F233. Association Between Cortical Gyrification and Negative Symptom Dimensions in Schizophrenia: A Neurodevelopmental Perspectiv


Toper M., Verim B., Demirlek C., Yalincetin B., Zorlu N., Bora İ. E.

2026 ANNUAL CONGRESS of the Schizophrenia International Research Society, Florence, İtalya, 25 - 29 Mart 2026, ss.879-880, (Özet Bildiri)

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Florence
  • Basıldığı Ülke: İtalya
  • Sayfa Sayıları: ss.879-880
  • Dokuz Eylül Üniversitesi Adresli: Evet

Özet

Background: Schizophrenia (SCH) is characterized by significant neurodevelopmental disruptions and associated structural brain alterations. Among morphometric indices, the local Gyrification Index (lGI) reflects cortical folding established early in development and provides a relatively stable neuroanatomical measure of neurodevelopmental structure, offering a useful approach to examine developmental contributions to clinical symptom dimensions in SCH. However, its relationship with negative symptoms remains relatively underexplored. While negative symptoms were traditionally reported as a homogeneous entity, growing evidence from factorial analyses of different psychometric scales shows that negative symptoms indicate two distinct dimensions: apathy (comprising the domains of anhedonia, avolition, and asociality) and diminished expression (comprising the domains of alogia and blunted affect). It has been previously hypothesized that the diminished expression dimension may have a more pronounced neurodevelopmental basis and tends to align more consistently with neurocognitive deficits and neurological soft signs than the apathy dimension. Integrating these perspectives, the present study aimed to investigate how neurodevelopmental morphometric features relate to these negative symptom domains in patients with SCH.

Methods: Structural MRI data from 62 clinically stable patients with SCH were preprocessed using FreeSurfer to extract lGI values across 17 bilateral regions of interest (ROIs). These

regions, including the prefrontal, temporal, cingulate and insular cortex, were selected based on their established roles in the neurobiology of SCH and their association with negative symptoms in prior morphometric research. Clinical symptoms were assessed using the Brief Negative Symptom Scale (BNSS) and the Scale for the Assessment of Negative Symptoms (SANS). Associations between regional lGI measures and clinical scores were assessed using Pearson correlations with FDR correction implemented in R.

Results: FDR-corrected Pearson correlation analyses revealed that lower lGI values in the left frontal pole were significantly associated with higher BNSS total scores (p=0.02), SANS scores (p=0.02), and alogia scores (p=0.001). Furthermore, reduced gyrification in both the left (p=0.04) and right (p=0.03) temporal poles was significantly correlated with blunted affect scores. Additional significant associations were observed between reduced lGI in the left pars opercularis both alogia (p=0.04) and asociality scores (p=0.03). No significant correlations were identified for the anhedonia and avolition scores after multiple comparison correction.

Discussion: This is the first study to investigate the direct association between lGI and negative symptom domains in SCH. Unlike relatively more state-dependent or transient measures -such as cortical thickness or functional activity that can be influenced by on medication and disease progression- lGI serves as a relatively more stable, trait-like measure of early neurodevelopment. Our findings indicate that alterations in early cortical folding within prefrontal and temporal regions are more prominently associated with the diminished expression domain, whereas associations with the apathy dimension are more limited. Together, these results are consistent with the broader literature indicating a relatively stronger neurodevelopmental contribution to diminished expression. Further research integrating longitudinal designs and multimodal approaches may help clarify the role of regional lGI patterns in distinguishing neurodevelopmentally distinct negative symptom profiles and their clinical trajectories.