Migraine surgery is any surgical operation undertaken with the goal of reducing or preventing migraines. Innovative surgical techniques have been developed to help patients with migraine headaches. Migraines affect an estimated 10% of the worldwide population annually  and cause significant loss of workdays and billions of dollars in productivity. It is well documented that migraine headaches cause significant disability, and reduce of quality of life that is as dire, if not worse than, debilitating chronic diseases. There have been major pharmacological advances for the treatment of migraine headaches, yet patients must still endure symptoms until the medications take effect. Furthermore, often they still experience a poor quality of life despite an aggressive regimen of pharmacotherapy. For these reasons, surgical solutions to migraines are actively being researched, particularly those involving the surgical cauterization of the superficial blood vessels of the scalp (the terminal branches of the external carotid artery), the removal of muscles in areas known as "trigger sites", and those involving the correction of a congenital heart defect. Despite the lack of evidence supporting the removal of muscles, there are over a dozen surgeons actively performing these operations in the US.
Minimally Invasive Arterial Surgery (The Shevel Procedure)
There is compelling evidence to show that migraine pain often originates in the terminal branches of the external carotid artery. In migraine sufferers with extracranial vascular pain, and in whom digital compression of the relevant artery reduces or abolishes the pain, surgical ligation or cauterization of the relevant vessel or vessels provides permanent relief from not only the pain of migraine, but also the associated symptoms such as the aura, light sensitivity (photophobia), sensitivity to sound (phonophobia), nausea, and vomiting. The Shevel procedure is highly successful in migraine sufferers where a definite positive diagnosis has been made (See below - How do we diagnose who will benefit from arterial surgery?).
Ligation of temporal vessels was first described by Abu al-Qasim al-Zahrawi (936 – 1013 AD), a Moorish physician. Historically, it has been reported that Ambroise Paré (1510–1590 AD), father of modern medicine, ligated his own temporal vessels for relief of his migraines. Since then the efficacy of arterial ablation for migraine treatment by ligation, cryotherapy, or cauterization of the relevant vessels has been confirmed repeatedly.
When is arterial surgery indicated?
This treatment modality is of particular value in: 1) patients who have not responded to conventional drug therapy, 2) patients who are unable to use drug therapy because they experience unacceptable side effects, or 3) patients who would prefer not to be on permanent medication. Included in this category are those with Chronic Daily Headache (headache on more than 15 days per month) and patients with what is known as "refractory headache" - headache that has not benefited from any other form of treatment. A recent study has shown that patients with chronic migraine experienced a significant reduction in pain levels and significant improvement in their quality of life following the surgery. The most common vessels involved in the pain of migraine are the terminal branches of the external carotid artery, and in particular, the superficial temporal artery and its frontal branch, and the occipital artery. These vessels are subcutaneous (just under the skin) and the small incisions required to access them mean that the surgery is minimally invasive and can be done in a day facility. As these vessels have no connection with the arterial supply to the brain, MIAS is exceedingly safe with no unpleasant side effects. The cosmetic effect is excellent as most of the incisions are within the hairline.
How do we diagnose who will benefit from arterial surgery?
There are a number of methods used to diagnose whether arterial surgery will be of benefit.
1) There are certain scalp arteries that most commonly cause the pain of migraine. These are compressed with the fingertip during an attack. If blocking the artery by pressure relieves the pain temporarily, and the pain returns when the finger pressure is removed, then arterial surgery is indicated.
2) Some migraine sufferers get relief from tying a tight band round the head just above the eyes and ears. This closes off the arteries that are causing the pain. If a tight band provides relief, then the surgery is indicated.
3) Certain medications provide relief from migraine pain by constricting or narrowing the scalp arteries. If these medications give relief, then the arterial surgery is indicated. These medications include the:
This type of migraine surgery is not offered as a first line of treatment, but after extensive evaluation and failure of traditional medical treatments. Trials are still ongoing to standardize the procedures of choice for definitive management of migraine headaches, but there have been successful guidelines for surgical therapy, which are being used by several migraine surgery specialists around the globe. Currently this treatment has institutional approval for adults, and trials for the pediatric population are ongoing.
