Abstract

Nine patients with chronic cluster headache were studied as to end-tidal PCO2, heart rate, blood pressure, common carotid artery blood flow, vascular resistance, and intensity and duration of pain before, during, and after breathing 6% CO2 in air for 6 minutes and before and after administration of 1 mg nitroglycerin sublingually. End-tidal PCO2 was low at rest without provocation indicating that chronic cluster headache patients hyperventilate. Carbon dioxide provocation induced an increase in common carotid artery blood flow. This provocation, previously shown to induce pain in episodic cluster headache patients, did not result in unilateral pain in chronic cluster headache patients. Nitroglycerin did not provoke any pain in 4 of 5 chronic cluster headache patients in contrast to the effects in episodic cluster headache patients in a cluster period. In one chronic cluster headache patient, a short-lasting attack of moderate pain intensity was provoked. The results agree with the hypothesis that chronic cluster headache patients have changed vascular reactivity due to permanent sympathicoplegia unilaterally in the middle fossa in contrast to episodic cluster headache patients who it has been suggested have a nonpermanent sympathicoplegia unilaterally in the same region.

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