ABSTRACT. 2. METhODS 3. RESULTS

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1 Laser induced retinal nerve fiber layer (NFL) damage H. Zwick, D.A. Gagliano, J.A. Zuclich, B.E. Stuck, M. Belkin USArmy Medical Research Detachment Walter Reed Army Institute of Research San Antonio, Tx ABSTRACT Retinal nerve fiber layer (NFL) damage can be induced by retinal laser photocoagulation. This type of thermal injury involves degeneration in both descending and ascending directions from the photic injury site. We have repeated early studies in evaluation of the acute phases of the injury process. Our findings indicate that the ascending or Wallerian portion of the NFL degeneration requires less time then the descending portion; an early neural debris channel occurs in close proximity to retinal vessels and appears to enter the optic disc in close proximity to the retinal vasculature. Angiography of the ascending debris sheath suggests possible capillary pattern modulation associated with this neural debris sheath. Retinal traction evident in with other acute injuries appears at 2 weeks and disappears after 8 weeks suggesting secondary control factors other than retinal hemorrhage in the development ofretinal traction bands. 1. INTRODUCTION The ability to damage the retinal nerve fiber layer (NFL) by laser exposure has not been widely recognized, although first reported by Frisch et al and recognized more recently in both human laser accident cases and in long term evaluation of acute laser retinal damage effects in non human primates (5), In all of these investigations damage to the retinal NFL is apparent in both ascending (Wallerian )and descending directions. Wallerian degeneration extends to through the optic nerve and presumably the forth order neuron, the lateral geniculate; descending neural degeneration travels from the retinal injury site back to the third order neuron, the lateral geniculate. Frish et al. found a reduction lateral geniculate neurons following NFL damage in the nonhuman primate. The purpose of this investigation was to explore the early dynamics of retinal NFL injury with regard to the time course of the development of retinal NFL damage and the differential development of Wallerian and descending portions ofthe retinal NFL injury. 2. METhODS An air cooled multiline Argon laser was used to make retinal lesions in the nonhuman primate retina. Single Argon laser exposures at 1 sec. 150 microns retinal spot size, at 300 mwatts Exposures were made in one rhesus monkey retina at three locations within the retinal arcades. Ophthalmoscopy was conducted immediately before and after retinal laser exposure. Followup measurements were made in roughly 1 to two week intervals over a period of six months. Both conventional and Scanning Laser Opthalmoscopy (SLO) were employed in acute and long term lesion evaluation. SLO evaluation involved both spectral in the visible and near IR as well as confocal evaluation 5) 3. RESULTS Figure 1 shows three Argon laser lesions at 1 hour after exposure. The lower lesion (lesion site 1) has a central confined retinal hemorrhage with surrounding edema. The region between this lesion and the optic disk shows evidence of retinal NFL disturbance indicated by possible NFL swelling and dark banding in this region as well.. Lesion site 2 shows a central white opacity with little or no NFL alteration. The exposure energy at this site was compromised by an iris occlusion at the time of exposure. Lesion site 3 shows a similar white lesion with some evidence of NFL alteration in both directions from the lesion site. Figure 2 shows a low and high magnification (2X) comparison of lesion site 1. The region between the lesion and the optic disk reveal shows evidence of both swelling and dark banding. Figure 3 was imaged 5 days post exposure showing a well defined diffuse like region of retinal NFL alteration at lesion site 1 in the ascending direction (Wallerian) and a somewhat less evident region in the descending region, toward the retinal ganglion cell layer or third order neuron. Similar alteration in the NFL is observable at lesion site 3; little or no alteration in the NFL is observable at lesion site 2. Figure 4 shows lesion site1 at one hour and at five days post exposure. At five days post exposure, the ascending portion of the NFL degeneration appears as a sheath of diffuse nerve fiber debris in close proximity to a retinal vessel passing into the optic disc. Figure 5 shows four 330 / SPIE Vol /951$6.OO

confocal images of lesion sites 3 and 1; the right upper image (lesion site 3) is at the retinal NFL level and shows a thicker arcuate region of NFL alteration than that shown at the right, where the

2 confocal images of lesion sites 3 and 1; the right upper image (lesion site 3) is at the retinal NFL level and shows a thicker arcuate region of NFL alteration than that shown at the right, where the confocal plane was more posterior revealing more of Figure 1 SLO low magnification (40 degree field) 1 hour post-exposure. Figure 2. Lesion #1 post 1 hour comparison of low and high magnification image of retinal NFL loss. SPIE Vol

3 Figure 3. Conventional fundus photograph showing NFL sites marked as N. Figure 4.. Comparison of high magnification lesion site 1 at 1 hour post and 5 days post. S marks neural debris sheath. 332 ISPIE Vol. 2393

4 Figure 5. Four images showing NFL defects at lesion sites #3 (upper) and #1 (lower). Figure 6 High magnification view of NFL defect at lesion sites #3 (Wallerian portion). SPIE Vol / 333

5 Figure 7. Lesion site #1 and WallerianNFL defect. Figure 8. Fluorescein of lesion site 1 shows capillary pattern alteration in NFL defect. 334 / SPIE Vol. 2393

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the underlying retinal blood vessel. The left lower image shows the Wallerian portion of lesion site 1 at the NFL level vs. a more posterior view at the right.

