Neuropeptide Changes in a case of Chronic Paroxysmal Hemicrania—Evidence for Trigemino-Parasympathetic Activation

Cephalalgia ◽  
1996 ◽  
Vol 16 (6) ◽  
pp. 448-450 ◽  
Author(s):  
P J Goadsby ◽  
L Edvinsson
Keyword(s):  
Cluster Headache ◽  
Vasoactive Intestinal Polypeptide ◽  
Successful Treatment ◽  
International Headache Society ◽  
Paroxysmal Hemicrania ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Autonomic Activation ◽  
Chronic Paroxysmal Hemicrania ◽  
Underlying Pathophysiology

Chronic paroxysmal hemicrania (CPH) is a rare headache syndrome of short-lasting attacks of pain, characterized clinically by trigemino-parasympathetic activation. The features of the headache are severe attacks of pain that generally last no more than minutes in association with autonomic activation, such as lacrimation or rhinorrhea. We report a patient fulfilling International Headache Society guidelines for the diagnosis of CPH in whom levels of calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were elevated in the cranial circulation during attacks. Moreover, successful treatment of the problem with indomethacin leads to normalization of the levels of both CGRP and VIP. Given that similar neuropeptide changes are seen in cluster headache the data suggest a shared underlying pathophysiology between CPH and cluster headache.

Nostril Capsaicin Application as a Model of Trigeminal Primary Sensory Neuronal Activation

Cephalalgia ◽  
1994 ◽  
Vol 14 (2) ◽  
pp. 134-138 ◽  
Author(s):  
M Nicolodi
Keyword(s):  
Substance P ◽  
Cluster Headache ◽  
Vasoactive Intestinal Polypeptide ◽  
Separate Study ◽  
Sensory Neurones ◽  
Related Peptide ◽  
Capsaicin Application ◽  
Episodic Cluster Headache ◽  
Calcitonin Gene ◽  
Neurochemical Changes

Capsaicin was applied unilaterally to the nostril mucosa of 18 episodic cluster headache sufferers in remission. Plasma and saliva levels of substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay. Increase of salivary SP-LI and CGRP-LI as well as of plasma CGRP-LI occurred after capsaicin stimulation. Capsaicin-induced neurochemical changes in saliva and in plasma were compared to the changes observed during cluster headache attacks measured in a separate study. The comparative changes in SP, CGRP and VIP characterizing these two conditions suggest that trigeminal capsaicin-sensitive sensory neurones are unlikely to play any fundamental role in the mechanics of cluster headache.

PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation

Cephalalgia ◽  
2021 ◽  
pp. 033310242110562
Author(s):  
Lanfranco Pellesi ◽  
Basit Ali Chaudhry ◽  
Anne Luise Haulund Vollesen ◽  
Agneta Henriette Snoer ◽  
Katrine Baumann ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cluster Headache ◽  
Vasoactive Intestinal Polypeptide ◽  
Plasma Levels ◽  
Cell Activation ◽  
Calcitonin Gene Related Peptide ◽  
Mast Cell Activation ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Headache Patients

Background Pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) and vasoactive intestinal polypeptide can provoke cluster headache attacks in up to half of cluster headache patients in their active phase. At present, it is unknown whether provoked attacks are mediated via calcitonin gene-related peptide or mast cell activation. Methods All enrolled patients with cluster headache were randomly allocated to receive a continuous infusion of either PACAP38 (10 pmol/kg/min) or vasoactive intestinal polypeptide (8 pmol/kg/min) over 20 min. We collected clinical data and measured plasma levels of calcitonin gene-related peptide and markers of mast cell activation (tryptase and histamine) at fixed time points: at baseline (T0), at the end of the infusion (T20), 10 min after the infusion (T30), and 70 min after the infusion (T90). Results Blood was collected from episodic cluster headache patients in active phase (n = 14), episodic cluster headache patients in remission (n = 15), and chronic cluster headache patients (n = 15). At baseline, plasma levels of calcitonin gene-related peptide, tryptase, and histamine were not different among the three study groups. Plasma levels of calcitonin gene-related peptide ( p = 0.7074), tryptase ( p = 0.6673), or histamine ( p = 0.4792) remained unchanged during provoked attacks compared to attack-free patients. Conclusion Cluster headache attacks provoked by either PACAP38 or vasoactive intestinal polypeptide were not accompanied by alterations of plasma calcitonin gene-related peptide, tryptase or histamine. The provoked attacks may not be mediated by calcitonin gene-related peptide or mast cell activation. Trial Registration: The study is registered at ClinicalTrials.gov (NCT03814226).

