This article is reprinted from a post originally published on Sphenopalatineganglionblocks.com
Neuromuscular Dentistry and Sphenopalatine Ganglio Blocks are a powerful combination for eliminating and relieving migraines. When utilized in conjunction with occipital or greater occipital nerve blocks and trigger point injections it is probably as close to a migraine cure as possible.
Sphenopalatine Ganglion Block: A New Article in Practical Pain Management
There is recent article in Practical Pain Management.
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.
By Soma Sahai-Srivastava, MD and Kellie Spector, BS
MY COMMENTS ARE IN ALL CAPITAL LETTERS.
PLEASE NOTE HOW THE ARTICLE OPENS SIMPLE, INEXPENSIVE PROCEDURE WITH LOW RISKS FOR PATIENTS.
THIS IS ACTUALLY A PRETTY AMAZING STATEMENT!
WE ARE TALKING ABOUT LIFE CHANGING TREATMENT THAT CAN DRASTICALLY IMPROVE PATIENTS LIVES AND COSTS ARE MINIMAL.
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
THIS IS A MAJOR PROBLEM WORLD WIDE THAT ESPECIALLY EFFECT FEMALE PATIENTS. 200-400% MORE FREQUENT IN WOMEN THAN MEN!
AGAIN SPG BLOCKS ARE A SIMPLE, INEXPENSIVE AND SAFE APPROACH TO CHRONIC HEADACHES AND MIGRAINE, AN SIGNIFICANTLY LARGER AMOUNT OF PATIENTS
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
CHRONIC MIGRAINE IS ONE OF AN ENORMOUS AMOUNT OF CHRONIC HEADACHES: International Classification of Headache Disorders
THIS IS FROM WIKIPEDIA ON THE HIERARCHY OF HEADACHES:
1.1 Primary headaches
1.1.1 ICHD 1, ICD10 G43: Migraine
1.1.2 ICHD 2, ICD10 G44.2: Tension-type headache (TTH)
1.1.3 ICHD 3, ICD10 G44.0: Cluster headache and other trigeminal autonomic cephalagias
1.1.4 ICHD 4, ICD10 G44.80: Other primary headaches
1.2 Secondary headaches
1.2.1 ICHD 5, ICD10 G44.88: Headache attributed to head and/or neck trauma
1.2.2 ICHD 6, ICD10 G44.81: Headache attributed to cranial or cervical vascular disorder
1.2.3 ICHD 7, ICD10 G44.82: Headache attributed to non-vascular intracranial disorder
1.2.4 ICHD 8, ICD10 G44.4 or G44.83: Headache attributed to a substance or its withdrawal
1.2.5 ICHD 9, ICD10 G44.821 or G44.881: Headache attributed to infection
1.2.6 ICHD 10, ICD10 G44.882: Headache attributed to disorder of homeostasis
1.2.7 ICHD 11, ICD10 G44.84: Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures
1.2.8 ICHD 12, ICD10 R51: Headache attributed to psychiatric disorder
1.3 Cranial neuralgias, central and primary facial pain and other headaches
1.3.1 ICHD 13, ICD10 G44.847, G44.848, or G44.85: Cranial neuralgias and central causes of facial pain
1.3.2 ICHD 14, ICD10 R51: Other headache, cranial neuralgia, central or primary facial pain
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
1% SUFFER CHONIC MIGRAINES! MILLIONS CAN BE HELPED WITH SPG BLOCKS EVEN IF THEY WERE ONLY 10% EFFECTIVE!
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
MOST RESEARCH IS FOCUSED ON PHARMOCOLOGIC APPROACH BECAUSE IT IS PAID FOR BY PHARMACEUTICAL COMPANIES.
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
IN ADDITION TO SPG BLOCKS NEUROMUSCULAR DENTISTRY CAN DRAMATICALLY TREAT AND ELIMINAT THE HEADACHES ARIVING FROM MYOFASCIAL SOURCES. THERE ARE MANY PATIENT TESTIMONIALS ABOUT THE EFFECTIVENESS OF SPG BLOCKS AND NEUROMUSCULAR DENTISTRY ALONE OR IN COMBINATION.
