The neurocognitive functioning in bipolar disorder: a systematic review of data
Tsitsipa and Fountoulakis Ann Gen Psychiatry
The neurocognitive functioning in bipolar disorder: a systematic review of data
Eirini Tsitsipa 2
Konstantinos N. Fountoulakis 0 1
0 Division of Neurosciences, 3rd Department of Psychiatry, School of Medicine, Aristotle University of Thessaloniki , 6, Odysseos street (1st Parodos, Ampelonon str.) 55536 Pournari Pylaia, Thessaloniki , Greece
1 Division of Neu- rosciences, 3rd Department of Psychiatry, School of Medicine, Aristotle Uni- versity of Thessaloniki , 6, Odysseos street (1st Parodos, Ampelonon str.) 55536 Pournari Pylaia, Thessaloniki , Greece
2 Aristotle University of Thessaloniki , Thessaloniki , Greece
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 MetaAnalyses 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.
Background
The neurocognitive dysfunction in BD has been the
focus of debate for many years. It was not clear whether
the observed neurocognitive deficit could be explained
by iatrogenic or alcohol and/or drug abuse effects or by
the temporary functional changes which constitute the
result of mood changes. Also, it was unclear whether
the impairment is the product of degenerative structural
brain changes or of some kind of structural changes of a
neurodevelopmental origin (trait), or it is secondary to
mood dysregulation (state). Recent data suggested that
the neurocognitive deficit is not only an enduring
component of the illness, but also represents a core primary
characteristic of the illness, rather than being
secondary to the mood state or medication [
1
]. It has been
suggested by recent data that 84 % of patients suffering from
schizophrenia, 58.3 % of psychotic major depressive
patients, and 57.7 % of psychotic BD patients are
neurocognitively impaired (at least one SD below healthy
controls in at least two domains) [
2
].
It has also been suggested that patients with BD are
more creative (e.g., artists, scientists, etc.) and have
higher IQ in comparison to the general population [
3–7
].
However, more recent data reported a significant and
broad neurocognitive deficit, which seems to be present
even before the first manifestation of mood symptoms,
and it persists across the different phases and even
worsens during the course of the illness [
8–13
]. Several
studies suggest that 40 % of BD patients are impaired in one
neurocognitive domain, one-third or more are impaired
in at least two neurocognitive domains and 22 % in three
or more domains [
14, 15
]. This deficit is rather stable and
relatively independent from mood changes, probably
reflecting trait features of BD [
16–19
] Even after
controlling for confounding variables, such as education and
social class and clinical symptoms, it has been indicated
that the neurocognitive impairment in BD is less
pronounced in comparison to that in schizophrenia [
20, 21
].
Gender, age, education, phase of the illness and
medication status constitute some of the identified
confounding factors. Additionally, patients in a severe depression
or mania cannot be tested.
A significant limitation in this kind of research is that
the performance in most tests is influenced by more than
one neurocognitive process. It is a fact that the
boundaries between neurocognitive processes are unclear and
no process is completely independent from the others.
Different approaches in their classification and
nomenclature have been proposed, adding to the confusion. The
domain of executive functions, particularly, is open to
several different approaches and conceptualizations.
Th (...truncated)