scholarly journals Calcitonin gene-related peptide and disease activity in cluster headache

Cephalalgia ◽  
2019 ◽  
Vol 39 (5) ◽  
pp. 575-584 ◽  
Author(s):  
Agneta Snoer ◽  
Anne Luise H Vollesen ◽  
Rasmus P Beske ◽  
Song Guo ◽  
Jan Hoffmann ◽  
...  
Keyword(s):  
Cluster Headache ◽  
Vasoactive Intestinal Polypeptide ◽  
Active Phase ◽  
Calcitonin Gene Related Peptide ◽  
Chronic Cluster Headache ◽  
Related Peptide ◽  
Episodic Cluster Headache ◽  
Calcitonin Gene ◽  
Headache Patients ◽  
Intestinal Polypeptide

Objective To investigate the role of calcitonin gene-related peptide, pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) and vasoactive intestinal polypeptide in cluster headache, we measured these vasoactive peptides interictally and during experimentally induced cluster headache attacks. Methods We included patients with episodic cluster headache in an active phase (n = 9), episodic cluster headache patients in remission (n = 9) and patients with chronic cluster headache (n = 13). Cluster headache attacks were induced by infusion of calcitonin gene-related peptide (1.5 µg/min) in a randomized, double-blind, placebo controlled, two-way cross-over study. At baseline, we collected interictal blood samples from all patients and during 11 calcitonin gene-related peptide-induced cluster headache attacks. Results At baseline, episodic cluster headache patients in remission had higher plasma levels of calcitonin gene-related peptide, 100.6 ± 36.3 pmol/l, compared to chronic cluster headache patients, 65.9 ± 30.5 pmol/l, ( p = 0.011). Episodic cluster headache patients in active phase had higher PACAP38 levels, 4.0 ± 0.8 pmol/l, compared to chronic cluster headache patients, 3.3 ± 0.7 pmol/l, ( p = 0.033). Baseline levels of vasoactive intestinal polypeptide did not differ between cluster headache groups. We found no attack-related increase in calcitonin gene-related peptide, PACAP38 or vasoactive intestinal polypeptide levels during calcitonin gene-related peptide-induced cluster headache attacks. Conclusions This study suggests that cluster headache disease activity is associated with alterations of calcitonin gene-related peptide expression. Future studies should investigate the potential of using calcitonin gene-related peptide measurements in monitoring of disease state and predicting response to preventive treatments, including response to anti-calcitonin gene-related peptide monoclonal antibodies.

Sensory Neuropeptides (Substance P, Calcitonin Gene-Related Peptide) and Vasoactive Intestinal Polypeptide in Human Saliva: Their Pattern in Migraine and Cluster Headache

Cephalalgia ◽  
1990 ◽  
Vol 10 (1) ◽  
pp. 39-50 ◽  
Author(s):  
Maria Nicolodi ◽  
Elena Del Bianco
Keyword(s):  
Substance P ◽  
Cluster Headache ◽  
Vasoactive Intestinal Polypeptide ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Control Subjects ◽  
Cluster Headache Attack ◽  
Calcitonin Gene ◽  
Symptomatic Side ◽  
Intestinal Polypeptide

