Research Article

Neuromodulation with pulsed radiofrequency of the sphenopalatine ganglion in selected forms of chronic headache

Todor Shamov^‡, Georgi Krasimirov Georgiev^‡, Demetrio Atanasov^‡

‡ Neurosurgical department, St. Anna University Hospital - Sofia, Sofia, Bulgaria

Corresponding author: Todor Shamov ( shamov@abv.bg )

This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: Shamov T, Krasimirov Georgiev G, Atanasov D (2026) Neuromodulation with pulsed radiofrequency of the sphenopalatine ganglion in selected forms of chronic headache. Folia Medica 68(4): e179522. https://doi.org/10.3897/folmed.68.e179522

Abstract

Introduction: The article examines the role of the sphenopalatine ganglion (SPG) in the pathogenesis of various pain syndromes involving the head and neck, particularly in trigeminal autonomic cephalalgias.

Materials and methods: A clinical study involving 17 patients from 2017 to 2025 is presented, in which pulsed radiofrequency (PRF) neuromodulation of the SPG was used to treat chronic facial pain and certain types of headache. The interventions, performed under fluoroscopic guidance and mild sedation, demonstrated good safety and a low risk of complications.

Results: The results showed that 77% of patients achieved significant pain reduction, especially those with cluster, post-traumatic, and post-dural puncture headaches. PRF proved to be a less invasive and safer alternative to conventional ablative techniques (RF), with its effect attributed to neuromodulation rather than destruction of neural structures.

Conclusion: The analysis of the study emphasizes PRF’s potential as a minimally invasive and successful treatment option for chronic cephalalgia, but it also recognizes its limitations, including its small sample size, heterogeneous diagnoses, and brief follow-up period. The authors suggest future controlled studies and exploration of implantable neuromodulation systems for the SPG as a next step in chronic pain management.

Keywords

chronic pain, headache, neuromodulation, pulsed radiofrequency therapy, sphenopalatine ganglion

Introduction

The sphenopalatine ganglion (SPG) is a complex anatomical structure involved in the genesis of various pain syndromes affecting the head and neck, typically accompanied by autonomic manifestations. Although the symptomatology may be quite variable, patients most commonly report a dull headache associated with pain in the maxillary region and teeth, together with autonomic signs such as lacrimation, rhinorrhea, and facial sweating, as well as vasomotor disturbances including conjunctival injection, facial flushing, and nasal congestion.

Headache types associated with this pathophysiology include cluster headache, paroxysmal hemicrania, SUNCT syndrome, SUNA syndrome, and Hemicrania continua. Similar mechanisms are implicated in post-dural puncture headache, post-traumatic headache, and pain syndromes following Herpes Zoster involving the ophthalmic and maxillary branches of the trigeminal nerve.^[1]

Treatment of these headache types is difficult and often insufficient. In cluster headaches, agents such as verapamil, corticosteroids, lithium medications, and anticonvulsants, including valproates and topiramate, are used. First-line medications for SUNCT include lamotrigine and topiramate. Gabapentin is considered first-line therapy for SUNA syndrome. Indomethacin is the treatment of choice for paroxysmal hemicrania and hemicrania continua. Nonsteroidal anti-inflammatory drugs are commonly used for post-traumatic and post-dural puncture headache.^[2]

In chronic cases, greater occipital nerve blocks and radiofrequency interventions targeting the sphenopalatine ganglion have proven useful.^[3] In radiofrequency (RF) procedures, temperatures reach 60–80°C for 80–90 seconds, producing ablative lesions and irreversible neurological functions. Pulsed radiofrequency (PRF), however, maintains a maximum temperature of 42°C, and tissue injury is not temperature-dependent. The principal lesional factor is the current density surrounding the electrode. PRF exerts a neuromodulatory effect without causing permanent neural damage, and its complication rate is extremely low, allowing repeat interventions.^[4] Recent literature increasingly highlights the neuromodulatory benefits of PRF for chronic pain.

Aim

The aim of the study was to evaluate the efficacy of PRF applied to the SPG in patients with chronic headache and facial pain.

Materials and methods

This is a retrospective study with 17 patients who underwent SPG neuromodulation procedures between 2017 and 2025. The interventions were performed at the Neurosurgery Clinic of the Military Medical Academy, Sofia, and the Neurosurgery Clinic of St. Anna University Hospital, Sofia, by the same team. The mean patient age was 53±7 years (range 27–76). The cohort included 12 women and 5 men. All patients had previously undergone conservative treatment for more than 6 months without satisfactory results. Diagnoses were confirmed in consultation with neurologists and based on the diagnostic criteria of the National Consensus on the Diagnosis and Treatment of Primary Headache Types.^[5] The cohort also included three patients without trigeminal autonomic cephalgia: two with post-traumatic headache and one with post-dural (lumbar puncture) headache.

