OC-11 | Corneal nerve plexus impairment in patients with trigeminal neuralgia

Daniel Litewczuk,¹ Gianfranco De Stefano,¹ Sabrina Compagno,² Mattia D’Andrea,² Ludovico Alisi,² Marco Marenco,² Giulia Di Stefano,¹ Andrea Truini¹ | ¹Department of Human Neuroscience, Sapienza University of Rome, ²Department of Sense Organs, Sapienza University of Rome, Italy

Background: Primary Trigeminal Neuralgia (TN) typically lacks overt signs of sensory impairment in association with pain paroxysms. Nevertheless, recent studies suggested that function impairment of small fibers could play a significant role in the pathophysiology of this peculiar condition. Corneal confocal microscopy (CCM) is a well established, non-invasive tool to assess the morphological changes of small fibers in the trigeminal territory. We aimed to assess whether TN is associated with a measurable reduction of nerve fibers in the cornea assessed by CCM.

Methods: Patients with a definite diagnosis of classical and idiopathic TN were consecutively enrolled. Clinical features were systematically recorded using a dedicated questionnaire. Each patient underwent CCM on both sides of the face to assess length and density of nerve fibers, density of branches, number of corneal cells, and tortuosity of nerve fibers.

Results: We enrolled 19 patients (12 females, 7 males, age 65.28 ± 8.69) with primary TN. The affected side of the face was characterized by a significant reduction of corneal nerve fiber length (p = 0.0119) and corneal nerve branch density (p = 0.03). No correlation was found between clinical characteristics and CCM parameters.

Conclusion: Our study shows that CCM revealed signs of small fiber loss on the affected side of TN patients. This finding is unexpected as the most implicated pathogenetic mechanism in TN is a pre-ganglionic compression by an offending vessel at the level of the trigeminal root. One possible explanation for this observation might be secondary denervation due to an otherwise undetected ganglionic involvement. Further studies are needed to clarify the role of small fiber impairment in TN and its clinical implications.