A method for determining when the superficial scalp arteries are the source of migraine pain.

In some patients the pain of migraine originates in the extracranial cranial arteries. This article describes the location and a logical examination sequence of the vessels most frequently involved in migraine pain.

TRPV1, CGRP and SP in scalp arteries of patients suffering from chronic migraine.

OBJECTIVE: The transient receptor potential vanilloid type-1 receptor (TRPV1) and the neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP) appear to be differently involved in migraine pain. A role of neurovascular scalp structures is also suggested by several data. We performed a quantitative study of TRPV1-like immunoreactive (LI), CGRP-LI and SP-LI innervation of scalp arterial samples from patients affected with chronic migraine (CM). METHODS: Short segments of scalp arteries were collected from 17 participants undergoing vascular surgery for treatment-resistant CM and from 6 controls who underwent neurosurgery for various indications. The immunoreactivity of the arterial innervation to TRPV1, CGRP, SP and to the pan-neuronal marker protein gene product 9.5 (PGP9.5) was examined. Immunoreactive nerve fibres in vessel cross-sections were quantified by computerised image analysis. RESULTS: A significant increase of TRPV1-LI nerve fibres was found in the arterial wall from CM compared with control patients (p<0.05), while no significant difference was found for CGRP and SP. CONCLUSIONS: This study yields the first evidence for the existence of a TRPV1-LI innervation in human scalp arteries and provides the first quantitative assessment of the TRPV1-LI, CGRP-LI and SP-LI innervation of those vessels. The increase of TRPV1-LI periarterial nociceptive fibres of scalp arteries may represent, at least in some participants, a structural condition favouring CM (and possibly migraine), for example, by causing a higher sensitivity to algogenic agents.

Arterial surgery for sporadic hemiplegic migraine: preliminary results.

My aim was to report for the first time (to my knowledge) the successful treatment of 3 patients with sporadic hemiplegic migraine by surgical cautery of terminal branches of the external carotid artery under conscious sedation. Since the operations (between 1 and 2 years) none of the patients have had further attacks of migraine or hemiplegia. This preliminary report suggests that for patients with sporadic hemiplegic migraine with a confirmed arterial component, surgical cautery of selected terminal branches of the external carotid artery may be effective treatment.

A new minimally invasive technique for cauterizing the maxillary artery and its application in the treatment of cluster headache.

PURPOSE: To describe a new, relatively atraumatic method of cauterizing the maxillary artery and its effectiveness in treating cluster headache. MATERIALS AND METHODS: Five patients with cluster headache were treated with arterial ligation of certain terminal branches of the external carotid artery. A new, atraumatic method of cauterizing the maxillary artery is described. RESULTS: The success rate and postoperative morbidity are presented. In four out of five patients the cluster attacks ceased immediately following surgery. CONCLUSION: A new intraoral technique for maxillary artery cauterization and the effectiveness of cauterization of the terminal branches of the external carotid artery in the treatment of cluster headache are described. Although the sample is small, the results are encouraging, and may offer permanent relief of cluster headache pain.

The extracranial vascular theory of migraine--a great story confirmed by the facts.

Over the years, there has been a considerable amount of controversy as to whether the vascular component of migraine pain arises from the intracranial or the extracranial vessels or both. Some have even questioned whether vasodilatation even plays a significant role in migraine pain and have described it as an unimportant epiphenomenon. In this review, evidence is presented that confirms (1) vasodilatation is indeed a source of pain in migraine; (2) this dilatation does not involve the intracranial vasculature; (3) the extracranial terminal branches of the external carotid artery are a significant source of pain in migraine.

The extracranial vascular theory of migraine: an artificial controversy.

Over the years there has been a considerable amount of controversy over whether the vascular component of migraine pain arises from the intracranial or the extracranial vessels, or both. Some have even questioned whether vasodilatation actually plays a significant role in migraine pain, and have described it as an unimportant epiphenomenon. The controversy is an artificial one though, which has been generated as a consequence of misrepresentation of the facts in the headache literature. In this review, some of the more blatant distortions in the literature are exposed.

Middle meningeal artery dilatation in migraine.

OBJECTIVE: To show that migraine pain is not related to dilatation of the dural meningeal arteries. BACKGROUND: The origin of the pain in migraine has not yet been adequately explained and remains the subject of vigorous debate. Current theories implicate changes in the trigeminovascular system, which is defined as comprising the large intracranial vessels, and in particular, the dural meningeal vessels, the dura mater, and their neural connections. METHODS: The anatomical relationships of the dural meningeal arteries to the dura mater and the inner surface of the calvarium are described. RESULTS: The dural meningeal arteries lie in grooves in the inner table of the calvarium, are encased in the unyielding fibrous dura mater, and are consequently unable to dilate. CONCLUSION: The pain of migraine is not related to dilatation of the dural meningeal arteries.