Vol. 114, No. 5 Letters to The Journal eye. The patient would not consent to laser treatment at any time during his treatment course. Unfortunately, further bleeding oc­ curred, which resulted in a dense vitreous hem­ orrhage. The left eye was monitored conservatively for several months, but showed no sign of clearing. Visual acuity in the right eye improved during this time to 20/70. On Aug. 28, 1991, the patient underwent pars plana vitrectomy in the left eye. The surgical procedure proceeded fa­ vorably, but marked preretinal fibrosis, retinal pigment epithelial atrophy, and metaplastic subretinal tissue were evident in the macula. Early preoperative cataract demonstrated pro­ gression that ultimately required extracapsular cataract and anterior chamber intraocular lens implantation, which were performed on Dec. 11, 1991. On Jan. 23, 1992, best-corrected visual acuity was R.E.: 20/40 and L.E.: 20/300. There was no clinical sign of hemorrhage in the left macula, but there was distortion caused by preretinal fibrosis and metaplastic subsensory retinal tis­ sue. Focal arterial wall damage is the likely pre­ cursor of retinal artery macroaneurysms. The rarity of emboli as the cause of this damage is evident from previous reports of macroaneu­ rysms. Some additional cases in which an embolus is noted near a macroaneurysm could have a similar origin. Palestine, Robertson, and Goldstein 3 noted that only one of ten cases had an embolus nearby. Thus, it is likely that most are not caused by embolie disease. Of course, most macroaneurysms are detected because of symptoms of loss in visual acuity. The appear­ ance of the retinal artery before the onset of the symptoms is not known in most cases, and the potential for an undetected embolus to have preceded the macroaneurysm cannot be exclud­ ed. Emboli have been demonstrated to be the definite cause of a retinal artery macroaneu­ rysm in three cases, including the present one. 1 · 5 The lack of macroaneurysms as a subse­ quent development in the large series of retinal artery emboli described by Arruga and Sand­ ers4 implies that most macroaneurysms are at­ tributable to other causes. References 1. Lewis, R. A., Norton, E. W. D., and Gass, J. D. M.: Acquired arterial macroaneurysms of the retina. Br. J. Ophthalmol. 60:21, 1976. 643 2. Cleary, P. E., Kohner, E. M„ Hamilton, A. M, and Bird, A. C: Retinal macroaneurysms. Br. J. Oph­ thalmol. 59:355, 1975. 3. Palestine, A. G., Robertson, D. M., and Gold­ stein, B. G.: Macroaneurysms of the retinal arteries. Am. J. Ophthalmol. 93:164, 1982. 4. Arruga, J., and Sanders, M.: Ophthalmologic findings in 70 patients with evidence of retinal embo­ lism. Ophthalmology 89:1336, 1989. 5. Khalil, M., and Lorenzetti, M. D.: Acquired reti­ nal macroaneurysms. Can. J. Ophthalmol. 14:163, 1979. Nonbacterial Thrombotic Endocarditis and Cortical Blindness J a m e s A. R u s h , M . D . Department of Ophthalmology, University of South Florida College of Medicine. Presented at the IX International Neuro-Ophthalmological Symposium, Williamsburg, Virginia, June 30, 1992. Inquiries to James A. Rush, M.D., 508S Habana Ave., Suite 100, Tampa, Fl 33609. A 73-year-old man had a two-week history of stepwise painless progressive visual loss in both eyes. No focal nonvisual neurologic symp­ toms occurred; however, he experienced four weeks of headaches and two weeks of mild confusion. His medical history was unremarka­ ble. Visual acuity was R.E.: 20/200 and L.E.: counting fingers at 2 feet. He identified none of the ten City University color plates with either eye. Pupillomotor responses were brisk without afferent defect in both eyes. Results of the examination of the ocular fundi were normal bilaterally. Computed perimetry showed abso­ lute superior altitudinal field loss with involve­ ment of fixation, along with moderate genera­ lized depression inferiorly in both eyes. Results of a left superficial temporal artery biopsy and bilateral carotid ultrasonograms were normal. Cranial magnetic resonance images showed a lesion in the left occipital lobe of mixed signal, suggesting hemorrhage, and mild gyral en­ hancement of the right occipital cortex (Fig. 1). Progressive confusion and weight and appetite loss resulted in hospitalization and death 11 days later. A chest x-ray film disclosed a left upper lobe infiltrate found on autopsy study to be a mucin-secreting pulmonary adenocarcinoma. Nonbacterial thrombotic endocarditis was present on the aortic and mitral valves, as well 644 November, 1992 AMERICAN JOURNAL OF OPHTHALMOLOGY Fig. 2 (Rush). Axial autopsy section through occipi­ tal cortex shows round area of hemorrhage in the left occipital lobe and bilateral calcarine cortical infarc­ tions. Fig. 1 (Rush). T 2 -weighted image shows the round hypointense lesion in the left occipital lobe and mild gyral enhancement of the right occipital cortex. as in b o t h posterior cerebral a r t e r i e s , a n d caused m u l t i p l e systemic infarctions, i n c l u d i n g t h o s e i m a g e d on m a g n e t i c r e s o n a n c e scans (Fig- 2). Occipital stroke is insufficiently r e c o g n i z e d as a cause of visual loss in p a t i e n t s w i t h cancer in w h o m n o n b a c t e r i a l t h r o m b o t i c e n d o c a r d i t i s d e v e l o p s . As m a n y as 8 5 % of p a t i e n t s w i t h nonbacterial thrombotic endocarditis have un­ derlying t u m o r s , especially m u c i n - s e c r e t i n g a d e n o c a r c i n o m a s of the lung a n d p a n c r e a s . 