This simple, inexpensive procedure may provide a relatively low-risk option for the treatment of chronic migraines.
Authors: Soma Sahai-Srivastava, MD and Kellie Spector, BS
Migraine is a common cause of disability leading to significant financial, societal, and personal burden, along with a diminished quality of life.1,2 According to the World Health Organization, migraine ranks in the top 20 causes of disability worldwide and accounts for 1.3% of life-years lost to disability.3 Migraine is 2 to 4 times more prevalent in women than men and disability from migraine is also more common in women.4
Chronic migraine became an established diagnosis in 2004 by the International Classification of Headache Disorders, and the criteria for diagnosing chronic migraine have been refined twice since then.5 Chronic migraine is currently defined as headache occurring on 15 or more days per month for more than 3 months, which has the features of migraine headache on at least 8 days per month.6
Compared with episodic migraines, chronic migraines cause a larger disease burden, increased healthcare utilization, and more associated comorbidities.7 In the United States, approximately 1% of the population (3 million people) suffers from chronic migraine.4
Most of the treatments aimed at migraines focus on management of high frequency episodic migraines.1 Despite its burden, clinical trials of pharmacological treatments for preventative or acute treatment for chronic migraines are lacking, with established treatments often ineffective or cause notable side effects (ie, medication overuse headache).8
When pharmacological interventions fail, patients often receive onabotulinumtoxin A injections (Botox), the only FDA-approved preventative treatment for chronic migraine.1,9 Other options include greater occipital nerve blocks.1 The most severe and debilitating cases of chronic migraine sometimes require surgery, including occipital nerve stimulation or deep brain stimulation.1
One procedure that has recently re-emerged in migraine treatment is the sphenopalatine ganglion (SPG) block.10-12 This procedure was first described in 1908 by Greenfield Sluder, MD, chairmen of Otolaryngology at Washington University in St. Louis.13
The SPG contains postganglionic sympathetic fibers, synapses between pre- and postganglionic parasympathetic fibers, and somatosensory fibers of the head and neck region, making it a good target for pain intervention14
The methods of administration of SPG blocks have been greatly expanded since Sluder’s time, as more anecdotal studies were published. SPG blocks are now used to treat pain of trigeminal neuralgia, persistent idiopathic facial pain, acute migraine, acute and chronic cluster headaches, Herpes Zoster neuralgia involving the ophthalmic nerve, and various facial neuralgias.15,16
This review will focus on the sphenopalatine ganglion anatomy relevant to pain structures (Figure 1), the historical advancement of SPG blocks, and its role in headache management.
The Role SPG Ganglion in Migraine Pain
The sphenopalatine ganglion (also called the pterygopalatine ganglion) is an extracranial parasympathetic ganglion found in the pterygopalatine fossa.14 There are two ganglia, one in each of the bilateral fossae.16 The pterygopalatine fossa is an inverted pyramidal space posterior to the middle nasal turbinate. The ganglion has 3 nerve roots: sensory, parasympathetic, and sympathetic.12,14-17
While the mechanism of migraine pain is still not completely understood, there are a few supported theories as to why SPG blocks may help relieve migraine pain.
