OCR Text |
Show Journal of Clinical Neuro-ophthalmology 7(2): 92, 1987. Editorial Comment Commentary on Ocular Toxicity Following Intracarotid Chemotherapy © 1987 Raven Press, New York Ocular toxicity was originally reported to have clinically occurred following BNCU infusion as a form of regional chemotherapy for recurrent gliomas. The acute toxicity consisted of discomfort in the area of the infusion (orbital) during the injection itself, with concurrent injection and edema of the orbital and periorbital structures for several days afterward. Some of the patients who received intracarotid BCNU infusions subsequently developed progressive loss of visual acuity, and funduscopic examination revealed changes most compatible with a vasculopathy of the retinal arterial vessels (1). Such visual loss rarely improved and often produced significant ipsilateral blindness, but at the same time was often tolerated by the patient provided the treatment was producing a significant response on the part of the intracranial glioma. We have attempted to study this phenomenon in a rat model, and have found that there are gross changes in the eye following carotid infusion with BCNU, which appear to be the counterpart of the orbital changes seen in the human. However, histological examination of the globes of these rats revealed that most of the histopathological changes took the form of changes in the choroid layer, with thinning of the photoreceptor and adjacent nerve cell layer, with no demonstrable changes in the retinal vessels (2). These observations in the rat retina may be the counterpart of the ciliary artery vasculopathy recorded by Purvin. Thus, carotid infusion of BCNU may lead to an ischemic vasculopathy of the retina, the ciliary artery circulation, or both. As serious as the loss of vision in one eye may be, even more potentially dangerous is the now recognized central neurotoxicity that may occur following intracarotid BCNU infusions in patients with gliomas, particularly if they are given concurrently with radiation therapy. The radiosensitizing characteristics of BCNU undoubtedly contribute heavily to the middle cerebral artery ischemic 92 vasculopathy that has been reported (3) and which had led to our own discontinuance of intracarotid BCNU concomitantly with radiotherapy. Incidentally, our own experience with over 30 cases of cisplatinum intracarotid infusion for recurrent gliomas (usually many months following radiation therapy) has been favorable from the standpoint not only of less ocular and neurotoxicity but also of equivalent or more effective antitumor response to treatment. When one applies intracarotid cisplatinum earlier in the course of treatment of these patients (prior to or during radiotherapy), it is prudent to observe very carefully for evidence of a radiosensitizing effect of cis-platinum upon the nervous system in the form of central neurotoxicity. Neuro-oncologists continue to tread a narrow path between potential antitumor effectiveness of radiotherapy and chemotherapy and the toxic effects of these treatments on normal nervous system structures. M. S. Mahaley, Jr., M.D., Ph.D Department of Surgery Division of Neurosurgery The University of Alabama at Birmingham Birmingham, AL REFERENCES 1. Grimson BS, Mahaley MS, Dubey HD, Dudka L. Opthalmic and central nervous system complications following intracarotid BCNU (carmustine). J Clin NeuroophthalmoI1981; 1:261-4. 2. EIHennawi Y, Mahaley MS. Retinopathic effects of single intracarotid BCNU injection in normal Fischer 344 rats. Neurosurgery 1987 (in press). 3. Mahaley MS, Whaley RA, Blue M, Bertsch L. Central neurotoxicity following intracarotid BCNU chemotherapy for malignant gliomas. JNeuro-OncoI1986;3:297-314. |