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Prof. Guy M. Goodwin

Guy M. Goodwin psiquiatra Controversias Psiquiatría Barcelona
University of Oxford, Reino Unido
Ponencia Síntomas cognitivos como objetivo para el tratamiento de la depresión
Fecha Sábado, 21 de Abril 2018
Hora 11:45 a 12:30
Mesa redonda Complejidades en Psiquiatría: trastornos afectivos

BIOGRAFÍA

Guy Goodwin, DPhil, FMedSci is currently a research fellow and former WA Handley Professor of Psychiatry at the University of Oxford, Oxford, UK. He completed his medical degree and DPhil in physiology at the University of Oxford and, following his training in psychiatry, became a Clinical Scientist and Consultant Psychiatrist at the MRC Brain Metabolism Unit at the Royal Edinburgh Hospital, Edinburgh, UK.

His research interests are in the treatment of bipolar disorder and the application of neuroscience in understanding the neurobiology of mood disorders, with a focus on developing new treatments. He has been a lead investigator in clinical trials for bipolar affective disorder, including the BALANCE and CEQUEL studies. He works with industry in developing translational models of psychotropic drug action in man.

He has served as a member of the Wellcome Trust Neurosciences Panel, the Council of the British Association for Psychopharmacology, the Clinical Fellowships Panel and Advisory Board of the Medical Research Council, INSERM's ANR panel. He is a Fellow of the American College of Neuropsychopharmacology, and has previously held the position of President of the British Association for Psychopharmacology (2004–2005). He is past president of the European College of Neuropsychopharmacology (ECNP) and a Senior Investigator on the faculty of UK National Institute for Health Research (NIHR).

RESUMEN

Major depression is commonly associated with impaired cognitive function. In other words, attention, memory and executive function when measured using standard neuropsychological tests are impaired compared with age and IQ matched controls. Patients also commonly say that their concentration and decision making are abnormal and that this limit their ability to execute everyday tasks. The DSM criteria for a major depressive episode (MDE) include diminished ability to think or concentrate, or more indecisiveness as an item.

What remains controversial is whether such cognitive impairment represents only an expression of the unitary concept we have of MDE. Obviously, the negative bias of depression means subjective descriptions of performance may simply be expressions of being depressed. The finding of objective deficits in cognitive performance means that they are real but could still secondary to depressed mood. Alternatively cognition may be a separable dimension. Indeed is cognitive impairment one of the scars attributable to repeated episodes and is it something we should manage separately as a treatment target also. Actual measurement of cognitive deficits is easy. It cannot be explained by current medication and it shows a marked diurnal swing in intensity in patients with melancholic depression with marked diurnal mood change. So, the subjective complaints of poor concentration are paralleled by objective measures and those measure are in part determined by the mental state. They suggest a common underlying neurobiology whereby depression expresses itself as a brain disease.

The other possibility, not excluded by the foregoing, is that cognitive impairment may be a more lasting consequence of one and particularly of repeated episodes of depression. This idea is sometimes referred to as neuroprogression. It is poorly characterized but receives some support from longitudinal and especially brain imaging studies. Clearly, cognitive impairment may limit functional outcomes in depression. This assumes increasing importance with the realization that failure to return to full employment after a MDE, or to return and underperform (‘presenteesm’) represents a major cost to developed economies as well as disappointing the ambitions of the individual patient.

The evidence in favour of cognitive impairment being a separate entity from depression, perhaps even trans-diagnostic will be reviewed together with evidence that it may reflect brain insult. Finally the limited evidence bearing on whether antidepressants improve cognitive function will be described.

REFERENCIAS

[PDF] Austin, MP et al (1992). Cognitive function in major depression, Journal of Affective Disorders 25, 21-30.

[PDF] Austin, MP et al (2001). Cognitive deficits in depression: possible implications for functional neuropathology, British Journal of Psychiatry, 178; 200-206.

[web] Gorwood P et al (2008). Toxic effects of depression on brain function: Impairment of delayed recall reflects the cumulative length of the depressive disorder in a large sample of depressed out-patients, Am J Psychiatry. 2008 Jun;165(6):731-9. doi: 10.1176/appi.ajp.2008.07040574. Epub 2008 Apr 1.

[web] Smith J et al (2017). Vortioxetine reduces BOLD signal during performance of the N-back working memory task: a randomised neuroimaging trial in remitted depressed patients and healthy controls, Mol Psychiatry. 2017 May 23. doi: 10.1038/mp.2017.104.