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Neuro-progressive effects of severely treatment-resistant depression

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3 papers 0 to 25 followers
Blair A Johnston, Serenella Tolomeo, Victoria Gradin, David Christmas, Keith Matthews, J Douglas Steele
Major depressive disorder is characterized by anhedonia, cognitive biases, ruminations, hopelessness and increased anxiety. Blunted responses to rewards have been reported in a number of recent neuroimaging and behavioural studies of major depressive disorder. In contrast, neural responses to aversive events remain an under-studied area. While selective serotonergic reuptake inhibitors are often effective in treating major depressive disorder, their mechanism of action remains unclear. Following a series of animal model investigations of depressive illness and serotonergic function, Deakin and Graeff predicted that brain activity in patients with major depressive disorder is associated with an overactive dorsal raphe nucleus with overactive projections to the amygdala, periaqueductal grey and striatum, and an underactive median raphe nucleus with underactive projections to the hippocampus...
September 2015: Brain: a Journal of Neurology
Claudi L H Bockting, Philip Spinhoven, Maarten W J Koeter, Luuk F Wouters, Aart H Schene
OBJECTIVE: Depression is a recurring disease. Identifying risk factors for recurrence is essential. The purpose of this study was to identify factors predictive of recurrence and to examine whether previous depressive episodes influence vulnerability for subsequent depression in a sample of remitted recurrently depressed patients. METHOD: Recurrence was examined prospectively using the Structured Clinical Interview for DSM-IV Axis I Disorders in 172 euthymic patients with recurrent depression (DSM-IV) recruited from February 2000 through September 2000...
May 2006: Journal of Clinical Psychiatry
P Gorwood, S Richard-Devantoy, F Baylé, M L Cléry-Melin, M L Cléry-Melun
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...
October 2014: European Neuropsychopharmacology: the Journal of the European College of Neuropsychopharmacology
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