4.6 Article

Mapping Convergent and Divergent Cortical Thinning Patterns in Patients With Deficit and Nondeficit Schizophrenia

Journal

SCHIZOPHRENIA BULLETIN
Volume 45, Issue 1, Pages 211-221

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/schbul/sbx178

Keywords

deficit schizophrenia; MRI; cortical thickness; surface area; temporo-parietal junction

Categories

Funding

  1. National Natural Science Foundation of China [81620108016, 91432115, 81571314, 81371474]
  2. National Key Research and Development Program [2016YFC1307000]
  3. Beijing Natural Science Foundation [Z161100004916027, Z161100000216152, Z151100003915082]
  4. Fundamental Research Funds for the Central Universities [2015KJJCA13, 2017XTCX04]
  5. Nanjing Technology Development Foundation [201505001]
  6. Six Talent Peaks Project in Jiangsu Province [2015-WSN-071]

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Deficit schizophrenia (DS) is a homogeneous subtype of schizophrenia characterized by primary and enduring negative symptoms. However, the underlying neuroanatomical substrate of DS remains poorly understood. Here, we collected high-resolution structural magnetic resonance images of 115 participants, including 33 DS patients, 41 nondeficit schizophrenia (NDS) patients, and 41 healthy controls (HCs), and calculated the cortical thickness and surface area for statistical comparisons among the 3 groups. Relative to the control group, both the DS and NDS groups exhibited convergent cortical thinning in the bilateral inferior frontal gyri and the left superior temporal gyrus. The cortical thinning in the right inferior frontal cortex in the patient group was significantly positively correlated with declines of cognitive flexibility and visuospatial memory. Importantly, compared to the NDS group, the DS group exhibited a more widespread cortical thinning pattern, with the most significant differences in the left temporo-parietal junction area. For the surface area measurement, no significant group differences were observed. Collectively, these results highlight the convergent and divergent cortical thinning patterns between patients with DS and NDS, which provide critical insights into the neuroanatomical substrate of DS and improve our understanding of the biological mechanism that contributes to the negative symptoms and cognitive impairments in DS.

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