Short-lasting, Unilateral, Neuralgiform Headache Attacks with Conjunctival Injection and Tearing (SUNCT Syndrome): IV. Respiratory sinus arrhythmia during and outside paroxysms
Article first published online: 19 MAY 2005
Headache: The Journal of Head and Face Pain
Volume 32, Issue 8, pages 377–383, September 1992
How to Cite
Kruszewski, P., Sand, T., Shen, J. M. and Sjaastad, O. (1992), Short-lasting, Unilateral, Neuralgiform Headache Attacks with Conjunctival Injection and Tearing (SUNCT Syndrome): IV. Respiratory sinus arrhythmia during and outside paroxysms. Headache: The Journal of Head and Face Pain, 32: 377–383. doi: 10.1111/j.1526-4610.1992.hed3208377.x
- Issue published online: 19 MAY 2005
- Article first published online: 19 MAY 2005
- Accepted for publication: May 14, 1992.
- Cited By
- cluster headache;
- sinus arrhythmia;
- vagus nerve, atropin
SUNCT is a headache syndrome characterized by short-lasting (usually 15-120 sec), unilateral head pain paroxysms localized in the peri-ocular area, accompanied by conjunctival injection, lacrimation, nasal stuffiness, rhinorrhea, and subclinical forehead sweating, all on the symptomatic side. A relative bradycardia seems to be an integral part of the paroxysm; a parasympathetic stimulation could theoretically be the causative factor for the bradycardia. In 3 SUNCT patients, vagal nerve function (E:I ratio) has been monitored outside and during pain paroxysms, while 3 other patients could be studied in the attack-free period only. E:I ratio is obtainable in the course of a maximally deep breath and represents the ratio of the longest R-R Interval during a 5 sec long expiration to the shortest R-R interval during a 5 sec long inspiration. The mean E:I ratio of SUNCT patients outside paroxysms was significantly higher than the mean E:I ratio in an aged-matched control group. The E:I ratio was, however, significantly decreased during paroxysms in comparison with ratios obtained outside the pain paroxysms. After 0.6 mg atropine administration s.c. to one of the patients in the symptomatic phase, the heart rate increased, and the relative bradycardia during headache paroxysm was diminished (but not completely abolished). The E:I ratio was lowered but it was still slightly larger outside than during attacks. The reason for the abrupt and seemingly clear attack-related decrement in E:I ratio together with the previously described relative bradycardia remains enigmatic, however the possibility of increased parasympathetic tone cannot be excluded.