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
IT WAS MADE FAMOUS IN 1986 BY THE BOOK “MIRACLES ON PARK AVENUE” I FIRST LEARNED OF THE PROCEDURE WHEN A PATIENT GAVE ME A COPY OF THE BOOK AND WANTED MY HELP IN FINDING A DOCTOR IN CHICAGO. ULTIMATELY, I LEARNED THE PROCEDURE AND HAVE TAUGHT HUNDREDS OR THOUSANDS OF PATIENTS AND DOCTORS HOW TO ADMINISTER SPG BLOCKS.
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
A SPHENOPALATINE GANGLION OF CRANIAL NERVES IS ACTUALLY PART OF THE BRAIN OUTSIDE THE CALVARIUM WHERE IT CAN BE TREATED EASILY.
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
THE TERM SLUDER’S NEURALGIA IS OFTEN THOUGHT TO BE FIRST DESCRIPTION OF CLUSTER HEADACHES, TMJ DYSFUNCTION HEADACHES, AND CONTACT HEADACHES.
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
SPHENOPALATINE GANGLION IS ADDITIONALLY KNOWN AS MECHEL’S GANGLION AND THE NASAL GANGLION. THE PTERYGOPALATINE FOSSA IS LOCATED WITHIN MAXILLA AND SPHENOID BONES.
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.
THERE ARE MANY FIBERS OF THE TRIGEMINAL NERVE PASSING THROUGH THE GANGLION. THE TRIGEMINAL NERVE IF THE CHIEF SENSORY NERVE!
ALMOST 100% OF HEADACHES AND MIGRAINES ARE AT LEAST PARTLY TRIGEMINAL IN ORGIN. THE TRIGEMINAL NERVE IS OFTEN CALLED THE DENTIST’S NERVE.
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
I LIE TO TALK ABOUT THE SPG BLOCK TURNING OFF THE “FIGHT OR FLIGHT” REFLEX WHICH CAN CAUSE SYMPATHETIC OVERLOAD AND ALLOWS PREDOMINANCE OF THE PARASYMPATHETIC “FEED AND BREED” OR EAT AND DIGET REFLEX”
The parasympathetic outflow from the SPG contributes to the vasodilation of cranial blood vessels that occurs during migraine.
THE TRIGEMINAL NERVE CONTROLS BLOOD FLOW TO ANTERIOR 2/3 OF MENINGES OF THE BRAIN.
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
I HAVE ROUTINELY SEE SPG BLOCKS WORK FOR VERY STRESSED PATIENTS WHICH IS SYMPATHETIC OVERLOAD.
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
IT SHOULD BE CLEARLY UNDERSTOOD THAT EACH AND EVERY PATIENT IS UNIQUE AND THE ABOVE SYMPTOMS MAY HAPPEN BUT CERTAINLY ARE NOT UNIVERSAL.
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.
NEUROMUSCULAR DENTISTRY ADDRESSES THE CENTRAL SENSITIIZATION BY DECREASING NOCICEPTIVE INPUT INTO THE TRIGEMINAL NERVOUS SYSTEM PARTICULARLY INTO THE MESENCEPHALIC NUCLEUS THE FASTEST AND ONLY ELECTRICAL SYNAPSE IN THE BODY.
”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
I LIKE TO TEACH MY PATIENTS HOW TO SELF ADMINISTER SPG BLOCKS FOR MORE FREQUENT REPETITIVE SPG BLOCKS AS OFTEN AS 2-3 TIMES DAILY IF NECESSARY INITIALLY.
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.MAY BE TMD OR CONTACT HEADACHE AND OTHER TRIGEMINAL AUTONOMIC CEPHALGIASHEADACHES
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
USE OF LIDOCAINE OR MARCAINE IS ALSO EFFECTIVE. I ADVISE AGAINST DESTRUCTION OF GANGLION. A STUDY AT MAYO CLINIC HAD DISASTEROUS RESULTS AND WAS ENDED DUE TO LITIGATION.
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
I SMETIMES DO INJECTIONS OF THE GANGLION THROUGH THE GREATER PALATINE FORAMEN AT THE BACK OF THE HARD PALATE.
