Having baseline knowledge of medications used to treat a migraine is important when assessing patients for migraine surgery. There are three main types of medication used to manage migraines: prophylactic agents, abortive agents, and acute analgesics. The triptans, including sumatriptan, represent an abortive type of therapy and are given to prevent a suspected early migraine or stop an attack once it has begun. They act on serotonin 5-HT receptors and inhibit release of neuropeptides. The frequency of triptan use is a useful guide to both the frequency and severity of migraine attacks. Recording a journal of triptan use is also helpful for comparison before and after intervention with botox injections or surgery. Prophylactic agents have the goal of reducing severity and frequency of migraine attacks. They are subclassified as beta-blockers (e.g., propranolol), calcium channel blockers (e.g., verapamil), antidepressants (e.g., amitriptyline), anticonvulsants (e.g., gabapentin or valproate), and antihistamines (e.g., diphenhydramine). Acute analgesics have the goal of relieving mild to moderate symptoms of migraine during an episode. These comprise nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, aspirin, or diclofenac. Another popular agent is acetaminophen.1,2
2. Whyte CA, Tepper SJ. Adverse effects of medications commonly used in the treatment of migraine. Expert Rev Neurother 2009;9(9):1379–1391 headaches? Migraine headaches have traditionally been treated with medications including analgesics, such as acetaminophen, anti-inflammatory agents such as ibuprofen, serotonin agonists such as the triptans, beta- blockers such as propranolol, or calcium channel inhibitors such as verapamil. However, migraines persist in many patients in spite of these medical treatments and as a result, surgical approaches to their management have been developed. These are based on the theory that extracranial sensory branches of the trigeminal and cervical spinal nerves can be irritated, entrapped, or compressed at points throughout their anatomic course. Surgical treatments are aimed at addressing the compression sites in order to reduce compression and ultimately the frequency and severity of migraine attacks.1 Specific compression of the facial, vagus, or glossopharyngeal nerves is not thought to be responsible for the development of migraines although patients can experience visual disturbances and abnormal smells or tastes before or during an attack. Nasal abnormalities such as a deviated septum may be implicated in migraines via irritation of the anterior and posterior ethmoid and nasopalatine nerves, which are branches of the trigeminal nerve, but the olfactory nerve, which is responsible for the sense of smell is not involved.
headaches? A number of different anatomic trigger points of the trigeminal nerve and cervical plexus have been implicated in the development of migraine headaches. A variety of tissue types have been attributed to the compression or irritation, but tendon is not one of them. Tissues implicated in causing compression and/or irritation of the nerves include muscle, fascia, bone, and vessel. For example, supraorbital nerve triggers may be caused by the corrugator or procerus muscles, bone, and fascia at the supraorbital foramen, or by the adjacent supraorbital artery. In addition, cartilage may be implicated in intranasal compression by the effects of septal deviation on paranasal branches of the trigeminal nerve (branches of the sphenopalatine ganglion).1–5
Compression of the supraorbital nerve is implicated in migraine headaches and can occur at a number of sites. In approximately 86% of cases there is a fascial band across the supraorbital notch that may be the cause of compression in this area. The anatomy of fascial compression is subclassified into the subgroups type I, type II, and type III, depending on the anatomic arrangement of fascia and bone. Type I represents a single fascial band over a single foramen and is the most common type. Type II bands have partial bony spicules that extend to the neurovascular bundle. Type III bands contain a horizontal (A) or vertical (B) septum that encases the nerve (Fig. 25.1). Muscular sites of compression beyond the supraorbital foramen include the corrugator and procerus muscles. Dilated arteries can cause irritation of nerves such as in the temple secondary to the action of the superficial temporal artery.1–4 Fig. 25.1 Bony, fascial, and vascular compression of the supraorbital nerve. Supraorbital artery Supraorbital vein Type I: Simple Type IIIA: Horizontal septum Type IIIB: Vertical septum Type II: Partial bony fibrous band nerve
5. Janis JE, Hatef DA, Hagan R, et al. Anatomy of the supratrochlear nerve: implications for the surgical treatment of migraine headaches. Plast Reconstr Surg 2013;131(4):743–750
Temporal migraine often occurs in the morning and is associated with bruxism (grinding of the teeth) overnight. Pain is often associated with the temporalis or masseter muscles and originates just lateral and cephalad to the lateral canthus. Patients with temporal headaches may describe improvement with manual pressure applied to the area of the superficial temporal artery during a migraine attack.1 It is postulated that pulsation of the superficial temporal artery causes irritation to local sensory nerve fibers.2 For this reason, some surgical treatments involve tying off the superficial temporal artery for such patients.
