Percutaneous Trigeminal Ganglion Stimulation as a Treatment Modality for Anesthesia Dolorosa

Neurosurgery Practice 2026;7(1):e000191.

This case report describes successful percutaneous trigeminal ganglion stimulation (TGS) in a 71-year-old woman with anesthesia dolorosa (AD) after multiple rhizotomies for trigeminal neuralgia related to multiple sclerosis. The authors detail implantation technique, trial and permanent lead placement, stimulation parameters, and sustained clinical improvement over three years without major complications.

The article situates TGS within neuromodulation strategies for refractory deafferentation pain, reviews prior peripheral nerve stimulation evidence, and discusses mechanisms, patient selection considerations, and hardware anchoring challenges. The authors conclude TGS is a promising option for refractory AD and call for further research to refine indications and device fixation.

Condition Anesthesia dolorosa (AD) is a rare, debilitating deafferentation pain syndrome (incidence ~0.3%–2%) that often follows iatrogenic trigeminal nerve injury such as trigeminal rhizotomy and is frequently refractory to medications.

Patient case A 71-year-old woman with trigeminal neuralgia secondary to multiple sclerosis developed severe, medically refractory AD after multiple rhizotomies, with burning jaw pain and substantial numbness that impaired eating, talking, and oral hygiene.

Intervention An off-label percutaneous trigeminal ganglion stimulation (TGS) externalized trial was offered because some sensation was preserved.

Procedure Under fluoroscopic guidance, an electrode was advanced via a Jamshidi needle through the foramen ovale to the trigeminal ganglion region and secured on the cheek/postauricular area; an external generator was connected for the trial.

Trial outcome Over ~2 weeks of continuous stimulation, pain during episodes improved from 9/10 to 0–1/10, and relief persisted until permanent implantation 2 months later.

Durability After permanent implantation (St. Jude Octrode lead; generator in left chest wall), the patient reported 0–1/10 burning pain with return to baseline activities, with stable relief for 3 years with minimal setting adjustments alongside baclofen and pregabalin.

Rationale TGS is proposed to help restore tonic signaling to the trigeminal nucleus to rebalance excitatory/inhibitory processing and alleviate pain, potentially even with severe peripheral deafferentation.

Implications/limits This single case supports TGS as a promising option for refractory AD and warrants further investigation; practical challenges include achieving robust facial lead anchoring and defining optimal indications/trial criteria.

Trigeminal and sphenopalatine ganglion stimulation for intractable craniofacial pain

Trigeminal and sphenopalatine ganglion stimulation for intractable craniofacial pain

Acta Neurochir (2016) 158:513–520

Facial pain is often debilitating and can be characterized by a sharp, stabbing, burning, aching, and dysesthetic sensation. Specifically, trigeminal neuropathic pain (TNP), anesthesia dolorosa, and persistent idiopathic facial pain (PIFP) are difficult diseases to treat, can be quite debilitating and an effective, enduring treatment remains elusive.

Methods We retrospectively reviewed our early experience with stimulation involving the trigeminal and sphenopalatine ganglion stimulation for TNP, anesthesia dolorosa, and PIFP between 2010–2014 to assess the feasibility of implanting at these ganglionic sites. Seven patients received either trigeminal and/or sphenopalatine ganglion stimulation with or without peripheral nerve stimulation, having failed multiple alternative modalities of treatment. The treatments were tailored on the physical location of pain to ensure regional coverage with the stimulation.

Results Fluoroscopy or frameless stereotaxy was utilized to place the sphenopalatine and/or trigeminal ganglion stimulator. All patients were initially trialed before implantation. Trial leads implanted in the pterygopalatine fossa near the sphenopalatine ganglion were implanted via transpterygoid (lateral-medial, infrazygomatic) approach. Trial leads were implanted in the trigeminal ganglion via percutaneous Hartel approach, all of which resulted in masseter contraction. Patients who developed clinically significant pain improvement underwent implantation. The trigeminal ganglion stimulation permanent implants involved placing a grid electrode over Meckel’s cave via subtemporal craniotomy, which offered a greater ability to stimulate subdivisions of the trigeminal nerve, without muscular (V3) side effects. Two of the seven overall patients did not respond well to the trial and were not implanted. Five patients reported pain relief with up to 24- month follow-up. Several of the sphenopalatine ganglion stimulation patients had pain relief without any paresthesias. There were no electrode migrations or post-surgical complications.

Conclusions Refractory facial pain may respond positively to ganglionic forms of stimulation. It appears safe and durable to implant electrodes in the pterygopalatine fossa via a lateral transpterygoid approach. Also, implantation of an electrode grid overlying Meckel’s cave appears to be a feasible alternative to the Hartel approach. Further investigation is needed to evaluate the usefulness of these approaches for various facial pain conditions.