Phone:(+39)010.55.54.580

Email:edoardo.raposio@unige.it

HUNDREDS AND HUNDREDS OF OPERATED PATIENTS

FIFTEEN YEARS OF SPECIFIC CLINICAL EXPERIENCE

THE LARGEST AND MOST IMPORTANT OPERATING CASUISTRY IN EUROPE

MIGRAINE HEADACHE

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 the seventh-highest specific cause of disability worldwide. The first approach is usually a combination of pharmacologic treatments (both abortive and preventive drugs) and nonpharmacologic interventions like behavioral and lifestyle changes. Despite all the available conservative options, a quite relevant group of MH patients remains refractory and does not achieve a satisfactory relief.

Although the pathophysiology of MHs remains a matter of debate, it is a common belief that chronic compression to the terminal branches of trigeminal nerve caused by surrounding structures (eg, muscles, vessels, or fascial bands) is responsible for its origin. In our experience, three main migraine trigger zones may be involved: frontal (supraorbital and supratrochlear nerves),temporal (auriculotemporal nerve), and occipital (greater and lesser occipital nerves).

MIGRAINE HEADACHE

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 the seventh-highest specific cause of disability worldwide. The first approach is usually a combination of pharmacologic treatments (both abortive and preventive drugs) and nonpharmacologic interventions like behavioral and lifestyle changes. Despite all the available conservative options, a quite relevant group of MH patients remains refractory and does not achieve a satisfactory relief.

Although the pathophysiology of MHs remains a matter of debate, it is a common belief that chronic compression to the terminal branches of trigeminal nerve caused by surrounding structures (eg, muscles, vessels, or fascial bands) is responsible for its origin. In our experience, three main migraine trigger zones may be involved: frontal (supraorbital and supratrochlear nerves),temporal (auriculotemporal nerve), and occipital (greater and lesser occipital nerves).

Detecting the precise site of pain onset (trigger point) is of paramount importance for a successful outcome. Indeed, partial or nonresponse to surgery may be primarily related to failure in recognizing all the trigger points. Botulinum toxin injections, nerve blocks, portable Doppler devices were all investigated. Botulinum toxin administration proved to be useless since lack or incomplete response does not automatically exclude the suspected trigger point, since close nerve-artery relationship might be the main cause of MH. Nerve blocks could be helpful; however, patients should be seen in the office during a MH attack. Finally, handheld Doppler devices proved to be useful in detecting migraine trigger points, especially because the nerve-artery crossover or close relationship might be the implicated in the headache pathogenesis. Nevertheless, clinical findings are still the best way to identify trigger points’ location. Patients suffering from temporal migraine usually report diffuse low temporal pain closer to the lateral canthus, localized in the temple or alternatively moderate-to-severe pain on the preauricular area, often spreading to the ipsilateral temple. Patients usually report diffuse headache; however, they can precisely pinpoint with one fingertip the precise location of the tender spot form where the MH attack begins, and that is where the surgical treatment should be carried out. Furthermore, simple compression of the tender spot by the fingertip of the surgeon during physical examination can usually evoke pain confirming the diagnosis. Therefore, it is my experience that accurate history and careful physical examination can safely detect all patient’s trigger points, while positive handheld Doppler signal can corroborate the diagnosis.

OCCIPITAL TRIGGER POINTS

With respect to the occipital site, the involvement of the occipital nerves (the greater occipital nerve (GON); the lesser occipital nerve (LON); the third occipital nerve (TON)) could apply to all the aforementioned types of trigger points: arising from branches of the second and third cervical nerves (coming from the cervical spine), GON, LON, and TON run toward the occipital region crossing or passing through muscles and fascial planes such as inferior obliquus capitis, semispinalis capitis, and trapezius. A close relationship with the occipital artery (OA) and its minor branches is also well documented. The diagnosis of occipital migraine can be difficult owing to the overlap with other disorders and a pathophysiology that is not well-understood. It is characterized by recurrent headaches of moderate to severe intensity localized to the occipital region, with the occasional irradiation to the neck and face. Occipital MH treatment has long been focused on GON compression by the semispinal capitis muscle and the obliquus capitis during forceful, flexion-extension movements of the neck or in cases of trauma. However, the pulsating nature of pain during occipital migraine reinforced the idea of neurovascular etiology for the disease. Pulsatile distension of terminal branches of external carotid artery can determine traction and pressure stimuli to local terminal branches of the occipital nerve, resulting in a pulsating headache. Afterward, it can determine a chronic antalgic contraction of the surrounding muscles of the head and neck that can overcome the original vascular pain and determined chronic headache. During the initial consultation, occipital trigger sites are identified precisely (in proximity of the superior nuchal ridge, left, right, or bilateral) by patients as the points from which attacks started. Manual compression of these points by the examiner usually cause a pain described by patients as linked characteristically to their headaches. A comprehensive questionnaire on headaches is submitted to each patient before surgery.

