Abstract
Anhedonia is a prominent symptom in neuropsychiatric disorders, most markedly in major depressive disorder (MDD) and schizophrenia (SZ). Emerging evidence indicates an overlap in the neural substrates of anhedonia between MDD and SZ, which supported a transdiagnostic approach. Therefore, we used activation likelihood estimation (ALE) meta-analysis of functional magnetic resonance imaging studies in MDD and SZ to examine the neural bases of three subdomains of anhedonia: consummatory anhedonia, anticipatory anhedonia and emotional processing. ALE analysis focused specifically on MDD or SZ was used later to dissociate specific anhedonia-related neurobiological impairments from potential disease general impairments. ALE results revealed that consummatory anhedonia was associated with decreased activation in ventral basal ganglia areas, while anticipatory anhedonia was associated with more substrates in frontal-striatal networks except the ventral striatum, which included the dorsal anterior cingulate, middle frontal gyrus and medial frontal gyrus. MDD and SZ patients showed similar neurobiological impairments in anticipatory and consummatory anhedonia, but differences in the emotional experience task, which may also involve affective/mood general processing. These results support that anhedonia is characterized by alterations in reward processing and relies on frontal-striatal brain circuitry. The transdiagnostic approach is a promising way to reveal the overall neurobiological framework that contributes to anhedonia and could help to improve targeted treatment strategies.Electronic supplementary materialThe online version of this article (doi:10.1007/s11682-015-9457-6) contains supplementary material, which is available to authorized users.
Highlights
A total of 57 articles (33 articles on major depressive disorder (MDD) and 24 on SZ) with 986 patients and 1041 healthy controls and reporting 453 foci were included in the transdiagnostic metaanalysis
For reward consummatory (16 studies and 160 foci), Activation likelihood estimation (ALE) revealed a set of subcortical areas, including bilateral globus pallidus (GPe), bilateral red nucleus, right caudate body, left substania nigra (SN) and right putamen, left parahippocampal gyrus, as well as left medial frontal gyrus
For the emotional processing (9 studies and 94 foci), several regions in frontal gyrus were activated to a greater degree, such as mPFC, MFG and IFG, as well as the middle temporal gyrus and fusiform gyrus (p400 mm3, Table 2 and Fig. 2)
Summary
Medical Psychological Institute, The Second Xiangya Hospital of Central South University, 139 Renmin (M) Road, Changsha, Hunan 410011, People’s Republic of China. Key Laboratory of Biomedical Information Engineering of Education Ministry, Institute of Biomedical Engineering, Xi’an Jiaotong University, Xi’an, Shanxi 710049, People’s Republic of China. Anhedonia has long been considered a prominent symptom in neuropsychiatric disorders, especially major depressive disorder (MDD) and schizophrenia (SZ) (Association and Association 1994), its underlying neurobiological mechanisms remain poorly understood. Evidence has emerged to indicate overlap of behavioral, cognitive processing and neurobiological abnormalities between MDD and SZ patients with marked clinical anhedonia (Gradin et al 2011; Whitton et al 2015). A quantitative meta-analysis of pooled neuroimaging studies of anhedonia in MDD and SZ, discussed within the RDoC framework, is a promising approach to investigate the neural substrates of anhedonia. It is important to be mindful of the complexity and multifaceted nature of clinical anhedonia to understand neuroimaging studies in this field
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