Post-Traumatic Trigeminal Neuropathy: Neurobiology and Pathophysiology

Abstract

Painful traumatic trigeminal neuropathy (PTTN) is a chronic neuropathic pain that may develop following injury to the trigeminal nerve. Etiologies include cranio-orofacial trauma that may result from dental, surgical, or anesthetic procedures or physical trauma, such as a motor vehicle accident. Following nerve injury, there are various mechanisms, including peripheral and central, as well as phenotypic changes and genetic predispositions that may contribute to the development of neuropathic pain. In this article, we review current literature pertaining to the cellular processes that occur following traumatic damage to the trigeminal nerve, also called cranial nerve V, that results in chronic neuropathic pain. We examine the neurobiology and pathophysiology based mostly on pre-clinical animal models of neuropathic/trigeminal pain.

Considerations in the Diagnosis and Treatment of Post-Traumatic Neuropathic Pain: A<strong> </strong>Narrative Review

“…Animal studies have been instrumental in elucidating the pathophysiology of PTTN [2,6,15,18,19]. These studies highlight the pivotal role of inflammatory responses in the injured nerve system [15,18,19].…”

“…Animal studies have been instrumental in elucidating the pathophysiology of PTTN [2,6,15,18,19]. These studies highlight the pivotal role of inflammatory responses in the injured nerve system [15,18,19]. Numerous inflammatory mediators contribute to peripheral and central sensitization over time, which includes modifications in the functional, biochemical, and physical properties of glial cells and neurons against the backdrop of their genetic makeup [15,18,19].…”

“…Nerve injury disrupts neuronal electrical activity, leading to peripheral sensitization and nociceptor activation [15,18,19]. This process involves the release of inflammatory mediators, which lower the thresholds and increase the excitability of the peripheral terminal membrane [15,18,19].…”

“…Nerve injury disrupts neuronal electrical activity, leading to peripheral sensitization and nociceptor activation [15,18,19]. This process involves the release of inflammatory mediators, which lower the thresholds and increase the excitability of the peripheral terminal membrane [15,18,19]. The resultant inflammatory response causes blood vessel dilation, white blood cell recruitment, and mast cell degranulation, further reducing the threshold [15,18,19].…”

“…This process involves the release of inflammatory mediators, which lower the thresholds and increase the excitability of the peripheral terminal membrane [15,18,19]. The resultant inflammatory response causes blood vessel dilation, white blood cell recruitment, and mast cell degranulation, further reducing the threshold [15,18,19]. Peripheral sensitization intensifies rapidly due to inflammation associated with the activation or sensitization of nociceptors, potentially manifesting early clinical signs of hyperalgesia and allodynia [15,18,19].…”