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Show Jounull of CIiPliCQI Neuro-ophthalmology 7(1): 49-57, 1987. Literature Abstracts Anterior Optic Nerve Blood Flow Decreases in Clinical Neurogenic Optic Atrophy. Sebag J, Deloria FC, Feke GT, Goger 0, Fitch K, Tagawa H, Deupree 0, Weiter JJ, McMeel JW. Ophthalmology 1986;93:858-65 (June). [Reprint requests to J. Sebag, M,D., Library, Eye Research Institute, 20 Staniford St., Boston, MA 02114.] Nine patients with unilateral "neurogenic" optic atrophy (secondary to optic neuritis or compression of the optic nerve) were studied with noninvasive laser Doppler and disk reflectometry, The techniques are explained in detail, but are not understood easily by the casual reader. Basically, they measure blood speed and volume. In all cases, speed and volume were reduced in the temporal part of the abnormal optic nerve compared to the normal fellow eye, and less striking differences were seen in the nasal optic nerve. The authors believe their techniques may have clinical application in the assessment of early optic nerve damage in glaucoma; however, this seems an optimistic prediction. Lyn A. Sedwick, M.D. Magnetic Resonance Imaging of Craniopharyngioma. Johnson LN, Hepler RS, Yee RD, Frazee JG, Simons KB. Am J Ophthalmol 1986;102:242-4 (Aug). [Reprint requests to Robert S. Hepler, M.D., Jules Stein Eye Institute, 800 Westwood Plaza, Los Angeles, CA 90024.] An interesting patient is presented who had visual field loss, first nasally in the right eye, but later an incongruous left homonymous hemianopia, and ultimately sudden visual loss in the right eye over 14 months' time. Two computerized tomographic scans showed no lesion, but metrizamide computed tomography and magnetic resonance imaging demonstrated a lesion that proved to be a craniopharyngioma. The authors note that such tumors may be missed even with high resolution views of the sella and parasellar space on computerized tomography, but are identified 49 © 1987 Raven Press, New York easily on T2-weighted magnetic resonance scans because of their hyperintensity. Lyn A. Sedwick, M.D. Treatment of Facial Spasm with Botulinum Toxin. Frueh BR, Musch DC. Ophthalmology 1986;93:917-23 (July). [Reprint requests to Bartley R. Frueh, M.D., W. K. Kellogg Eye Center, 1000 Wall St., Ann Arbor, MI48105.] These authors give a follow-up report on 48 patients with hemifacial spasm or blepharospasm treated over 2 years' time with botulinum toxin injections. Their data are tabulated in easy-to-read tables and show, for example, the following: how many needed repeat injections; who was "cured" following the second or third or fourth injection; the length of the follow-up; the time to recurrence; and a breakdown of complications for each series of injections (i.e., after the third injection of 25 units/lid, 11 of 14 patients had side effects, four with exposure keratitis, eight ptosis, seven diplopia, etc.). They also measured lid force and found that injections reduced force from a normal level of about 150 g to about 20-30 g (even if the injection was unsuccessful in relieving spasm!), and clinical recurrence occurred with recovery of lid force to about 60-70 g. They make observations regarding lid force, the role of ancillary lid protractors, and the number of side effects related to the size of the botulinum dose. It certainly is a pity to see yet another nice article on the use of botulinum toxin for both hemifacial spasm and blepharospasm, considering that one cannot currently act on this further knowledge due to the unavailability of Oculinum. Lyn A. Sedwick, M.D. Perimetric Findings in Pseudotumor Cerebri Using Automated Techniques. Smith Tj, Baker RS. Ophthalmology 1986;93:887-94 (July). [Reprint |