All patients were hospitalized for three days, and interventions were performed in the operating room. Preoperative antibiotic prophylaxis with 2 g IV ceftriaxone was administered two hours prior to the procedure. Patients were positioned supine with slight head extension and forehead fixation. Vital signs (blood pressure, heart rate, oxygen saturation) were continuously monitored. Mild sedation using 2.5–5 mg of midazolam or a low dose of propofol was administered while maintaining verbal contact. Fluoroscopic guidance was used for all procedures. A lateral skull projection was obtained with the C-arm centered at the mid-zygomatic arch, ensuring avoidance of overlapping images from the anterior cranial fossa and planum sphenoidale.

The sphenoid sinus and pterygomaxillary fissure were clearly visualized. After sterile preparation, the skin entry point was marked using a K-wire at the intersection of the projection line of the sphenoid sinus and the lower margin of the zygomatic arch, aligned with the fluoroscopic projection of the mandibular incisura.

A Cosman G4 (Boston Scientific) RF generator was used. A 20G SMK electrode with an active tip of 0.5 cm and a length of 3.5 inches was introduced. The dispersive electrode was placed on the abdomen ipsilateral to the intervention. Under lateral fluoroscopy, the electrode was advanced into the pterygomaxillary fissure; anterior-posterior projection confirmed placement adjacent to the lateral wall of the nasal cavity, without entering it (Fig. 1).

Figure 1.

Fluoroscopic positioning of the electrode in lateral and AP projection. Morphography: 1. maxillary sinus, 2. sphenoidal sinus, 3. pterigo-maxillary fissure, 4. pterygoid bone, 5. nasal wall, 6. orbit, 7. with arrow -electrode.

After C-arm verification of the position, it was advanced to sensory stimulation that confirmed the target neural structure’s proximity to the electric field of the electrode. Sensory thresholds were typically 0.4–0.6 V. Proper positioning produced paresthesia inside the nasal cavity and ipsilateral lacrimation. Paresthesia behind the incisors indicated stimulation of the maxillary division of CN V, requiring slight caudal adjustments. Paresthesia of the soft palate indicated stimulation of the greater palatine nerve, requiring posterior repositioning for a couple of millimeters.

Once verified, PRF was applied in 3 cycles with the following parameters:

– Frequency: 2 Hz

– Pulse width: 20 ms

– Interpulse interval: 480 ms

– Duration: 120 seconds

– Temperature: 42°C

– Impedance: <400 Ω

Following PRF, 2–3 mL of 0.5% bupivacaine (Marcaine Spinal) and 4 mg dexamethasone were injected through the cannula.

Pain intensity was assessed using the Visual Analog Scale (VAS) pre-procedure, on postoperative day 2, and at 3-month follow-up.^[6]

Results

The intervention was performed on the right side in 6 patients (30%), on the left side in 9 patients (50%), and bilaterally in 2 patients (post-traumatic and post-dural puncture headache cases). All procedures were performed for chronic pain except in the post-dural puncture headache cases. The procedure was ineffective in 4 patients (≈25%), defined as VAS ≥7 at 3 months post-procedure.

A very good effect (VAS <2 and discontinuation of medications) was observed in 5 patients (30%), 3 months post-procedure.

A good effect (VAS 3–5) was recorded in 8 patients (47%), three of whom discontinued medication by month 3.

Overall, discontinuation of analgesic medication at 3 months was achieved in 8 patients (≈50% of the cases).

Two patients underwent repeat intervention after 3 months, with good subsequent outcomes.

Fig. 2 shows the declining levels of pain based on the visual analogue scale before the procedure, three days after the procedure and three months after the procedure.

Figure 2.

Distribution based on procedure efficacy.

In our data, in half of the cases (8 people), discontinuation of the medical treatment was achieved. The second procedure was performed in 2 patients after 3 months with good clinical results.

Table 1 shows the distribution of the patients based on efficacy and nosology.

Table 1.

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Efficacy by diagnosis

Diagnosis	Very Good (VAS 0–2)	Good (VAS 2–5)	Poor (VAS 7–10)
Cluster headache (5 pts)	3	1	1
Paroxysmal hemicrania (1 pt)	–	1	–
SUNCT (1 pt)	–	–	1
Hemicrania continua (2 pts)	–	2	–
Post-traumatic headache (4 pts)	2	1	1
Post-dural puncture headache (2 pts)	2	–	–
Post-herpetic pain (2 pts)	1	–	1

The data demonstrates good efficacy in cluster headache, post-traumatic headache, post-dural puncture headache, and post-herpetic pain affecting V1 and V2. Moderate efficacy was observed in paroxysmal hemicrania and hemicrania continua.

