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Baseline Anhedonia Phenotypes Reveal Divergent Neurophysiological Effects of Intermittent Theta Burst Stimulation in
Jiang Wu1, Zhengzhi Deng1, Xinyuan Cheng1
1Clinical Hospital of Chengdu Brain Science Institute, Sichuan Institute for Brain Science and Brain-Inspired Intelligence, China-Cuba Belt and Road Joint Laboratory on Neurotechnology and Brain-Apparatus Communication, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.
Background:
Anhedonia is a core but underrecognized symptom of major depressive disorder (MDD). Whether remission defined by Hamilton Depression Rating Scale (HAMD) and Hamilton Anxiety Rating Scale (HAMA) reflects improvement in anhedonia capacity measured by the Snaith-Hamilton Pleasure Scale (SHAPS) remains unclear. Evidence regarding repetitive transcranial magnetic stimulation (rTMS) efficacy for anhedonia is inconsistent. In this study, we examined SHAPS-stratified neurophysiological phenotypes using resting-state electroencephalography (EEG) spectra and functional connectivity to evaluate differential responses to intermittent theta burst stimulation (iTBS).
Methods:
Fifty MDD patients with anhedonia were classified into high-anhedonia (HA) (n = 25) and low-anhedonia (LA) (n = 25) groups based on SHAPS score, alongside 25 healthy control (HC) participants. All patients received a 2-week course of iTBS over the left dorsolateral prefrontal cortex. Resting-state EEG and clinical assessments were acquired at baseline and posttreatment.
Results:
At baseline, both patient groups exhibited lower alpha power compared with HC group, with region-specific deficits in the LA group and bilateral reductions in the HA group. Following iTBS, the LA group demonstrated the HAMD, HAMA, and SHAPS scores and alpha power recovery to the state of HC group and increased frontal/central-posterior connectivity. Conversely, although HAMD and HAMA scores improved in the HA group, SHAPS scores remained higher and alpha power deficits persisted and exhibited decreased bilateral connectivity, particularly in the right hemisphere.
Conclusions:
Remission of depressive and anxiety symptoms does not necessarily indicate recovery from anhedonia. Distinct neurophysiological responses to iTBS suggest divergent pathophysiological mechanisms in anhedonia subtypes, which may inform personalized treatment strategies for MDD.
