Am I hallucinating or is my fusiform cortex activated? Functional activation differences in schizophrenia patients with and without hallucinations

Kunzelmann, Katharina; Grieder, Matthias; Swam, Claudia van; Homan, Philipp; Winkelbeiner, Stephanie; Hubl, Daniela; Dierks, Thomas

doi:10.1016/j.ejpsy.2018.06.002

Cited by 5 publications

(1 citation statement)

References 31 publications

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“…As STG contains the primary auditory cortex, hypermyelination in this area could affect auditory function (Tzourio-Mazoyer et al, 2018). Structural and functional abnormalities in STG were related to verbal hallucination in SZ (Kose, Jessen, Ebdrup, & Nielsen, 2018;Kunzelmann et al, 2019). Level of gamma-aminobutyric acid (GABA) was found increased in temporal gyrus in SZ patients, which may suggest that hypermyelination in the STG could relate to GABAergic pathway disruption in the disease (Galinska-Skok et al, 2018).…”

Section: Depth-dependence Of Abnormal Regional Myelination In Fesmentioning

confidence: 99%

Depth‐dependent abnormal cortical myelination in first‐episode treatment‐naïve schizophrenia

Wei

Zhang

et al. 2020

Human Brain Mapping

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Myelination is key to effective message passing in the central nervous system and is likely linked to the pathogenesis of schizophrenia (SZ). Emerging evidence indicates that a large portion of intracortical myelin insulates inhibitory interneurons that are highly relevant to pathogenesis of schizophrenia. Here for the first time, we characterized intracortical myelination across the entire cortical surface in first‐episode treatment‐naïve patients with schizophrenia (FES) using T1w/T2w ratio of structural MRI, FES patients exhibited significantly higher myelin content in the left inferior parietal lobe, supramarginal gyrus, and superior temporal gyrus in the superficial layer, as well as left IPL in the middle layer, but significantly lower myelin content in the left middle insula and posterior cingulate gyrus. Years of education, a proxy for onset of functional decline, significantly altered the relationship between abnormal parietal and posterior cingulate myelination and clinical symptoms, indicating that the pathoplastic role of myelination hinges on the age of onset of functional decline. In addition, higher myelination generally related to better cognitive function in younger subjects but worse cognitive function in older subjects. We conclude that FES is characterized by increased myelination of the superficial layers of the parietal–temporal association cortex, but reduced myelination of the cingulo‐insular midcortical layer cortex. Intracortical myelin content affects both cognitive functioning and symptom burden in FES, with the effect conditional upon age and timing of onset of functional decline. These results suggest myelination might be a critical biological target for procognitive interventions in SZ.

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