The Extracranial Vascular Theory of Migraine

A Great Story Confirmed by the Facts

Elliot Shevel, BDS, Dip MFOS, MB, BCh

Disclosures

Headache. 2011;51(3):409-417. 

In This Article

Abstract and Introduction

Abstract

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.

Introduction

Following the work of Leaõ[1] on cortical spreading depression (CSD) and Sicuteri's work with serotonin,[2] the major focus of headache research shifted almost exclusively to the intracranial structures and centrally located pathophysiological changes. Since then, some of the extracranial peripheral links in the complex chain of events that occur in migraine have largely been ignored and forgotten.

Great strides have been made in understanding certain of the changes that occur during the course of migraine attack, such as central sensitization,[3–6] peripheral sensitization,[7–12] cutaneous allodynia,[4,13–16] and the influence of genetic factors.[17,18] However, our understanding of migraine has been hampered because a major element, the role of the extracranial terminal branches of the external carotid artery, inexplicably has been relegated to the sidelines in recent years.

HaroldWolff and his co-workers were the first to subject the phenomenon of vasodilation to rigorous scientific testing.Wolff's vascular theory of migraine consisted of 2 elements: (1) that intracranial vasospasm of the cerebral arteries causes the aura of migraine, and (2) that extracranial vasodilatation (together with lowered pain threshold, concurrent intramural vascular edema, and local sterile inflammation) is a cause of migraine pain.[16,19,20]

Wolff's theory held sway for about 30 years, until Olesen and the "Copenhagen Group" were able to demonstrate by measuring regional cerebral blood flow during migraine aura that the pattern of spread of oligemia (and, presumably, CSD) did not conform to the anatomical boundaries of the major cerebral blood vessels.[21] This was felt to indicate that cerebral artery vasospasm could not account for CSD, and the first part of Wolff's theory was correctly discredited. As Olesen's study was not conducted on the extracranial vessels, it had no relevance to—and consequently neither contradicted nor discredited—the second part ofWolff's theory.

It is only this latter portion ofWolff's theory that is discussed in this review, and the wealth of evidence to be presented serves strongly to suggest that not only does vasodilatation play a role in migraine pain, but that this dilatation is extracranial and not intracranial. Wolff did not merely theorize on the role of dilatation of these vessels in migraine; he confirmed his theory with a series of elegant and meticulously executed experiments, the results of which have never been successfully challenged.

Such attempts as have been made to repudiate Wolff's theory have been based on evidence that is irrelevant with regard to the extracranial arteries. One such instance is the investigation by Olesen et al, wherein evidence was provided that the painful phase of migraine did not correlate with intracranial vasodilatation, a study that has been cited on more than one occasion in the attempt to disproveWolff's theory.[22–27] What Wolff's detractors omitted to mention, however, is that Olesen's research involved regional cerebral blood flow and had nothing to do with the extracranial arteries or blood flow (Fig. 1).

Figure 1.

Computed tomography angiogram showing the superficial temporal and occipital arteries which form the basis of Wolff's theory of extracranial vascular pain.

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