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
THE DEVELOPMENT OF MEDICATIONS AND THE PHARMACEUTICAL COMPANIES ROLE IN FUNDING RESEARCH WAS ONE OF MANY REASONS. ANOTHER WAS A LESS HANDS ON APPROACH TO MEDICINE BY PHYSICIANS.
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.
DR MILTON REDER IN NYC BECAME INTERNATIONALLY KNOWN FOR UTILIZING THE SPG BLOCK DURING THIS TIME PERIOD.
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
THIS IS MY MOST FAVORED METHOD BUT I USE A VARIATION WHERE WE UTILIZE A HOLLOW NASAL CATHETER THAT IS COTTON TIPPED WHICH THEN GIVE A CONTINUAL FLOW OF ANAESTHETIC OVER THE AREA OF MUCOSA OVER THE PTERYGOPALATINE FOSSA WHERE IN INFILTRATES TO THE GANGLIA.
THE BEST FEATURE IS PATIENTS CAN SELF-ADMINISTER BILATERAL BLOCKS FOR LESS THAN $1.00 PER APPLICATION.
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
IN MY OPINION THIS IS AN OUTDATED PROCEDURE THAT SHOULD RARELY IF EVER BE UTILIZED.
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.
I LOVE THE SPHENOCATH AND CONSIDER IT MY FIRST CHOICE BECAUSE OF EASE OF USE. I CAN ALSO TEACH PATIENTS TO SELF ADMINISTER THE BLOCK WITH A SPHENOCATH. I HAVE TAUGHT COURSES IN INJECTION TECHNIQUES AND WITH NASAL CATHETERS AND SPHENOCATH DEVICE.
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.
IT IS MY UNDERSTANDING THAT ALLEVIO COPIED THE SPHENOCATH AND THAT THEY ONCE MANUFACTURED IT FOR DOLOR INDUSTRIE THE ORIGINATOR. IT BOTHERS ME WHEN INTELLECTUAL PROPERTY IS TAKEN WITHOUT BEING BOUGHT.
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 (Figure 3).21 The catheter tip then sprays 0.5% buvipicaine superiorly, laterally, and anteriorly to bathe the ganglion.20,35
THIS IS A RATHER UNIQUE DEVICE THAT IS SINGLE USE BUT GIVES ACCURATE PLACEMENT. MY ISSUE WITH SINGLE USE IS THAT THE DEVICE RUNS APPROXIMATELY$75 MAKING IT OUT OF REACH OF MANY PATIENTS.
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 SPG BLOCKS THAT ARE APPLIED WITH $75 DEVICES IN DOCTORS OFFICES ARE NOT INEXPENSIVE IN TERMS OF COST OR PATIENT’S TIME.
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 TWICE A WEEK PROTOCOL FOR 6 WEEKS IS 12 VISITS AND AT A COST OF $700 PER ADMINISTRATION THE TOTAL COST IS $8500 BUT TIME IN DOCTORS OFFICES AND TRAVEL TIME FOR PATIETS.
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
THIS IS CERTAINLY NOT TRUE OR SLANTED. TH USE OF PALATAL ANASTHETIC IS VERY COMMON ON A DAILY BASIS BY DENTIST AND AFTER 1 OR 2 DROPS OF ANAESTHETIC THERE IS NO FEELING. MANY DENTISTS CAN DO THIS WITHOUT PAIN. I USED TO USE THIS TECHNIQUE FOR YEARS ON A REGULAR BASIS. VERY PREDICTABLE.
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
THIS IS A DIFFICULT AND RATHER PINFUL PROCEDURE AND THE USE FLUOROSCOPY MAKES IT VERY EXPENSIVE.
I PREFER THE SUPRAZYGOMATIC APPROACH TO GIVE INJECTIONS TO THE SPHENOPALATINE GANGLION INTO THE PTERYGOPALATINE FOSSA AREA. AS A DENTIST THERE IS INITIAL DISCOMFORT COMING FROM AN EXTRA-ORAL APPROACH BUT ONCE COMFORTABLE WITH THE TECHNIQUE IT IS EASIER THAN AN MANDIBULA BLOCK ROUTINELY UTILIZED BY DENTISTS.
