When light hurts: Comparative Morphometry of Human Brainstem in Traumatic Photalgia

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

Feasibility of using normobaric hypoxic stress in mTBI research

Studies of mild traumatic brain injury (mTBI) recovery generally assess patients in unstressed conditions that permit compensation for impairments through increased effort expenditure. This possibility may explain why a subgroup of individuals report persistent mTBI symptoms yet perform normally on objective assessment. Accordingly, the development and utilization of stress paradigms may be effective for enhancing the sensitivity of mTBI assessment. Previous studies, discussed here, indirectly but plausibly support the use of normobaric hypoxia as a stressor in uncovering latent mTBI symptoms due to the overlapping symptomatology induced by both normobaric hypoxia and mTBI. Limited studies by our group and others further support this plausibility through proof-of-concept demonstrations that hypoxia reversibly induces disproportionately severe impairments of oculomotor, pupillometric, cognitive and autonomic function in mTBI individuals