Neurocognitive impairment and evidence-based treatment options in Bipolar disorder
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Annals of General Psychiatry Open Access
REVIEW
Neurocognitive impairment and evidence‑based treatment options in Bipolar disorder Konstantinos N. Fountoulakis*
Abstract Background: The current paper briefly summarizes the literature on the neurocognitive deficit and its treatment in BD patients. Methods: The material was chosen on the basis of previous systematic reviews the author has taken part in. Results: The data so far suggest that the deficit is qualitatively similar but quantitatively milder in comparison to schizophrenia, it is present already since the first episode, is weakly related to mood symptoms and somewhat stronger to psychotic symptoms, it probably determines much of the disability and treatment is problematic. This deficit is also present during periods of euthymia. The possible adverse effect of psychotropic medication is rather small if any at all and is confounded by the specific clinical symptoms, for which medication is used for their treatment. This is especially true concerning antipsychotics and psychotic symptoms. The origin and the etiopathogenesis of the core neurocognitive impairment remain elusive. The presence of a neurodegenerative and of a neurodevelopmental component has both data in favor and against and they are both the focus of debate. Conclusions: Treatment of the neurocognitive deficit and restoration of functioning is problematic. The data are limited and treatment options are few and with a weak overall effect. Pharmacological treatments, ECT and rTMS present some hard data, while the literature is inconclusive concerning psychotherapeutic interventions. Keywords: Bipolar disorder, Neurocognitive disorder, Cognitive disorder, Cognitive remediation, Functional remediation, treatment Background The nature of the neurocognitive dysfunction in mood disorders, and particularly in Bipolar disorder (BD), has been the focus of debate for long and only during the last couple of decades the picture became clearer. It seems that the neurocognitive deficit is not only an enduring component of BD, but also represents a core primary characteristic, rather than being secondary to the mood state or medication. A number of other questions are also *Correspondence: [email protected] 3rd Department of Psychiatry, School of Medicine, Aristotle University of Thessaloniki, 6, Odysseos str (1st Parodos Ampelonon str.), Pylaia, 55535 Thessaloniki, Greece
important, that is whether it is the result of a neurodevelopmental or neurodegenerative process and what is its relationship to the widely believed higher creativity of BD patients. Today, there is a number of studies suggesting that almost half of BD patients are impaired in one neurocognitive domain, one-third or more are impaired in at least two neurocognitive domains and more than one-fifth in three or more domains [1, 2]. This deficit is rather stable and relatively independent from mood changes, probably reflecting trait features [3–6] Importantly, even after controlling for confounding variables, like education and social cla
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