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.36 The 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
THE USE OF NEUROSTIMULATION MAY BE VERY POWERFUL BUT THE USE OF DAILY SELF ADMINISTERED BLOCKS MAY MAKE IT OBSOLETE IN MOST PATIENTS.
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
EFFECTIVENESS APPEARS LOW AND COSTS ARE HIGH, ESPECIALLY IN PROCEDURE MORBIDITY AND HOSPITAL COSTS.
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.
THIS MAKES MORE SENSE BUT AGAIN THE EFFICACY IS STILL RATHER LOW COMPARED TO USE OF ANAESTHETIC. I PROPOSE THAT A DEVICE COULD BE USED TO AUTOMATICALLY DELIVER ANAESTHETIC TO THE GANGLION SIMILAR TO AN INSULIN PUMP.
I PUT THIS IDEA FOR FREE INTO THE PUBLIC DOMAIN. TO MY KNOWLEDGE IT HAS NEVER BEEN PUBLISHED. I HOPE SOMEONE INVESTIGATES IT AND ALL I ASK IS REFERENCING THIS POST, NO FINANCIAL COMPENSATION.
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
AGAIN PLEASE VISIT MAYO CLINIC STUDY THAT SHOWED VERY SEVERE ADVERSE OUTCOMES.
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.
IT IS ESSENTIAL TO UNDERSTAND THAT PERSONAL APPLICATION BY PATIENTS AT HOME IS BY FAR THE BEST METHOD ADMINISTERING THESE BLOCKS. IN PATIENTS WIRH DIFFICULT NASAL PASSAGES INSURANCE COMPANIES WILL SAVE MONEY AND PREVENT PATIENT SUFFERING BY DECLARING THAT THERE IS COVERAGE FOR TURBINATE REDUCTION AND CORRECTION OF DEVIATED SEPTUMS TO ALLOW EASY ADMINISTERATION OF SPG BLOCKS.
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.
THE COST IS SO INEXPENSIVE THAT TRIAL SPG BLOCKS SHOULD BE CONSIDERED IN CHRONIC PAIN PATIENTS ON A TRIAL BASIS TO EVALUATE EFFECTIVENESS. THIS ISESPECIALLY TRUE WHEN WE ARE TRYING TO STOP AND REVERSE THE PRESCRIPTION OPIOD EPIDEMIC.
THE FOLLOWING IS A LIST OF HEADACHES FROM WIKIPEDIA AND THE INTERNATIONAL CLASSIFICATION OF HEADACHES. ALL OF THESE COULD BE AREAS WHERE SPG BLOCKS MIGHT BE UTILIZED FOR TREATMENT OF SYMPTOMS. IT IS IMPORTANT THAT WE ALSO LOOK FOR UNDERLYING ORGANIC CAUSES OF PAIN. WHEN MY LATE WIFE WAS SUFFERING SEVERE PAIN FROM OVARIAN CANCER SPG BLOCKS OFTEN CONSIDERABLY REDUCED HER PAIN LEVELS AND DECREASED THE AMOUNT OF PAIN MEDICATION, FENTANYL. IT IMPROVED HER QUALITY OF LIFE BUT DID NOT TREAT THE CANCER.
