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Show 140 LITERATURE ABSTRACTS Progressive Visual Loss Caused by an Arachnoidal Brain Cyst in a Patient with an Optic Nerve Coloboma. Rosenberg LF, Burde RM. Am J OphthalmoI1988; 106: 322- 5 ( Sept). [ Reprint requests to Dr. R. M. Burde, Department of Ophthalmology, Montefiore Hospital, 111 East 210th Street, Bronx, NY 10467.] An adult patient with an optic nerve coloboma had gradual visual loss over years in this eye with decreased acuity and visual field. Computerized tomography demonstrated a probable arachnoid cyst anterior to the right temporal lobe in the right middle cranial fossa, which was evacuated and subtotally resected. The authors discuss this first report of colobomatous optic nerve occurring with arachnoidal brain cyst and point out the need for investigation when a patient with what should be a stable optic nerve abnormality develops visual loss. Lyn A. Sedwick, M. D. Afferent Pupillary Defect Caused by Hyphema. Striph GG, Halperin LS, Stevens JL, Chu Fe. Am J Ophthalmol 1988; 106: 352- 3 ( Sept). [ Inquiries to Dr. G. Striph, Department of Ophthalmology, Washington University School of Medicine, Box 8096, 660 South Euclid Avenue, St. Louis, MO 63110.] The authors described two children with dense, total, or near- total hyphema, who initially had an afferent pupillary defect (" marked" in one) that resolved to normal vision and, at least in one, normalization of pupil responses. The authors comment that total hyphema may act more to block light than diffuse it and although severe retinal or optic nerve damage may be coexistent, causing the pupil signs, patients with total hyphema may guardedly be encouraged about possible visual outcome even when an afferent defect is seen. Lyn A. Sedwick, M. D. Diabetic Superior Division Oculomotor Nerve Palsy. Bregman OK, Harbour R. Arch Ophthalmol 1988; 106: 1169- 70 ( Sept.) [ Reprint requests to Dr. J Clin Neuro- ophthalmol, Vol. 9, No. 2, 1989 D. K. Bregman, Ophthalmology Service, Walter Reed Army Medical Center, Washington, DC 20307- 5000.] A 68- year- old man with diabetes had the acute onset of right ptosis and a right supraduction deficit worse in abduction, which resolved in 8 weeks. The authors note that this palsy of the superior division of the third cranial nerve can be caused by a variety of lesions, including vasculopathic. Lyn A. Sedwick, M. D. Oblique Muscle Palsies Fixating with the Paretic Eye. Dickey CF, Scott WE, Cline RA. Surv Ophthalmol 1988; 33: 97- 107 ( Sept- Oct). [ Reprint requests to Librarian, Department of Ophthalmology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242.] This review discusses findings in patients who have superior oblique or inferior oblique muscle palsies who prefer fixation with the paretic eye and hence show not only secondary deviation but also " inhibitional palsy of the contralateral antagonist." Three- step testing, ductions versus versions, and forced ductions may help to solve the dilemma of which muscle is truly palsied. This is a nice review but no new insights are presented. Lyn A. Sedwick, M. D. Current Concepts of the Pathogenesis of Optic Neuritis Associated with Multiple Sclerosis. Sergott RC, Brown MJ. Surv Ophthalmol 1988; 33: 10816 ( Sept- Oct). [ Reprint requests to Dr. R. e. Sergott, Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, PA 19104.] These authors discuss current evidence of " viral, cell mediated, and antibody- induced etiologies of MS ( multiple sclerosis) and optic neuritis." It is an easily read article that comes to no specific conclusions but presents the information intelligibly. Lyn A. Sedwick, M. D. |