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Show LETTERS TO THE EDITOR Tonic Pupil as the Presenting Sign of Relapsed Acute Myeloid Leukemia A 23- year- old woman complained of photophobia, lacrimation, and redness of the left eye of 1 week's duration and a dilated left pupil. Acute myeloid leukemia ( AML) had been diagnosed 5 years earlier and treated with a stem cell transplant. She had developed graft vs host disease ( GVHD) affecting her skin and had undergone psoralen plus UVA ( PUVA) treatment. The AML had been in remission for 3 years before her ophthalmic visit. Medications included acyclovir, fluconazole, penicillin, cyclosporine, and mycophenolate. Systemic corticosteroid treatment had recently been discontinued. Best- corrected visual acuities were 20/ 20 in the right eye and 20/ 40 in the left eye, improving to 20/ 30 with pinhole. In the left eye, the palpebral fissure was slightly narrow but with normal levator function, the tear break- up time was reduced, and there was punctate staining of the cornea. The pupils measured 2 mm in the right eye and 4 mm in the left eye in minimal illumination. On bright light stimulation with the indirect ophthalmoscope light, the right pupil constricted to 1 mm and the left remained at 4 mm. After stimulation by a near target the left pupil also constricted to 1 mm. The left eye showed vermiform movements of the iris on slit lamp examination. Dilute pilocarpine ( 0.125%) was then instilled in both eyes. After this both pupils measured 2 mm, demonstrating hypersensitivity of the left pupil. She was orthophoric and had a full range of ocular movements. Posterior subcapsular lens opacities were present in both eyes. Ophthalmoscopy was normal. The punctuate epitheliopathy of the cornea was attributed to GVHD and the cataracts to the use of systemic corticosteroids. Left tonic pupil was diagnosed. Lubricants were prescribed for the epitheliopathy. Two days later, she returned complaining of blurred vision. Best- corrected visual acuities were 20/ 80 in the right eye and 20/ 40 in the left eye. There was no change in the anterior segment findings of either eye. Ophthalmoscopy showed localized elevation of the retina in the macular region in both eyes. B scan ultrasound showed thickening and irregular elevations of the choroid in both eyes ( Fig. 1). Fluorescein angiography showed pinpoint areas of hyper-fluorescence of increasing brightness in the macular region of both eyes. Blood tests showed an elevated white cell count, indicating relapse of leukemia. Brain and orbit MRI showed only faint mucosal thickening of the sinuses. Chemotherapy was begun. The leukemia could not be controlled, and she subsequently died of systemic complications. Tonic pupil can be caused by Adie syndrome, systemic neuropathic diseases, or local lesions ( 1). Adie syndrome is characterized by tonic pupil and disturbance of deep tendon reflexes without evidence of local ocular or orbital disease or generalized peripheral or autonomic system dysfunction. Orbito- ocular causes of tonic pupil include inflammation, infection, or infiltration that affects ciliary ganglion or the ciliary nerves in the retrobulbar region or in the suprachoroidal space. Tonic pupil has been reported in siderosis caused by retained intraocular foreign body ( 2); injury to the final cholinergic fibers within the suprachoroidal space was postulated as the likely pathologic mechanism. Postganglionic denervation by damage within the suprachoroidal space has also been reported with retinal detachment surgery using explants ( 3) and after laser photocoagulation for diabetic retinopathy ( 4). Leukemia can cause tonic pupil by direct infiltration of the orbit or the choroid. However, postganglionic nerve injury at the level of the eye in choroidal cancer has been reported only once ( 5). In our patient, there was no imaging evidence of orbital infiltration at presentation. The ultrasound study showed extensive choroidal thickening and irregularity. The fluorescein evidence of pinpoint leaks and serous retinal detachment indirectly indicated dysfunction of the retinal pigment epithelium. A similar phenomenon FIG. 1. B scan ultrasound of the left eye shows thickening and irregularity of the choroid ( arrowhead) and overlying serous retinal detachment. 310 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Letters to the Editor J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 caused by choroidal infiltration has been reported ( 6). Hence it is likely that the damage to the ciliary nerves occurred at the suprachoroidal level. Mandagere R. Vishwanath, FRCSEd Stephen J. Charles, MA, MD, FRCOphth Manchester Royal Eye Hospital Manchester, United Kingdom m. vishwanath@ virgin. net REFERENCES 1. Thompsons HS, Miller NR. Disorders of pupillary function, accommodation, and lacrimation. In: Miller NR, Newman NJ. Walsh and Hoyt's Clinical A'euro- Ophthalmology, Vol 1, 5th ed. Baltimore: Williams & Wilkins; 1998: 977- 8. 