Hierarchy Primary headaches ICHD 1, ICD10 G43: Migraine See also: ICHD classification and diagnosis of migraine
Migraine without aura
Migraine with aura
Childhood periodic syndromes that are commonly precursors of migraine
Complications of migraine
ICHD 2, ICD10 G44.2: Tension-type headache (TTH) Infrequent episodic tension-type headache
Frequent episodic tension-type headache
Chronic tension-type headache
Probable tension-type headache
ICHD 3, ICD10 G44.0: Cluster headache and other trigeminal autonomic cephalagias Cluster headache
Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT)
Probable trigeminal autonomic cephalagia
ICHD 4, ICD10 G44.80: Other primary headaches Primary stabbing headache
Primary cough headache
Primary exertional headache
Primary headache associated with sexual activity
Primary thunderclap headache
New daily persistent headache (NDPH)
Secondary headaches ICHD 5, ICD10 G44.88: Headache attributed to head and/or neck trauma Acute post-traumatic headache
Acute post-traumatic headache attributed to moderate or severe head injury
Acute post-traumatic headache attributed to mild head injury
Chronic post-traumatic headache
Chronic post-traumatic headache attributed to moderate or severe head injury
Chronic post-traumatic headache attributed to mild head injury
Acute headache attributed to whiplash injury
Chronic headache attributed to whiplash injury
Headache attributed to traumatic intracranial haematoma
Headache attributed to epidural haematoma
Headache attributed to subdural haematoma
Headache attributed to other head and/or neck trauma
Acute headache attributed to other head and/or neck trauma
Chronic headache attributed to other head and/or neck trauma
Acute post-craniotomy headache
Chronic post-craniotomy headache
ICHD 6, ICD10 G44.81: Headache attributed to cranial or cervical vascular disorder Headache attributed to ischaemic stroke or transient ischaemic attack
Headache attributed to ischaemic stroke (cerebral infarction)
Headache attributed to transient ischaemic attack (TIA)
Headache attributed to non-traumatic intracranial haemorrhage
Headache attributed to intracerebral haemorrhage
Headache attributed to subarachnoid haemorrhage (SAH)
Headache attributed to unruptured vascular malformation
Headache attributed to saccular aneurysm
Headache attributed to arteriovenous malformation (AVM)
Headache attributed to dural arteriovenous fistula
Headache attributed to cavernous angioma
Headache attributed to encephalotrigeminal or leptomeningeal angiomatosis
(Sturge Weber syndrome)
Headache attributed to arteritis
Headache attributed to giant cell arteritis (GCA)
Headache attributed to primary central nervous system (CNS) angiitis
Headache attributed to secondary central nervous system (CNS) angiitis
Carotid or vertebral artery pain
Headache or facial or neck pain attributed to arterial dissection
Carotid angioplasty headache
Headache attributed to intracranial endovascular procedures
Headache attributed to cerebral venous thrombosis (CVT)
Headache attributed to other intracranial vascular disorder
CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical
Infarcts and Leukoencephalopathy)
MELAS (Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like
Headache attributed to benign angiopathy of the central nervous system
Headache attributed to pituitary apoplexy
ICHD 7, ICD10 G44.82: Headache attributed to non-vascular intracranial disorder Headache attributed to high cerebrospinal fluid pressure
Headache attributed to idiopathic intracranial hypertension (IIH)
Headache attributed to intracranial hypertension secondary to metabolic, toxic
or hormonal causes
Headache attributed to intracranial hypertension secondary to hydrocephalus
Headache attributed to low cerebrospinal fluid pressure
Post-dural puncture headache
CSF fistula headache
Headache attributed to spontaneous (or idiopathic) low CSF pressure
Headache attributed to non-infectious inflammatory disease
Headache attributed to neurosarcoidosis
Headache attributed to aseptic (non-infectious) meningitis
Headache attributed to other non-infectious inflammatory disease
Headache attributed to lymphocytic hypophysitis
Headache attributed to intracranial neoplasm
Headache attributed to increased intracranial pressure or hydrocephalus
caused by neoplasm
Headache attributed directly to neoplasm
Headache attributed to carcinomatous meningitis
Headache attributed to hypothalamic or pituitary hyper- or hyposecretion
Headache attributed to intrathecal injection
Headache attributed to epileptic seizure
Headache attributed to Chiari malformation type I (CM1)
Syndrome of transient Headache and Neurological Deficits with cerebrospinal fluid Lymphocytosis (HaNDL)
Headache attributed to other non-vascular intracranial disorder
ICHD 8, ICD10 G44.4 or G44.83: Headache attributed to a substance or its withdrawal Headache induced by acute substance use or exposure