The SPG is the main source of cranial and facial parasympathetics.12 A widely proposed theory is that SPG blocks interfere with the parasympathetic outflow from the SPG and that is the main mechanisms for the pain relief.15 Various migraine triggers activate brain areas that converge on the superior salvatory nucleus.18 When a trigger is encountered, the trigeminoautonomic reflex is stimulated. The afferent trigeminal sensory neurons from meningeal vessels project through the thalamus to the pons. The neurons in the pons reflexively stimulate the Superior Salvatory Neucleus (SSN), which increases parasympathetic output from the SPG, otic, and carotid ganglia via the facial nerve.19
The parasympathetic outflow from the SPG contributes to the vasodilation of cranial blood vessels that occurs during migraine. This allows inflammatory mediators to be extravasated from blood vessels and activate meningeal nociceptors, causing migraine pain.15,16,19 Yarnitsky demonstrated that patients experiencing parasympathetic symptoms are more likely to have pain relief from an SPG block with lidocaine.17 Additionally, it is clear that the autonomic pathway is activated during migraine because of the common symptoms experienced by migraneurs, including lacrimation, nausea, emesis, nasal congestion, rhinorrhea, forehead/facial sweating, conjunctival infection, salivation, diarrhea, and polyuria.14
Another common feature of migraine that has been proven is central sensitization to pain via hypersensitivity of neurons.15,20According to Levin, migraine is a “centrally mediated primary neuropathic phenomena.”20 SPG blocks, especially repetitive blocks, may provide a way to break the autonomic pain cycle. Modulating the trigeminal nucleus caudalis via the afferent sensory fibers through an SPG block could slowly change pain processing centers and lead to reduced pain.16,21
A Brief History SPG Blocks
In Sluder’s original 1908 article, he described a variety of neuralgic, motor, sensory, and gustatory symptoms, referred to as Sluder’s neuralgia, which are now called cluster headaches.12,22 Dr. Sluder was the first to propose and use transnasal injections of cocaine to anesthetize the SPG, and described using a straight needle to enter the naris, reach the pterygomaxillary fossa, push posteriorly 0.66 cm, and inject topical cocaine to bathe the ganglion. Four years later, Sluder reported that injecting a 5% solution of phenol (carbolic acid), a neurolytic substance, dissolved into alcohol instead of cocaine provided longer term pain relief from these neuralgias in 10 of his patients.23
Simon L. Ruskin, MD, an attending Otolaryngologist from New York Hospitals, further developed the technique that Sluder had implemented, as well as expanded the indications for SPG blocks.22 In 1925, Ruskin became the first to use SPG blocks for trigeminal neuralgia.24 He also introduced transoral approaches for blocking the ganglion.25,26
By 1930, the SPG block had quickly gained momentum amongst physicians. Byrd and Byrd described over 2,000 patients who had undergone the procedure, on whom the SPG block had been performed over 10,000 times.27 Despite this success and for reasons that are unclear, the use of SPG blocks dwindled and not much was published in the literature until the 1980s.22
Then, in 1982 Barré tried using a dropper that patients administer themselves to drip cocaine hydrochloride into the nose to abort cluster headaches.28 Two further papers, one by Diamond and another by Hardebo and Elner described using SPG blocks for cluster headaches, which lead to positive outcomes.29,30 In the past few years there has been a resurgence of interest in SPG blocks.
Recent Advances in SPG Block Techniques
There are many methods now available for blocking or modulating the SPG, with their respective advantages and disadvantages.31 The most common methods for SPG blocks using local anesthetic (2% to 4% lidocaine or 0.5% bupivacaine) are transnasal, transoral, and lateral infratemporal approaches.
The traditional transnasal topical approach involves using a cotton tipped applicator soaked in lidocaine. Introduced by John Bonica in 1952, the anesthetic is applied posteriorly to the middle nasal turbinate on the nasopharyngeal mucosa.32 While the transnasal approach is simple and well tolerated, the variability in anatomy amongst patients makes it uncertain that the anesthetic will reach the SPG. Side effects may include epistaxis and infection.11,16
An endoscopic transnasal approach was developed in 1993, and is also sometimes used. In this case, a physician directs a needle to deliver the anesthetic under direct vision via sinuscope, allowing the needle to directly penetrate the pterygopalatine fossa. This procedure, however, carries an increased risk for damage to the mucosa.16
Three inexpensive and low-risk transnasal devices have recently been made available that allows the procedure to be completed in a few minutes and address the limitations of earlier techniques. The first device, called the SphenoCath (Dolor Technologies, Salt Lake City, UT) (Figure 2), is offered in 2 versions.33 Both versions have flexible sheaths, angled tips, and directional arrows.
