What is old is new again in Headache Management. The Sphenopalatine Ganglion Block is an amazing back door to the brain for treating all types of Headaches, Migraines and Autonomic Cephalgias as well as multiple other conditions. This new article is available as an open access journal available to everyone. I will post the abstract here and the walk through the high points of this excellent paper.
Abstract
Headache disorders are among the most prevalent and disabling neurological conditions worldwide, affecting more than three billion individuals and contributing to a substantial socioeconomic burden. Despite the availability of pharmacologic treatments such as triptans, NSAIDs, and CGRP monoclonal antibodies, a significant proportion of patients remain refractory or intolerant to these therapies. The sphenopalatine ganglion (SPG), a parasympathetic neural structure in the pterygopalatine fossa, is increasingly recognized as a critical node in the pathophysiology of primary headache disorders. SPG blocks—using local anesthetics, neurolytic agents, or electrical neuromodulation—offer a minimally invasive therapeutic approach by disrupting nociceptive transmission and autonomic activation. This narrative review synthesizes the anatomical and physiological rationale for SPG intervention, details various procedural techniques, evaluates clinical evidence across headache subtypes, and explores future research directions. Conditions covered include migraine, cluster headache, tension-type headache, trigeminal neuralgia, and persistent idiopathic facial pain. With expanding evidence and evolving technologies, SPG-targeted interventions have the potential to reshape the management of refractory headaches and facial pain syndromes.
Link to original article in full: https://www.mdpi.com/2076-3425/15/7/672#
Keywords: sphenopalatine ganglion; SPG block; headache; cluster headache; migraine; trigeminal neuralgia; facial pain; craniofacial pain; neuromodulation; refractory headache
My paper on this subject in CRANIO Journal is not available open access, but this is a link to last prepublication version of my article: Neuromuscular dentistry and the role of the autonomic nervous system:
Neuromuscular dentistry and the role of the autonomic nervous system: Sphenopalatine ganglion blocks and neuromodulation.
https://www.sphenopalatineganglionblocks.com/spg-blocks-and-neuromodulation/
The first item I would like to note that all headaches are products in part or in full of the Trigeminal Nervous System, the Trigemino-vascular system and the autonomic components, both sympathetic and parasympathetic divisions of the of the autonomic nervous system. I often refer to the Trigeminal Nerve because dentists have the most experience in use of anesthetics in this area. The Sphenopalatine Ganglion lies in the Pterygopalatine Fossa along with the Maxillary (Afferent) Division and the Maxillary artery.
The Transoral injection technique is routine in general Dentistry, Endodontics and especially Maxillofacial surgery. “This technique inserts a needle through the greater palatine foramen in the hard palate and advances superiorly into the pterygopalatine fossa under fluoroscopic or neuronavigation guidance. It allows direct anesthetic or neurolytic injection to the SPG. Though more invasive and requiring expertise, it offers deeper access and longer-lasting effects.” This procedure does not actually require any imaging for use of anesthetic but I would definitely advise for use of neurolytic injections. THAT SAID, I WOULD HIGHLY DISCOURAGE THE USE OF NEUROLYTIC SOLUTIONS BEING INJECTED. My preferred method for anesthetic is the Suprazygomatic Approach, which is basically easier that a mandibular block that dentists do routinely in their offices. It does require a longer needle (50 ml) than most general dentist have in their offices. This approach does not have to go through significant tissues and deposits anesthetic at the Pterygopalatine Fissure into Pterygopalatine Fossa (wikipedia, has an excellent illustration). This area is very easy to access and could easily have a port and internal catheter put in for easy home administration.
The Transnasal Approach makes that catheter unnecessary. This is described in the article as
“The transnasal technique is the most commonly used approach due to its simplicity and minimal invasiveness. Local anesthetic (usually 4% lidocaine or 0.5% bupivacaine) is delivered to the posterior nasal cavity via the following:
Cotton-tipped applicators;
Flexible catheters;
Commercially available devices such as Tx360® or Sphenocath®.
