The effect of intranasal cocaine and lidocaine on nitroglycerin-induced attacks in cluster headache

Citation
A. Costa et al., The effect of intranasal cocaine and lidocaine on nitroglycerin-induced attacks in cluster headache, CEPHALALGIA, 20(2), 2000, pp. 85-91
Citations number
34
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
CEPHALALGIA
ISSN journal
03331024 → ACNP
Volume
20
Issue
2
Year of publication
2000
Pages
85 - 91
Database
ISI
SICI code
0333-1024(200003)20:2<85:TEOICA>2.0.ZU;2-I
Abstract
The administration of nitroderivatives in cluster headache (CH) sufferers i s the most reproducible experimental paradigm to induce spontaneous-like pa in attacks. Previous uncontrolled studies have reported that the local use of anaesthetic agents in the area of the sphenopalatine fossa is able to ex tinguish nitroglycerin (NTG)-induced pain in CH. The present study, carried out according to a double-blind placebo-controlled design, included 15 CH patients, six with episodic CH (mean +/- so age of 36.8 +/- 5.6 years), and nine with chronic CH (37.8 +/- 10.4 years). Patients had undergone a stand ard NTG test (0.9 mg sublingually), during which the intensity of pain was scored using a visuoanalogic scale (VAS, range 0-10). Nine patients (two wi th the episodic form, seven with the chronic form) experienced a typical, s pontaneous-like attack on the usual side, occurring in all cases within 45 min. In these patients, the test was repeated with an interval of 2 days, a nd once pain intensity reached 5 on the VAS, a 10% solution of cocaine hydr ochloride (1 ml, mean amount per application 40-50 mg), or 10% lidocaine (1 ml), or saline was applied using a cotton swab in the area corresponding t o the sphenopalatine fossa, under anterior rhinoscopy. This was done in bot h the symptomatic and the non-symptomatic side, for 5 min. Treatments were always performed randomly, in separate sessions. All patients responded pro mptly to both anaesthetic agents, with complete cessation of induced pain o ccurring after 31.3+/-13.1 min for cocaine and 37.0+/-7.8 min for lidocaine (M+/-SD). In the case of saline application, pain severity increased there after, and extinction of the provoked attacks occurred with a latency of 59 .3+/-12.3 min (P<0.01 and P<0.01 vs. cocaine and lidocaine, respectively, M ann-Whitney U-test). While further suggesting that the sphenopalatine gangl ion participates in the mechanisms of pain, these findings indicate that th e local administration of the anaesthetic agents cocaine and lidocaine is e ffective on NTG-induced CH attacks, and may be used in the symptomatic trea tment of this disorder.