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Show Journal of Clinical Neuro- ophthalmology 8( l); 61--{ j5, 1988. Literature Abstracts Persistent Strabismus Presenting After Cataract Surgery. Catalano RA, Nelson LB, Calhoun JH, Schatz NJ, Harley RD. Ophthalmology 1987; 94: 4914 ( May), [ Reprint requests to Dr. L. B. Nelson, Wills Eye Hospital, Department of Pediatric Ophthalmology, 9th and Walnut Streets, Philadelphia, PA 19107.] Persistent Binocular Diplopia After Cataract Surgery. Hamed LM, Helveston EM, Ellis FD. Am J OplztlzalmoI1987; 103: 741- 4 Oun). [ Reprint requests to Dr. E. M. Helveston, Department of Ophthalmology, Indiana University Medical Center, Indiana Lions Eye Care Center, 702 Rotary Circle, Indianoplis, IN 46223.] In the first article, eight patients are discussed who experienced persistent diplopia following cataract surgery, one combined with trabeculectomy. In all cases, superior rectus bridle sutures were used and the combined procedure also used an inferior rectus bridle suture. Six patients had retrobulbar anesthesia and two general anesthesia. An intraocular pressure- reducing device was used in three patients. Detailed discussion of each case is given as well as a concise summary table. The authors conclude that direct trauma to and scarring of the rectus muscles vis- a- vis bridle sutures is the etiology of most postcataract surgery diplopia, not myopathy from anesthetic agents or hypoxia from the intraocular pressure reducer. The second article discusses 38 patients with diplopia following cataract surgery. These 38 are not presented in detail and it is interesting to contrast the conclusions reached by these authors. First, they found 10 categories of muscle imbalance including superior oblique palsy presurgery, superior oblique palsy postsurgery, childhood exotropia and esotropia, and skew, with the largest category being " idiopathic." Second, they doubt that bridle suture injury usually plays any role in the diplopia as ( a) only two of the 38 patients had superior rectus paresis evident on ductions and ( b) many postoperative hyperdeviations were oppposite to the operated eye. Catalano et aL would probably reply that bridle sutures can cause either scar or palsy and result in hypo- or 61 ,. 1988 Raven Press, Ltd, New York hypertropia ( as their cases demonstrate). It is hard to completely reconcile the disparate conclusions reached by these authors. A larger series in the paper by Catalano et ai. and more complete discussion of the cases in their intrasurgical findings ( those who underwent strabismus surgery) for the paper by Hamed et ai. would help the confused reader come up with a firm take- home lesson about strabismus postcataract surgery. LYIl A. Sedwick, M. D. Posterior Ischemic Optic Neuropathy During General Surgery. Rizzo JF III, Lessell S. Am JOphthalmol 1987; 103: 808- 11 Oun). [ Reprint requests to Dr. J. F. Rizzo III, 243 Charles Street, Boston, MA 02114.] Two patients are described who awoke from general anesthesia with profound or total visual impairment. Neither patient initially or subsequently had optic nerve edema and both patients developed optic atrophy, in one patient asymmetric with partial visual recovery in the eye with less atrophy. Both were anemic and sustained moderate blood loss intraoperatively and one patient had two documented periods of hypotension intraoperatively. The authors conclude that these are cases of posterior ischemic optic neuropathy and contrast this entity to " shock- induced" optic neuropathy, which purportedly will result in glaucoma- like cupping as well as segmental or total optic disk pallor. Also their patients noted blindness immediately postanesthesia, not several days later as has bee'n previously reported with pe~ ioperative posterior ischemic optic neuropathy. LYIl A. Sedwick, M. D. Ocular Symptoms of Moyamoya Disease. Noda S, Hayasaka S, Setogawa T, Matsumoto S. Am J Ophtlwlmol 1987; 103: 812- 6 0un). [ Reprint requests to Dr. S. Noda, Department of Ophthalmology, Shi- |