Brain Blood Flow Shifts Reveal Hidden Dynamics of Reversible Cerebral Vasoconstriction

Reversible cerebral vasoconstriction syndrome (RCVS) is a neurovascular condition marked by thunderclap headaches and transient constriction of cerebral arteries, with serious potential complications including stroke, subarachnoid hemorrhage, and posterior reversible encephalopathy syndrome. Despite its clinical significance, how cerebral blood flow actually behaves across the disease course—particularly the interplay between large-vessel vasoconstriction and small-vessel autoregulation—has remained poorly characterized, with prior perfusion data limited to isolated case reports.

This prospective, single-center study enrolled 316 participants (281 RCVS patients and 35 age- and sex-matched healthy controls) between 2018 and 2023 at a major tertiary hospital in Taiwan. Patients were stratified as acute RCVS (aRCVS; MRI within 30 days of onset) or remission RCVS (rRCVS; MRI ≥90 days after onset). Cerebral blood flow was measured noninvasively using pseudocontinuous arterial spin labeling (pCASL) MRI at 3 Tesla, with voxelwise and whole-brain gray matter analyses conducted using SPM12. Transcranial color-coded duplex sonography (TCCS) was performed on the same day as MRI to assess large-vessel flow velocities.

Acute RCVS patients had significantly lower global CBF compared to healthy controls (49.0 ± 10.2 vs. 53.9 ± 6.7 mL/100 g/min; p = 0.033), with the most pronounced hypoperfusion in posterior brain regions. Importantly, CBF values returned to normal by approximately two weeks after headache onset and were fully normalized by the remission stage (rRCVS: 52.8 ± 9.3 mL/100 g/min; p = 0.005 vs. aRCVS). A critical window of abrupt CBF fluctuation was identified between days 2–16 and 7–21 after headache onset—a finding that remained robust across multiple statistical thresholds and sliding time-interval models, underscoring its biological significance rather than analytic artifact.

Ultrasound-based flow velocities of the middle cerebral artery and internal carotid artery showed strong positive correlations with CBF during the 2nd and 4th weeks of the acute phase (MCA 2nd week: r = 0.628, p < 0.001; ICA 2nd week: r = 0.626, p < 0.001), suggesting that downstream perfusion is directly tied to upstream large-vessel hemodynamics during the critical acute period. The study also examined whether nimodipine treatment affected CBF measurements in aRCVS, adding clinical nuance to the findings.

These results provide the most comprehensive spatiotemporal map of cerebral perfusion in RCVS to date, identifying a narrow, biologically critical fluctuation window that may correspond to the period of greatest ischemic risk. The posterior predominance of hypoperfusion aligns with the known predilection of RCVS complications for the posterior circulation and may help explain why PRES and posterior ischemic stroke are common in this syndrome. While causality cannot be established from this observational design, the data support further investigation into whether early CBF monitoring could guide risk stratification or treatment timing in RCVS.