Details of the procedure
Patients have to be screened preoperatively with a full neurological examination, and subsequent Botox injection and nasal endoscopy. A positive response to Botox has been a positive predictor of a successful outcome. However, in patients with trigger-point tenderness, a failure of Botox may mean compression of the nerve by a non-muscular structure (ie: band of connective tissue or a tight bony canal). Single or multiple TSs may be treated. It is important to identify the initial trigger sites rather than address all the areas of pain, after the inflammation involves the entire trigeminal tree. In patients with chronic migraine pain, a single trigger point may be dominant, with subsequent minor trigger points becoming unmasked after the initial surgery which can then be addressed at separately. Four main trigger points have been identified, with two other (more rare) areas of trigeminal nerve compression having been recently identified as other nerves to be treated.
Forehead migraine headaches: In the glabellar area (between the eyebrows) the supra-orbital and supra-trochlear nerves are skeletonized by resecting the corrugator and depressor supercilii muscle using an endoscopic approach similar that of used for cosmetic forehead lift. In patients in whom an endoscopic approach is not advisable due to forehead anatomy, an upper eyelid incision can be used for direct exposure and muscle resection. To avoid a noticeable contour deformity in the area of the brows, fat harvested from a separate site (lower abdomen or buccal fat pad) is used to fill in the defect and act as a barrier to scar formation around the skeletonized neurovascular bundles.
Temporal migraine headaches: The temporal area, where the zygomaticotemporal branch of trigeminal nerve passes through the temporalis muscle, is addressed using a similar endoscopic approach but involves removing a segment of the nerve rather than transecting the muscle. This results in a slight sensory defect over temporal skin area, but cross-innervation from other sensory nerves helps to limit the area of numbness (which is quite small). An open approach can also be used in patients in whom an endoscopic approach is not feasible.
Rhinogenic migraine headaches: The nasal trigger points where enlarged turbinates are in contact with the nasal septum are addressed with a septoplasty and a turbinectomy. The superior turbinate has been implicated in rhinogenic migraines, where abnormal turbinate-septal contact is thought to provide noxious stimuli along the trigeminal tree. Conchal or septal bullae (bony, air-filled sacs in either the turbinates or septum) have also been implicated in the development of rhinogenic migraines, and their resection or unroofing at the time of surgery has eliminated symptoms in patients who manifest this pathology.
The auriculotemporal nerve has also recently been implicated in development or perpetuation of migraine headaches. Decompression of this nerve via a small incision in front of the ear allows constricting bands of connective tissue to be released, which may also eliminate this nerve as a migraine trigger. Patients with auriculotemporal pain have point tenderness in front of and slightly above the ear which is usually worse with pressure and will not respond to Botox injections due to a lack of overlying muscle in this area.
Patent foramen ovale closure
Several clinical trials are currently under way in an effort to determine the existence of a causal linkage between migraines and the presence of a patent foramen ovale (PFO), a hole between the upper chambers (the atria) of the heart. There is significant evidence that a link exists between migraine with aura and the presence of a PFO.
It is estimated that 20-25% of the general population in the United States has a PFO. Medical research studies have shown that migraineurs are twice as likely as the general population to have a PFO, that over 50% of sufferers of migraine with aura have a PFO, that patients with a PFO are 5.1 times more likely to suffer from migraines and 3.2 times more likely to have migraines with aura than the general population, and that patients with migraine with aura are much more likely to have a large opening than the general PFO population.
