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The Relationship Between Frontostriatal Connectivity and Striatal Dopamine Function in Schizophrenia: An18F-DOPA PET and Diffusion Tensor Imaging Study in Treatment Responsive and Resistant Patients

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Sangho Shin, Wi Hoon Jung, Robert McCutcheon, Mattia Veronese, Katherine Beck, Jae Sung Lee, Yun Sang Lee, Oliver D. Howes, Euitae Kim, Jun Soo Kwon

Original languageEnglish
Pages (from-to)570-579
Number of pages10
JournalPsychiatry Investigation
Issue number7
Accepted/In press13 May 2022
Published21 Jul 2022

Bibliographical note

Funding Information: This work was supported by the National Research Foundation of Korea (NRF) grants funded by the Korea government (MSIT) (No. 2022R1A2B5B02002400, NRF-2019M3C7A1032472). Publisher Copyright: © 2022 Korean Neuropsychiatric Association.


King's Authors


Objective Striatal dopamine dysfunction caused by cortical abnormalities is a leading hypothesis of schizophrenia. Although prefrontal cortical pathology is negatively correlated with striatal dopamine synthesis, the relationship between structural frontostriatal connectivity and striatal dopamine synthesis has not been proved in patients with schizophrenia with different treatment response. We therefore investigated the relationship between frontostriatal connectivity and striatal dopamine synthesis in treatment-responsive schizophrenia (non-TRS) and compared them to treatment-resistant schizophrenia (TRS) and healthy controls (HC). Methods Twenty-four patients with schizophrenia and twelve HC underwent [18F] DOPA PET scans to measure dopamine synthesis capacity (the influx rate constant Ki cer) and diffusion 3T MRI to measure structural connectivity (fractional anisotropy, FA). Connectivity was assessed in 2 major frontostriatal tracts. Associations between Ki cer and FA in each group were evaluated using Spearman’s rho correlation coefficients. Results Non-TRS showed a negative correlation (r=-0.629, p=0.028) between connectivity of dorsolateral prefrontal cortex-associative striatum (DLPFC-AST) and dopamine synthesis capacity of associative striatum but this was not evident in TRS (r=-0.07, p=0.829) and HC (r=-0.277, p=0.384). Conclusion Our findings are consistent with the hypothesis of dysregulation of the striatal dopaminergic system being related to prefrontal cortex pathology localized to connectivity of DLPFC-AST in non-TRS, and also extend the hypothesis to suggest that different mechanisms underlie the pathophysiology of non-TRS and TRS. Psychiatry Investig 2022;19(7):570-579.

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