Correspondence
Vol. 110, No. 1
drochloride in all probability can now be added to this list. The National Registry of Drug-Induced Ocular Side Effects appreciates reports from clinicians of suspected drug-induced or chemicalinduced ocular side effects. Without these, this report would not have occurred.
References 1. Pearlman, J. T., Kadish, A. H., and Ramseyer, J. c.: Vision loss associated with amantadine hydro-
chloride use. lAMA 237:1200,1977. 2. Postma, l. D., and van Tilburg, W.: Visual hallucinations and delirium during treatment with amantadine (Symmetrel). Am. J. Psychiatry 136:111, 1979. 3. Fraunfelder, F. T.: Drug-Induced Ocular Side Effects and Drug Interactions, ed. 3. Philadelphia, Lea and Febiger, 1989. 4. Bleidner, W. E., Harmon, J. B., Hewes, W. E., Lynes, T. E., and Hermann, E. c.: Reported amantadine present in a saliva sample 30 hours after dosing at a concentration approximating that in blood. J. Pharmacol. Exp. Ther. 150:484, 1965. 5. Hayden, F. G., Minocha, A., Spyker, D. A., and Hoffman, H. E.: Reported amantadine concentrations present in nasal mucus at 1, 4, and 8 hours after dosing. Antimicrob. Agents Chemother. 28:216, 1985.
6. Ubels, J. L., and MacRae, S. M.: Vitamin A is present in retinol in the tears of humans and rabbits. Curro Eye Res. 3:815, 1984.
Correspondence Correspondence concerning recent articles or other material published in THE JOURNAL should be submitted within six weeks of publication. Correspondence must be typed double-spaced, on 81/2 x Ll-inch bond paper with 1 V2-inch margins on all four sides and should be no more than two typewritten pages in length. Every effort will be madeto resolve controversies between the correspondents and the authors of the article before publication.
Anatomy of Arteriovenous Crossings in Branch Retinal Vein Occlusion EDITOR:
In the article, "Anatomy of arteriovenous crossings in branch retinal vein occlusion," by D. Weinberg, D. G. Dodwell, and S. A. Fern
97
(Am. J. Ophthalmol. 109:298, March 1990), the authors describe the occurrence of venous overcrossings at two of 82 vein occlusion sites. They did not consider that those two cases might not have been overcrossings. I have observed the development of a bridge-type overcrossing collateral at a branch vein undercrossing obstruction site. The angiegraphic appearance was identical to that depicted in the article and termed, by the authors, as an overcrossing obstruction. I believe it remains to be proven that venous obstruction develops to any significant degree at an overcrossing. W.
_ _ _ _ _ _ _ Reply EDITOR:
REX HAWKINS, M.D.
Houston, Texas
_
We appreciate Dr. Hawkins's interest in and comments on our article. Based on a previous observation, he proposes that the two cases that we reported as branch retinal vein occlusions at venous overcrossings could actually represent occlusions at arterial overcrossings, with secondary bridging venous collaterals. Although we cannot categorically dismiss this possibility, we are confident of our observations and have scientific evidence to support our conclusions. Vein-to-vein collaterals form because of expansion of preexisting capillary channels.' In experimental branch retinal vein occlusions, these collaterals were seen to originate from capillaries deep in the retina.' This information is inconsistent with the development of a collateral vessel bridging over a large artery, which lies in the superficial layers of the retina. We would be most interested to see the case Dr. Hawkins described. If it evolved as he states, an alternate mechanism of collateral formation must be considered. Clemmetr' reported the appearance of a branch retinal vein occlusion at a venous overcrossing three weeks after the onset of symptoms. It would be unusual for such a welldeveloped collateral to form in such a short time. If Dr. Hawkins's argument is correct, it does not contradict our basic assertion that branch vein occlusion at venous overcrossings are rare. The question is whether or not branch retinal vein occlusions ever occur at venous
Vol. 110, No. 1
drochloride in all probability can now be added to this list. The National Registry of Drug-Induced Ocular Side Effects appreciates reports from clinicians of suspected drug-induced or chemicalinduced ocular side effects. Without these, this report would not have occurred.
References 1. Pearlman, J. T., Kadish, A. H., and Ramseyer, J. c.: Vision loss associated with amantadine hydro-
chloride use. lAMA 237:1200,1977. 2. Postma, l. D., and van Tilburg, W.: Visual hallucinations and delirium during treatment with amantadine (Symmetrel). Am. J. Psychiatry 136:111, 1979. 3. Fraunfelder, F. T.: Drug-Induced Ocular Side Effects and Drug Interactions, ed. 3. Philadelphia, Lea and Febiger, 1989. 4. Bleidner, W. E., Harmon, J. B., Hewes, W. E., Lynes, T. E., and Hermann, E. c.: Reported amantadine present in a saliva sample 30 hours after dosing at a concentration approximating that in blood. J. Pharmacol. Exp. Ther. 150:484, 1965. 5. Hayden, F. G., Minocha, A., Spyker, D. A., and Hoffman, H. E.: Reported amantadine concentrations present in nasal mucus at 1, 4, and 8 hours after dosing. Antimicrob. Agents Chemother. 28:216, 1985.
6. Ubels, J. L., and MacRae, S. M.: Vitamin A is present in retinol in the tears of humans and rabbits. Curro Eye Res. 3:815, 1984.
Correspondence Correspondence concerning recent articles or other material published in THE JOURNAL should be submitted within six weeks of publication. Correspondence must be typed double-spaced, on 81/2 x Ll-inch bond paper with 1 V2-inch margins on all four sides and should be no more than two typewritten pages in length. Every effort will be madeto resolve controversies between the correspondents and the authors of the article before publication.
Anatomy of Arteriovenous Crossings in Branch Retinal Vein Occlusion EDITOR:
In the article, "Anatomy of arteriovenous crossings in branch retinal vein occlusion," by D. Weinberg, D. G. Dodwell, and S. A. Fern
97
(Am. J. Ophthalmol. 109:298, March 1990), the authors describe the occurrence of venous overcrossings at two of 82 vein occlusion sites. They did not consider that those two cases might not have been overcrossings. I have observed the development of a bridge-type overcrossing collateral at a branch vein undercrossing obstruction site. The angiegraphic appearance was identical to that depicted in the article and termed, by the authors, as an overcrossing obstruction. I believe it remains to be proven that venous obstruction develops to any significant degree at an overcrossing. W.
_ _ _ _ _ _ _ Reply EDITOR:
REX HAWKINS, M.D.
Houston, Texas
_
We appreciate Dr. Hawkins's interest in and comments on our article. Based on a previous observation, he proposes that the two cases that we reported as branch retinal vein occlusions at venous overcrossings could actually represent occlusions at arterial overcrossings, with secondary bridging venous collaterals. Although we cannot categorically dismiss this possibility, we are confident of our observations and have scientific evidence to support our conclusions. Vein-to-vein collaterals form because of expansion of preexisting capillary channels.' In experimental branch retinal vein occlusions, these collaterals were seen to originate from capillaries deep in the retina.' This information is inconsistent with the development of a collateral vessel bridging over a large artery, which lies in the superficial layers of the retina. We would be most interested to see the case Dr. Hawkins described. If it evolved as he states, an alternate mechanism of collateral formation must be considered. Clemmetr' reported the appearance of a branch retinal vein occlusion at a venous overcrossing three weeks after the onset of symptoms. It would be unusual for such a welldeveloped collateral to form in such a short time. If Dr. Hawkins's argument is correct, it does not contradict our basic assertion that branch vein occlusion at venous overcrossings are rare. The question is whether or not branch retinal vein occlusions ever occur at venous