This method targets the Sphenopalatine Foramen, approximating the SPG by capillary absorption and diffusion. Relief is often rapid, occurring within 15–30 min, but may be short-lived, lasting hours to a few days [14]. Repeated sessions are commonly required in chronic migraine or cluster headache.”
This is an excellent explanation, however the use of cotton-tipped applicators is a point I would like to discuss further. It is much better procedure to use sterile cotton tipped catheters that can be filled with 2% Lidocaine while I usually utilize or 4% as the article describes. I usually avoid bupivicaine because it can be irritating to tissues while Lidocaine is a natural anti-inflamatory agent. This is primarily an issue when it is not used by injection as it can cause increased nasal irritation.
This is an AI review of that comparison:
“Based on the information from the search results, it appears there are some nuances regarding the inflammatory effects of bupivacaine compared to lidocaine.
Here’s a breakdown:
Bupivacaine is not considered a natural anti-inflammatory like lidocaine. While it primarily works as a local anesthetic, it has shown both pro-inflammatory and anti-inflammatory effects depending on the concentration and context.
Studies have shown that bupivacaine can increase certain inflammatory mediators like prostaglandin E2 (PGE2) in some situations, potentially leading to increased post-operative pain. However, other studies found that ultralow concentrations of bupivacaine can have anti-inflammatory effects by attenuating the upregulation of IL-1β secretion and interacting with various receptor systems in inflammation-reactive astrocytes. It has also been shown to relieve inflammation-induced pain by suppressing the activation of the NF-κB signaling pathway and inhibiting the activation of spinal microglia and astrocytes.
Lidocaine, on the other hand, is known for its anti-inflammatory properties and is considered a potent anti-inflammatory agent, even compared to steroids and NSAIDs. It reduces the activation of neutrophils and macrophages, decreases the release of pro-inflammatory cytokines and prostaglandins, and preserves endothelial integrity, helping to control excessive inflammatory responses.
The potential for irritation from bupivacaine is generally related to the dose and route of administration. While some studies suggest it may cause more post-operative pain and inflammation compared to lidocaine, other studies found that it could provide more efficient pain control with topical administration in some cases. It is important to note that both bupivacaine and lidocaine can cause temporary local side effects like pain, redness, or swelling at the injection site.
In summary, while lidocaine is more consistently recognized for its anti-inflammatory properties, bupivacaine’s effects on inflammation are more complex and depend on the specific context and concentration. “
The advantage is that the catheter will gradually release lidocaine over and extended period of time. The catheter can be bent to achieve ideal placement and loosening the cotton tip can give a larger area for capillary action. It is easy to add additional anesthetic through the catheter which can be used for long periods. A very important concept is that the Lidocaine anesthetic acts like a reset button of the CNS, especially the autonomic division, like hitting control/alt/delete on a computer. Just like a computer, sometimes that reset needs to be done multiple times for the best results. That is why since I began doing Sphenopalatine Ganglion Blocks in 1986 after a patient brought me a copy of the book “MIRACLES ON PARK AVENUE” I have always taught patient to Self-Administer SPG Blocks and had planned on producing a product line for OTC and Medical Prescription for Self-Administration. I file for a trademark for “SASPGB” but was told because of my frequent use of that it was now in common usage (my mistake for using that on wikipedia). I would still like to see a OTC market device and advanced medical version for home use by prescription.
The article states “
“Reduction in Neurogenic Inflammation’
“Headache disorders, particularly migraines, involve the release of pro-inflammatory neuropeptides, such as calcitonin gene-related peptide (CGRP) and substance P, from trigeminal nerve endings [10, 11]. These neuropeptides lead to vasodilation, increased vascular permeability, and neurogenic inflammation, which amplify headache pain.”
“SPG blocks have been shown to reduce the release of these inflammatory mediators. By doing so, they attenuate the neurogenic inflammation and vascular changes that contribute to headache pathophysiology” I believe this is 100% correct and is actually the mechanism of the Con/alt/del reset mechanism. Also, a reason not to utilize bupivicaine if lidocaine will suffice.
