How We Do It: Sphenopalatine Ganglion Blockade for Migraine Treatment

INTRODUCTION

Migraine is a common, often disabling neurologic disorder characterized by its pulsatile nature, unilateral location, and prolonged duration. It can be associated with nausea, vomiting, photophobia, or phonophobia and potentially with sensory (most commonly visual), verbal, or motor aura. Common triggers include emotional stress, hormonal changes, inconsistent meals, weather, and sleep disturbances. Migraine affects one out of seven Americans annually, with the highest prevalence in women aged 25–55.^[1] The pathophysiology of migraine is complex, involving activation of the trigeminovascular system that leads to inflammatory changes in the pain-sensitive meninges and alters the permeability of the blood–brain barrier.^[2] Given the complex neurobiology of this disorder, treatment of migraine is often difficult and refractory.

Current management of migraine includes abortive therapy for acute attacks and preventive therapy to reduce the frequency and severity of recurrent headaches. Abortive therapy includes nonsteroidal anti-inflammatory drugs (NSAIDs) and analgesics, with level A recommendations for acetylsalicylic acid, ibuprofen, naproxen, diclofenac, and acetaminophen.^[1] These therapies may also be combined with caffeine. Many migraine-specific therapies target the 5-HT serotonin receptors, as agonists at these receptors result in intracranial extra-cerebral vasoconstriction and inhibition of peripheral and central trigeminal nociceptive terminals. Triptans are 5-HT1B/1D agonists that can be used in moderate-to-severe migraines and are effective in 60% of NSAID non-responders; however, sustained relief may not occur, with headache recurrence in 15–40% of patients.^[1] The most common side effects of triptan use include paresthesia, flushing, tingling, and mild transient chest pressure. Triptan use is contraindicated in patients with myocardial infarction, stroke, peripheral vascular disease, or untreated vascular risk factors.^[3]

A common complication of episodic acute migraine treatment is the development of a medication overuse headache (MOH). Development of MOH can be limited by reducing triptan use to fewer than 10 days per month.^[1] Chronic migraine, defined as 15 or more headache days per month for more than 3 months, occurs in 1% of the United States and commonly occurs in the setting of MOH.

In patients with a chronic migraine or frequent and/or disabling episodic migraine, preventive treatment should be explored to improve quality of life and decrease disability. Preventive treatment for migraine has multiple aims, including decreasing attack frequency by 50%, decreasing headache intensity and duration, improving acute therapy responsiveness, improving overall function, and decreasing occurrence of MOH. The choice of preventive treatment includes consideration of patient comorbidities, drug interactions, and side effects.^[1] In addition to non-pharmacologic methods such as stress management and relaxation techniques, commonly used medications for migraine prevention include beta-blockers and antiepileptics.^[4] On average, 40–45% of patients taking prophylactic medications experience a 50% reduction in migraine frequency, possibly limited by adherence due to drug side effects.^[3]

OnabotulinumtoxinA (BTA) is approved for the management of chronic migraine. This treatment is delivered as intramuscular injections targeting 31 different head and neck sites every 12 weeks. BTA blocks acetylcholine release at the synaptic cleft, resulting in the autonomic blockade. In a meta-analysis by Jackson et al., BTA was associated with fewer headaches per month and a greater likelihood of experiencing a 50% reduction among patients with chronic migraine headaches, compared to placebo.^[5] Further, Hepp et al. showed that when compared to oral migraine prophylaxis, BTA was associated with a significantly lower likelihood of headache-related ED visits and hospitalizations at 6, 9, and 12 months after initiating treatment.^[6]

Sphenopalatine ganglion (SPG) blockade, the focus of this instructional article, is another emerging therapy for patients with chronic migraine. Greenfield Sluder first described the SPG in association with facial pain syndromes in 1909, and it is now targeted in the treatment of multiple disorders including sphenopalatine neuralgia, atypical facial pain, migraine, cluster headache, and herpes zoster.^[7]

The SPG is located in the pterygopalatine fossa and is one of the four cranial parasympathetic ganglia. Activation of parasympathetic synapses within the SPG releases vasoactive peptides that contribute to neurogenic inflammation, vasodilation, and the symptoms of migraine.^[8] Cranial autonomic symptoms commonly associated with migraine, such as lacrimation, conjunctival injection, eyelid edema, nasal congestion, and facial swelling, may be mediated by this parasympathetic outflow of the SPG.^[9] By applying topical local anesthetic to the SPG, parasympathetic and sensory outflow may be attenuated, thereby treating migraine and its associated autonomic symptoms.

Blockade of the SPG has been achieved through transnasal, transoral, and infrazygomatic arch application of local anesthetics. Today, there are three FDA approved devices exist for delivery of blocking agents, namely SphenoCath^® (Dolor Technologies, Scottsdale, Arizona, USA), Allevio™ (Jet Medical, Schwenksville, PA, USA), and Tx360^® (Tian Medical Inc., Lombard, IL, USA), all which approach the ganglion transnasally.^[10]

The effectiveness of this treatment in acute and long-term relief of migraine has been shown. Cady et al. described SPG blockade in patients with a chronic migraine using the Tx360^® device. In this setup, the device is advanced below the middle turbinate to the pterygopalatine fossa, where 0.3 cc of 0.5% bupivacaine is injected. In 26 patients treated with bupivacaine compared to 12 patients treated with saline, significant headache relief was noted at 15 and 30 min with sustained relief at 24 h.^[11] In follow-up of the same patient group, decreased number of headache days at 1 month post-treatment, decreased acute medication usage at 6 months, and improved quality of life at 6 months were all reported.^[12]

Similar effectiveness of SPG blockade was reported in a study by Mandato et al. They studied the response of 112 patients with a chronic headache who were treated with 4% of xylocaine using the Allevio™ device. At 30 days, 88% of patients required less medication for ongoing migraine relief, with a 36% point reduction in the visual analog scale score used to quantify the degree of debilitation.^[13]

Preliminary evidence shows SPG blockade is an effective and safe option for treatment and prevention of migraine disorders. We will describe how the authors use the SphenoCath^® device.

CONCLUSIONS

Sphenopalatine ganglion blockade is a treatment option for those who suffer an episodic or chronic migraine, as it shown to be effective as acute migraine treatment and prevention of recurrent migraine. The SphenoCath^® method described above is a safe and reproducible method to achieve SPG blockade. Research is currently being conducted to further characterize the effectiveness of this device in both acute and long-term migraine treatment.