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A New Look at Sphenopalatine Ganglion Blocks for Chronic Migraine

This simple, inexpensive procedure may provide a relatively low-risk option for the treatment of chronic migraines.
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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.15,20 According 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

Last updated on: February 9, 2016
First published on: January 1, 2016
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New Technique Shows Promise as Adjunct In Chronic Pain Management