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Cognition and volition: a melancholic condition

Published online by Cambridge University Press:  24 June 2014

M Green,
D Hadzi-Pavlovic and
G Malhi
M Green
Affiliation:
School of Psychiatry, University of New South Wales
D Hadzi-Pavlovic
Affiliation:
School of Psychiatry, University of New South Wales
G Malhi
Affiliation:
Academic Discipline of Psychological Medicine, Northern Clinical School, The University of SydneyThe Black Dog Institute, SydneyPrince of Wales Medical Research Institute, Sydney, Australia
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Abstract

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Information

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Information
Acta Neuropsychiatrica , Volume 18 , Issue 6 , December 2006, pp. 252
Copyright
Copyright © 2006 Blackwell Munksgaard

Background:

Melancholia, a subtype of depression described as a specifier in DSM-IV, also forms a component of bipolar disorder (BD) and is distinguished from nonmelancholic depression on the basis of additional psychomotor disturbance (PMD). The latter comprises both retardation and agitation; concomitant cognitive disturbances are clinically observable and identified by patients as ‘a difficulty in thinking’, with lapses in concentration and decision-making impairments.

Methods:

A literature review of experimental studies of cognition in melancholia was undertaken alongside a review of literature on bradyphrenia (slowed cognition) within various neuropsychiatric conditions. Particular emphasis was assigned to studies that attempted to distinguish PMD from processing speed on cognitive tasks, in terms of both functional neuroanatomy and relationships with impaired volition. The implications for future studies of cognition in melancholia are carefully critiqued.

Results:

There has been relatively little empirical investigation of cognition and volition in melancholia. Studies thus far report partitioning of the neuropsycho-logical profile of depression across melancholic and nonmelancholic subtypes implicating distinct neural dysfunction within dorsal and ventral prefrontal networks. In comparison, research examining psychomo-tor retardation and impaired volition has gravitated toward abnormal functioning within basal ganglia and related networks, with the archetypal example of this being Parkinson's disease.

Conclusions:

Further empirical examination of cognition in depressive subtypes is required to evaluate the potential contribution of impaired volition to psycho-motor retardation and distinct neuropsychological deficits in melancholia. Evidence for a cognitive marker of melancholia may prove useful for refining diagnostic criteria and elucidating functional brain networks that subserve endogeneity.