7 the underlying retinal blood vessel. The left lower image shows the Wallerian portion of lesion site 1 at the NFL level vs. a more posterior view at the right. The NFL debris still obscures the retinal vessel in this image as opposed to that shown in the upper right.. Figure 6 is a close up view of Wallerian NFL debris of lesion site 3 in conjunction with the retinal vessel. This image shows that the nerve fiber debris is independent of the vessel with several diffuse whitish areas emanating along this debris channel. Lesion site 2 is observable with two thin connections to the optic disk. These connections appear similar but small to the debris channel just described for lesion site 3. Figure 7 shows the Wallerian portion of the NFL defect between lesion site 1 and the optic disk This region of debris appears thicker than that observed at either sites 3 or 2 with a discrete entiy point into the optic disk. A corresponding Fluorescein image shows a marked alteration in the retinal capillaiy pattern corresponding to the NFL debris channel (Figure 8). Figure 9 shows lesion site 1 with traction bands emanating from it. These traction bands became prominent at two weeks post exposure and disappeared about 2 months post exposure. Figure 9 was taken at 2 months post exposure showing little or no evidence of retinal traction but significant darkening of the nerve fiber layer in both directions for all lesion sites. A complete ring of retinal NFL degeneration is obvious emanating from both lesions sites 1 and 3 in both Wallerian and descending directions from the lesion sites. Lesion site 2 also shows evidence of mild retinal NFL alteraüon, evidenced by short, thick dark bands emanating in both directions from the lesion site. 4. DISCUSSION In this study we have detailed the early development of laser induced NFL damage. Our observations indicate that the descending portion ofthe NFL retinal injuiy is slower to develop than the ascending or Wallerian portion probably because the descending portion of the injury involves ganglion cell death The ascending or Wallerian portion of the NFL injuiy develops within 5 days post exposure. This more rapid development may occur because this portion of the axon has been cut off from its cell body, the retinal ganglion cell, initiating relatively immediate axonal degeneration. The smooth globular appearance of this portion of the injury at 5 days suggests a loss of nerve fiber differention. as well as a sheath like structure containing neural "debris". A close association with the retinal vasculature is apparent from Figure 3, where the neural debris is observed to enter the optic disk in close proximity to a retinal vessel. The entrance of the ensheathed debris into the optic disk raises the distinct possibility that the ascending NFL injury might extend into the optic disk and into the lateral geniculate neuronal level of the ascending visual pathway. Furthermore, the alteration in capillaiy perfusion associated with the ascending injuiy site suggests that the ascending neural degenerative process may involve the release of trophic factors influential in the control of the micro-vascular network in the retina as well as in that of the optic disk and higher visual centers. In previous investigations of retinal NFL injury, retinal traction bands were often observed. Similarly in this study, traction emanating from the impact zone oflesion 1 to the macular region and lesion site 2 became prominent within 2 to 6 weeks post exposure, and resolved nearly completely by 8 weeks post exposure. As in previous investigations, these traction bands were imaged more prominently in the anterior retina within the retinal NFL layer, unlike previous investigations, their appearance was transient, suggestive of control factors other than retinal hemorrhage.8 The functional effects of retinal NFL damage have been shown to effect peripheral visual fields (4) as well as macular function. Long wavelength sensitivity loss have been reported in human cases of optic neuritis 9as well as in animal studies of laser macular injuiy (5) Human clinical findings confirm the potential NFL disruption and visual field loss following retinal laser photocoagulation to at least four contiguous clock hours around the optic disc across the perimacular bundle00'. The injuiy reported here would also be complicated by retinal traction that might cause mechanical as well as central neural factor alteration to visual function. 5. REFERENCES 1. G.D. Frisch, P.D. Shawalulç and D.O. Adams "Remote nerve fiber bundle alterations in retina as caused by argon laser photocoagulation, "Nature, Vol. 248, pp , H.Zwick, B.E. Stuck, D.A. Gagliano, et al., "Two infonnative cases of Q-switched laser eye injury, "Presidio of San Francisco, Ca: Letterman Army Institute of Research, Institute ofresearch No E.E. Boidrey, H.L. Little, M. Flocks, and A. Vassiliadis. "A retinal eye injury due to industrial laser burns," Ophthalmology. Vol. 88, pplol-lo7, / SPIE Vol. 2393

8 4. A. Athalel, Y. Glovinsky, G. Treister, E. Bartov, M. Blumenthal, M. Belkin. "Long-term follow up of accidental parafoveal laser burns.", Retina. Vol. 13, pp , H2wick, Schuschereba, D.A. GagJianoB.E. Stuck et al, "Morphological and functional effects of induced laser retinal fibrosis," In S.T. Melamed,, Proceedings of Laser Applications in Ophthalmology, Europto Series, SPIE, VoL 2079, pp 20-43, }L Zwick D.J. Lund, D.A. Gagliaio, and BE. Stuck "Functional and ophtbalmoscopic observations in human laser accident cases using scanning laser ophthalmoscopy, "In: Parel, J.M., Ren, Q. (Et), Proceedings of Ophthalmic Technologies, SPIE, VoL 2126, pp , H Zwick, "Visual function changes associated with low-level light effects," Health Physics. VoL 56, pp , M. Hull and M. Bahr. "Differential regulation of JUN expression in rat retinal ganglion cells after optic nerve transection and during regeneration," Soc. Neurosci. Abstr., VoL 20, pp. 697, Mi. Klein, Personal communication, J. Francois and G. Verriest "Clssification et symptomatologie des dyschromatopsies acquises," Bull. Soc. Beige Ophthalmol. VoL 116, , 195Th. Keywords: Scanning laser ophtbalmoscopy, confocal, retinal nerve fiber layer, rhesus, retina,laser SP1E Vol /337

Photocoagulation of disciform macular lesions

British Journal of Ophthalmology, 1979, 63, 669-673 Photocoagulation of disciform macular lesions with krypton laser A. C. BIRD AND R. H. B. GREY From the Institute of Ophthalmology, Moorfields Eye Hospital,