Anhedonia, suicide ideation and Dexamethasone nonsuppression in depressed patients

Oei, T.I.; Verhoeven, W.M.A.; Westenberg, H.G.M.; Zwart, F.M.; Ree, Jan M. van

doi:10.1016/0022-3956(90)90022-i

Cited by 32 publications

(20 citation statements)

References 16 publications

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“…Although anhedoniais present in up to 50% of individuals with MDD (Fawcett et al, 1983; Oei et al, 1990; Pelizza and Ferrari, 2009), it transcends diagnostic boundaries and plays prominent roles in other disorders, including schizophrenia and substance abuse (Diekhof et al, 2008; Dowd and Barch, 2010). In the context of a rich theoretical background postulating that a genetic predisposition to hedonic deficits may leave individuals vulnerable to the development of depression (Klein, 1987; Loas, 1996; Meehl, 1975; Myerson, 1922; Willner, 1993) and evidence that reward-related behavior is heritable (Bogdan and Pizzagalli, 2009; Loas, 1996), research has begun to investigate how genetic background and environmental experience contribute to the vast array of individual differences in reward-related behavior and brain function with important implications for our understanding of depression.…”

Section: Reward Processingmentioning

confidence: 99%

“…While the lack of cross-association between polymorphisms linked to depression and those linked to reward-related brain function and behavior (in predominantly healthy or clinically unassessed populations) may be disappointing, it is not entirely surprising. In light of evidence suggesting that anhedonia may reach clinical significance in half of patients with MDD (Fawcett et al, 1983; Oei et al, 1990; Pelizza and Ferrari, 2009), a large portion of patients included in studies of depressed individuals will likely not feature reward processing deficits, thereby suppressing the detection of genetic effects increasing vulnerability to MDD via anhedonia-related mechanisms. Such heterogeneity highlights the potential utility of using continuous and specific measures in clinical and healthy populations to better represent distinct disorder components associated with given pathophysiological processes.…”

Section: Genetics Of Reward Processingmentioning

confidence: 99%

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Neurogenetics of depression: A focus on reward processing and stress sensitivity

Bogdan

Nikolova

Pizzagalli

2013

Neurobiology of Disease

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Major depressive disorder (MDD) is etiologically complex and has a heterogeneous presentation. This heterogeneity hinders the ability of molecular genetic research to reliably detect the small effects conferred by common genetic variation. As a result, significant research efforts have been directed at investigating more homogenous intermediate phenotypes believed to be more proximal to gene function and lie between genes and/or environmental effects and disease processes. In the current review we survey and integrate research on two promising intermediate phenotypes linked to depression: reward processing and stress sensitivity. A synthesis of this burgeoning literature indicates that a molecular genetic approach focused on intermediate phenotypes holds significant promise to fundamentally improve our understanding of the pathophysiology and etiology of depression, which will be required for improved diagnostic definitions and the development of novel and more efficacious treatment and prevention strategies. We conclude by highlighting challenges facing intermediate phenotype research and future development that will be required to propel this pivotal research into new directions.

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Section: Reward Processingmentioning

confidence: 99%

Section: Genetics Of Reward Processingmentioning

confidence: 99%

Neurogenetics of depression: A focus on reward processing and stress sensitivity

Bogdan

Nikolova

Pizzagalli

2013

Neurobiology of Disease

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“…In fact, anhedonia was linked to anxiety and adjustment disorders (Silverstone, 1991), suicidal ideation (Oei et al, 1990), and successful suicide (Fawcett, 1993). On the other hand, in the model proposed by Loas (1996), a genetically determined low hedonic capacity was regarded as a specific character trait, which, together with aspects like introversion, obsessive-compulsivity, pessimism, and passivity, could represent a risk factor, which could lead, under stress conditions, to unipolar endogenomorphic depression.…”

