A commentary: Aetiology of depression, negative symptoms and cognitive dysfunction

Either the presence of depressed mood or/and the presence of anhedonia (inability to experience physical and social pleasure) is needed for the diagnosis of major depression disorder (MDD) (5th ed., DSM-V, American Psychiatric Association). Anhedonia is also the core feature of melancholia and the first symptom to consider for the severity of a depression episode (DSM-V). Anhedonia, flat affect, alogia (deteriorated fluency and efficiency of thought) and avolition/asociality (severely diminished self initiated activities/lack of social interaction or avoidance of social interaction) are often present in MDD.

The cause of depression is unknown, however, aetiology of depression is widely thereorised as multifactorial and in specific biopsychosocial. Despite the aforementioned and oppositely to the DSM’s conceptualisation of anhedonia as a core symptom of depression (hence, an effect of depression), other researchers as for example Loas (1996) have theorized the presence of anhedonia as being a constitutional “hedonic deficit”  that comprises “vulnerability to depression” (Loas, 1996). The vulnerability to depression model suggests that anhedonia, being a genetically defined trait causes “endogenomorphic” depression on the presence of a stressful life event, rather than being a symptom of depression (Loas, 1996).

However, research findings are mixed, as studies have reported that anhedonia may or may not be present in major depression disorder.   There has been evidence that a significant subset of patients with MDD do not present anhedonia (Pelizza & Ferrari, 2009) or other negative symptoms (Bottlender, Sato, Groll, Jäger, Kunze, Möller, 2003). Therefore, anhedonia should not be considered as the cause of depression, intrinsic, endogenomorhic etc.

Similarly, mixed are the findings for the presence of cognitive dysfunction, such as attention and short-term verbal memory problems. Findings derive from self-report, computerized cognitive measures and neuroimaging methods and are mixed largely due to diverse methods, diversity of included patient samples and cognitive domains under investigation (Snyder, 2013). 

For example, in depression research there are  studies that have suggested that attention, verbal memory and fluency dysfunction persist during remission (Kupferberg, Bicks & Hasler; Weiland-Fiedler et al.,  2016), do not persist during remission of depression (Biringer et al., 2005) or that deficits are associated with the increasing number of previous MD episodes (Kessing, 1998), implying that cognitive dysfunctions might be an issue of patients’ fatigue due to recurrent depression.

Also, there are reports such as the study of Grant, Thase & Sweeny (2001) with unmedicated MDD patients suggesting that cognitive dysfunction as measured with a battery of cognitive tests was minor (Grant et al., 2001), suggesting that pharmacotherapy requires close communication between the patient and the psychiatrist - physician.

For example, a meta-analytic research (Snyder, 2013) that included 113 studies with 3,939 participant with MDD (and 3,771 participants healthy control) found significant lower performance in all executive function and cognitive domains assessed (inhibition, mind set-shifting, information updating, processing speed, verbal working memory, visuospatial working memory, planning and verbal fluency) as compared to participants in the control groups.

However, the statistical analysis in the same study also revealed that effect sizes of inhibition, set-shifting, verbal fluency and processing speed increased with severity of depression and in this research set-shifting, verbal fluency and processing speed were found independent of medication (Snyder, 2013). In addition, there has been a significant amount of evidence suggesting that when cognitive dysfunction is present, improvement is not analogues to improvement of depression symptoms, as subsequent to treatment (Hammar & Ardal, 2009).

In addition, affective (i.e. depressive symptoms), negative and cognitive dysfucntion symptoms are present not specifically MDD but in plenty other psychiatric (i.e. anxiety disorders, schizophrenia) and non-psychiatric disorders as well as in general population (Kaiser, 2011), such as: in chronic pain (Elvemo, Landrø, Borchgrevink & Aberg, 2015; Ferreira, Foss, Thomaz, Teixeira & Oliver, 2016), in disabled population (Prince, Harwood, Thomas & Mann, 1998), in psoriasis (Ritchlin & Fitzgerald, 2007) and arthritis (Marbach & Lund, 1981).

Indeed, a consistently reported risk factor for cognitive function is physical pain (Ferreira et al., 2016), however there is lack of research in mental disorders in regard to chronic pain.In other words, the relationship of physical fatigue symptoms with depression and other mental disorders (Kapfhammer, 2006); Lyrakos, Hatziagelaki, Spinaris, Damigos, Spyropoulos & Kostopanagiotou, 2012) might at some extent explain the presence of cognitive dysfunction in depression and also might explain symptoms’ independency from the core symptomatology of these disorders. Apostolia Alizioti, B.Sc. (Psychol), M.Sc. (Health Psychol), M.B.A., GBC member of the British Psychological Society.

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References

Grant, M. M., Thase, M. E. & Sweeney, J. A. (2001). Cognitive disturbance in outpatient depressed younger adults: Evidence of modest Impairment. Biological Psychiatry, 50(1), pp. 35–43.  doi: 10.1016/S0006-3223(00)01072-6

Biringer, E., Lundervold, A., Stordal, K., Mykletun, A., Egeland, J., Bottlender, R. & Lund, A. (2005). Executive function improvement upon remission of recurrent unipolar depression. European Archives of Psychiatry Clinical Neuroscience, 255, pp. 373-380. doi: 10.1007/s00406-005-0577-7

Bottlender, R., Sato, T., Groll, C., Jäger, M., Kunze, I. & Möller, H. J. (2003).  Negative symptoms in depressed and schizophrenic patients: how do they differ? Journal of Clinical Psychiatry, 64(8), pp. 954-8. PMID: 12927013

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Lyrakos, G., Hatziagelaki, E., Spinaris, B., Damigos, D., Spyropoulos, I. & Kostopanagiotou, G. (2012). The comparison of fatigue between patients with diabetes melittus, psychiatric outpatients and general population in Greece. European Psychiatry, 27(1), pp. 1. doi: 10.1016/S0924-9338(12)74399-7

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Pelizza, L. & Ferrari, A. (2009). Anhedonia in schizophrenia and major depression: state or trait? Annals of General Psychiatry, 8(22).  doi:10.1186/1744-859X-8-22 no pages

Prince, M. J., Harwood, R. H., Thomas, A. T. & Mann, A. H. (1998). A prospective population-based cohort study of the effects of disablement and social milieu on the onset and maintenance of late-life depression. The Gospel Oak project VII. Psychological Medicine , 28(2), pp. 337-350. doi: 10.1017/S0033291797006478

Ritchlin, C. T. & FitzGerald, O. (2007). Psoriatic and reactive arthritis. Philadelphia, USA:  MOSBY Elsevier Health Sciences

Snyder, H. R. (2013). Major depressive disorder is associated with broad impairments on neuropsychological measures of executive function: A meta-analysis and review. Psychological Bulletin, 139(1), pp. 81-132. doi:10.1037/a0028727

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