Vulnerability to depression: A model centered on anhedonia

Loas, Gwenolé

doi:10.1016/0165-0327(96)00065-1

Cited by 166 publications

(130 citation statements)

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“…Nonetheless, it is self-report trait anhedonia measured in non-clinical individuals that has been shown in past studies to be predictive of the future development of psychiatric disorders. 2,7,[22][23][24][25] Thus, we are confident that the structural and the functional neural correlates of trait anhedonia reported in this study have an important clinical value for the identification of neural markers of vulnerability.…”

Section: Discussionsupporting

confidence: 54%

“…24,25 Moreover, anhedonia could characterize a specific subform of SZ 26 and is a key symptom for the diagnostic of melancholia, a specific subtype of MDD. 27 As a result, the characterization of the structural and functional correlates of trait anhedonia in non-clinical individuals may provide new insights for the early detection of SZ and MDD and eventually for the identification of more homogeneous forms of diseases.…”

Section: Introductionmentioning

confidence: 99%

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Individual differences in trait anhedonia: a structural and functional magnetic resonance imaging study in non-clinical subjects

et al. 2007

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Anhedonia, the reduced capacity to gain pleasure from pleasurable experiences, is a key symptom of major depression and schizophrenia. Reduced hedonic capacity can also be measured as an enduring trait in non-clinical subjects. Such altered hedonic capacity is likely the result of a basic neuropsychophysiological dysfunction and a vulnerability marker that potentially precedes and contributes to the liability of developing psychiatric disorders. The characterization of the structural and functional neural correlates of trait anhedonia in nonclinical individuals may provide new insights for the early detection of such psychiatric diseases. Twenty-nine non-clinical subjects were scanned at the Montreal Neurological Institute. Trait anhedonia was measured using the Chapman Revised Physical Anhedonia Scale. Semi-automated and automated structural MRI segmentation techniques were used to explore structural correlates of trait anhedonia. Seventeen of the 29 subjects also underwent a functional imaging task where responses to the viewing of affective stimuli were examined to identify the functional correlates of trait anhedonia. Trait anhedonia was inversely related to anterior caudate volume, but positively related to ventromedial prefrontal cortex activity during the processing of positive information. These findings may reflect a specific kind of vulnerability for the development of psychiatric affective disorders and suggest that trait anhedonia may be linked to a volumetric reduction in the basal ganglia and to a prefrontal functional abnormality during hedonic processing.

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Individual differences in trait anhedonia: a structural and functional magnetic resonance imaging study in non-clinical subjects

et al. 2007

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“…We hypothesize that our specific treatment modality with a target in the reward system might positively influence this symptom, possibly by restoring normal function of this system. But anhedonia has been implicated with other chronic and debilitating psychiatric disorders such as obsessive-compulsive disorders (Loas, 1996), substance abuse disorders (Wise, 1996), and schizophrenia (Wolf, 2006). These initial observations that DBS to striatal regions indeed might restore dysfunc- The reported behavioral changes that occurred in these patients beg the question of what neurobiological changes occurred that underlie these behavioral and clinical shifts.…”

mentioning

confidence: 99%

Deep Brain Stimulation to Reward Circuitry Alleviates Anhedonia in Refractory Major Depression

Schläepfer

Cohen

Frick

et al. 2007

Neuropsychopharmacol

901

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Deep brain stimulation (DBS) to different sites allows interfering with dysfunctional network function implicated in major depression.Because a prominent clinical feature of depression is anhedoniaFthe inability to experience pleasure from previously pleasurable activitiesFand because there is clear evidence of dysfunctions of the reward system in depression, DBS to the nucleus accumbens might offer a new possibility to target depressive symptomatology in otherwise treatment-resistant depression. Three patients suffering from extremely resistant forms of depression, who did not respond to pharmacotherapy, psychotherapy, and electroconvulsive therapy, were implanted with bilateral DBS electrodes in the nucleus accumbens. Stimulation parameters were modified in a double-blind manner, and clinical ratings were assessed at each modification. Additionally, brain metabolism was assessed 1 week before and 1 week after stimulation onset. Clinical ratings improved in all three patients when the stimulator was on, and worsened in all three patients when the stimulator was turned off. Effects were observable immediately, and no side effects occurred in any of the patients. Using FDG-PET, significant changes in brain metabolism as a function of the stimulation in fronto-striatal networks were observed. No unwanted effects of DBS other than those directly related to the surgical procedure (eg pain at sites of implantation) were observed. Dysfunctions of the reward systemFin which the nucleus accumbens is a key structureFare implicated in the neurobiology of major depression and might be responsible for impaired reward processing, as evidenced by the symptom of anhedonia. These preliminary findings suggest that DBS to the nucleus accumbens might be a hypothesis-guided approach for refractory major depression. Neuropsychopharmacology (2008) 33, 368-377; doi:10.1038/sj.npp.1301408; published online 11 April 2007 Keywords: deep brain stimulation; major depression; anhedonia; nucleus accumbens; brain stimulation; Cg25 INTRODUCTIONTraditional methods of alleviating depression largely stem from serendipitous observations of antidepressant effects of substances such as iproniazid (originally developed as a treatment for tuberculosis) or imipramine (originally developed as a treatment for schizophrenia). In particular, increasing levels of monoamine neurotransmitters in the synaptic cleft are associated with improvements of depressive symptoms. This insight led to a more targeted drug discovery process, resulting in drugs with fewer side effects, such as SSRIs. These medication treatments, in conjunction with certain methods of psychotherapy and electroconvulsive therapy, are effective at alleviating depressive symptomatology in most patients (Andrews and Nemeroff, 1994;Mann, 2005). However, these treatments do not work for all patients. A sizable minority of patients does not respond. Indeed, twelve percent of patients suffering from major depression have a poor outcome even after 5 years of treatment (Keller et al, 1992). Patien...

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“…Anhedonia is characterized by diffi culties experiencing positive affect in response to typically rewarding situations (Loas 1996). Recognized as a prominent characteristic in major depressive episodes (Berenbaum and Oltmanns 1992), anhedonia is also conceptualized as a personality characteristic in the general population (Meehl 2001).…”

mentioning

confidence: 99%