2. Weiss MJ, Hofeldt AJ, Behrens M, et al. Ocular siderosis: diagnosis and management. Retina 1997; 17: 105- 8. 3. Newsome DA, Einaugler RB. Tonic pupil following retinal detachment surgery. Arch Ophthalmol 1971; 86: 233^ k 4. Lobes LA Jr, Bourgon P. Pupillary abnormalities induced by argon laser photocoagulation. Ophthalmology 1985; 92: 234- 6. 5. Liegl O, Kohn K. Zur pathogenese der pupilotonie. Klin Monatsbl Augenheilkd 1962; 140: 324- 38. 6. Miyamoto K, Kashii S, Honda Y, et al. Serous retinal detachment caused by leukemic choroidal infiltration during complete remission. Br J Ophthalmol 2000; 84: 1318- 9. [CLcataractsurgery] Generalized Myasthenia Gravis Triggered by Cataract Surgery There have been many case reports describing onset of myasthenia gravis ( MG) after cardiac surgery ( 1- 3) and after administration of neuromuscular blocking agents in preparation for surgery ( 4). We describe a patient in whom severe generalized MG developed immediately after cataract surgery, requiring thymectomy and long- term immunosuppressive therapy. A 52- year- old right- handed white man developed progressive weakness 1 day after outpatient cataract surgery on the right eye. His past medical history was significant for insulin- dependent diabetes treated with an insulin infusion pump. He had diabetic peripheral neuropathy. Before surgery, he reported no other neurologic symptoms. The cataract surgery was uncomplicated, and routine topical analgesics had been applied on the eye before the procedure. The patient noticed nothing unusual until he removed the eye patch the day after surgery and experienced diplopia followed by bilateral ptosis. Over the next 2 weeks, he noted progressive fatigue and limb weakness. A Tensilon test performed 3 weeks after surgery showed subjective and objective strength improvement, and pyridostigmine and prednisone were started. One week later, he developed neck weakness and difficulty swallowing and was hospitalized. On admission, he had 4 mm of ptosis bilaterally. The right eye had no movement in any direction. The left eye had 80% adduction and abduction and full vertical duc-tions. He was hoarse and had difficulty swallowing liquids. He had 4/ 5 weakness in distal and proximal muscles. His reflexes were 1 + throughout. Plantar reflexes were flexor. Sensory signs included bilateral decreased temperature, vibration, and joint position sense distal to the knees. Results of laboratory studies were negative for acetylcholine receptor binding and blocking antibody, anti- striated muscle antibody, anti- muscle- specific tyrosine kinase ( MuSK) antibody, serum cytomegalovirus ( CMV) IgG and IgM, and anti- ganglioside GDI a IgG and IgM antibody. Results of a paraneoplastic workup were negative. A chest CT scan was negative for thymoma, and cerebrospinal fluid ( CSF) showed a red blood cell count of 0, white blood cell count of 1, glucose of 157 mg, and protein of 89 mg. Slow repetitive nerve stimulation ( 3 Hz) of the bilateral median nerve at rest and 1 minute after exercise showed compound muscle action potential ( CMAP) amplitude decrements of 35% and 20%, respectively, consistent with a diagnosis of neuromuscular junction disorder. The baseline CMAP amplitude was normal without an incremental response of CMAP amplitude after 10 seconds of maximum isometric contraction, making it less likely to be a presynaptic condition. Sensory nerve action potentials were absent, indicating a polyneuropathy. Surprisingly, the patient had moderate to severely prolonged CMAP onset latencies with decreased conduction velocity in all extremities and preserved CMAP amplitudes, indicating a demyelinating polyneuropathy, which is unlike the findings seen in typical diabetic neuropathy. The patient was treated with a course of plasmapheresis and his bulbar symptoms improved. Three months after his initial symptoms, he underwent thymectomy, with the specimen showing normal thymic tissue. With 60 mg prednisone, 80 mg pyridostigmine 3 times/ day, and 250 mg mycophenolate mofetil 2 times/ day, he continues to have binocular oblique diplopia that is worse in up- and- left gaze and is ambulatory with minimal assistance. It is rare to identify a trigger for the onset of MG. With respect to cardiothoracic surgery ( 1- 3), it has been presumed that manipulation of thymic remnants provided a trigger for autoimmune damage. It is possible that damage induced during the surgical procedure could induce a new wave of autoantibody production that is not readily subject to immune regulation in susceptible individuals. A well- documented effect of neuromuscular blockade agents such as vecuronium, which are administered during