1 U n d e t e c t a b l e by cardiac a u s c u l t a t i o n a n d con­ v e n t i o n a l e c h o c a r d i o g r a p h y b e c a u s e of their smaller size, the friable fibrin-platelet excres­ cences frequently e m b o l i z e to t h e m i d d l e cere­ bral arteries a n d cause n o n v i s u a l stroke, w h i c h m i g h t b e the initial clinical s y m p t o m of c a n ­ cer. 2 H o m o n y m o u s h e m i a n o p s i a with ipsilateral sensory 3 or motor 4 deficits h a s b e e n r e p o r t e d , b u t occipital visual loss w i t h o u t focal n o n v i s u a l n e u r o l o g i c s y m p t o m s , as in this case, m i g h t b e the earliest s y m p t o m . Nonbacterial thrombotic endocarditis should b e c o n s i d e r e d in any stroke p a t i e n t in w h o m a source of emboli c a n n o t be found. As a r e m o t e effect of cancer o n the visual system, its early d e t e c t i o n m i g h t lead to l i f e - p r o l o n g i n g a n t i c o ­ agulation.5 References 1. Barron, K. D., Siqueira, E., and Hirano, A.: Ce­ rebral embolism caused by non-bacterial thrombotic endocarditis. Neurology 10:391, 1960. 2. Biller,J., Challa, V. R., Toole, J. F., and Howard, V. J.: Non-bacterial thrombotic endocarditis. A neu­ rologic perspective of clinicopathologic correlations of 99 patients. Arch. Neurol. 39:95, 1982. 3. Case 41491, Case Records of the Massachusetts General Hospital. N. Engl. J. Med. 253:1030, 1955. 4. Case 36-1991, Case Records of the Massachu­ setts General Hospital. N. Engl. J. Med. 325:714, 1991. 5. Rogers, L. R., Cho, E.-S., and Posner, J. B.: Ce- Vol. 114, No. 5 Letters to The Journal 645 rebral infarction from non-bacterial thrombotic en­ docarditis. Clinical pathological study including the effects of anticoagulation. Am. J. Med. 83:746, 1987. Visual Recovery After Radiation Therapy of Orbital Lymphoma Darius M. M o s h f e g h i , B.S.E., Paul T. Finger, M.D., Ronald B. Cohen, M.D., Woomyung C h o e , M.D., and Thorn Smilari, M . D . Department of Ophthalmology, Division of Ocular Tumor and Orbital Disease, North Shore University Hospital-Cornell Medical College (D.M.M., P.T.F., R.B.C.); Department of Radiotherapy, South Nassau Community Hospital (W.C.); and Department of Pa­ thology, North Shore University Hospital-Cornell Medical College (T.S.). Inquiries to Paul T. Finger, M.D., Division of Ocular Tumor and Orbital Disease, North Shore University Hospital-Cornell University Medical College, 300 Community Dr., Manhasset, NY 11030. An 84-year-old white man with glaucoma had a history of transitional cell carcinoma of the urinary bladder, disseminated well-differ­ entiated lymphocytic follicular lymphoma, and squamous metaplasia of the prostate. On Dec. 5, 1991, the patient had visual acuity of R.E.: 20/25 and L.E.: 20/30 (ascribed to nuclear sclerotic cataracts). On Jan. 6, 1992, he returned because of decreased vision in his left eye. Ophthalmic examination then disclosed visual acuity of R.E.: 20/30 and L.E.: no light perception. Applanation tensions were 16 mm Hg in both eyes. His pupils were miotic and nonreactive as the result of pilocarpine thera­ py. Both exotropia and exophthalmos were not­ ed in his left eye. Hertel exophthalmometry showed 5 mm of proptosis at 16 mm in the right eye and 21 mm in the left eye, with a base diameter of 95 mm. Slit-lamp biomicroscopy disclosed edema of the left upper eyelid. Computed axial tomography of the left orbit showed an ovoid area of soft tissue 3.0 cm long and 18 mm wide surrounding the left optic nerve and extending to the orbital apex (Fig. 1). Intratumoral microcalcifications were noted. Because of the patient's desire to have pros­ tate surgery, he was first examined in consulta- Fig. 1 (Moshfeghi and associates). Computed axial tomography shows a 3.0 x 1.8-cm tumor surround­ ing the optic nerve in the left eye (arrow). tion on Jan. 30, 1992. Visual acuity was R.E.: 20/40 and L.E.: no light perception. Results from an ultrasonically guided fine-needle aspi­ ration biopsy of the left orbital tumor were consistent with small cell malignant orbital lymphoma (Fig. 2). Fifty-one days after documentation of the patient's loss of light perception in his left eye, external beam radiotherapy was initiated. Through a paired wedge technique, a 4 x 5-cm field, and 6-MEV photons, our patient received a total dose of 36 Gy (18 fractions of 200 cGy over a period of 24 days). Two weeks later, visual acuity was L.E.: 2 0 / 40. The patient had normal ocular motility and decreased eyelid edema. Indirect ophthalmoscopy showed no evidence of maculopathy, vasculopathy, or optic neuropathy. Three months after treatment Hertel exophthalmometry showed symmetry at 16 mm in both eyes with a base diameter of 95 mm. Though the patient's visual acuity had stabilized at 20/40 in both eyes, relative optic nerve pallor was noted in the left eye. Orbital lymphomas are the most common malignant orbital tumors and account for 10% of tumors of the orbit and adnexa. 1,2 Though these tumors are relatively radiosensitive (as was illustrated by our case),3·4 it was remarkable that our patient started treatment 51 days after the first documentation of no light perception in the involved eye, and recovered to 20/40. This case suggests that when orbital lympho-