Richard J Porter1, Lucy J Robinson2, Gin S Malhi3,4, Peter Gallagher5,6. 1. Department of Psychological Medicine, University of Otago, Christchurch, New Zealand. 2. School of Psychology, Newcastle University, Newcastle, UK. 3. CADE Clinic, Department of Psychiatry, Royal North Shore Hospital, Sydney, Australia. 4. Discipline of Psychiatry, Kolling Institute, Sydney Medical School, University of Sydney, Sydney, Australia. 5. Institute of Neuroscience, Newcastle University, Newcastle, UK. 6. Newcastle University Institute for Ageing, Newcastle, UK.
Abstract
OBJECTIVES: Cognitive abnormalities are an established part of the symptomatology of mood disorders. However, questions still exist regarding the exact profile of these deficits in terms of the domains most affected, their origins, and their relationship to clinical subtypes. This review aims to examine the current state of the evidence and to examine ways in which the field may be advanced. METHODS: Studies examining cognitive function in bipolar disorder (BD) and unipolar major depression (MDD) were examined. Given the number and variability of such studies, particular attention was paid to meta-analyses and to meta-regression analyses which examined the possible mediators of cognitive impairment. RESULTS: Meta-analyses are available for MDD and BD in both depression and euthymia. Several analyses examine mediators. Results do not support the presence of domain specific deficits but rather a moderate deficit across a range of domains in BD and in MDD. The data on clinical mediators is inconsistent, even with regard to the effect of mood state. CONCLUSIONS: A two-tiered approach, with the broad-based application of standardized measures on a large-scale, and the refined application of theoretically driven experimental development would significantly further our understanding of neurocognitive processing in mood disorder.
OBJECTIVES:Cognitive abnormalities are an established part of the symptomatology of mood disorders. However, questions still exist regarding the exact profile of these deficits in terms of the domains most affected, their origins, and their relationship to clinical subtypes. This review aims to examine the current state of the evidence and to examine ways in which the field may be advanced. METHODS: Studies examining cognitive function in bipolar disorder (BD) and unipolar major depression (MDD) were examined. Given the number and variability of such studies, particular attention was paid to meta-analyses and to meta-regression analyses which examined the possible mediators of cognitive impairment. RESULTS: Meta-analyses are available for MDD and BD in both depression and euthymia. Several analyses examine mediators. Results do not support the presence of domain specific deficits but rather a moderate deficit across a range of domains in BD and in MDD. The data on clinical mediators is inconsistent, even with regard to the effect of mood state. CONCLUSIONS: A two-tiered approach, with the broad-based application of standardized measures on a large-scale, and the refined application of theoretically driven experimental development would significantly further our understanding of neurocognitive processing in mood disorder.
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