Neuronal Signal Substances as Biomarkers of Migraine

@article{Edvinsson2006NeuronalSS,
  title={Neuronal Signal Substances as Biomarkers of Migraine},
  author={Lars Edvinsson},
  journal={Headache: The Journal of Head and Face Pain},
  year={2006},
  volume={46}
}
  • L. Edvinsson
  • Published 1 July 2006
  • Biology, Medicine
  • Headache: The Journal of Head and Face Pain
Of the sensory nervous system associated signal substances it is only calcitonin generelated peptide (CGRP) that is reliably associated with the degree of pain in the acute attacks of primary headaches. The treatment with triptans alleviates both the pain and the associated CGRP release, putatively via a presynaptic effect on the sensory nerves. The studies of opoids and other sensory neuropeptides are inconsistent and require further analysis. Initial positive data on endothelin and its… 

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References

SHOWING 1-10 OF 47 REFERENCES

The Nitric Oxide Hypothesis of Migraine and Other Vascular Headaches

TLDR
The importance of NO as a potential initiator of the migraine attack indicates new directions for the pharmacological treatment of migraine and other vascular headaches.

Nitric Oxide Metabolites, Prostaglandins and Trigeminal Vasoactive Peptides in Internal Jugular Vein Blood During Spontaneous Migraine Attacks

TLDR
The results support early activation of the l-arginine/NO pathway which accompanies the release of vasoactive peptides from trigeminal endings and a late rise in the synthesis of prostanoids with algogenic and vaso active properties which may intervene in maintaining the headache phase.

Human in vivo evidence for trigeminovascular activation in cluster headache. Neuropeptide changes and effects of acute attacks therapies.

TLDR
Patients with episodic cluster headache fulfilling the criteria of the International Headache Society were examined during an acute spontaneous attack of headache to determine the local cranial release of neuropeptides to demonstrate in vivo human evidence for activation of the trigeminovascular system and the cranial parasympathetic nervous system.

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

TLDR
A patient fulfilling International Headache Society guidelines for the diagnosis of CPH is reported in whom levels of calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were elevated in the cranial circulation during attacks.

Vasoactive peptide release in the extracerebral circulation of humans during migraine headache

TLDR
A substantial elevation of the calcitonin gene‐related peptide level in the external jugular but not the cubital fossa blood was seen in both classic and common migraine, and may have importance in the pathophysiology of migraine.

Raised Plasma Endothelin During Acute Migraine Attack

TLDR
It is hypothesized that ET-1 may constrict cerebral vessels during the initial stage of the migraine attack, and be elevated in all migraine patients above the range of normal subjects.

Release of vasoactive peptides in the extracerebral circulation of humans and the cat during activation of the trigeminovascular system

TLDR
The observation of elevation of substance P—like and CGRP‐like immunoreactivity after activation of the nociceptive afferent system of the head provides new insights into a putative role of peptides in the pathophysiology of migraine and cluster headache, and suggests new areas of possible therapeutic intervention.

Regulation of Calcitonin Gene-Related Peptide Secretion by a Serotonergic Antimigraine Drug

TLDR
The results suggest that 5-HT1 agonists may block a deleterious feedback loop in migraine at the trigeminal neurons and provide a general mechanism by which this class of drugs can attenuate stimulated neuropeptide release.

Responsiveness of the trigeminovascular system to nitroglycerine in cluster headache patients.

TLDR
The results of this study suggest that the provocative action of nitroglycerine in cluster headache is due, at least in part, to activation of the trigeminovascular system, which seems to be slow and unrelated to the well-known rapidly occurring vasodilator effects of the drug.

Substance P Mechanism in Cluster Headache: Evaluation in Plasma and Cerebrospinal Fluid

TLDR
During spontaneous and histamine induced attacks in the cluster phase, plasma EKA was increased in comparison with the values in controls and it remains to be seen whether variations of plasma SPLI and EKA levels play a role in the CH mechanism.