Purpose: We investigated the effects of term neonatal encephalopathy on retinal function and structure.
Methods: A rat model of term neonatal hypoxic-ischemic (HI) encephalopathy (Vannucci model) was used. Hypoxia-ischemia was induced by a left common carotid ligation followed by a 2-hour period of hypoxia (8% oxygen) in Long-Evans rat pups at postnatal day 10 (P10). Sham operated rats served as controls.. Retinal function was assessed at P30 and P60 by electroretinograms (ERGs), after which retinal histology was performed. Retinocortical function was assessed with visual evoked potentials (VEPs) at P60 and subsequently brain histology was performed.
Results: The ERGs of the HI animals at P30 and P60 demonstrated a significant reduction in the scotopic and photopic b-wave amplitudes, but a preserved a-wave amplitude. The retinal histology of the HI animals confirmed that the photoreceptor layer remained intact, whereas the inner layers of the retina were damaged. The HI animals also showed reduced VEP P100 amplitudes, which correlated with reduced left cerebral hemisphere surfaces. There was no correlation between the severities of retinal versus cerebral injuries.
Conclusions: Our findings suggest that term neonatal encephalopathy resulting from HI induces functional and structural damages to the inner retina, while relatively sparing the photoreceptors. These findings raise the possibility that retinal injuries may contribute to visual impairments with or without the presence of brain injury in term asphyxiated newborns and, thus, warrant further studies with humans and animals to better understand the disease process.
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