Anhedonia in depression and schizophrenia: A transdiagnostic challenge

Lambert, Clare; Silva, Susana Da; Ceniti, Amanda K.; Rizvi, Sakina J.; Foussias, George; Kennedy, Sidney H.

doi:10.1111/cns.12854

Cited by 116 publications

(89 citation statements)

References 119 publications

(229 reference statements)

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“…Anhedonia, or the inability to experience pleasure, emerges in some people in the aftermath of psychological trauma. Anhedonia is a transdiagnostic phenomenon that is observed across various psychiatric disorders, including depression, PTSD, and schizophrenia (Krynicki et al, 2018;Lambert et al, 2018;Vujanovic et al, 2017). Specific symptoms of post-traumatic stress disorder (PTSD) reflect anhedonia: feelings of detachment from others, diminished emotional responsiveness, and decreased interest in activities (American Psychiatric Association, 1994).…”

Section: Introductionmentioning

confidence: 99%

Structural connectivity and risk for anhedonia after trauma: A prospective study and replication

Fani

Michopoulos

Rooij

et al. 2019

Journal of Psychiatric Research

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Anhedonia emerges in some people after psychological trauma, reflected by a loss of interest, diminished affect, and detachment. Structural abnormalities in specific neural pathways at the time of trauma may influence the development of these posttraumatic anhedonia (PTA) symptoms. In this prospective study, we determined whether white matter connectivity at around one month post-trauma predicts PTA and other PTSD symptoms at six months post-trauma. Thirty men and women aged 19-62 were recruited from the emergency department of a Level I trauma center. Participants received diffusion tensor imaging at approximately one month post-trauma and clinical assessments at one and six months post-trauma. Probabilistic tractography was used to examine connectivity of select pathways. A replication sample (N = 57) in an independent, crosssectional dataset of traumatized women was similarly analyzed. Logistic regression results indicated that, after accounting for early PTSD symptoms (at one month) and other clinical risk factors, the integrity of the uncinate fasciculus (UF) uniquely predicted the presence of PTA at six months post-trauma (Beta = −225.6, p < .05). Together, these factors contributed to 76% of the variance in PTA. Integrity of the UF also predicted re-experiencing PTSD symptoms at six months post-trauma. These results were supported in our replication analyses. Our findings indicate that the integrity of the UF around 1 month post-trauma affects vulnerability for the development of anhedonic PTSD symptoms as well as re-experiencing symptoms. Connectivity of this amygdalaventromedial prefrontal pathway appears to be a salient predictor of anhedonia, above and beyond clinical risk factors.

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Section: Introductionmentioning

confidence: 99%

Structural connectivity and risk for anhedonia after trauma: A prospective study and replication

Fani

Michopoulos

Rooij

et al. 2019

Journal of Psychiatric Research

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“…[45] This theory has recently been extended to anhedonia in schizophrenia, although the latter's mesolimbic dopamine dysfunction is characterized more by disorganization rather than the deficiency typical in MDD. [46,47] This has led to the recognition that many mood disorders have a systemic component or even a systemic foundation. A few associations have been unexpected, such as obesity and MDD (metabolic syndrome affects both populations at disproportionately high rates).…”

Section: Mental Disorders and Brain Energy Metabolismmentioning

confidence: 99%

Exploring the Rationale for the Use of the Ketogenic Diet in the Treatment of Mental Health Disorders

Pergolizzi¹,

Tabor²,

LeQuang³

et al. 2019

obm icm

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Background: The ketogenic diet (KD) was developed in the 1920s as a treatment for pediatric epilepsy and is emerging as a possible treatment option for certain mental health disorders. There is a link between certain mental health disorders and epilepsy, suggesting some commonality among underlying mechanisms. Methods: The literature relating to mental disorders and the KD is sparse. The authors attempt to a narrative review of the existing literature to show that there may be validity to studying the KD as a treatment for certain mental health disorders. Results: Various types of mitochondrial dysfunction and impaired oxidative metabolism have been identified in many mental health disorders (bipolar disorder, major depressive disorder, autism, schizophrenia, and others). Mitochondrial deficits may affect neuroplasticity and cause synaptic dysfunction, which could change brain structure and function in a way that might affect behavior. The KD has been associated with epigenetic changes in the genes associated with mitochondrial function. Chronic oxidative stress and inflammation have also been implicated in mental health disorders and may be reduced by the KD. The KD regulates

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“…anticipatory or motivational anhedonia, disorganization) can hinder the individual from generating pleasurable experiences and could then present as (secondary) consummatory anhedonia [13]. There are findings indicating that patients with depression experience consummatory and anticipatory anhedonia whereas patients with schizophrenia mainly show a deficit in anticipatory pleasure [13–15]. The emergence of anticipatory pleasure is more complex than the experience of consummatory pleasure and hints at motivational deficits in schizophrenia as opposed to deficits in experiencing emotions [16].…”

Section: Introductionmentioning

confidence: 99%

Measurement of negative and depressive symptoms: Discriminatory relevance of affect and expression

et al. 2019

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There is conceptual overlap between negative and depressive symptoms: Mainly the ‘avolition’ factor of negative symptoms also encompasses main symptoms of depression. However, whereas in depression mood is low, mainly anticipatory anhedonia can be found in negative symptoms. Moreover, patients with schizophrenia (SCZ) show greater expressive deficits than those with Major Depressive Episode (MDE). We investigated if measures of depressive and negative symptoms differentiate SCZ subjects, subjects with MDE, and healthy controls (HC). 21 SCZ, 22 MDE, and 25 HC subjects were examined with a rater assessment and a self-rating for negative symptoms (Clinical Assessment Interview for Negative Symptoms (CAINS); Motivation and Pleasure – Self-Report (MAP-SR)) and depressive symptoms (Hamilton Rating Scale for Depression (HAMD-17); Beck Depression Inventory (BDI)). All measures differentiated the psychiatric samples from HC (all p’s < 0.01). The ratings of depressive symptoms (HAMD-17, BDI) and rater assessment of negative symptoms (CAINS) – specifically its sub scale measuring expressive deficits – managed to discriminate between subjects with schizophrenia and those with MDE (SCZ > MDE > HC for negative, MDE > SCZ > HC for depressive symptoms, all p’s < 0.05). The self-rating of negative symptoms (MAP-SR) did not. To differentiate negative symptoms and depression clinicians might look for (self-)reported low mood and observer-rated reduction in speech as well as in gestures and facial expression. Reduced expression and moderate levels of depression point towards a negative syndrome, whereas mostly unimpaired expression and high scores of self-reported depressive symptoms are more likely to indicate a depressive syndrome.

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Anhedonia in depression and schizophrenia: A transdiagnostic challenge

Abstract: Anhedonia as a clinical presentation of reward circuit dysregulation is an important and relatively undertreated symptom of both SZ and MDD. In order to improve patient outcomes and quality of life, it is important to consider how anhedonia fits into both diagnoses.

Cited by 116 publications

References 119 publications

Structural connectivity and risk for anhedonia after trauma: A prospective study and replication

Structural connectivity and risk for anhedonia after trauma: A prospective study and replication

Exploring the Rationale for the Use of the Ketogenic Diet in the Treatment of Mental Health Disorders

Measurement of negative and depressive symptoms: Discriminatory relevance of affect and expression

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