Abstract

Traumatic brain injury is an increasingly common affliction, although many of its serious repercussions are still underappreciated. A frequent consequence is the development of light-induced pain, or ‘photalgia’, which can often lead to prolonged debilitation. The mechanism underlying the sensitivity to light, however, remains unresolved. Since tissue oedema (swelling) is a common feature of traumatic brain injury, we propose that the brainstem oedema, in particular, might sensitize the brainstem trigeminal complex to signals from ocular mechanisms activated in bright light. To assess this hypothesis, we ran high-resolution Magnetic Resonance Imaging of the brainstems of concussion groups with mild and severe photalgia, without photalgia, and healthy controls. The 3D configuration of the brainstem was determined by Tensor-Based Morphometry (TBM) for each participant. The TBM revealed significant deviations in the brainstem morphology of all concussion groups, with a characteristic signature for each group. In particular, concussion without photalgia showed bilateral expansion at the pontine/medulla junction, whereas concussion with photalgia showed mid-pontine shrinkage, consistent with degeneration of nuclei of the trigeminal complex. These results support the hypothesis that brainstem shrinkage/degeneration represents a morphological substrate of the photalgic sensitization of the trigeminal pathway.

Highlights

  • Mild traumatic brain injury is a term generally applied to cases of non-penetrating trauma to the head that results in damage to the brain

  • A common link in many of the theories of photalgia is a sensitization of the trigeminal nerve to bright light[12,13,14,15], which has been demonstrated in animal models[16], the mechanism by which the trigeminal nerve is sensitized to light remains unresolved

  • Oedema has two basic origins: vasogenic and cellular[17,19]. Both origins are associated with Mild traumatic brain injury (mTBI), especially the cellular oedema that results from axonal damage[20,21,22]. This line of reasoning led us to the hypothesis that the initial oedema might be followed by a chronic shrinkage/degeneration that results in sensitization of the trigeminal nuclear complex to overactivation by light stimulation

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Summary

Introduction

Mild traumatic brain injury (mTBI) is a term generally applied to cases of non-penetrating trauma to the head that results in damage to the brain. As such, it can present a diagnostic and treatment challenge, since the damage is internal to the closed head and is difficult to directly assess, persistent symptoms may markedly affect the patients’ quality of life. Oedema has two basic origins: vasogenic (breakdown of the blood-brain barrier) and cellular (accumulation of fluids inside or outside cell walls)[17,19] Both origins are associated with mTBI, especially the cellular oedema that results from axonal damage[20,21,22]. Activity in the human TNC can be recorded by standard fMRI techniques to both painless (tactile) and noxious (heat) stimulation, with opposite effects on the BOLD activation of the TNC; activation for the noxious and reduction for the painless stimulation[30]

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