The foramen ovale (literally oval hole) is present in all fetuses. Because a fetus' blood is oxygenated through the mother's placenta and not through breathing, the pulmonary system is unneeded. To make the fetal circulatory system more effective, the hole exists so that blood can travel from the right atrium to the left atrium without entering the pulmonary circulation. When the baby is born and begins breathing, the resistance in the lungs decreases dramatically, and blood begins to travel into the pulmonary system. This results in increased pressure in the left atrium, which then forces the flap down and effectively seals the hole. Once fully fused, the resulting structure is called the fossa ovalis (literally oval ditch). If the hole is not fully sealed, it is said to be patent (literally open).
In certain scenarios, such as when a person sneezes, the pressure in the left atrium decreases and the flap over the still-present foramen ovale opens temporarily. When this happens, blood is able to bypass the lungs and therefore the filtration process in the pulmonary system. There are at least 4 theories as to how this defect leads to migraines.
Early speculation regarding this link centered on the idea that, because blood bypasses the detoxificaiton process in the lungs and reenters the circulatory system uncleaned, this "toxic blood" may contain various substances that then trigger migraines. There is speculation that one of these substances is 5-HT, more commonly known as serotonin. Normally, 5-HT is filtered in the pulmonary circulation. However, if blood is bypassing that filtration process, 5-HT can re-enter systemic circulation and travel to and enter the brain. Numerous studies have related 5-HT to migraine pathogenesis, and the current pharmacological treatment of choice is a triptan drug, which binds to serotonin receptors in the brain and leads to the migraine being cured. This evidence lends support to the theory that 5-HT is one of the substances that triggers a migraine in a patient with a PFO.
It has been shown that the changes in interarterial pressure that occur with a PFO cause an increase in atrial natriuretic peptide (ANP), and that the ANP concentration in migraineurs with aura is lower than the concentration in control subjects. A study has shown that when the cortical spreading depression phenomenon was induced in mice, ANP was expressed in the brain. As well, ANP levels are elevated in patients with a PFO. All together, this suggests a possible correlation between ANP concentration and migraine with aura.
It has been shown that migraine frequency and severity is reduced if the hole is patched surgically. Mark Reisman, cardiologist at Seattle's Swedish Medical Center explained an advantage to non-pharmacological migraine relief. He said, "In contrast to drugs, PFO closure appears highly effective against migraines and usually has no side effects". Because PFO closure continues to prove successful, new devices are being produced to make the surgery easier to perform and less invasive.
Recent studies, however, have emphasised caution in relating PFO closure surgeries to migraines, stating that the favourable studies have been poorly-designed retrospective studies and that insufficient evidence exists to justify the dangerous procedure. As well, at least one patient with infrequent migraines who underwent the surgery ended up with daily migraines for at least 6 months, and others have reported short-term increases in migraine frequency and intensity following the surgery.
Coherex FlatStent Closure System
From Coherex Medical Inc. of Salt Lake City, a device called the Coherex FlatStent PFO Closure System is being tested as a new product for PFO closure. This device is first being studied by a European clinical study in Frankfurt, Germany. If this study proves to be a success, the device will begin to undergo FDA approval. The Coherex Closure System is an alternative to the typical method of repairing a PFO by placing a disk on each side of the defect and clamping them together to form a solid wall. The typical method doesn't always work particularly well with PFOs because the lengths, widths and dimensions of the defect are always different. The Coherex device is small and looks delicate, although it's not. One of its unique features is that it's deployed inside the tunnel of the PFO, so it closes the defect from within Because of its construction, it adapts to a PFO's individual shape in terms of length and width, thus avoiding the typical problem with PFO closure. Besides pulling the opening closed, it has a sponge polymer that encourages tissue to grow into it and integrate it into the heart's structure.
Another closure system is in use right now called CardioSEAL. This device looks like a small umbrella made out of Dacron fabric and folded into a special catheter. This catheter is inserted into a vein in the leg like the Coherex device. To close the PFO valve, each umbrella opens up and the device is pushed out of the catheter. The device is absorbed into the heart as the heart tissues grow over the implant in time.
