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Show LITERATURE ABSTRACTS 253 A 55-year-old man with esophageal carcinoma was found to have an isolated inferior rectus palsy. Magnetic resonance scan demonstrated a brainstem lesion of the third nerve nucleus, although computerized tomography did not show this lesion, and autopsy verified a subnuclear metastasis. Kudos to the persistent resident, Dr. Pusateri, who obtained the autopsy, which demonstrated the first reported pathologically verified isolated inferior rectus palsy secondary to a subnuclear lesion as prophesied by Warwick and others. Lyn A. Sedwick, M.D. Retinal Venous Sheathing in Optic Neuritis. Lightman S, McDonald WI, Bird AC, Francis DA, Hoskins A, Batchelor JR, Halliday AM. Brain 1987;110:405-14 (April). [Reprint requests to Professor W. 1. McDonald, Institute of Neurology, National Hospital, Queen Square, London WClN 3BG, England.] The authors studied 50 patients presenting with acute optic neuritis for retinal vascular abnormalities and cells in the media. They noted abnormalities in 14 patients (fluorescein leakage in 10, perivenous sheathing in six, and cells in the vitreous in six and in the anterior chamber in four). After a mean follow-up of 3.5 years, multiple sclerosis developed in eight of 14 patients with vascular abnormalities and/or evidence of inflammation and in five of 32 without. The authors suggest that sheathing of retinal vessels observed ophthalmoscopically is the visible sign of perivascular lymphocytic infiltration and accompanying edema. Since this perivascular cuffing occurs in the retina in a region free of myelin or oligodendrocytes, they argue that the primary events leading to demyelination occur at the vascular endothelium. Although the authors offer an interesting hypothesis on the pathogenetic significance of perivascular cuffing, they do not offer an explanation of why their patients with vascular abnormalities and/or evidence of inflammation should have a higher incidence of documented multiple sclerosis at the end of their study. Presumably, the same pathogenetic process is occurring in the optic nerves of both groups. It is not clear why the presence or absence of intraocular vascular abnormalities and/or inflammation should have implications for the development of a generalized systemic disease such as multiple sclerosis. Walter M. Jay, M.D. Symptoms of Amaurosis Fugax in Atherosclerotic Carotid Artery Disease. Goodwin JA, Gorelick PB, Helgason CM. Neurology 1987;37:829-32 (May). [Reprint requests to Dr. C. M. Helgason, Department of Neurology, University of Illinois at Chicago, 912 S. Wood Street, Room 855-N, Chicago, IL 60612.] Two major causes of transient monocular visual loss are atherosclerotic amaurosis fugax and retinal migraine. Differentiating between the two is important, in that the former may be surgically treated whereas the latter usually is approached with medications. Traditionally, amaurosis fugax is said to last only a few minutes and scintillations or other positive visual phenomena are rare. Retinal migraine, on the other hand, is said to last between 15 and 60 min and commonly exhibits positive visual phenomena. In the present study the authors evaluated 37 patients with amaurosis fugax and angiographic evidence of carotid atherosclerosis unilateral to the symptomatic eye. Nearly one-third had long attacks or positive visual phenomena, episodes previously thought to be more typical for retinal migraine. Clearly, there is considerable overlap in the clinical pictures of atherosclerotic amaurosis fugax and retinal migraine. The authors emphasize the importance of appropriate diagnostic workups (carotid duplex scanning or angiography) in middle-aged and elderly patients with transient visual loss, even when the clinical picture might seem more compatible with retinal migraine. Walter M. Jay, M.D. I Clill Neuro-ophthalmol. Vol. 7. No.4. 1987 |