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The neurocognitive functioning in bipolar disorder: a systematic review of data.

Tsitsipa E, Fountoulakis KN - Ann Gen Psychiatry (2015)

Bottom Line: There are no differences between BD subtypes.Its origin is unclear.This core deficit is confounded (either increased or attenuated) by the disease phase, specific personal characteristics of the patients (age, gender, education, etc.), current symptomatology and its treatment (especially psychotic features) and long-term course and long-term exposure to medication, psychiatric and somatic comorbidity and alcohol and/or substance abuse.

View Article: PubMed Central - PubMed

Affiliation: Aristotle University of Thessaloniki, Thessaloniki, Greece.

ABSTRACT

Background: During the last decades, there have been many different opinions concerning the neurocognitive function in Bipolar disorder (BD). The aim of the current study was to perform a systematic review of the literature and to synthesize the data in a comprehensive picture of the neurocognitive dysfunction in BD.

Methods: Papers were located with searches in PubMed/MEDLINE, through June 1st 2015. The review followed a modified version of the recommendations of the Preferred Items for Reporting of Systematic Reviews and Meta-Analyses statement.

Results: The initial search returned 110,403 papers. After the deletion of duplicates, 11,771 papers remained for further evaluation. Eventually, 250 were included in the analysis.

Conclusion: The current review supports the presence of a neurocognitive deficit in BD, in almost all neurocognitive domains. This deficit is qualitative similar to that observed in schizophrenia but it is less severe. There are no differences between BD subtypes. Its origin is unclear. It seems it is an enduring component and represents a core primary characteristic of the illness, rather than being secondary to the mood state or medication. This core deficit is confounded (either increased or attenuated) by the disease phase, specific personal characteristics of the patients (age, gender, education, etc.), current symptomatology and its treatment (especially psychotic features) and long-term course and long-term exposure to medication, psychiatric and somatic comorbidity and alcohol and/or substance abuse.

No MeSH data available.


Related in: MedlinePlus

The PRISMA flowchart
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Related In: Results  -  Collection

License 1 - License 2
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Fig1: The PRISMA flowchart

Mentions: The initial search returned 110,403 papers. Αfter the deletion of duplicates 11,771 remained. The reference lists of review papers and books were scanned and eventually and after assessing these papers on the basis of title and abstract 250 papers remained for further study (Fig. 1).Fig. 1


The neurocognitive functioning in bipolar disorder: a systematic review of data.

Tsitsipa E, Fountoulakis KN - Ann Gen Psychiatry (2015)

The PRISMA flowchart
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4666163&req=5

Fig1: The PRISMA flowchart
Mentions: The initial search returned 110,403 papers. Αfter the deletion of duplicates 11,771 remained. The reference lists of review papers and books were scanned and eventually and after assessing these papers on the basis of title and abstract 250 papers remained for further study (Fig. 1).Fig. 1

Bottom Line: There are no differences between BD subtypes.Its origin is unclear.This core deficit is confounded (either increased or attenuated) by the disease phase, specific personal characteristics of the patients (age, gender, education, etc.), current symptomatology and its treatment (especially psychotic features) and long-term course and long-term exposure to medication, psychiatric and somatic comorbidity and alcohol and/or substance abuse.

View Article: PubMed Central - PubMed

Affiliation: Aristotle University of Thessaloniki, Thessaloniki, Greece.

ABSTRACT

Background: During the last decades, there have been many different opinions concerning the neurocognitive function in Bipolar disorder (BD). The aim of the current study was to perform a systematic review of the literature and to synthesize the data in a comprehensive picture of the neurocognitive dysfunction in BD.

Methods: Papers were located with searches in PubMed/MEDLINE, through June 1st 2015. The review followed a modified version of the recommendations of the Preferred Items for Reporting of Systematic Reviews and Meta-Analyses statement.

Results: The initial search returned 110,403 papers. After the deletion of duplicates, 11,771 papers remained for further evaluation. Eventually, 250 were included in the analysis.

Conclusion: The current review supports the presence of a neurocognitive deficit in BD, in almost all neurocognitive domains. This deficit is qualitative similar to that observed in schizophrenia but it is less severe. There are no differences between BD subtypes. Its origin is unclear. It seems it is an enduring component and represents a core primary characteristic of the illness, rather than being secondary to the mood state or medication. This core deficit is confounded (either increased or attenuated) by the disease phase, specific personal characteristics of the patients (age, gender, education, etc.), current symptomatology and its treatment (especially psychotic features) and long-term course and long-term exposure to medication, psychiatric and somatic comorbidity and alcohol and/or substance abuse.

No MeSH data available.


Related in: MedlinePlus