The neurobiological reward system in Prolonged Grief Disorder (PGD): A systematic review

• Published in: Psychiatry research. Neuroimaging Vol. 303; p. 111135
• Main Authors: Kakarala, S.E., Roberts, K.E., Rogers, M., Coats, T., Falzarano, F., Gang, J., Chilov, M., Avery, J., Maciejewski, P.K., Lichtenthal, W.G., Prigerson, H.G.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 30.09.2020
• Subjects: Bereavement; Brain - diagnostic imaging; Complicated Grief (CG); Grief; Humans; Neuroimaging; Nneurobiology; Prolonged Grief Disorder (PGD); Reward; Time Factors; Neuroimaging; Bereavement; Prolonged Grief Disorder (PGD); Complicated Grief (CG); Nneurobiology
• ISSN: 0925-4927; 1872-7506; 1872-7506
• DOI: 10.1016/j.pscychresns.2020.111135

•Prolonged Grief Disorder (PGD) likely involves the neural reward system.•Evidence associates the mesolimbic dopamine system and cortical regions with PGD.•Oxytocin function may also be altered in PGD.•Further research on disordered reward processing in PGD is needed. Prolonged Grief Disorder (PGD) is a debilitating condition affecting between 7% and 10% of bereaved individuals. Past imaging and psychological studies have proposed links between PGD's characteristic symptoms - in particular, profound yearning - and the neural reward system. We conducted a systematic review to investigate this connection. On December 19, 2019, we searched six bibliographic databases for data on the neurobiology of grief and disordered grief. We excluded studies of the hypothalamic-pituitary-adrenal (HPA) axis, animal studies, and reviews. After abstract and full-text screening, twenty-four studies were included in the final review. We found diverse evidence for the activation of several reward-related regions of the brain in PGD. The data reviewed suggest that compared to normative grief, PGD involves a differential pattern of activity in the amygdala and orbitofrontal cortex (OFC); likely differential activity in the posterior cingulate cortex (PCC), rostral or subgenual anterior cingulate cortex (ACC), and basal ganglia overall, including the nucleus accumbens (NAc); and possible differential activity in the insula. It also appears that oxytocin signaling is altered in PGD, though the exact mechanism is unclear. Our findings appear to be consistent with, though not confirmative of, conceptualizing PGD as a disorder of reward, and identify directions for future research.