Four patients with SUNCT syndrome (Short-lasting, Unilateral, Neuralgiform headache attacks with Conjunctival injection and Tearing) were investigated with Doppler ultrasonography. Blood flow velocity (V) was measured in all intracranial arteries during both normocapnia and voluntary hyperventilation in 4 patients outside attacks (2 during remission; 2 during bout, but outside attacks) and in 8 healthy individuals. Vasomotor reactivity (VMR) was calculated on the basis of the formula of percentage change in V divided by the reduction in end-tidal PCO2 (PETCO2). Under the basal condition, the patients had a slightly, but non-significantly higher V in the middle cerebral artery (MCA) (P > 0.1) and lower V in the basilar artery (P > 0.05) than controls. During hyperventilation, a significant reduction in V was observed in the anterior and posterior cerebral arteries, at a level 1.5-2 SD above that in controls (P < 0.05), but a non-significant difference in VMR in comparison with controls. VMCA was continuously insonated during spontaneous (n = 8) and precipitated (n = 4) attacks in one particular patient on different days. Prior to attack, VMCA was significantly lower on the symptomatic side than on the non-symptomatic side (P < 0.014). VMCA decreased significantly during spontaneous attacks on both sides (P < 0.01) in comparison with the pre-attack stage, and returned to baseline before the cessation of attack. Similar findings were made during precipitated attacks. PETCO2, was rather constant throughout the entire attack study. Our data suggest that abnormal cerebral circulation may be part of the SUNCT syndrome. The vascular changes may have underlying mechanisms differing from those of the pain.