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Show i\;. 19116 Raven Press. New York Papilledema in Traumatic Lesion of Optic Nerve with Amaurosis Riri S. Manor, M.D., Shimon Cohen, M.D., Eduardo Svetliza, a.p., and Isaac Ben Sira, M.D. A patit?nt with subdural ht?matoma and right amaurosis resulting from traumatic injury to the optic nerve developed papilledema in both eyes a few days after the trauma. This was.interpreted as supplementary proof of the existence of axonal flow in the first weeks after incurrence of the optic axon lesion. In the amaurotic eye, the papilledema was less pronounced and disappeared more rapidly (after 3 wet?ks, as opposed to 6 weeks for the other eye). The nerve fiber layer disappeared between 4 and 6 weeks after the trauma. From the Unit of Neuro-Ophthalmoillgy, Dt!partment of Ophthalmology, Beilinson Medical Center, Petah Tiqva, Sackler School of Medicine, Tel Aviv University, Israt?1. Address corrt.>spondence and reprint rt.>quests to Dr. R. S. Manor at N~~ro-Ophth~lmologyUnit, Department of Ophthalmology, Belhnson Medical Center. Petah Tiqva 49100, Israel. !OO Conditions that change the normal pressure differential at the primate optic nerve head, i.e., increased intraocular pressure, ocular hypotony, or raised intracranial pressure, were experimentally found to induce axoplasmic transport stasis and papilledema (1-5). This experimental work in nonhuman primates is consistent with the clinical observation that an atrophied optic nerve having no more axonal flow will not develop axoplasmic flow stasis-related papilledema. We had the opportunity to observe a patient with unilateral amaurosis resulting from optic nerve injury who developed, a few days after the trauma, bilateral papilledema due to increased intracranial pressure and subdural hematoma. This case is of interest because it provides supplementary proof of the dynamics ofaxoplasmic flow during the first 3 weeks following axonal injury. CASE REPORT A 24-year-old man fell from a height while at work. Upon examination, he was conscious, but there were multiple contusions of the body as well as a hematoma of the right lids. Motility of the right eye was markedly limited in all directions and the right pupil showed an amaurotic reaction. Visual acuity was 20/20 in the left eye, with no light perception in the right eye. The intraocular pressure was normal. The appearance of the fundi was normal. X-ray films of the skull revealed a right frontoparietal fracture. The electroencephalogram showed a slow disturbance, more pronounced on the right side. Three days later, the patient complained of a severe headache and at this time examination revealed a blurring of both disc margins with some edema of the discs, more prominent on the left side (Fig. 1). Computed tomography demon- PAPiLLEDEMA IN AMAur~OTlCEYE FIG. 1. Narrow-band (540 nm) green-light stereoscopic photography of the fundus 1 week after the head injury. Top: Amaurotic right eye. There is strong blurring of optic disc margins and bulging. The nerve fiber layer appears normal. Bottom: left eye, The area of disc edema appears to be larger and the bUlging more prominent than in the right eye. 101 strated the presence of a sma II Sli bJ ur,ll IWIll.ltoma located bilaterally in the frontoparil'l.ll rl'gion. The ventricles appeared small. Thl' p<ltil'nt received appropriate medical treatment. Ell'vl'n days after the head injury, the blurring of th~ disl' margins and edema of the right disc had lessl'n~d. whereas the left disc showed the same degree of edema (Fig. 2). Temporal to the right optic disc there were some choroidal folds seen. The clinical pidll1'l' illlpnl\'l'd, ,1I1d .3 \V~t'ks "fter the head injury tIll' l'dl'lll,l of the ri~ht disc had completely dis.'ppl'Ml'd whik in thl' left disc it still persisted, tlH1u~h to .1 Il's5l'r dl'~rl'e. At this time, the nerve fibl'r layer W,lS still present in the right amaurotic l'yl' (Fig. 3). althou~h some toss of papillomacular bundll' wuld be observed. Six weeks after tht' hecld injury, there was a total disappl'arance of the nerve fiber layer in the right I Clil/ Nt'll'tl·""I,lImllllol. V",. 6. No.1. 1986 102 R. S. MANOR £T AL. FIG. 2. Narrow-band (540 nm) green-light stereoscopic photography of the fundus 11 days after the head injury. Top: Amaurotic right eye. The blurring of disc margins and the bulging are less pronounced. There are some choroidal folds seen temporally from the disc area. Bottom: Left eye. Note that there is no lessening of the edema. eye, with evolving optic atrophy. In the left eye, the border of the optic disc also became sharper (Fig. 4). DISCUSSION Experimental and clinical studies relating to the transection of optic nerve axons (6-12) indicate that "the entire length of individual axons seems to degenerate simultaneously as early as three I C/in Nturo'ophthalmol, Vol. 6. No.2. 