Cutaneous Sensory Stimulation Leading to Facial Flushing and Release of Calcitonin Gene-Related Peptide

Cephalalgia ◽  
1992 ◽  
Vol 12 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Peter J Goadsby ◽  
Lars Edvinsson ◽  
Rolf Ekman

A patient is described with a 17-year history of intractable left-sided facial pain. The pain occurred daily in 5 sec spasms to a maximum of one every 2–3 min and was restricted to the left upper face. It was associated with rhinorrhoea on the left and often with ipsilateral facial flushing. Conventional therapy, including carbamazepine, baclofen and three posterior fossa explorations, had not provided lasting relief. Local facial stimulation by tapping a painful trigger point led to both pain and flushing of the face ipsilaterally. During this flushing, blood was collected and assayed using sensitive radioimmunoassays for several neuropeptides (neuropeptide Y, substance P, vasoactive intestinal polypeptide and calcitonin gene-related peptide). A marked (119%) increase in calcitonin gene-related peptide was noted in the external jugular vein blood ipsilaterally during the flushing with no change in the other peptides measured. To quantitate the effect of calcitonin gene-related peptide on human extracranial vessels, standard pharmacological procedures were used to examine the potency of the peptide as a vasodilator of human facial artery. The 1C50 of calcitonin gene-related peptide for the prostaglandin F2a -precontracted human facial artery was 10-9 mol/1. The relevance of these observations to the clinical problem of migraine is considered.

Cephalalgia ◽  
1993 ◽  
Vol 13 (3) ◽  
pp. 180-183 ◽  
Author(s):  
Richard D Piper ◽  
Lars Edvinsson ◽  
Rolf Ekman ◽  
Geoffrey A Lambert

There is circumstantial evidence that cortical spreading depression (SD) may account for the scotoma and the “spreading cortical oligemia” seen during migraine with aura. It has been shown that calcitonin gene-related peptide (CGRP) is increased in blood taken from the external jugular vein (EJV) in humans during migraine and after stimulation of the trigeminal ganglion. To test the hypothesis that cortical SD may elevate the concentration of this vasoactive peptide in the EJV during migraine, we have measured its concentration in the external jugular vein of cats during cortical SD. This study demonstrates that SD has no effect on the concentration of CGRP either during the passage of a wave of spreading depression across the cortex or, 60 min later, during the period of post-SD cortical oligemia.


1988 ◽  
Vol 74 (4) ◽  
pp. 413-418 ◽  
Author(s):  
C. W. Howden ◽  
Catherine Logue ◽  
Karen Gavin ◽  
Lizbeth Collie ◽  
P. C. Rubin

1. The effects of intravenous bolus doses of human calcitonin-gene-related peptide (hCGRP) were studied in ten healthy male volunteers. 2.5, 10 and 25 μg of hCGRP and placebo were administered to each subject in a randomized double-blind study. 2. hCGRP had no effect on systolic or diastolic blood pressure in the supine or standing position. 3. hCGRP increased supine and standing heart rate. Both the extent and duration of the tachycardia were dose related. 4. Plasma noradrenaline levels were transiently increased after 10 and 25 μg of hCGRP. 5. All subjects displayed marked facial flushing after the two higher doses of hCGRP. 6. We conclude that systemic administration of hCGRP produces tachycardia and stimulation of the sympathetic nervous system in the absence of any change in blood pressure.


Neuropeptides ◽  
1999 ◽  
Vol 33 (3) ◽  
pp. 244-250 ◽  
Author(s):  
I. Dawidson ◽  
B. Angmar-Månsson ◽  
M. Blom ◽  
E. Theodorsson ◽  
T. Lundeberg

Cephalalgia ◽  
1989 ◽  
Vol 9 (10_suppl) ◽  
pp. 290-291
Author(s):  
Peter J. Goadsby ◽  
Lars Edvinsson ◽  
Rolf Ekman

Cephalalgia ◽  
2005 ◽  
Vol 25 (9) ◽  
pp. 700-703 ◽  
Author(s):  
A Frese ◽  
M Schilgen ◽  
L Edvinsson ◽  
E Frandsen ◽  
S Evers

Trigeminovascular activation is involved in the pathophysiology of migraine and cluster headache. The marker evaluated best for trigeminovascular activation is calcitonin gene-related peptide (CGRP) in the cranial circulation. It is unknown whether trigeminovascular activation plays any role in cervicogenic headache (CEH). The objective of this study was to investigate CGRP plasma levels in CEH patients in relation to headache state. To compare plasma CGRP levels between the peripheral and the cranial circulation. Blood from both external jugular veins and from the antecubital vein was drawn from 11 patients with CEH. Plasma CGRP levels were measured by radioimmunoassay. No difference was found between CGRP levels assessed on days with and without headache. There was no difference beween CGRP levels from the symptomatic and the asymptomatic external jugular vein and the antecubital vein. There is no evidence for an activation of the trigeminovascular system in CEH. In certain cases, clinical differentiation between CEH and migraine without aura is difficult. Plasma CGRP levels might serve as a biological marker to distinguish the two headache entities.


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