 

OCCIPITAL TRIGGER POINTS

With respect to the occipital site, the involvement of the occipital nerves (the greater occipital nerve (GON); the lesser occipital nerve (LON); the third occipital nerve (TON)) could apply to all the aforementioned types of trigger points: arising from branches of the second and third cervical nerves (coming from the cervical spine), GON, LON, and TON run toward the occipital region crossing or passing through muscles and fascial planes such as inferior obliquus capitis, semispinalis capitis, and trapezius. A close relationship with the occipital artery (OA) and its minor branches is also well documented. The diagnosis of occipital migraine can be difficult owing to the overlap with other disorders and a pathophysiology that is not well-understood. It is characterized by recurrent headaches of moderate to severe intensity localized to the occipital region, with the occasional irradiation to the neck and face. Occipital MH treatment has long been focused on GON compression by the semispinal capitis muscle and the obliquus capitis during forceful, flexion-extension movements of the neck or in cases of trauma. However, the pulsating nature of pain during occipital migraine reinforced the idea of neurovascular etiology for the disease. Pulsatile distension of terminal branches of external carotid artery can determine traction and pressure stimuli to local terminal branches of the occipital nerve, resulting in a pulsating headache. Afterward, it can determine a chronic antalgic contraction of the surrounding muscles of the head and neck that can overcome the original vascular pain and determined chronic headache. During the initial consultation, occipital trigger sites are identified precisely (in proximity of the superior nuchal ridge, left, right, or bilateral) by patients as the points from which attacks started. Manual compression of these points by the examiner usually cause a pain described by patients as linked characteristically to their headaches. A comprehensive questionnaire on headaches is submitted to each patient before surgery.

 

Patients whose trigger sites are identified in the GON bilaterally undergo horizontal incision in the occipital scalp (length, about 6 cm) along the superior nuchal midline. In patients with mono-lateral trigger sites, a lateral incision (starting from the midline; length, about 4 cm) is made. The occipital muscle is dissected first to visualize the GON and vascular bundle. In 85 % of cases, we find a dilated (or frankly aneurysmatic) occipital artery in close connection with the GON. In these patients, we ligate the vessel without any other surgical maneuvers except for accurate hemostasis and skin closure. In the remaining patients (in whom vascular compression is not found), we adopt a more conventional approach based on neurolysis of the GON and LON by undermining the trapezius muscle and semispinalis capitis muscle and following the nerve course caudally for ≈3 cm. Patients are advised to keep ice above the undermined area for 6 h postoperatively. The expected success rate of the procedure is 90% of treated patients.

TEMPLE AND TEMPORAL REGION

For auricolotemporal nerve (ATN) decompression surgery, we usually mark a 1.5-cm incision where patients pinpoint the tender spot.

A handheld Doppler is regularly used to locate the superficial temporal artery (STA), since we observed 100% correlation rate between the trigger point identified and a close ATN-STA relationship (being either a simple crossover or a helical intertwining).

Once the incision is made (always without shaving the haits), dissection is taken with the help of blunt tipped scissors to expose and isolate both ATN and STA, which is ligated both proximally and caudally to the area of nerve-artery intersection.

After a mean follow-up of 21 months, patients complaining for temporal MH usually have 85% positive surgical outcome (50% complete MH elimination, 35% significant improvement).

Only rare minor complications are reported (eg, edema, hematoma/ecchymosis, numbness, and paresthesia). Numbness can occur (lasting <1 year on average) in 5.7% of the patients. Furthermore, 25% of patients can experience secondary trigger point emergence following primary migraine surgery.

MH recurrence may occur from 1 up to 3 months after surgery; thus, the result may be regarded as permanent only after the third postoperative month.

FRONTAL TRIGGER SITE

Patients who suffer from frontal MH can be treated with an endoscopic approach or a transpalpebral approach. We performe both procedures to decompress supraorbital and supratrochlear nerves.

Endoscopic nerve decompression, however, is not performed in patients with long foreheads (8 cm measured from the anterior hairline to the supraorbital ridge) or in patients with significant curvature to the forehead because endoscopic access would have been difficult or impossible.

