Psychomotor retardation is a scar of past depressive episodes, revealed by simple cognitive tests

• Published in: European neuropsychopharmacology Vol. 24; no. 10; pp. 1630 - 1640
• Main Authors: Gorwood, P, Richard-Devantoy, S, Baylé, F, Cléry-Melun, M.L
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.10.2014
• Subjects: Acetamides - therapeutic use; Antidepressive Agents - therapeutic use; Attention - drug effects; Attention - physiology; Cognition; Cognition - drug effects; Cognition - physiology; Depressive Disorder - drug therapy; Depressive Disorder - physiopathology; Depressive Disorder - psychology; Female; Follow-Up Studies; Humans; Internal Medicine; Major depressive disorder; Male; Middle Aged; Neuropsychological Tests; Neurotoxic; Psychiatry; Psychomotor Performance - drug effects; Psychomotor Performance - physiology; Psychomotor retardation; Recurrence; Scar; Severity of Illness Index; Recurrence; Cognition; Neurotoxic; Psychomotor retardation; Scar; Major depressive disorder
• ISSN: 0924-977X; 1873-7862
• DOI: 10.1016/j.euroneuro.2014.07.013

Abstract The cumulative duration of depressive episodes, and their repetition, has a detrimental effect on depression recurrence rates and the chances of antidepressant response, and even increases the risk of dementia, raising the possibility that depressive episodes could be neurotoxic. Psychomotor retardation could constitute a marker of this negative burden of past depressive episodes, with conflicting findings according to the use of clinical versus cognitive assessments. We assessed the role of the Retardation Depressive Scale (filled in by the clinician) and the time required to perform the neurocognitive d2 attention test and the Trail Making Test (performed by patients) in a sample of 2048 depressed outpatients, before and after 6 to 8 weeks of treatment with agomelatine. From this sample, 1140 patients performed the TMT-A and -B, and 508 performed the d2 test, at baseline and after treatment. At baseline, we found that with more past depressive episodes patients had more severe clinical level of psychomotor retardation, and that they needed more time to perform both d2 and TMT. When the analyses were performed again after treatment, and especially when the analyses were restricted to patients with clinical remission, the cognitive tests were the only ones correlated with past depressive episodes. Psychomotor retardation tested at a cognitive level was therefore systematically revealing the burden of past depressive episodes, with an increased weight for patients with less remaining symptoms. If prospectively confirmed, interventions such as cognitive remediation therapy could benefit from a more specific focus on neurocognitive retardation.