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Background: There are many theories about the cause of trigeminal neuralgia (TN). None of them satisfactorily explains how demyelination alone through the ephaptic mechanism can contribute to the development of the TN crisis. The main characteristic of TN pain is its dynamic nature, which is difficult to explain based only on anatomical findings. With these antecedents, the exact mechanism by which radiosurgery produces pain relief in TN is unknown. Methods: It is based on the trigeminal ganglion (TG) cytoarchitecture and the pathophysiological findings observed after an injury to a trigeminal branch. TG seems to have a predominant role given its cellular structure. The neuronal component in sensory ganglia is generally surrounded by a single layer of satellite glial cells (SGC), which forms a sheath around each body cell. There is increasing evidence that SGCs play a key role in nociception. This depends on their ability to influence the neuronal excitability that occurs in conditions of neuropathic and inflammatory pain; contributing to both the generation and maintenance of pain. Results: We have already published the beneficial effects of radiosurgery on the TG for the treatment of idiopathic TN and secondary to vertebrobasilar ectasia. Now, we are investigating the functioning of the TG and how radiosurgery could act on the SGC, deactivating them, and contributing to the decrease or disappearance of the painful condition. Conclusion: We are postulating a theory on how radiosurgery in TG produces changes in the SGC, with implications in the pathological mechanisms initiated by the alteration caused in the neuron after a nerve injury.

Novel theory about radiosurgery’s action mechanisms on trigeminal ganglion for idiopathic trigeminal neuralgia: Role of the satellite glial cells