AMPLATZER PFO Occluder
Another device for PFO Closure is called the AMPLATZER PFO Occluder device.
It consists of two wire mesh discs filled with polyester fabric. It is folded into a special delivery catheter, similar to the catheter used during a catheterization. The catheter is inserted into a vein in the leg, advanced into the heart and through the defect.
When the catheter is in proper position, the device is slowly pushed out of the catheter until the discs of the device sit on each side of the defect (like a sandwich). The two discs are linked together by a short connecting waist. The discs and the waist are filed with polyester fabric to increase the device’s closing ability.
Over time, heart tissue grows over the implant, and it becomes part of the heart. The tissue grows over the device over time.
University of Washington Medical Center tests the effectiveness of PFO closure in eliminating migraines in a clinical trial called the Premium Trial. All patients must meet certain criteria to qualify for the study including a diary that recounts the severity and frequency of migraines and undergoing tests to eliminate other medical reasons for migraines. A random selection process is then used to determine which patients have their PFO repaired and which ones do not. After a year, the patients will find out if they had the actual procedure and physicians will be able to determine if the process really worked.
The surgery is not performed by cutting open the chest and working on the heart. Instead, a catheter is pushed up to the hole in the heart after it is inserted in a vein in the leg. To keep the study blind, all patients are blindfolded and wear headphones while being mildly sedated. All patients receive a catheter in the leg, but not all catheters are pushed up to the heart.
ESCAPE migraine trial
This study was terminated due to insufficient enrollment.
Spinal cord stimulation
Spinal cord stimulators are medical stimulators implanted in the region of the spinal cord. They are sometimes used in cases of severe migraine headache on patients who tend to have multiple attacks per month.
In 2008, a subcommittee of the American Academy of Neurology (AAN) assessed the effectiveness of botulinum toxin in numerous disorders, with one report focusing on autonomic disorders and pain, including 'chronic daily headache'—they noted that this group's headaches were "mainly transformed migraines", and 'chronic tension-type headaches' were not included—and 'episodic migraines'. For chronic daily headaches, four studies were analyzed where the reduction in headache frequency when injected with BoNT-A was compared to a placebo-injected control group. While two of these studies showed favourable results, others observed no significant benefits. The AAN has thus reported that they can not yet draw any conclusions on the effectiveness of BoNT-A injections in chronic daily headaches. It was noted that, in one study where subjects were stratified based on whether or not they were currently being treated with a prophylactic medication, patients who were not taking prophylactic medications concomittantly fared significantly better than those who were.
In the same report, the AAN concluded that the injections were "probably ineffective" in treating episodic migraines. Other studies have reached the same conclusion.
Studies examining the effectiveness of BoTN-A injections that were not included in the AAN report have yielded positive results. It has been noted, however, that repeated injections are required to keep the headaches under control—the BoTN-A may have a cumulative effect—and they do not address the headaches which are triggered from the septum and turbinates.
^Rasmussen BK, Jensen R, Schroll M, Olesen J (1992). "Interrelations between migraine and tension-type headache in the general population". Arch Neurol. 49(9) (9): 914–8. PMID1520080.
^Bloudek LM, Stokes M, Buse DC, Wilcox TK, Lipton RB, Goadsby PJ, Varon SF, Blumenfeld AM, Katsarava Z, Pascual J, Lanteri-Minet M, Cortelli P, Martelletti P. (2012). "Cost of healthcare for patients with migraine in five European countries: results from the International Burden of Migraine Study (IBMS)". J Headache Pain13: 361–78. doi:10.1007/s10194-012-0460-7. PMC3381065. PMID22644214.
^Stokes M, Becker WJ, Lipton RB, Sullivan SD, Wilcox TK, Wells L, Manack A, Proskorovsky I, Gladstone J, Buse DC, Varon SF, Goadsby PJ, Blumenfeld AM (2011). "Cost of health care among patients with chronic and episodic migraine in Canada and the USA: results from the International Burden of Migraine Study (IBMS)". Headache51: 1058–77. doi:10.1111/j.1526-4610.2011.01945.x. PMID21762134.