Transpalpebral approach for frontal trigger site deactivation is performed by means of a cutaneous incision involving up to two-thirds of the medial limit of the caudal portion of the conventional upper blepharoplasty incision.

After selective myotomy of depressor and corrugator supercilii muscles, the lateral fibers of the procerus muscle encasing the supratrochlear nerve are dissected. Once the supraorbital and supratrochlear nerves are isolated, they are decompressed by the cauterization of the concomitant (usually ectatic) arteries.

The endoscopic selective myotomies technique is performed with a single access by means of a specifically modified endoscope. With the patient supine and the head in a neutral position, frontal trigger nerves are located.

Skin markings are drawn above the eyebrow bilaterally, at the mid-pupillary line (supraorbital nerve) and about 1.5 cm medially (supratrochlear nerve).

A single, 1.5-cm incision is then performed on the midline, 1 cm behind the frontal hairline.

The modified endoscope is used to perform endoscopically assisted section of the corrugator supercilii, depressor supercilii, and procerus muscles bilaterally, with the purpose of decompressing the supraorbital and supratrochlear nerves bilaterally.

At the end of the procedure, a compressive bandage is positioned all around the undermined region.

FRONTAL TRIGGER SITE

Patients who suffer from frontal MH can be treated with an endoscopic approach or a transpalpebral approach. We performe both procedures to decompress supraorbital and supratrochlear nerves.

Endoscopic nerve decompression, however, is not performed in patients with long foreheads (8 cm measured from the anterior hairline to the supraorbital ridge) or in patients with significant curvature to the forehead because endoscopic access would have been difficult or impossible.

Transpalpebral approach for frontal trigger site deactivation is performed by means of a cutaneous incision involving up to two-thirds of the medial limit of the caudal portion of the conventional upper blepharoplasty incision.

After selective myotomy of depressor and corrugator supercilii muscles, the lateral fibers of the procerus muscle encasing the supratrochlear nerve are dissected. Once the supraorbital and supratrochlear nerves are isolated, they are decompressed by the cauterization of the concomitant (usually ectatic) arteries.

The endoscopic selective myotomies technique is performed with a single access by means of a specifically modified endoscope. With the patient supine and the head in a neutral position, frontal trigger nerves are located.

Skin markings are drawn above the eyebrow bilaterally, at the mid-pupillary line (supraorbital nerve) and about 1.5 cm medially (supratrochlear nerve).

A single, 1.5-cm incision is then performed on the midline, 1 cm behind the frontal hairline.

The modified endoscope is used to perform endoscopically assisted section of the corrugator supercilii, depressor supercilii, and procerus muscles bilaterally, with the purpose of decompressing the supraorbital and supratrochlear nerves bilaterally.

At the end of the procedure, a compressive bandage is positioned all around the undermined region.

Success rate is close to 90%. Migraine surgery is regarded as a minimally invasive procedure, but all patients undergoing frontal decompression surgery experience frontal and/or upper eyelid edema of various degrees. Usually, the edema resolves by the fifth postoperative day. Ecchymosis of both upper and lower eyelids follows surgery. No treatment needs to be given because these collateral events resolve by themselves; boric water applications 3 times a day may help the process of reabsorption of the edema. Patients with particularly thin skin of the frontal region may develop postoperative burn-like scar because of the endoscopic electrocautery. Temporarily,anesthesia occurs in almost all patients, which lasts 150 days on average.

Based on our experience, because the operation does not cause any serious complication or side effects and provides excellent results, surgical decompression of supraorbital and supratrochlear nerves can be recommended to patients who suffer from a moderate to severe chronic frontal migraine not responding to medications. With the same results, at present, we prefer to adopt a transpalpebral approach that allows a better anatomic exposure of the nerves and related structures.

AUTHOR AND EDITOR OF THE WORLDWIDE BEST SELLER “ATLAS OF SURGICAL THERAPY FOR MIGRAINE AND TENSION-TYPE HEADACHE”.

