Trisha Chakrabarty

Anhedonia presents in various psychiatric disorders and is a core symptom of depression. It involves disruptions in temporally and anatomically distinct subcomponents of reward processing, including reward anticipation and consumption. Studies using electroencephalography (EEG) to examine both anticipatory and consummatory reward processing components are limited, and study paradigms that incorporate psychological constructs like decision-making and reinforcement learning often overlap and confound the electrophysiological markers that are unique to anticipatory and consummatory reward processing. This study aims to validate an EEG-based Monetary Incentive Delay (MID) paradigm in a college population to examine relevant anticipatory and consummatory reward-related event-related potentials (ERPs), P3 and stimulus-preceding negativity (SPN), during different stages of reward processing. We found that the paradigm successfully elicited reward-related ERPs. Cue-P3 amplitudes and latency were modulated by reward magnitudes, however, no significant effect of reward magnitudes and valence was found on SPN and Feedback-P3, respectively. The paradigm was adjusted following the initial study to eliminate potential interfering visual effects from the cue and feedback stimuli. Additional data were collected in a new group of participants, and we found similar results, but without the confounding potentials. The paradigm also incorporated behavioural measurements of reward anticipation and consumption, and higher anticipatory and consummatory ratings and shortened response time towards the target stimuli were elicited as reward magnitudes increased. We concluded that the validated MID paradigm allows for a precise examination of reward-related ERPs, especially at early anticipation stage, and offers a valuable tool for investigating reward processing and related symptoms in clinical populations. Future studies should consider recruiting larger and more diverse samples besides college populations to investigate symptoms of anhedonia and reward processing in clinical populations.

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Background: While there is evidence of widespread grey matter (GM) changes in bipolar I disorder (BD-I), it is unclear how early in the illness such changes emerge. However, to date there has been little systematic examination of longitudinal grey matter changes early during BD-I. We conducted a systematic review to examine the literature regarding GM changes in BD-I patients following the first episode of mania (FEM), in addition to a quantitative analysis of grey matter changes in a prospective cohort of BD-I patients in the first three years of disease.Methods: Following PRISMA guidelines, we conducted a systematic review of studies examining longitudinal changes in GM volume (GMV), cortical thickness and/or surface area in patients with BD-I following FEM. We qualitatively synthesized results regarding baseline differences between BD-I patients and HCs, and longitudinal GM changes in BD-I patients. For the longitudinal study, FEM patients and HCs were recruited and completed structural 3T MRI at pre-determined intervals. Images were analyzed using FreeSurfer’s longitudinal pipeline and linear mixed models used to examine longitudinal changes in cortical thickness, surface area and subcortical volume. Results: Fifteen studies met inclusion criteria for the systematic review, all examining changes in GMV. While results were highly heterogeneous, one replicated finding was decreased anterior cingulate cortex (ACC) volumes in first episode BD-I patients versus HC at baseline, and greater longitudinal ACC volume decrease in patients in the months following FEM. The potential impact of episode recurrence, substance use, age of onset and prior depressive episodes was inconsistently examined.In the longitudinal study, BD-I patients and HCs showed comparable reductions in cortical surface area and subcortical volumes over 3 years. No significant time*group effects were found; BD-I patients had smaller right thalamic volumes versus HCs at year 3 at trend-level significance.Limitations: The literature regarding GM changes early in BD-I is inconsistent. The sample size in our longitudinal study may have been insufficient to detect statistically significant changes. Conclusions: Evidence for longitudinal grey matter changes in the early phases of BD-I is inconsistent. Larger longitudinal studies are needed to fully understand neuroprogression in early BD-I.

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