^Solomon GD, Skobieranda FG, Gragg LA (1993). "Quality of life and well-being of headache patients: measurement by the medical outcomes study instrument.". Headache33 (7): 351–8. PMID8376093.
^Clark D, Hough H, Wolff HG (1934). "Experimental studies on headache". A Research Nerv. and Ment. Dis15: 417.
^Graham JR, Wolff HG (1938). "Mechanism of migraine headache and action of ergotamine tartrate". Arch. Neurol. Psychiat39: 737–763.
^Schumacher GA, Wolff HG (1941). "Experimental studies on headache: A. Contrast of histamine headache with the headache of migraine and that associated with hypertension. B. Contrast of vascular mechanisms in pre-headache and in headache phenomena of migraine". Arch. Neurol. Psychiat45: 199–214.
^Wolff HG, Tunis MM (1952). "Analysis of cranial artery pressure pulse waves in patients with vascular headache of the migraine type". Trans. Assn. Am. Phys65 (5): 240–244. PMID13005666.
^Wolff HG, Tunis MM, Goodell H (1953). "Evidence of tissue damage and changes in pain sensitivity in subjects with vascular headaches of the migraine type". Arch. Int. Med92: 332–341. PMID13136278.
^Tunis MM, Wolff HG (1953). "Long term observations on the reactivity of the cranial arteries in subjects with vascular headaches of the migraine type". Arch. Neurol. Psychiat70 (5): 551–557. PMID13091503.
^Brazil P, Friedman AP (1956). "Craniovascular studies in headache; a report and analysis of pulse volume tracings". Neurology6 (2): 96–102. PMID13288761.
^Ostfeld AM, Chapman LF, Goodell H, Wolff HG (1957). "Studies in headache; summary of evidence concerning a noxious agent active locally during migraine headache". Psychosom Med19 (3): 199–208. PMID13432093.
^Olesen IJ, Gulbenkian S, Valenca A (1995). "The peptidergic innervation of the human superficial temporal artery: immunohistochemistry, ultrastructure, and vasomotility". Peptides16 (2): 275–287. doi:10.1016/0196-9781(94)00165-0. PMID7540293.
^Goadsby PJ, Edvinsson L (1993). "The trigeminovascular system and migraine: studies characterizing cerebrovascular and neuropeptide changes seen in humans and cats". Annals of Neurology33 (1): 48–56. doi:10.1002/ana.410330109. PMID8388188.
^Goadsby PJ, Edvinsson L, Ekman R (1990). "Vasoactive peptide release in the extracerebral circulation of humans during migraine headache". Annals of Neurology28 (2): 183–187. doi:10.1002/ana.410280213. PMID1699472.
^Verheggen R, Bumann K, Kaumann AJ (2002). "BIBN4096BS is a potent competitive antagonist of the relaxant effects of alpha-CGRP on human temporal artery: comparison with CGRP(8-37)". Br J Pharmacol136 (1): 120–126. doi:10.1038/sj.bjp.0704682. PMC1762122. PMID11976276.
^Drummond PD, Lance JW (1983). "Extracranial vascular changes and the source of pain in migraine headache". Annals of Neurology13 (1): 32–37. doi:10.1002/ana.410130108. PMID6830162.
^Lipton SA (1986). "Prevention of classic migraine headache by digital massage of the superficial temporal arteries during visual aura". Annals of Neurology19 (5): 515–516. doi:10.1002/ana.410190521. PMID3717913.
^Shevel E, Spierings E (2004). "Role of the Extracranial Arteries in Migraine Headache: a Review". Cranio:the Journal of Craniomandibular Practice22 (1): 132–6. PMID15134413.
