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Show J. Clill. Neuro-ophthalmol. 4: 141-142, 1984. Therapeutic Temporal Artery Biopsy To the Editor: I would like to briefly present for your consideration and review, a case history that is amazing and extraordinary. On September 13, 1983, I saw a 69-year-old white male who on September 12, 1983, noted a marked decrease in visual acuity in the left eye. This was sudden and nonprogressive. He had no complaints in the right eye. Past medical history revealed that the patient had a long history of adenocarcinoma of the colon that is presently in remission. He had a known history of systemic hypertension that was easily controlled with Dyazide. He had taken no other medication other than Dyazide. He had no known allergies to medicine and no prior history of eye disease, other than an aunt with adult onset diabetis mellitus. There is no other significant family history. Examination revealed a corrected visual acuity of 20/60 in the right eye, and 3/200 in the left eye. External examination revealed the globes and orbits to be quiet and white on each side. He had a marked decrease in color and brightness perception in the left eye. Pupillary examination revealed a +4 out of 4 positive swinging light test in the left eye. Motility examination was totally unremarkable. Visual fields were full in the right eye and full in the left eye peripherally, but a large central scotoma was noted centrally. Intraocular pressure was 20 mm Hg in each eye. Hertel exophthalmometry revealed no evidence of proptosis. There were no orbital or carotid bruits. Slit lamp examination was unremarkable except for modest lenticular opacities. There was a decrease in the amplitude of the pulsation of the left carotid artery, but no bruit was heard. Dilated examination of the fundi, including Goldmann three-mirror lens examination revealed an unremarkable retinal periphery in each eye. The posterior pole of the left eye revealed a translucent appearance of the retina with nerve fiber layer hemorrhage on the surface and at the edge of the superior left disc. There were few scattered macular hemorrhages in the superficial retina. There were no spontaneous venous pulsations on the left side, but spontaneous venous pulsations were present on the right side. The patient had a sedimentation rate of 81, by the Westergren method. A left superficial temporal artery biopsy was undertaken on September 15, 1983. At the time of ligation of the left superficial temporal artery June 1984 and before the skin sutures were applied, the patient exclaimed that his visual acuity in the affected eye had improved dramatically. At that time in the operating room, he was able to read fine print with the left eye. The biopsy of the left superficial temporal artery with multiple serial sections was negative for giant cell arteritis. The patient was seen again on September 16, 1983. At that time, his visual acuity in the left eye was 20/30 +2. There was a negative swinging light test on the left side. He had equal color and brightness perception. Digital subtraction angiography, undertaken on September 20, 1983, showed mild irregularities about the left carotid bifurcation. No evidence of high-grade stenosis was seen. The patient has maintained his visual acuity and has no complaints whatsoever. I consider this as an unusual and dramatic case report; to my knowledge, this is the first example of a therapeutic temporal artery biopsy. Robert A. Laibovitz, M.D. Austin, Texas Response: And now to the case of the millennium! The first assumption I am going to make about this man is that his problem has a vascular substrate. I also assume it is neither neoplastic nor traumatic. The vasculopathies obviously include aneurysms and arteriovenous malformations which seem to be ruled out easily, and the more pedestrian entities like central retinal artery or branch artery occlusion, venous obstructive processes, and ischemic optic neuropathies. The description of the fundus leaves me perplexed, but the lack of hemorrhages in the periphery and the absence of venous congestion would seem to make a central retinal vein occlusion ordinaire unlikely. In some ways, the description sounds like an arterial occlusive process, but perhaps with an excess of hemorrhages. I think that a fluorescein angiogram and fundus photographs would go a long way toward explaining the nature of the process responsible for the visual loss, and a late photograph and description of the fundus so we could know what the fundus looked like when "the smoke cleared" might be helpful. Unfortunately, we have none of these. Could some of the changes that were described have reflected subretinal accumulations of liquid perhaps related to a vascular choroidopathy? I will proceed on the assumption that this is not an 141 Letters to the Editor ordinary vein occlusion, aneurysm, or arteriovenous malformation, but that it could be any other kind of vascular process involving retina, optic nerve, or even choroid. I would then consider the events that occur when a temporal artery is biopsied. There are three possibilities. One is the position