Background <p>Although abnormal amygdala functional connectivity (FC) has been reported in schizophrenia, most studies have treated the amygdala as a single structure. This study aimed to explore the association between amygdala subregional FC and anhedonia in patients with first-episode schizophrenia (FES).</p> Methods <p>Resting-state functional magnetic resonance imaging (fMRI) was conducted in 31 FES patients (including 11 drug-naïve) and 33 matched healthy controls (HCs). Clinical symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS), and anhedonia was evaluated via the Snaith-Hamilton Pleasure Scale (SHAPS). Whole-brain FC analyses of amygdala subregions were performed, followed by group comparisons and correlation analyses with anhedonia scores.</p> Result <p>Compared to HCs, FES patients showed significantly reduced FC between specific amygdala subregions and cortical regions, particularly within the frontal, temporal, parietal, and limbic lobes (<i>P</i> &lt; 0.05, GRF correction). Anhedonia severity was positively correlated with altered FC in the centromedial (CM) subregion of the amygdala (AMY_CM), especially with the supplementary motor area (SMA) and paracentral lobule (PLG). Notably, the association between right AMY_CM and right SMA FC and anhedonia remained significant after adjusting for clinical symptom severity (<i>r</i> = 0.46, <i>P</i> = 0.02).</p> Conclusions <p>FES patients exhibit disrupted FC between amygdala subregions and cortical areas, with specific patterns linked to anhedonia. These findings suggest that anhedonia may be associated with a potential neurobiological marker independent of general clinical symptoms and may be indicative of amygdala–cortical dysconnectivity in schizophrenia.</p> Trial registration <p>Data used for this analysis came from case-control studies. Clinical trial number: not applicable. (April 2018 through March 2021).</p>

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Subregional amygdala functional connectivity abnormalities and anhedonia impairments in first-episode schizophrenia

  • Qijie Kuang,
  • Sumiao Zhou,
  • Guangxing Deng,
  • Nvnan Zhou,
  • Xiangzhu Zeng,
  • Hengyu Zhang,
  • Yongjie Deng,
  • Yingjun Zheng,
  • Shenglin She

摘要

Background

Although abnormal amygdala functional connectivity (FC) has been reported in schizophrenia, most studies have treated the amygdala as a single structure. This study aimed to explore the association between amygdala subregional FC and anhedonia in patients with first-episode schizophrenia (FES).

Methods

Resting-state functional magnetic resonance imaging (fMRI) was conducted in 31 FES patients (including 11 drug-naïve) and 33 matched healthy controls (HCs). Clinical symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS), and anhedonia was evaluated via the Snaith-Hamilton Pleasure Scale (SHAPS). Whole-brain FC analyses of amygdala subregions were performed, followed by group comparisons and correlation analyses with anhedonia scores.

Result

Compared to HCs, FES patients showed significantly reduced FC between specific amygdala subregions and cortical regions, particularly within the frontal, temporal, parietal, and limbic lobes (P < 0.05, GRF correction). Anhedonia severity was positively correlated with altered FC in the centromedial (CM) subregion of the amygdala (AMY_CM), especially with the supplementary motor area (SMA) and paracentral lobule (PLG). Notably, the association between right AMY_CM and right SMA FC and anhedonia remained significant after adjusting for clinical symptom severity (r = 0.46, P = 0.02).

Conclusions

FES patients exhibit disrupted FC between amygdala subregions and cortical areas, with specific patterns linked to anhedonia. These findings suggest that anhedonia may be associated with a potential neurobiological marker independent of general clinical symptoms and may be indicative of amygdala–cortical dysconnectivity in schizophrenia.

Trial registration

Data used for this analysis came from case-control studies. Clinical trial number: not applicable. (April 2018 through March 2021).