependent cognitive asymmetries: active (word > faces); withdrawn (faces > words), except active females who showed a word deficit. The results support selective lateralized temporoparietal impairment of either hemisphere in schizophrenia, with laterality related to active (face memory/right-sided impairment) and withdrawn (word memory/left-sided impairment) syndromes, except active syndrome females. These syndrome-related asymmetries moderated the sexually dimorphic asymmetries found in normal subjects. Consideration of individual differences both in sex and syndromes based on activity and withdrawal, and of left and right hemisphere memory modality, may assist in unraveling heterogeneity in schizophrenic cognition. The superior memory of recovered patients indicates that some memory impairment in schizophrenia is functional. (+info)