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Cluster Headache: Transcranial Doppler Assessment of Dynamic Cerebral Circulatory Changes During Hypocapnia and Attack
Author(s) -
Shen Jie Ming,
Johnsen HansJørgen,
Juul Roar
Publication year - 1993
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.1993.hed3309488.x
Subject(s) - hypocapnia , hyperventilation , transcranial doppler , medicine , middle cerebral artery , anesthesia , posterior cerebral artery , cerebral blood flow , cardiology , ischemia , hypercapnia , acidosis
SYNOPSIS 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 PCO 2 (P ET CO 2 ) (kPa), i.e. V/P ET CO 2 . TCD with simultaneous P ET CO 2 monitoring, was also performed in 5 patients during spontaneous attacks. Prior to hyperventilation, there was bilaterally lower anterior cerebral artery velocity (V ACA ) during the bout than during remission (P <0.05 on the symptomatic side), and also lower than in the controls. During remission, V ACA 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, P ET CO 2 started to decrease gradually from 4.65 to 4.10 kPa in one patient with severe attack. The V ACA 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.