^Wolff HG, Tunis MM, Goodell H. (1953). "Studies on headache: evidence of tissue damage and changes in pain sensitivity in subjects with vascular headaches of the migraine type.". Transactions of the Association of American Physicians66 (4): 332–341. PMID13136278.
^Holland JT (1976). "Three cases of vascular headache treated by surgery". Proc Aust Assoc Neurol13: 51–4. PMID1029006.
^Florescu V, Florescu R (1975). "[Value of resection of the superficial temporal vasculo-nervous bundle in some cases of vascular headache.]". Rev Chir Oncol Radiol O R L Oftalmol Stomatol Otorinolaringol. (Romanian)20 (2): 113–7. PMID127294.
^Bouche J, Freche C, Chaix G, Dervaux JL. (1974). "[Surgery by cryotherapy of the superficial temporal artery in temporo-parietal neuralgia]". Ann Otolaryngol Chir Cervicofac. (French)91 (1): 56–9. PMID4603862.
^Totonchi, A.; Pashmini, N.; Guyuron, B. (Jan 2005). "The zygomaticotemporal branch of the trigeminal nerve: an anatomical study". Plastic and reconstructive surgery115 (1): 273–277. ISSN0032-1052. PMID15622263. edit
^ abChim, H (August 2012). "The Auriculotemporal Nerve in Etiology of Migraine Headaches: Compression points and anatomic variations". Plastic & Reconstructive Surgery130 (2).
^ abcdYankovsky, A. E.; Kuritzky, A. (2003). "Transformation into Daily Migraine with Aura Following Transcutaneous Atrial Septal Defect Closure". Headache the Journal of Head and Face Pain43 (5): 496–498. doi:10.1046/j.1526-4610.2003.03096.x.edit
^Schwerzmann, M. W. (Apr 2004). "Percutaneous closure of patent foramen ovale reduces the frequency of migraine attacks". Neurology62 (8): 1399–1401. ISSN0028-3878. PMID15111681. edit
^ abcdNaumann, M.; So, Y.; Argoff, E.; Childers, K.; Dykstra, D.; Gronseth, S.; Jabbari, B.; Kaufmann, C.; Schurch, B.; Silberstein, S. D.; Simpson, D. M.; Therapeutics Technology Assessment Subcommittee of the American Academy of Neurology (May 2008). "Assessment: Botulinum neurotoxin in the treatment of autonomic disorders and pain (an evidence-based review): Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology". Neurology70 (19): 1707–1714. doi:10.1212/01.wnl.0000311390.87642.d8. ISSN0028-3878. PMID18458231. edit
^ abcDodick, W.; Mauskop, A.; Elkind, H.; Degryse, R.; Brin, F.; Silberstein, D.; Botox Cdh Study, P. (Apr 2005). "Botulinum Toxin Type a for the Prophylaxis of Chronic Daily Headache: Subgroup Analysis of Patients Not Receiving Other Prophylactic Medications: A Randomized Double-Blind, Placebo-Controlled Study". Headache the Journal of Head and Face Pain45 (4): 315–324. doi:10.1111/j.1526-4610.2005.05068.x. ISSN0017-8748. PMID15836567. edit
^Mathew, T.; Frishberg, M.; Gawel, M.; Dimitrova, R.; Gibson, J.; Turkel, C.; Botox Cdh Study, P. (Apr 2005). "Botulinum Toxin Type A (BOTOXR) for the Prophylactic Treatment of Chronic Daily Headache: A Randomized, Double-Blind, Placebo-Controlled Trial". Headache the Journal of Head and Face Pain45 (4): 293–307. doi:10.1111/j.1526-4610.2005.05066.x. ISSN0017-8748. PMID15836565. edit
Totonchi, A.; Pashmini, N.; Guyuron, B. (Jan 2005). "The zygomaticotemporal branch of the trigeminal nerve: an anatomical study". Plastic and reconstructive surgery115 (1): 273–277. ISSN0032-1052. PMID15622263. edit