The second device is the Allevio SPG Nerve Block Catheter (Jet Medical, Schwenksville, PA).34 Similar to the SphenoCath, this device has an angled tip, radiopaque ring, contrasted depth markings, flexible sheath, and directional arrow.
A third transnasal device is the Tx360 (Tian Medical, Lombard, Il, USA), which has a syringe in the barrel that is placed through the nares and then a flexible microcather is directed through the device posteriorly to the inferior nasal turbinate.21 The catheter tip then sprays 0.5% buvipicaine superiorly, laterally, and anteriorly to bathe the ganglion.20,35
According to Levin, this technique accommodates varying anatomy, ensures that the anesthetic reaches the ganglion, and is minimally invasive. In addition, the procedure can be performed as quickly as 10 seconds on each side and is inexpensive.20
There is no information available on the efficacy of the first two devices, and studies comparing the efficacy of the three devices are lacking. However, Cady et al used the Tx360 to study the effectiveness of SPG blocks for the treatment of chronic migraine.10,11 The investigators administered a repetitive anesthetic twice a week for 6 weeks in chronic migraineurs and controls. Numerous endpoints were measured, including number of headache days, pain, activity interference, HIT-6 scores, acute medication usage, and adverse events. The trends in the study suggest a possible role for SPG blocks in treating acute episodes of chronic migraine and for prevention of future attacks when repetitive blocks are administered.10,11
The transoral approach, also known as the greater palatine foramen approach, is performed by dentists.11 The SPG is reached by passing a needle through the greater palatine foramen at the posterior end of the hard palate. However, this approach can be very painful and is technically difficult. It is more unpredictable in terms of making sure the anesthetic reaches the ganglion. The side effects include orbital hematoma or infection.11,16
Another administration technique is the lateral infratemporal approach, also called the infrazygomatic arch approach.11,16 The clinician uses fluoroscopy to direct a cannula percutanously and laterally through the pterygo-maxillary fissure. The cannula is placed superiorly to the pterygopalatine fossa, and then anesthetic is delivered through the cannula.11 While this technique allows for the anesthetic to be delivered precisely, it is technically difficult—a rare side effect is infection.11,16
Another possible SPG intervention for migraine is neurostimulation. In 2009, Tepper et al conducted a trial using an implanted electrical neurostimulator device, which contained a lead and generator, in 11 patients with intractable migraine.36The authors reported that “2 patients were pain-free within 3 minutes of stimulation. Three had pain reduction; 5 had no response; and 1 patient was not stimulated. Five patients had no pain relief.” They concluded that the “lack of headache relief appeared linked to suboptimal lead placement, poor physiologic sensory response to localization stimulation, and diagnosis of medication overuse headache.”36
In 2010, a trial conducted by Ansarinia et al used stimulation electrodes inserted via an infrazygomatic transcoronoid approach to electrically stimulate the SPG in patients with cluster headache.37 In that study, 6 patients underwent up to 1-hour stimulation of the SPG during an acute, chronic migraine attack. The authors wrote that “SPG stimulation resulted in complete resolution of the headache in 11 attacks, partial resolution (>50% VAS reduction) in 3, and minimal to no relief in 4 attacks.” Pain relief was noted within several minutes of stimulation.37
In 2013, Schoenen et al used a transoral, gingival buccal technique to implant a neurostimulator in 32 patients suffering from cluster headache.38 Of the 28 patients who completed the study, headache relief was achieved in 67.1% of patient who received full stimulation-treated attacks compared to 7.4% of sham-treated attacks and 7.3% of “sub-perception-treated attacks.” All told, 68% patients experienced a clinically significant improvement—25% achieved pain relief in ≥50% of treated attacks; 36% achieved a ≥50% reduction in attack frequency; and two patients (7%), who achieved both.38 Adverse events were frequent (81%), and included transient, mild/moderate loss of sensation within distinct maxillary nerve regions that usually resolved within 3 months, noted the investigators.
