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Show 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 |