Nitric oxide (NO) donor-induced headache
Immediate NO donor-induced headache
Delayed NO donor-headache
Phosphodiesterase (PDE) inhibitor-induced headache
Carbon monoxide-induced headache
Immediate alcohol-induced headache
Delayed alcohol-induced headache
Headache induced by food components and additives
Monosodium glutamate-induced headache
Immediate histamine-induced headache
Delayed histamine-induced headache
Calcitonin gene-related peptide (CGRP)-induced headache
Immediate CGRP-induced headache
Delayed CGRP-induced headache
Headache as an acute adverse event attributed to medication used for other
Headache attributed to other acute substance use or exposure
Medication-overuse headache (MOH)
Combination analgesic-overuse headache
Medication-overuse headache attributed to combination of acute medications
Headache attributed to other medication overuse
Probable medication-overuse headache
Headache as an adverse event attributed to chronic medication
Exogenous hormone-induced headache
Headache attributed to substance withdrawal
Headache attributed to withdrawal from chronic use of other substances
ICHD 9, ICD10 G44.821 or G44.881: Headache attributed to infection Headache attributed to intracranial infection
Headache attributed to bacterial meningitis
Headache attributed to lymphocytic meningitis
Headache attributed to encephalitis
Headache attributed to brain abscess
Headache attributed to subdural empyema
Headache attributed to systemic infection
Headache attributed to systemic bacterial infection
Headache attributed to systemic viral infection
Headache attributed to other systemic infection
Headache attributed to HIV/AIDS
Chronic post-infection headache
Chronic post-bacterial meningitis headache
ICHD 10, ICD10 G44.882: Headache attributed to disorder of homeostasis Headache attributed to hypoxia and/or hypercapnia
Sleep apnoea headache
Headache attributed to arterial hypertension
Headache attributed to phaeochromocytoma
Headache attributed to hypertensive crisis without hypertensive
Headache attributed to hypertensive encephalopathy
Headache attributed to pre-eclampsia
Headache attributed to eclampsia
Headache attributed to acute pressor response to an exogenous agent
Headache attributed to hypothyroidism
Headache attributed to fasting
Headache attributed to other disorder of homoeostasis
ICHD 11, ICD10 G44.84: Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures Headache attributed to disorder of cranial bone
Headache attributed to disorder of neck
Headache attributed to retropharyngeal tendonitis
Headache attributed to craniocervical dystonia
Headache attributed to disorder of eyes
Headache attributed to acute glaucoma
Headache attributed to refractive errors
Headache attributed to heterophoria or heterotropia (latent or manifest squint)
Headache attributed to ocular inflammatory disorder
Headache attributed to disorder of ears
Headache attributed to rhinosinusitis
Headache attributed to disorder of teeth, jaws or related structures
Headache or facial pain attributed to temporomandibular joint (TMJ) disorder
Headache attributed to other disorder of cranium, neck, eyes, ears, nose, sinuses,
teeth, mouth or other facial or cervical structures
ICHD 12, ICD10 R51: Headache attributed to psychiatric disorder Headache attributed to somatization disorder
Headache attributed to psychotic disorder
Cranial neuralgias, central and primary facial pain and other headaches ICHD 13, ICD10 G44.847, G44.848, or G44.85: Cranial neuralgias and central causes of facial pain ICHD 13.1, ICD10 G44.847: Trigeminal neuralgia
Nervus intermedius neuralgia
Superior laryngeal neuralgia
Other terminal branch neuralgias
External compression headache
Constant pain caused by compression, irritation or distortion of cranial nerves or upper cervical roots by structural lesions
Ocular diabetic neuropathy
Head or facial pain attributed to herpes zoster
Head or facial pain attributed to acute herpes zoster
Central causes of facial pain
Central post-stroke pain
Facial pain attributable to multiple sclerosis
Persistent idiopathic facial pain (the IHS’s preferred term for atypical facial pain)
Burning mouth syndrome
Other cranial neuralgia or other centrally mediated facial pain
ICHD 14, ICD10 R51: Other headache, cranial neuralgia, central or primary facial pain Headache not elsewhere classified
Ira L Shapira DDS, D,ABDSM, D,AAPM, FICCMO
Chair, Alliance of TMD Organizations
Diplomat, American Academy of Pain Management
Diplomat, American Board of Dental Sleep Medicine
Regent & Fellow, International College of CranioMandibular Orthopedics
Board Eligible, American Academy of CranioFacial Pain
Dental Section Editor, Sleep & Health Journal
Member, American Equilibration Society
Member, Academy of Applied Myofunctional Sciences