Abstract
BACKGROUND: Cerebral venous congestion (CVC), including internal jugular vein stenosis (IJVS) and cerebral venous sinus stenosis (CVSS), can impair venous drainage, leading to secondary reductions in cerebral blood flow (CBF) and neurological symptoms such as non-auditory tinnitus (NAT). While arterial spin labeling (ASL) primarily measures arterial perfusion, it also provides insights into global perfusion changes in venous pathologies. This study investigates CBF alterations in CVC patients, particularly those with NAT. METHODS: A cross-sectional study was conducted with 87 participants, including 34 NAT+ patients, 17 NAT- patients, and 36 healthy controls (HC). Multi-delay pseudo-continuous ASL was used to quantify whole-brain and regional CBF based on the anatomical automatic labeling atlas version 3 (AAL3v1), adjusted for arterial transit time. Group differences in CBF were assessed, and correlations with clinical variables were analyzed, including tinnitus duration, sleep quality, anxiety, depression, and cognitive function. RESULTS: Patients in the NAT+ group exhibited significant CBF reductions in the left hemisphere, cerebrum, and specific regions, including the insula, paracentral lobule, and precentral gyrus, compared to those in the NAT- and HC groups. Reduced CBF in NAT+ patients was correlated with longer tinnitus duration, poorer sleep quality, and worse depression scores. Further analysis revealed that the affected regions were part of the attention, sensorimotor, default mode, and cerebellar networks. CONCLUSION: This study identified a distinct pattern of cerebral perfusion alterations in patients with CVC, particularly those with NAT. The findings highlight characteristic regional reductions in CBF associated with impaired venous outflow, offering new insights into the venous pathophysiological mechanisms underlying NAT. Moreover, reduced CBF was found to be associated with clinical symptoms such as sleep disturbances and emotional dysregulation. These findings support a link between venous pathology and altered cerebral perfusion patterns with symptom correlations, warranting confirmation in larger and longitudinal cohorts. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11682-026-01144-8.