Section: Anhedonia In Axis I Disordersmentioning

confidence: 99%

Anhedonia and Substance Dependence: Clinical Correlates and Treatment Options

Hatzigiakoumis¹,

Martinotti²,

et al. 2011

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Anhedonia is a condition in which the capacity of experiencing pleasure is totally or partially lost, and it refers to both a state symptom in various psychiatric disorders and a personality trait. It has a putative neural substrate, originating in the dopaminergic mesolimbic and mesocortical reward circuit. Anhedonia frequently occurs in mood disorders, as a negative symptom in schizophrenia, and in substance use disorders. In particular, we focus our attention on the relationships occurring between anhedonia and substance use disorders, as highlighted by many studies. Several authors suggested that anhedonia is an important factor involved in relapse as well as in the transition from recreational use to excessive drug intake. In particular, anhedonia has been found to be a frequent feature in alcoholics and addicted patients during acute and chronic withdrawal as well as in cocaine, stimulant, and cannabis abusers. Furthermore, in subjects with a substance dependence disorder, there is a significant correlation between anhedonia, craving, intensity of withdrawal symptoms, and psychosocial and personality characteristics. Therefore treating anhedonia in detoxified alcohol-dependent subjects could be critical in terms of relapse prevention strategies, given its strong relationship with craving.

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“…In contrast, elevated cortisol levels have been reported in MDE (Westrin et al, 1999), and about half of the in-patients with MDE fail to suppress cortisol secretion after dexamethasone (Brown et al, 1987;Duval et al, 2001;Yehuda et al, 1996;Halbreich et al, 1989). Most (Coryell and Schlesser, 2001;Meltzer et al, 1984;Norman et al, 1990;Oei et al, 1990;Inder et al, 1997;Roy, 1992), but not all, (Cleare et al, 1996;Duval et al, 2001;Westrin et al, 1999) studies of HPA axis in suicidal behavior suggest that there is elevation of cortisol or dexamethasone resistance in future suicide completers. Some of these discrepancies may be related to the spectrum of suicidal behavior that is assessed, such that suicidal ideation or the presence of attempts in a subject's history may have less of an effect on cortisol secretion than the violence of the attempt (Roy, 1992) or ultimate suicide completion (Coryell and Schlesser, 2001).…”

Section: Introductionmentioning

confidence: 98%

Lower Cortisol Levels in Depressed Patients with Comorbid Post-Traumatic Stress Disorder

Oquendo

Echavarría

Galfalvy

et al. 2002

Neuropsychopharmacol

104

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Post-traumatic stress disorder (PTSD) is often comorbid with major depressive episodes (MDEs) and both conditions carry a higher rate of suicidal behavior. Hypothalamic-pituitary-adrenal (HPA) axis and serotonin abnormalities are associated with both conditions and suicidal behavior, but their inter-relation is not known. We determined cortisol response to placebo or fenfluramine in MDE, MDE and PTSD (MDE+PTSD), and healthy volunteers (HVs) and examined the relation of cortisol responses to suicidal behavior. A total of 58 medication-free patients with MDE (13 had MDE+PTSD) and 24 HVs were studied. They received placebo on the first day and fenfluramine on the second day. Cortisol levels were drawn before challenge and for 5 h thereafter. The MDE+PTSD group had the lowest plasma cortisol, the MDE group had the highest, and HVs had intermediate levels. There were no group differences in cortisol response to fenfluramine. Suicidal behavior, sex, and childhood history of abuse were not predictors of baseline or postchallenge plasma cortisol. Cortisol levels increased with age. This study finds elevated cortisol levels in MDE and is the first report of lower cortisol levels in MDE+PTSD. The findings underscore the impact of comorbidity of PTSD with MDE and highlight the importance of considering comorbidity in psychobiology.

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Anhedonia, suicide ideation and Dexamethasone nonsuppression in depressed patients

Cited by 32 publications

References 16 publications

Neurogenetics of depression: A focus on reward processing and stress sensitivity

Neurogenetics of depression: A focus on reward processing and stress sensitivity

Anhedonia and Substance Dependence: Clinical Correlates and Treatment Options

Lower Cortisol Levels in Depressed Patients with Comorbid Post-Traumatic Stress Disorder

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