Transcranial Doppler ultrasound (TCD) investigations have been carried out in cluster headache patients (8 during remission and 6 during bout) and 14 healthy subjects, to assess cerebral vasomotor reactivity (VMR) to hypocapnia induced by voluntary hyperventilation. VMR was expressed as the relative change in blood flow velocity (V) (%) as a function of the reduction in end-tidal PCO2 (PETCO2) (kPa), i.e. V/PETCO2. TCD with simultaneous PETCO2 monitoring, was also performed in 5 patients during spontaneous attacks.
Prior to hyperventilation, there was bilaterally lower anterior cerebral artery velocity (VACA) during the bout than during remission (P <0.05 on the symptomatic side), and also lower than in the controls. During remission, VACA was higher on the symptomatic side than on the other side (P <0.05). ACA also showed a lower VMR during the bout than during remission, and it was also lower than in controls (bout vs. remission on the non-symptomatic side, P <0.01; on the symptomatic side, P > 0.1). Approximately 30 minutes after the onset of attack, PETCO2 started to decrease gradually from 4.65 to 4.10 kPa in one patient with severe attack. The VACA decreased markedly and bilaterally already at an early stage of the attack, i.e. prior to the hyperventilation. Middle cerebral artery velocity tended to decrease 30 minutes after the onset of attack on the symptomatic side, and 50 minutes after onset on the non-symptomatic side. It is concluded that the vascular hanges observed most likely are secondary phenomena during the cluster headache attack.