Abstract
Purpose: :
The objective of this study was to correlate visual evoked potential, electroretinogram(ERG) and ocular coherence tomography(OCT) in response to trauma to the optic nerve.
Methods: :
Ten NZW rabbits (average weight=2.4 kg, age>15 weeks) using a 50g or 125g pressure gauge clamp to clamp the optic nerve (OPN)(n=5 per group). Peritomy was performed and the OPN was located and exposed. The clamp was applied perpendicularly at 2-3 mm away from the base of the OPN for one minute and released. Scotopic and photopic ERG responses were evaluated. Fundus photography, OCT, fVEP, and clinical ophthalmic examinations were performed at baseline and weekly for 36 weeks. Statistical analysis was performed using ANOVA with multiple comparison procedures (p<0.05).
Results: :
After 125-g pressure clamping, bilateral absence of afferent pupillary reflex, papilloedema, deformed optic nerve head, pallor and atrophied optic streaks of the OPN persisted through day 41. The photopic negative response (PhNR) amplitude on clamped eyes was significantly different from the baseline value and had decreased in average of 56% on day 109 at -4dB(or 0.96 cd-s/m^2) flash intensity. The contralateral control eyes also responded to the trauma with an average decrease in the PhNR at -4dB of 47% on day 109. The fVEP response was absent on the injured eye and a 50% reduction of signal strength on the contralateral eye. In 50-g pressure clamping, the PhNR amplitudes decreased on the clamped eye by 20% and decreased on the contralateral eye by 29% at -4 dB on day 109. The fVEP on the injured eye showed a gradual diminishing response by day 123, and a 70% signal visual reduction was seen in the contralateral eye on day 123. Two of five rabbits in the 50 g pressure clamp model regained pupillary and blink reflexes to light on the clamped eye on day 41 and remained responsive on day 123.
Conclusions: :
Traumatic injury to the optic nerve caused sudden drop and complete suppression of the fVEP on the injured eyes accompanied by rapid, decreased in PhNR. Contralateral eyes responded with slower and partial suppression of the fVEP, indicating a possible trans-chiasmatic contralateral optic nerve injury. Further studies are warranted to show the mechanistic and biological association between PhNR and the various cellular components of the inner retina involved in ocular neurodegenerative diseases.
Keywords: optic nerve • ganglion cells • electrophysiology: non-clinical