Assessment of the CO2 response by means of non diffusible contrast media and angio-CT in patients with cluster headache.

We analyzed the possibility of assessing functional vasomotor changes by means of Arm-Brain Circulation Time (rABCT) and Vascular volume images (Vv) obtained with Angio-CT, in basal condition and following CO2 inhalation, in a sample of 48 patients with cluster headache. CO2 inhalation resulted in the appearance of local changes, which were detected in 28 regions. Analysis by indicator images of Vv-dependent rABCT distribution showed two main patterns: abnormal rABCT mostly evident at the smallest Vv pixels and abnormal rABCT dependent on abnormal Vv distribution. The former pattern was linked to abnormality at the circle of Willis; the latter to abnormal local vasomotor responses. Patients with cluster headache showed both patterns, which prompted us to conclude for the presence of low-degree stenosis in carotid arteries and vasomotor instability in peripheral brain vessels.

Cluster headache: transcranial Doppler assessment of dynamic cerebral circulatory changes during hypocapnia and attack.

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/P ETCO2. 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 changes observed most likely are secondary phenomena during the cluster headache attack.