[Behind the left eye, behind the right eye, the back of both eyes, left temporal side, right temporal side, in both temporal sides, above the left eyebrow, above the right eyebrow, above both eyebrows, left back of head, right back of head, both sides of the head.]
When did your pain disappear? Immediately after, 1 month after, 6 months after.
After hair transplantation, each migraine sufferer was checked once in the first month and then once every 3 months. Those who could not appear in person after the first year were evaluated by phone every 3 months. Migraine headaches had ceased in all 6 patients, none of whom used medical treatments for migraines thereafter. The postoperative improvement each patient experienced was dramatic (P < 0.001). Overall, the mean intensity of headaches declined from 6.6 ± 1.47 to 0, on an analog scale of 1–10 (P < 0.001), and mean headache frequency was reduced from 5.83 ± 1.03/mo to 0/mo (P < 0.001). Likewise, the migraine pain index fell from a mean of 149.33 ± 19.21/mo to mean of 0/mo (P < 0.001; Table 3).
It is currently conceded that migraine headaches are not fully treatable through symptomatic medical intervention, and the possibility of better results by surgical means is echoed in recent studies.10–16 In the past 15 years, various authorities (primarily Guyuron) have conducted numerous studies (e.g., anatomic, retrospective, prospective/randomized) aimed at surgical (or sham) treatment of migraine headaches.10–16 Based on the 5-year follow-up data, it would appear that surgery is indeed effective,9–16 but the underlying pathophysiology of migraines remains unclear. Related theories have implicated neuronal mediators, cortical neuronal hyperexcitability, peripheral and central activation of trigeminal nerves, and abnormal sensitization of the nociceptive system, the latter reflecting periaqueductal gray matter dysfunction.24–27 Given these influences, meningeal inflammation ensues, activating trigeminal nerves and perivascular sensory fibers.27–30 Vasodilation is then triggered through release of calcitonin gene-related peptide, substance P, and neurokinin A, all residing in trigeminal neurons.31–34 The result is central sensitization and abnormal excitability.35–39 However, the cause of neuropeptide release is not entirely understood. According to most current surgical studies, the target in migraine surgery is actually peripheral nerves. Chemodenervation of peripheral nerves by botulinum toxin and surgical decompression or avulsion (rarely ablation) have confirmed this.10–16 Hair transplantation impacts peripheral nerves, thus explaining postoperative benefits in migraine sufferers. We have also observed fewer forehead wrinkles in most patients after hair transplantation, similar to botulinum toxin effect. The hair transplantation donor field starts at temporal region and is extended to nearby occipital area, moving toward opposite temporal zone (Figs. 4, 5). Destruction of nerves, veins, and soft tissue is unavoidable in doing so. Occasionally, the superficial temporal artery is injured if a large number of grafts are collected. In the donor field, particularly the area of greater occipital nerve domain, both auriculotemporal and zygomaticotemporal branches of trigeminal nerve may be destroyed bilaterally from excessive grafting.38 Receiver areas for hair grafts are usually frontal area, apex, and vertex (Fig. 5). In these regions, approximately 50 pores (average depth, 5–6 mm) are opened in each square centimeter,39 damaging veins, nerves, and soft tissues (Fig. 5). Depending on the nature of hair loss, the auriculotemporal and zygomaticotemporal branches of trigeminal nerve, the distal branches of supraorbital and supratrochlear nerves (extending toward frontal area), the distal branches of occipital nerve at vertex, and the arteries and veins accompanying these nerves may be damaged as well. In grafts incorporating 0.4 mm2 of tissue (skin surface area), roughly 15 cm2 of tissue is lost for every 3,000 grafts procured from donor areas (graft radius, r = 0.4 mm; area [πr2] = 3.14 × 0.4 × 0.4 × 3,000 grafts = 1,500 mm2 = 15 cm2). Such extensive tissue loss may alter occipital skin and subcutis, which then tightens. Hair transplants are composite in nature, combining skin, connective tissue, aponeurosis, and loose areolar tissue, so donor side tissue losses impact both appearance and contours.39 The genetics of hair in occipital region differs from that in frontal region and apex. Hair follicles are capable of self-regulating responses to androgens through expressions of 5-alpha reductase and androgen receptors.23 , 40 , 41 The latter elements quantifiably differ in areas of alopecia and hair-bearing scalp.23 , 40–43 Accordingly, occipital hairs maintain resistance to male androgens when transplanted to vertex, and scalp hairs transplanted from vertex to forearm regress at the same pace as donor site.44 Both tissue destruction and genetic underpinnings may account for differences within receiver fields. It is at these sites where migraine-triggering neurotransmitters are released, thus serving as points of neuromodulation. After hair transplantation, blood circulation increases substantially in both donor and receiver areas,38 whereas disrupted vascular networks and fibrofatty tissues no longer contribute to vasospasm. As confirmed by Guyuron et al.,13 transecting the zygomaticotemporal branch of trigeminal nerve and repositioning temporal soft tissues minimizes the potential for neural coaptation, diminishing migraine headache recurrence. Hair transplantation may affect receiver and donor areas in a similar manner. Given the enhanced regional blood flow, growth factors are apt to penetrate faster, facilitating wound recovery and maturation. Regenerating nerves also undergo change, especially myelin sheaths, leading to improved sequencing of neurotransmitter release and propagation and stem cells conveyed via perifollicular fat of composite grafts aid in tissue recovery. Trigger sites of migraine headaches in occipital, frontal, and temporal regions that occupy donor and receiver fields are likely impacted by tissue injury and posttransplantation hypoaesthesia.23 In our patients, anesthesia and hypoesthesia (prominent in frontal region) typically lasted 3–6 months and dissipated gradually, with donor fields impacted comparatively less. Such developments were anticipated and were strictly temporary, not qualifying as complications.23 From our perspective, the chief reason for rapid resolution of migraine attacks after hair transplantation is the hypoesthesia of donor/receiver fields that follows.39 Subsequent benefit may be linked to regulatory control of perivascular sensory fibers. The positive effects of hair transplantation may well extend to psychosomatic aspects of migraine headaches. Although not an uncommon disorder, it was surprising that only 6 of our hair transplant patients were actual migraine sufferers, each treated medically for many years. Ultimately, all medications for migraine were abandoned during follow-up periods (6 months to 5 years), with no reported recurrences. The most striking part of this study is that the number of migraine patients is low compared with the hair plantation population. For this reason, we retrospectively and prospectively rescanned the patients more than once. But the rate did not change. This low rate can be entirely coincidental. Or, in patients who need hair transplantation, the rate of incidence of migraine may be low.
The seemingly curative effect of hair transplantation on migraine headaches has no clear explanation as yet. However, clinical and experimental studies of larger populations are surely forthcoming. Results were decisive in these few patients. It is remarkable that both alopecia and migraine headache may be easily remedied through a simple and easily applied procedure. As a result of this study, hair plantation in bald migraine patients may be an alternative to migraine treatment. In nonbald patients, the mechanism of action of hair transplantation may be a guide for migraine treatment. Previously, various mechanisms of central and peripheral origin have been emphasized in the treatment of migraine. In recent years, however, the focus has been on the origin of peripheral nerves. This study supports that the main cause of migraine originates from peripheral nerves. This study shows that migraine symptoms may improve in patients who do not need hair transplantation when they are damaged in the transcutaneous peripheral nerve, both in donor and recipient areas, as in hair transplantation. Our work will be a reference for such a study on patients in the future.
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