1.1 Background

Migraine headache (MH) is a common disabling disorder with high prevalence (it affects 1.7–4% of the world’s adult population) and high socioeconomic and personal impacts [1]. Indeed, it is ranked as the third most prevalent disorder and seventh highest specific cause of disability worldwide [2].

Despite its economic burden and debilitating nature, MH pathophysiology and treatment have been a matter of debate for more than a millennium with no clear consensus yet [3].

Various theories have been proposed to describe MH etiology. Central neurovascular phenomena, cortical neuronal hyperexcitability, cortical spreading depression, and abnormal modulation of brain nociceptive system were all investigated by researchers as potential cause of MH [4]. Until nowadays, when extracranial origin of MH came to be popularized by the works of Guyuron et al. and other independent groups, they demonstrated that chronic compression to the terminal branches of trigeminal nerve caused by surrounding structures (e.g., muscles, vessels, and fascial bands) was responsible for its origin [5–25]. And therefore, MH trigger deactivation surgeries started being performed in different cutting-edge centers all over the word with a success rate ranging from 68 to 95% [3].

More recently, the “vascular theory” is emerging as the leading cause of terminal branches of trigeminal nerve irritation [4, 18, 25–29]. Indeed, anatomical and clinical works have highlighted a close nerve/artery relationship (regarding especially temporal- and occipital-triggered MH) that intersect or intertwine each other, perhaps promoting irritation and therefore triggering MH attacks [18, 25, 26, 28, 29]. Indeed, pulsatile distention of terminal branches of external carotid artery can determine traction and pressure stimuli to surrounding terminal branches of the trigeminal nerve, thus resulting in throbbing and pulsating headache. Lately, antalgic contraction of surrounding muscles of the head and neck can overcome the original vascular pain, resulting in chronic, dull headache.

Nevertheless, both component of the neurovascular bundle might play a role in triggering MH attacks and current techniques involve decompression, neurectomy, arterial ligation, and arteriectomy depending on trigger site and surgeons experience [4, 27–45].

1.2 Historical Perspective

The first known report of MH extracranial theory and relative treatment dates back to the first century AD, when one of the most celebrated Greek physicians, Aretaeus of Cappadocia, described the first known detailed classification of MH and its surgical approach [46]. Indeed, he believed that “cutting out the bigger arteries where they lie on the bone, because it is very good if one removes these arteries” [47].

Nine centuries later, in the tenth century AD, the Andalusian physician Al-Zahrawi (936–1013 AD) also described his technique for MH relief in his book Kitab al-Tasrif [48]. His approach focused on blood vessel cauterization for MH treatment over the area of the skull where MH attacks were perceived by patients [49, 50].

Maimonides (1135–1204), which was an outstanding medical practitioner other than a great philosopher and theologian, also advocated the vascular etiology of MH and wrote: “Bloodletting from the pulsating arteries which are not visible to the surface, and which rise to the base of the brain” [51].

Almost five centuries later, Ambroise Paré (1510–1590), a famous French barber surgeon that was considered as a pioneer of battlefield medicine and surgical methods, believed that blood vessels of the skull were the origin of MH [52]. However, he refused to use cauterization as treatment strategy; instead he suggested the ligature of the vessels. Indeed, Paré ideated for this purpose an instrument known as bec de corbin, much similar to a hemostat used nowadays [52]. In his book, Treatise on Surgery, he described the ligation of the superficial temporal artery as remedy for temporally triggered migraine [52]. Furthermore, it is said that Paré successfully treated his temporal MH by removing by himself his very own superficial temporal artery while looking at the mirror [53].

Even more recently, other authors proposed either arteriotomies [Thomas Willis (1621–1675), Robert Whytt (1714–1766)] or arterial compression (W. Möllendorff) for MH treatment [3, 54].

Of historical note, arterial compression for MH treatment was behind the use of the “imposition crown” during the Middle Ages [3]. The iron was to be received in gift during the pilgrimage leading to the place where the holy healer was revered. After being blessed on the altar, the crown was placed on the head of the patient by the priest and was meant to treat MH by applying pressure to the MH trigger point.

Back to the nineteenth century, Harold Wolff and co-workers (1954) were fervent advocates of the extracranial vascular etiology of MH [55–59]. They were the first to subject the phenomenon of vasodilation to rigorous scientific testing [60]. Wolff’s vascular theory of MH consisted of two main postulates: the intracranial vasospasm of the cerebral arteries was responsible for the MH aura and the extracranial vasodilatation (along with lowered pain threshold, concurrent intramural vascular edema, and local sterile inflammation) caused migraine pain [61–63].

Thirty years later, Hildebrand and Jensen’s study corroborated the work of Wolff and colleagues [64]. Indeed, they were the first to demonstrate that MH attack could be provoked by the administration of vasodilating medication (nitroglycerine), while vasoconstricting preparation such as ergotamine determined pain relief.

And indeed, the fact that the most widely used MH rescue medications (e.g., ergots, triptans, and gepants) share the same vasoconstricting effect on abnormally dilated extracranial arteries once more suggest the importance of vasodilatation in the etiology of MH [60].

1.3 MH Trigger Point