Provocation of unilateral pain in cluster headache patients by breathing CO2.

Ten patients with cluster headache in an active period and 6 controls were studied as to heart rate, blood pressure, blood flow in the common carotid arteries (CCA), end-tidal PCO2 and pain before, during and after 6 minutes of breathing 6% CO2 in air. Heart rate increased significantly during CO2 breathing in controls but not in patients. The cluster headache patients had significantly lower baseline end-tidal PCO2 than controls. CCA blood flow increased significantly during CO2 breathing in both groups. Vascular resistance decreased during CO2 provocation and increased above baseline levels 5 minutes after provocation in both groups and related to the end-tidal PCO2. Six of eight cluster headache patients, who had an increase of blood flow at provocation, reported slight to moderate unilateral pain in relation to the CO2 provocation in contrast to controls. One patient treated with 6 mg sumatriptan 2.5 hours before the provocation had an end-tidal PCO2 within the range of the controls, and did not get an increase of CCA blood flow or pain at provocation. Six of the cluster headache patients were restudied when out of the active period. There was still no heart rate increase during CO2 breathing and end-tidal PCO2 was still lower than in the controls. Unilateral headache was not provoked.