Discussion

The SPG is the largest extracranial parasympathetic ganglion. It contains postganglionic parasympathetic neurons and traverses sympathetic and sensory fibers. Parasympathetic preganglionic fibers originate in the superior salivatory nucleus, travel via the nervus intermedius in the structure forming the VII CN, pass through the geniculate ganglion, form the greater petrosal nerve, and afterwards merge with the deep petrosal nerve to form the Vidian nerve and reach the SPG through the pterygoid canal. Sympathetic fibers that pass through the ganglion originate from the superior cervical ganglion (which receives preganglionic fibers from Th1–Th3) and reach the deep petrosal nerve via the internal carotid plexus. Postganglionic parasympathetic fibers innervate the lacrimal gland, nasal mucosa, and soft palate. Sympathetic fibers traverse the ganglion and join sensory fibers of V2 and leave the pterygopalatine fossa through the foramen rotundum.^[7]

Sluder identified the role of the SPG in cluster headache pathogenesis in 1908, when the condition was known as “Sluder’s neuralgia.”^[8]

Pathophysiologically, irritative changes in the SPG are central to trigeminal autonomic cephalalgias. One hypothesis proposes that parasympathetic, sympathetic, and C-fibers from the SPG innervate branches of the external carotid artery. C-fibers release substance P, while parasympathetic fibers release enkephalins, which antagonize substance P. Neurochemical imbalance leads to pain generation. Parasympathetic fibers also produce nitric oxide and vasoactive intestinal peptide, which are potent vasodilators.^[9]

Another hypothesis suggests that focal demyelination within the SPG produces abnormal ectopic discharges, leading to depolarization of parasympathetic fibers and resulting in lacrimation, rhinorrhea, vasodilation, and other autonomic signs. Support for this comes from the effectiveness of local anesthetic infiltration of the SPG, which leads to disruption of these pathophysiological mechanisms and relief of symptoms. Early in the 20th century, Alajouanine treated cluster headaches with cocaine infiltration of the SPG.^[10]

Historically, alcohol and phenol injections, surgical excision, and stereotactic radiosurgery have all been used to treat cluster headaches.

RF technology entered clinical pain practice in the 1960s, while PRF was introduced only in 1996. During RF thermocoagulation, 80°C is reached around the tip of the electrode, and the duration of the intervention lasts for around 80 sec. Interventions on the SPG are effective in about 80% of cases, with recurrence rates of about 45% over 72 months.^[11] PRF shows efficacy of 50–80% with effects lasting 3–12 months.^[12] PRF produces neuromodulation rather than thermolesion; the lesional effect is dependent on current density, not heat. When it comes to temperature, the thermotoxic effect of RF is absent, and the temperature reached is around 42 degrees C. The lesion zone is larger and can encompass a sphere with a diameter of one centimeter around the electrode tip. Lower tissue impedance enhances lesioning. PRF is a safer alternative, as it avoids thermal neurodestruction, thus avoiding damage to neural structures. In its core, the method is described as neuromodulation, as it affects the permeability of C-fiber membranes without leading to destruction. The supported lower temperature avoids long-term sensitive disorders or neuropathy development. It influences gene expression and protein synthesis and reduces pro-inflammatory mediators such as IL-6 and TNF-α, also mitigating central sensitization.^[13]

Our retrospective study serves as a preliminary confirmation and shows our initial results of using PRF on SPG. Limitations include heterogeneity of diagnoses, small sample size, short follow-up, and the confounding analgesic effect of local anesthetic and steroid injection.

Future perspectives include studies focused on specific diagnoses, sham-controlled designs, and development of implantable SPG stimulation systems.

Conclusion

PRF of the SPG is an effective and safe intervention for chronic headache and facial pain, especially in cluster headache, post-traumatic headache, and post-dural puncture headache. Limitations include the small and heterogeneous cohort, short follow-up duration, and the concurrent use of local anesthetics and corticosteroids. Future directions include diagnosis-specific studies, sham-controlled trials, and evaluation of implantable stimulation devices.

References

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Additional information

Ethical statements

The authors declared that no clinical trials were used in the present study.
The authors declared that no experiments on humans or human tissues were performed for the present study.
The authors declared that written informed consent was obtained from all participants in the study.
This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of St. Anna Military Hospital.
The authors declared that no experiments on animals were performed for the present study.
The authors declared that no commercially available immortalized human and animal cell lines were used in the present study.

Conflict of interest

The authors have declared that no competing interests exist.

Artificial Intelligence (AI) use

The authors accept full responsibility for the content of the manuscript, including the disclosure of any use of AI. No AI tools were used in the preparation of this manuscript.

Funding

No funding was reported

Author contributions

All authors have contributed equally.

Author ORCIDs

Georgi Krasimirov Georgiev https://orcid.org/0000-0002-4317-9624

Todor Shamov https://orcid.org/0000-0002-1257-6758

Data availability

All of the data that support the findings of this study are available in the main text.