MIGRAINE SURGERY SCIENTIFIC PAPERS

1) Caruana G, Bertozzi N, Boschi E, Pio Grieco M, Grignaffini E, Raposio E. Endoscopic forehead surgery for
migraine therapy Personal technique. Ann Ital Chir. 2014;85:583-6.
2) Caruana G, Grignaffini E, Raposio E. Endoscopic forehead muscle resection for nerve decompression: a
modified procedure. Plast Reconstr Surg Glob Open. 2015 Apr 7;3(3):e342.
3) Raposio E, Caruana G. Frontal endoscopic myotomies for chronic headache. J Craniofac Surg. 2015.
26;3:e201-3.
4) Polotto S, Simonacci F, Grignaffini E, Grieco MP, Raposio E. Surgical treatment of frontal and occipital
migraines: A comparison of results. Plast Reconstr Surg Glob Open. 2016 Mar 18;4(3):e653.
5) Raposio E, Caruana G. Tips for the surgical treatment of occipital nerve-triggered headaches. Eur J Plast
Surg. 2017.40(3):177-82.
6) Bertozzi N, Simonacci F, Lago G, Bordin C, Raposio E. Surgical therapy of temporal triggered migraine
headache. Plast Reconstr Surg Glob Open. 2018 Dec 17;6(12):e1980. doi: 10.1097/GOX.0000000000001980.
eCollection 2018 Dec.
7) Raposio E, Bertozzi N. Trigger site inactivation for the surgical therapy of occipital migraine and tensiontype headache: Our experience and review of the literature. Plast Reconstr Surg Glob Open. 2019;7:e2507.
8) Simonacci F Lago G, Bertozzi N, Raposio E. Surgical deactivation of occipital migraine trigger site.
Chirurgia. 2020;33(3):143-.9.
9) Raposio E, Simonacci F. Frontal trigger site deactivation for migraine surgical therapy. Plast Reconstr
Surg Glob Open. 2020;8(4):e2813.
10) Baldelli I, Mangialardi ML, Raposio E. Site V surgery for temporal migraine headaches. Plast Reconstr
Surg Glob Open. 2020;8(6):e2886.
11) Baldelli I, Mangialardi ML, Salgarello M, Raposio E. Nummular headache and its surgical treatment.
Plast Reconstr Surg Glob Open. 2020;8(7):e2989.
12) Mangialardi ML, Baldelli I, Salgarello M, Raposio E. Decompression surgery for frontal migraine
treatment. Plast Reconstr Surg Glob Open. 2020;8(10):e3084.
13) Baldelli I, Mangialardi ML, Salgarello M, Raposio E. Peripheral occipital nerve decompression surgery
in migraine headache. Plast Reconstr Surg Glob Open. 2020;8:e3019.
14) Cortese K, Tagliatti E, Gagliani MC, Frascio M, Zarcone D, Raposio E. Ultrastructural imaging reveals
vascular remodeling in migraine patients. Histochem Cell Biol. 2022 Apr;157(4):459-465.
15) Raposio G, Raposio E. Temporal surgery for chronic migraine treatment: A minimally-invasive
perspective. Ann Med Surg, 2022, 76, 103578.
16) Raposio G, Cortese K, Raposio E. An easy and reliable way to preoperatively identify the auriculotemporal nerve in Migraine Surgery. J Plast Reconstr Aesthet Surg 2022 Jul;75(7):2387-2440.
17) Raposio G, Raposio E. Surgical therapy of occipital (Arnold) neuralgia: A case series. Ann Med Surg,
2022, 80, 104237.
18) Raposio E, Raposio G, Del Duchetto D, Tagliatti E, Cortese K. Morphologic Vascular Anomalies detected
during Migraine Surgery. J Plast Reconstr Aesthet Surg 2022; 75(11): 4069-73.
19) Raposio G, Raposio E. Principles and techniques of migraine surgery. Eur Rev Med Pharmacol Sci,
2022; 26: 6110-3.
20) Raposio E, Raposio G. Surgical therapy of migraine: a 12-year single-center experience. Eur J Plast
Surg, 2023, 46(5), pp. 699–705.
21) Raposio G, Raposio E. Occipital site deactivation for the treatment of chronic migraine: A minimally
invasive approach. Eur Rev Med Pharmacol Sci 2023;27(9):4065-68.
22) Raposio G, Antonini A, Gualdi A, Raposio E. Frontal site surgery for chronic migraine therapy. Acta Biomed, 2023; 94(6): e2023253.

23) Raposio G, Baldelli I, Gualdi A, Raposio E. Surgical therapy of nummular headache. Am J Otolaryngol Head Neck Surg. 2023;6(6):1248.

24) Raposio E, Raposio G, Baldelli I, Peled Z. Active occipital motion with digipressure as preoperative screening in migraine surgery.  Plast Reconstr Surg Glob Open.2024; 12(5):p e5784).

25) Raposio G, Raposio E. Temporal aneurysms and migraine surgery. JPRAS Open 2024; 41:9-13.

26) Raposio G, Baldelli I, Raposio E. Surgical therapy for primary headaches: Techniques and results. Chirurgia. 2024; 37(3):173-6.