Occipital migraines can be triggered by heavy exercise and stress. Patients often have tight posterior neck musculature. Pain originates just lateral to the midline, a few centimeters caudal to the occipital tuberosity and there is often a tender site on manual palpation close to the origin of trapezius. Irritation of the greater occipital nerve, which is a branch of C2 (see Fig. 25.2), is thought to be implicated in this type of migraine and may be due to muscle or fascial compression, or irritation from the occipital artery.1,2
When meeting a new patient in clinic for assessment of suitability of surgical treatment of migraine, there are a number of key steps that must be taken during the consultation. Of these, a really useful and simple approach to guide the consultation early on is to ask the patient to use a single finger to describe precisely where the pain originates from during a typical attack. This will guide the clinician to determine which trigger sites are likely to be involved. Once this is established it can be useful to inject lidocaine into suspected compression or trigger sites. This can only be done once all of the other information is obtained and examination is complete. The use of a handheld Doppler in clinic may also be useful once the main pain/trigger point location has been identified by the patient in order to see if it corresponds closely to arterial location. Imaging in the form of CT is sometimes useful for patients with migraine, although this is less commonly needed. Plain films are not part of the usual workup. Physical examination should include intranasal examination with a speculum to identify deviated septum, septal spur, or turbinate hypertrophy, particularly where patients describe migraines associated with pain behind the eye, rhinorrhea, or nasal obstruction.1–3
If the patient’s constellation of symptoms suggests a specific trigger site, and if the patient has active pain in this location at the time of presentation, a local nerve block can be performed to help confirm the diagnosis. She is already taking a triptan so there is no benefit in adding in other triptans in this case. Furthermore, manipulation of medications is best left to the treating neurologist. Injection of Botox to the trigger sites in question will also provide diagnostic information (and potentially therapeutic effect) but does not have immediate action and would require a separate visit, usually 1 month later, to review the migraine log and determine the benefit. Although this is a potential option, blocks are typically preferred over Botox if the patient has active pain. Moving to surgical decompression is only indicated for this patient once the diagnostic workup has been completed.1
The auriculotemporal nerve is a branch of CN V3 and extends through the parotid gland, then travels over the temporomandibular joint (TMJ) before dividing over the zygomatic arch and within the layers of the temporoparietal fascia. It provides sensation to the tragus, the anterior portion of the ear, and posterior temple. Compression may be caused by soft tissues of the temple or oftentimes the superficial temporal artery. Due to its intimate proximity to the superficial temporal vessels, Doppler is particularly useful in this location.1,2
Temporal migraines can be triggered by compression of the zygomaticotemporal or auriculotemporal nerves which are branches of the trigeminal nerve. The zygomaticotemporal nerve arises from the maxillary division (V2), and the auriculotemporal nerve arises from the mandibular division (V3). The zygomaticotemporal nerve supplies a small patch of skin on the parietal scalp and is a nerve that is avulsed rather than decompressed in order to improve symptoms of migraine.1
Greater occipital nerve release is performed with either a vertical or horizontal approach. It involves release at a number of compression sites: Musculofascial release between obliquus capitis and semispinalis capitis muscles, partial resection of semispinalis capitis muscle, partial resection of trapezius muscle and fascial bands, and ligation/ablation of the occipital artery. Supraorbital nerve decompression (SON) may be achieved through endoscopic, open brow, or transpalpebral approaches. The transpalpebral approach is gaining favor due to ease of exposure.1,2 This surgery involves complete or partial resection of the corrugators, foraminotomies if needed, and release of all compression points to release the trunk and all branches of the SON and supratrochlear nerve (STN). Surgery should not be the mainstay of treatment for most migraine patients. It is used for patients who have an established diagnosis of migraine by a neurologist and where traditional medication has failed. Most surgical approaches involve decompression of muscle, fascial bands, and ablation of blood vessels as the primary aim and do not require osteotomies or foraminotomies except on rare occasion.
symptoms? Outcomes at 5 years after migraine surgery were described by Guyuron’s team.1 They found that more than 80% of patients who had surgery reported improvement in terms of reduced frequency of attacks and improved symptoms. They found that patients who had multiple trigger sites treated were more likely to have a successful outcome. This applied to targeting both frontal and temporal trigger sites together and targeting all four sites where appropriate (including nasal and occipital). In patients treated surgically at all trigger sites, 57% reported complete elimination of migraine headaches. Factors associated with better outcomes also included an older age at first onset of migraine symptoms, fewer baseline migraines per month, and daily use of over-the-counter medications. Factors associated with worse outcomes included a history of head or neck injury, increased intraoperative bleeding, and single-site surgery that could result in inadequate treatment of all trigger sites.