Substance P, calcitonin gene-related peptide and vasoactive intestinal polypeptide-like immunoreactivities have been evaluated in the saliva of 15 subjects suffering from migraine without aura and 16 control subjects. All three peptides were also measured in the symptomatic/non-symptomatic side saliva sampled from 10 cluster headache sufferers during the cluster period, 5 cluster headache sufferers out of the cluster period, as well as in the right and left side saliva of 18 control subjects. The most interesting result gives a clear difference in common migraine and cluster headache salivary vasoactive intestinal polypeptide-like immunoreactivity contents. In fact, these are enhanced during cluster headache attack and decreased during migraine attack when compared with the interictal period vasoactive intestinal polypeptide-like immunoreactivity levels. Another remarkable finding concerns the significant increase of substance P-like immunoreactivity and calcitonin gene-related peptide-like immunoreactivity levels, from basal values, in the saliva sampled during both migraine and cluster headache attacks. Control subjects showed a calcitonin gene-related peptide-like immunoreactivity and substance P-like immunoreactivity salivary contents significantly higher than migraine sufferers' saliva sampled in basal conditions. Conversely, calcitonin gene-related peptide-like immunoreactivities levels in controls were lower than in cluster headache sufferers' saliva obtained during intervals. Finally, during cluster headache attacks the enhancement of substance P-like immunoreactivity and vasoactive intestinal polypeptide-like immunoreactivity salivary contents interest the non-symptomatic side, whereas the symptomatic side salivary substance P-like immunoreactivity and vasoactive intestinal poly-peptide-like immunoreactivity contents remain unchanged. These findings do not allow any final conclusion. However, this biochemical evaluation indicates relevant changes of the salivary neuropeptides in diseases, such as migraine and cluster headache, in which pain transmission is surely involved.

Chronic Paroxysmal Hemicrania in a Patient with a Macroprolactinoma

Cephalalgia ◽  
2006 ◽  
Vol 26 (6) ◽  
pp. 738-741 ◽  
Author(s):  
M Sarov ◽  
D Valade ◽  
C Jublanc ◽  
A Ducros
Keyword(s):  
International Headache Society ◽  
Paroxysmal Hemicrania ◽  
Chronic Paroxysmal Hemicrania ◽  
International Headache Society Classification

We report a patient with headaches meeting the criteria of chronic paroxysmal hemicrania, as defined by the International Headache Society classification. Headaches were fully responsive to indomethacin during the first 3 months of treatment but recurred when daily doses were lowered. Investigations revealed a macroprolactinoma. Headaches stopped after cabergoline treatment. This report further suggests that patients with paroxysmal hemicrania should be investigated for pituitary abnormalities.

scholarly journals Multiple cranial nerve blocks for the transitional treatment of chronic headaches

Cephalalgia ◽  
2019 ◽  
Vol 39 (12) ◽  
pp. 1488-1499 ◽  
Author(s):  
Sarah Miller ◽  
Susie Lagrata ◽  
Manjit Matharu
Keyword(s):  
Cluster Headache ◽  
Chronic Migraine ◽  
Cranial Nerve ◽  
Chronic Cluster Headache ◽  
Hemicrania Continua ◽  
Paroxysmal Hemicrania ◽  
Nerve Blocks ◽  
Greater Occipital Nerve ◽  
Chronic Paroxysmal Hemicrania ◽  
Multiple Cranial Nerve

Background Multiple cranial nerve blocks of the greater and lesser occipital, supraorbital, supratrochlear and auriculotemporal nerves are widely used in the treatment of primary headaches. We present efficacy and safety data for these procedures. Methods In an uncontrolled open-label prospective study, 119 patients with chronic cluster headache, chronic migraine, short lasting unilateral neuralgiform attack disorders, new daily persistent headaches, hemicrania continua and chronic paroxysmal hemicrania were examined. All had failed to respond to greater occipital nerve blocks. Response was defined as a 50% reduction in either daily attack frequency or moderate-to-severe headache days after 2 weeks. Results The response rate of the whole cohort was 55.4%: Chronic cluster headache, 69.2%; chronic migraine, 49.0%; short lasting unilateral neuralgiform attack disorders, 56.3%; new daily persistent headache, 10.0%; hemicrania continua, 83.3%; and chronic paroxysmal hemicrania, 25.0%. Time to benefit was between 0.50 and 33.58 hours. Benefit was maintained for up to 4 weeks in over half of responders in all groups except chronic migraine and paroxysmal hemicrania. Only minor adverse events were recorded. Conclusion Multiple cranial nerve blocks may provide an efficacious, well tolerated and reproducible transitional treatment for chronic headache disorders when greater occipital nerve blocks have been unsuccessful.

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