A Systematic Review and Meta-Analysis of Arterial Spin Labeling Magnetic Resonance Imaging Studies in Psychosis Spectrum Disorders

Introduction: Alterations in cerebral blood flow (CBF) in subjects with psychosis spectrum disorders (PSD) and clinical high-risk (CHR) states may provide insights into the pathophysiologyofthese disorders. Arterial spin labeling (ASL) facilitated a more comprehensive examination of CBF in these subjects. This meta-analysis synthesizes findings on CBF in PSDs and CHR states, addressing literature gaps. Methods: A systematic literature search of the PubMed database was performed using a protocol based on the PRISMA statement and the recommendations of the MOOSE group. Studies eligible for inclusion in the review involved: I) individuals with PSD, first-episode psychosis or CHR state, II) had healthy controls for comparison, III) neuroimaging should be performed with MRI using the pseudo-continuous ASL method, IV) resting cerebral blood flow (rCBF) should be recorded. Information related to participants, CBF analyses, and results were systematically extracted. Results: The PubMed search for the meta-analysis identified 69 publications, including 24 articles that met the inclusion criteria for the meta-analysis, representing 491 SSD patients, 185 CHR states, and 554 controls. Studies included rCBFs for the whole brain, gray matter, and striatum. The meta-analysis results indicated that patients with PSD had decreased gray matter rCBF compared to controls (Hedge's g=0.33, 95% CI [0.08, 0.57]), but no difference in the whole brain (Hedge's g=0.09, 95% CI [-0.70, 0.88] and striatum rCBF (Hedge's g=0.38, 95% CI [-0.23, 1.00]). Additionally, subjects with CHR state showed no differences in the striatum rCBF compared to the controls (Hedge's g=-0.15, 95% CI [-0.80, 0.51]). Conclusions: This suggests that although perfusion changes in gray matter are present in PSD, they may not extend to wider brain regions or specific structures such as the striatum. Furthermore, the results imply that rCBF may be differentially regulated in subjects with PSD and CHR. Updated findings highlight hemodynamic correlations in PSD pathophysiology.