1986 weeks and as late as six weeks after injury" (7). Quigley et al. (7) found in two squirrel monkeys that, 2 weeks after transection of the optic nerve, the amount and pattern of slow axonal transport were no different from normal, whereas 3 weeks after transection they became abnormal. Three weeks after transection the population of ganglion cells was also seen to decrease, a process terminating 6 weeks after transection with the disap- PAPILLEDEMA IN AMAUROTIC EYE FIG. 3. Narrow-band (540 nm) green-light stereoscopic photography of the fundus 3 weeks after the head injury. Top: Amaurotic right eye. There is no disc edema. The nerve fiber layer is still present. although some deletion of papillomacular bundle fibers seems evident. Bottom: Left eye. Note the lessened but still present disc edema. 103 pearance of the nerve fiber layer and the ganglion cells. Lundstrom and Frisen (9) described a case of descending optic atrophy in a man after a suicide attempt; there was also bilateral papilledema, but this was of slight degree and was present from the first examination after trauma. It was of interest that the papilledema disappeared in the third week after trauma, as would be expected from the above-noted experimental work, in which normalcy of axonal flow was demonstrated only up to this point. In the case described by Lundstrom and Frisen, however, the papilledema also disappeared from the sound eye after 3 weeks, an event that can be interpreted as coincidental with the decrease in intracranial pressure. In our case, the bilateral papilledema appeared a / Clin Nturo-ophllullmol. Vol. 6, No.2, 1986 104 R. S. MANOR ET AL. FIG. 4. Narrow-band (540 nm) green-light stereoscopic photography of the fundus 6 weeks after the head injury. Top: Amaurotic right eye. Note total disappearance of the nerve fiber layer. Bottom: Left eye. The optic disc margin is again sharp. few days after the traumatic lesion of the right optic nerve and was due to a subdural hematoma. The development of right papilledema seems to prove that there had been an obstruction in the still-existing axonal flow in the injured nerve. The asymmetry of the papilledema in our case, I eli" Nrurc>-op/!Iholmol. Vol. 6. No.2. 1986 less prominent in the right eye, raises a number of questions. Could this have been merely an asymmetrical papilledema without any particular significance? Is it possible that if the perioptic sheath was injured, it had a lesser capability for transmitting the increased intracranial pressure? Or could PAPILLEDEMA IN AMAUROTIC EYE 105 it have been that the axonal flow was quantitatively somewhat impaired even in the first wl'ck after the axonal lesion? Whatever the answer to these qUl'stions, the papilledema persisted in the sound l'yl' but dis"ppeared from the amaurotic eyt' aftcr .1 wl'eks, thl' timing of which coincides ex,lCtI~! with thl' d,,'wlopment of abnormal axon"I flow ,lS dl'munstr,ltl'd in the experimental work of Quiglt,y l't <11. (7). When the papilledem" dis,lppeclrl'd fmm thl' right eye. there was onl~' <1 slight rl'lhICtion of papillomacular fibers seen. The m,lssive dis,lppearance of all of the nerw fiber I"yl'r occurred later. between the fourth and sixth weeks "fter the trauma. The present case therefore appears to support the supposition that in a damaged optic axon there is a cumulative effe·ct of impaired axonal flow on the metabolism of the cell. which eventually results in cell death. REFERENCES 1. Iso, K. O. M., and Fine, B.S.: Electron microscopic study of human papilledema. Alii. I. OplJllmlllwl. 82: 424-434, 1976. 2. Minckler. D. 5., Tso. M. O. M.. and Zimmerman, L. E.: A light microscopic autoradiographic stud~' uf a"oplasmic transport in the optic nerve head during ocular hypotony, inCrl'.lSl'd inlr,lIll"ulclr pressure and papilledema. Alii. ,. OI'/llllIIllIIfl/. 82: 741-7S7, 1976. 3. Minckk'r, D. S., and Bunt, A. H.: Axoplasmic transport in ll<:uIM hypotony and p.lpillcdcma in the monkey. Arclr. 0l'lJIlttlllll"l. 95: 1431J-143n, 1977. 4. Tso, M. O. M., and H.lyreh. S. 5.: OptiC disc edema in r.lisl·d intr,Krilnial pressurl'. IV axuplasmic transport in expl'riml'ntal papilll'dem'l. An'll. 0l'lItltnlll,,'/. 95: 1458-1462. 11l77. S. R.ldius, R. L., Schwartz, E. L., and Anderson. D. R.: f.lilurl' uf unilatl'ral carotid drtery ligation to affect pres· surl··inducl'd intl'rruptinn uf rapid axunal transport in pri· m.ltl' uptil" nl'n'l·S. /"'~'';1. Ol'lItlm/III"/. 19: 153-157, 1980. h. Andl·rsun. D. R.: Ascending and dl'sn'ndin/; optic atrophy produl"l'd l'xpl'riml'ntally in squirrl'l monkt'ys. Alii. ,. 0/,lIllml",,'/. 76: 793. I1l73. 7. Qui~lcy. tl. A.. Dilvis, E. Bo, and Andcr~on, D. R.: De· scending opli{- nl'rve de~cncratjlln in primate". 1I11'<'sl. O"lIl1ml",,,/. V;';WI/ $,1. 16: /loll, 1977. 1:1. Radius, R. Lo, and Andl'rson, D. R.: Retinal ganglion ct'll degeneration in experimental optic atrophy. Alii. /. 01'11tlral""'/. 86: 673, 1971:1. 9. Lundstrom, M., and Frisen. L.: Evolution of descending optic atrophy: a case report. Acln Opllti/alllloi. 53: 738, 1975. 10. Bell. F. C, and Behrens. M. D.: Observation of retinal nen'e fiber degeneration after optic nerve injurv. In N<'lIro,' pllt/lt/I",n/flgl/, J. S. Glaser. Ed. C V. Mosb}', St. Louis. 1977, pp. 207-214. 1I. Enoksson, Po, and Johansson. J. 0.: Altitudinal field defects and retinal nerve fibre degeneration in optic nen'e lesion. Actn Op//Illt/I",o/. 56: 957, 1978. 12. Manor, R. 5 .• Svetliza, E.. Reichenthal. E.. Yassur. Y.. Shalit, M.• and Ben Sira, I.: Ocular changes in invasive ostl'ogenic sarcoma l,f the skull. AJlJI. Oplll/lt/IIJlt'l. 16: 68. 1984. I Clin Nruro-ophlhall/lo/. Vol. 6, No.2. 1986 |
