Skip to main content
  • Macular Perfusion and Neuronal Loss in TBI

    By Lynda Seminara
    Selected by Prem S. Subramanian, MD, PhD
    Retina/Vitreous

    Journal Highlights

    Investigative Ophthalmology & Visual Science
    2023;64(4):35

    Download PDF

    Traumatic brain injury (TBI) may cause structural and functional damage to the visual system, with retinal ganglion cell (RGC) degeneration often occurring in the absence of vision-related symptoms. This degeneration correlates with di­minished retinal blood flow, but wheth­er the perfusion reductions precede or follow neurodegeneration has been unclear. To learn more, Hepschke et al. analyzed ophthalmic data for patients with TBI, hypothesizing that perfusion reductions would precede and predict neurodegeneration. Instead, they found that in patients with reduced visual function after TBI, macular perfusion remained normal until the ganglion cell layer (GCL) thinned—indicating that the perfusion changes are secondary to local GCL loss.

    Included in this prospective single-center case series were patients admitted to the hospital after acute TBI (moderate or severe) who under­went early ophthalmic examinations, including OCT and OCT angiography. The exams were conducted within 14 days of injury, as well as two to six months later. Measurements included thickness of the GCL and density of the superficial vascular plexus (SVP) and intermediate capillary plexus. Only patients with complete datasets for both eyes were included. Excluded from the analysis were patients who had any direct penetrating or nonpenetrating injury to the eye, those with a preexisting pathology of the retina or optic nerve, and patients who were unable to cooperate for the exams.

    Twenty-one adults met the inclu­sion criteria (mean age, 38 years). At initial examination, macular struc­ture and perfusion were normal in all patients. At this point, visual function was abnormal for three patients; the observed neurodegeneration and loss of perfusion in these patients coincided with the visual function deficits. At the follow-up visit, nine of the 21 patients had reduced macular GCL thickness. Perfusion in the SVP correlated strong­ly with local GCL thickness; the sum of vessel density was the metric with the strongest association (p < .0001).

    Per the authors, this is the largest published study of patients with moderate or severe TBI that includes comprehensive ophthalmic data. “We have shown for the first time that macular SVP retinal perfusion after anterior visual pathway damage reduces in proportion to the structural loss of macular RGC, rather than directly in response to injury,” said the authors. They emphasized that this can occur independently of detectable changes in visual function.

    The original article can be found here.