Radiofrequency ablation is also sometimes used to modulate the SPG. In 2009, Narouze et al enrolled 15 chronic cluster headache patients, who received percutaneous radiofrequency ablation of the SPG by a fluoroscopic-guided approach through the infrazygomatic arch.39 The authors concluded that “percutaneous radio-frequency ablation of the SPG is an effective modality of treatment for patients with intractable chronic cluster headaches. Precise needle placement with the use of real-time fluoroscopy and electrical stimulation prior to attempting radiofrequency lesioning may reduce the incidence of adverse events.”39
These more invasive procedures carry a larger risk of side effects and more imprecise localization.11
The sphenopalatine ganglion, which sits posteriorly to the middle nasal turbinate, is in important modulator of head and neck pain. Three transnasal devices that have been recently introduced, the SphenoCath, Allevio, and Tx360, provide a safe and effective way to block the ganglion with minimal risk to patients. We are currently conducting a trial using the Tx360 device in the headache clinic at Keck Medical Center of USC (manuscript in progress). This emerging treatment for chronic migraine is a simple, inexpensive procedure, which is relatively low-risk.
Certainly, additional research is needed to elucidate which pathways are responsible for the pain relief from SPG blocks. More clinical trials on SPG blocks in chronic migraine patients should be done in order to establish efficacy, determine procedure guidelines, predict which patients are good candidates, and study long-term outcomes.
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- Buse DC, Manack AN, Fanning KM, Serrano D, Reed ML, Turkel CC, Lipton RB. Chronic migraine prevalence, disability, and sociodemographic factors: results from the American Migraine Prevalence and Prevention Study.Headache. 2012;52(10):1456-1470.
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- Hazard E, Munakata J, Bigal ME, Rupnow MFT, Lipton RB. The burden of migraine in the United States: current and emerging perspectives on disease management and economic analysis.Value Health. 2009;12(1):55-64.
- Lipton RB, Fanning KM, Serrano D, Reed ML, Cady R, Buse DC. Ineffective acute treatment of episodic migraine (EM) is associated with new-onset chronic migraine (CM): Results of the American Migraine Prevalence and Prevention (AMPP) Study.2015;84:688-695.
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- Cady RK, Saper J, Dexter K, Cady RJ, Manley HR. Long-term efficacy of a double-blind, placebo-controlled, randomized study for repetitive sphenopalatine blockade with bupivacaine vs saline with the Tx360® device for treatment of chronic migraine.2015;55(4):529-542.
- Cady R, Saper J, Dexter K, Manley HR. A double-blind, placebo-controlled study of repetitive transnasal sphenopalatine ganglion blockade with Tx360® as acute treatment for chronic migraine.Headache. 2015;55(1):101-116.
- Khan S, Schoenen J, Ashina M. Sphenopalatine ganglion neuromodulation in migraine: what is the rationale?Cephalagia. 2014;34(5):382-391.
- Sluder G. The role of the sphenopalatine ganglion in nasal headaches.N Y State J Med. 1908;27:8-13.
- Láinez MJA, Puche M, Garcia A, Gascón F. Sphenopalatine ganglion stimulation for the treatment of cluster headache.Ther Adv Neurol Disord. 2014;7(3):162-168.
- Yarnitsky D, Goor-Aryeh I, Bajwa ZH, et al.
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- Wei J, Yan L, Liu T, Xu W, Shi Z, Wu T, Wan Q. Cervical sympathectomy reduces neurogenic vasodilation in dura mater of rats.Auton
- Burstein R, Jakubowski M. Unitary hypothesis for multiple triggers of the pain and strain of migraine.J Comp Neurol. 2005;493(1):9-14.
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- Candido KD, Massey ST, Sauer R, Darabad RR, Knezevic NN. A novel revision to the classical transnasal topical sphenopalatine ganglion block for the treatment of headache and facial pain.Pain Physician. 2013;16(6):E769-E768.
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