I am not a fan of TX-360 or Sphenocath devices as they are expensine, but more importantly designed to be less effective in giving continues capillary action to deliver the anesthetic. They are basically squirt guns, to maximize effect the block could be done one side at a time and let patient lay in place for 20-30 minutes and the repeat for the opposite side. This would be difficule to maintain in active practice.
The section on Contraindications is very revealing and important for financial considerations as well. Before going through ablation, neurolysis, neurotoxin or even implanted neurostimulation I would suggest common sense demands the least invasive method as a starting point. The contraindications I will addressone at a time:
Sphenopalatine ganglion (SPG) interventions, including blocks, radiofrequency ablation (RFA), and neurostimulation, are generally safe but require careful patient screening. The following contraindications should be considered when evaluating candidates for SPG-targeted procedures:
Absolute contraindications include the following [37,38]:
Patient refusal or inability to provide informed consent. Dr Shapira: Absolute Contraindication to work on patient without informed consent!
Known allergy to local anesthetics or chemical neurolytic agents (e.g., ethanol, phenol). Dr Shapira: Lidocaine allergies are very rare especially is not using epinephrine.
Active infection at the site of injection or systemic infection. DrShapira: Does not effect SASPGB
Uncorrected coagulopathy or ongoing anticoagulation therapy, particularly when procedures involve non-compressible or vascular-adjacent areas. Dr Shapira Could be a problem but safest with Self Administration
Presence of a pacemaker (in the case of planned RFA) without prior consultation with cardiac electrophysiology for device interrogation and safety clearance. Dr Shapira: Never hurts to get additional experts involved who possibly could do the procedure while in their offices
Relative contraindications include the following [37,38]:
Anatomical barriers such as severe nasal septal deviation, facial trauma, or obstructive polyposis that may impede access (especially for transnasal techniques). Dr Shapira: Obstructions can removed in various ways including ENT surgical intervention, reducing turbinate or correcting deviated septums, dentalyy by Maxillary Expansion by SARPE, MARPE, MSE or non-surgically with epigenetic orthopedics with devices like Vivos DNA or MRNA Aplliiances. THIS COULD ALSO HAVE THE ADVANTAGE OF TREATING CONTACT HEADACHES, CAUSED BY CONTACT BETWEEN SEPTUM AND TURBINATES. IN MY OFFICE I UTILIIZE OXYMETAZOLINE TO SHRING MUCOSA PRIOR TO TRANSNASAL APPROACH.
Preexisting neurologic deficits in the distribution of the maxillary nerve (CN V2), which may confound post-procedural assessments. Dr Shapira: True but may actually found to be diagnstic! Good reason to always start with non-invasive trans-nasal approach.
Psychological factors such as severe procedural anxiety or inability to tolerate awake interventions. Dr Shapira: Patient mangement techniques are important but most patients looking for answers will go ahead with procedure.
Recent midfacial surgery or implanted hardware that increases risk during needle-based or surgical approaches.
Diagnostic lidocaine blocks may help predict response and tolerability in borderline cases, especially before more invasive neurolytic or neuromodulatory treatments [37, 38]. Dr Shapira: I would never use anything other than anesthetic initially.
Economic Considerations:
Cost-effectiveness is critical in adopting SPG-targeted interventions, particularly given the high procedural costs associated with neurostimulation and ablative techniques. While short-term relief can often be achieved with anesthetic blocks, longer-lasting modalities such as SPG stimulation and radiofrequency ablation (RFA) entail significant upfront investment.
Dr Shapira: The cost must be considered in many ways including patient suffering and lost wages and production in patients living with headaches. SASPGB means that patients can use prophylactically or on an as needed basis. Extremely cost effective with minimal if any negative results other than mild nasal irritation. Patients can avoid most ER visits if they can shut it off right at the start. SASPGB seems effective for medication overuse headaches but that is a more complex issue.