of the patient, the second is the obliteration of a patent artery, and the third is an injection of an anesthetic (probably containing epinephrine diluted 1-10,000). The position of the patient should not be the answer since one can assume that in the 72 hours following the accident he had other occasions to lie down for 10 minutes! The two possible explanations would seem to lie with either the anesthetic injection or the ligation of the artery. The next item to consider is whether this kind of reversibility of visual function occurring from a process in or near the eye is possible! First, I have seen several individuals who had amaurosis premonitory to ischemic optic neuropathy, central retinal artery occlusion, or ipsilateral carotid stroke that lasted for more than 12 hours. In one of these cases, a woman who went on to have an ipsilateral central retinal artery occlusion and carotid stroke, there was a period of transient blindness of the left eye that lasted 72 hours and which recovered fully prior to the final episode of central retinal artery occlusion. Evidence indicates that patients may have a remarkable capacity for recovery following some forms of transient blindness afflicting only one eye and of which the mechanism is presumably vascular. Further support for this view comes from the reports of visual urescuesN in some cases of central retinal artery occlusion treated many hours after the onset of blindness. There is also experimental evidence to indicate that the neural tissues of the eyes seem to have a great resistance to ischemia from work done on the brain and eyes of monkeys. Those experiments consisted or occluding the ascending aorta with a Blalock clamp for up to about 30 minutes. Providing that cardiac function was promptly restored, many monkeys survived 20 minutes or more of ischemia without incurring behavioral abnormalities or significant lesions in the eye or brain. Admittedly, none of these experiments used periods of ischemia in the range under consideration in the clinical cases described or in the patient in question, but they certainly proved the belief that several minutes of complete ischemia produced irreversible damage to neural tissue is wrong! What could the anesthetic injection have accomplished to restore vision? Evidence from various medical accidents indicates that injections in the soft tissues of the face and scalp occasionally reach the orbital circulation. This might have occurred, and either the epinephrine or the local anesthetic may have effected a salutary change in the vascular dynamics. Perhaps it alleviated vasospasm. Vasospasm was once commonly invoked as an explanation for transient neurological dysfunction and, while it seems out of vogue, medical thinking is sufficiently fickle to suspect that it might one day be accepted again. This is the only way in which I can think of crediting the anesthetic injection for the reversal of near blindness in this patient. How could the ligation of the temporal artery have accomplished the remarkable improvement in acuity? Ligating the temporal artery must cause a miniscule rise in pressure in the other vessels that stem ultimately from the common carotid artery on that side, but the change would be so small that it is hard to imagine it had any important effects on the circulation of the eye. It is easy to think of ways in which tying off the temporal artery might theoretically impair circulation to the eye, but impossible for me to generate anything beyond what I suggested to explain an improvement! Another possibility in this man is that his visual acuity had improved prior to the surgical procedure, and that for some reason he happened to become aware of the improvement at the time the artery was ligated. All of us are familiar with pseudo-sudden visual loss (the patient with a mature cataract in one eye who thinks his vision has gone suddenly because he chances to cover his other eye), but this may be an example of pseudo-sudden improvement. It may be that he improved shortly after being seen initially by Dr. Laibovitz and was not aware of the improvement. Dr. Laibovitz does not indicate whether his vision was checked immediately before the procedure was done. If that were the case, it would free us from having to explain how anesthesia or surgery helped him, but would not explain the underlying pathophysiology of the original loss of vision. Simmons Lessell, M.D. Lexington, Massachusetts Comment: I would publish Dr. Laibovitz's letter and Dr. Lessell's response together. From my own point of view, there is little doubt that this is an example of psuedo-sudden visual improvement. The description of the patient's retina, especially the glistening, suggests relative swelling of the ganglion cell layer, probably secondary to an ischemic event which had already passed at the time the patient was seen. During the subsequent 48 to 72 hours, the ganglion cells began to work, and the patient, when retested appropriately either by himself accidently or by Dr. Laibovitz, noticed that his vision had returned. Ronald M. Burde, M.D. St. Louis, Missouri Journal of Clinical Neuro-ophthalmology |