Treatment with amisulpride and olanzapine improve neuropsychological function in schizophrenia

Mortimer, Ann; Joyce, Eileen M.; Balasubramaniam, Krishnapillai; Choudhary, Prasoon C.; Saleem, P.

doi:10.1002/hup.865

Cited by 24 publications

(11 citation statements)

References 44 publications

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“…Patients were found to perform markedly worse than control subjects for all six cognitive domains, and for all individual tests, except for a few concentration, visuo-spatial construction, and motor speed tasks. More pronounced cognitive dysfunctions found in patients compared to siblings and controls could be partially explained by side effects of psychotropic medications that can exert significant effects on cognitive functions (Keefe et al 2007;Mortimer et al 2007;Voruganti et al 2007). Siblings performed worse than the control group with P values indicating a trend towards statistical significance for a number of cognitive variables.…”

Section: Discussionmentioning

confidence: 86%

Cognitive profiles of healthy siblings of schizophrenia patients: Application of the cognitive domains of the MATRICS consensus battery

Nam

Kim

Park

et al. 2009

The World Journal of Biological Psychiatry

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Even though a large body of data suggests the presence of various types of cognitive deficits in the unaffected relatives of schizophrenia patients, more study is needed to clarify the comparative sensitivities of specific cognitive measures for relative-control differences. In this study, the authors compared the cognitive profiles of unaffected siblings of schizophrenia patients and those of patients and normal controls, and attempted to identify cognitive markers that might be associated with genetic liability to schizophrenia. Eighty-eight clinically stable schizophrenia patients, 44 healthy patient siblings, and 100 normal controls were evaluated using comprehensive neuropsychological tests. The domain structure of the MATRICS consensus cognitive battery was adopted, and both domain scores and individual test scores were used in the analysis. Performances of the sibling group were intermediate between those of patients and controls on most measures. A significant difference between the sibling and control groups was observed only in the Category Fluency Test. This cognitive deficit might be caused by familial predisposition to schizophrenia and could be a candidate of endophenotype for schizophrenia.

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Section: Discussionmentioning

confidence: 86%

Cognitive profiles of healthy siblings of schizophrenia patients: Application of the cognitive domains of the MATRICS consensus battery

Nam

Kim

Park

et al. 2009

The World Journal of Biological Psychiatry

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“…This was partly replicated98 in a comparison of amisulpride and olanzapine: patients’ cognition improved on both drugs, thus detracting from the notion that 5HT2A antagonism was a necessary prerequisite for antipsychotic drug induced enhancement of cognition in schizophrenia. A more recent randomized 6-month trial of acute patients again demonstrated cognitive improvements on both olanzapine and amisulpride99 but there was a particular advantage for amisulpride in a verbal memory test.…”

Section: Amisulpride and Cognitionmentioning

confidence: 96%

Update on the management of symptoms in schizophrenia: focus on amisulpride

Mortimer¹

2009

NDT

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Amisulpride is an atypical antipsychotic drug with a unique receptor pharmacology which is dose dependent. It is a standard treatment in dysthymia as well as in psychosis. Amisulpride is efficacious, effective and well tolerated in positive symptoms of schizophrenia: there is extensive evidence that it treats negative symptoms when given in low doses, although relative lack of EPS and an antidepressant effect may contribute. In first-episode patients amisulpride is an option, although there is little comparative work available. Amisulpride has the best evidence as an effective adjunct to clozapine treatment. Regarding intellectual function, amisulpride appears cognitive sparing but the clinical relevance of this remains obscure. There is evidence that amisulpride can improve social function but again there is little comparative work to demonstrate any particular advantages. Regarding the current conventional versus atypical antipsychotic controversy, amisulpride did better in switching studies and meta-analyses than in the single large pragmatic randomized trial reported to date. It is a versatile drug, and may offer advantages over other atypical antipsychotic drugs in the treatment of negative and depressive symptoms, and tolerability advantages such as the avoidance of weight gain. Essentially it rests with the treating clinician to employ a rational psychopharmacological approach towards the individual patient: there will be few circumstances in which amisulpride will not be a likely contender as a treatment choice.

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“…Thus, despite having a pharmacological profile reminiscent of a typical antipsychotic in that it exhibits high D 2 affinity and low 5-HT 2A affinity, amisulpride therapeutically resembles atypical antipsychotics. Amisulpride has also been reported to improve the cognitive domains of attention, executive function, and working memory, as well as the global cognitive index in patients with schizophrenia (Deeks and Keating 2008), and declarative memory in another study (Mortimer et al 2007). However, it has also been shown to impair recognition memory in normal subjects (Gibbs et al 2008), (Mortimer et al 2007).…”

Section: Introductionmentioning

confidence: 95%

Amisulpride is a potent 5-HT7 antagonist: relevance for antidepressant actions in vivo

et al. 2009

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Rationale Amisulpride is approved for clinical use in treating schizophrenia in a number of European countries and also for treating dysthymia, a mild form of depression, in Italy. Amisulpride has also been demonstrated to be an antidepressant for patients with major depression in many clinical trials. In part because of the selective D2/D3 receptor antagonist properties of amisulpride, it has long been widely assumed that dopaminergic modulation is the proximal event responsible for mediating its antidepressant and antipsychotic properties. Objectives The purpose of these studies was to determine if amisulpride’s antidepressant actions are mediated by off-target interactions with other receptors. Materials and Methods We performed experiments that: (1) examined the pharmacological profile of amisulpride at a large number of CNS molecular targets and (2) after finding high potency antagonist affinity for human 5-HT7a serotonin receptors, characterized the actions of amisulpride as an antidepressant in wild-type and 5-HT7 receptor knock-out mice. Results We discovered that amisulpride was a potent competitive antagonist at 5-HT7a receptors and that interactions with no other molecular target investigated here could explain its antidepressant actions in vivo. Significantly, and in contrast to their wildtype littermates, 5-HT7 receptor knockout mice did not respond to amisulpride in a widely used rodent model of depression, the tail suspension test. Conclusions These results indicate that 5-HT7a receptor antagonism, and not D2/D3 receptor antagonism, likely underlies the antidepressant actions of amisulpride.

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Treatment with amisulpride and olanzapine improve neuropsychological function in schizophrenia

Abstract: Both amisulpride and olanzapine produce sustained improvement in certain measures of neuropsychological performance in patients with schizophrenia; a significant improvement in score on the AVLT was observed only with amisulpride.

Cited by 24 publications

References 44 publications

Cognitive profiles of healthy siblings of schizophrenia patients: Application of the cognitive domains of the MATRICS consensus battery

Cognitive profiles of healthy siblings of schizophrenia patients: Application of the cognitive domains of the MATRICS consensus battery

Update on the management of symptoms in schizophrenia: focus on amisulpride

Amisulpride is a potent 5-HT7 antagonist: relevance for antidepressant actions in vivo

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