tracheal intubation, is to unmask undiagnosed MG. The diagnosis is made when patients fail to maintain adequate 311 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Letters to the Editor spontaneous ventilation after the procedure ( 4,5). Subsequently, it is discovered that such patients have a history of ptosis, diplopia, dysphagia, dysarthria, fatigue, and weakness. We postulate that the cataract surgery itself or local anesthetics triggered an autoimmune response or aggravated a preexisting subclinical MG in this patient. Soma Sahai- Srivastava, MD Tina C. Lin, DO Department of Neurology, Los Angeles County and University of Southern California Medical Center Los Angeles, California sahai@ usc. edu REFERENCES 1. Resatoglu AG, Tok M, Yemisci M, et al. Autoimmune myasthenia gravis after coronary artery bypass surgery. Ann Thorac Surg 2006; 81: 725- 6. 2. Scopetta C, Onorati P, Eusebi F, et al. Autoimmune myasthenia gravis after cardiac surgery. J Neurol Neurosurg Psychiatry 2003; 74: 392- 3. 3. Sleeman K, Rajani R, Chabers J, et al. Autoimmune neurological disease after cardiac surgery. J Neurol Neurosurg Psychiatry 2004; 75: 1078- 9. 4. Dunsire MF, Clarke SG, Stedmon JJ. Undiagnosed myasthenia gravis unmasked by neuromuscular blockade. Br JAnaesth 2001; 86: 727- 30. 5. Bailey C, Menon G, Saxena H. An unusual first presentation of myasthenia gravis. Anaesthesia 2004; 59: 515- 6. Benztropine- induced Esotropia and Mydriasis We recently examined a patient with esotropia and dilated pupils who had received haloperidol and benztropine mesylate to treat Tourette syndrome. Immediate resolution of the esotropia and mydriasis after discontinuation of benztropine mesylate indicates a causal relationship. This is the first report of esotropia induced by anticholinergic medication. A 16- year- old girl who had pseudohypoparathyroidism and mild mental retardation began to take 3 mg haloperidol and 2 mg benztropine mesylate per day for a diagnosis of Tourette syndrome, which had manifested with involuntary vocalization, snorting, frequent troublesome motor behaviors, and occasional aggressive impulses. Five days after starting the medications, she experienced sudden dizziness, diplopia, and blurred vision. There was no preceding systemic or ocular infection or physical or psychic shock. She had no history of strabismus or visual dysfunction. Seven days after she started the medications, neuro-ophthalmologic examination revealed a visual acuity of 20/ 20 in both eyes, esotropia of 35 prism- diopters when fixating a distant ( 20- foot) target ( Fig. 1), and esotropia of 45 prism- diopters when fixating a near ( 14 inch) target. Refraction with cycloplegia showed no hyperopia. Ocular ductions and versions were full. Anterior and posterior segments were normal with clear and sharp disc margins in both eyes. Both pupils were enlarged at 7 mm and unreactive to light and near stimuli ( Fig. 2). The dilated pupils did not constrict in response to 0.1% or 1.0% solutions of pilocarpine eye drops ( Fig. 2). There were no other neurologic findings. Results of routine laboratory tests, including complete blood cell count, routine blood chemistry analyses, urinalysis, and chest x- ray, were negative. Brain and orbital MRI showed small symmetric calcifications of the basal ganglia. The benztropine mesylate was discontinued, and the diplopia, dizziness, and esotropia disappeared within 2 weeks. A follow- up ophthalmologic evaluation 2 months later disclosed no esodeviation by alternate cover tests, but a reduced fusional divergence amplitude of 4 prism-diopters ( normal 6- 8 prism- diopters). The pupils were normal in size and reactivity. Anticholinergic medications may cause dry mouth, bladder dysfunction, constipation, impaired cognition, and visual disturbance. With repeated doses of certain anticholinergics, reduction in the near point of accommodation has been reported ( 1). Benztropine mesylate, a tertiary amine muscarinic receptor antagonist frequently used to antagonize the parkinsonian side effects of antipsychotics, may impair accommodation and near visual acuity, especially when used with neuroleptics ( 1,2). Various anticholinergic drugs, including amitripty-line, oxybutynin, propantheline, and atropine, can cause pupillary dilatation ( 3). In children, topical anticholinergics increase the accommodative convergence- to- accommodation ratio transiently and exacerbate an underlying esotropia ( 4). FIG. 1. Comitant esotropia is present with distant fixation. 312 © 2007 Lippincott Williams & Wilkins Letters to the Editor J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 sf^*^*? « ^\ • . - ^ / * . I J ^ *=- S= « > /^ HPT^ ,£ pP" Moreover, esotropia may develop after anticholinergic eye drops without preexisting esotropia ( 5). The synkinetic near triad consists of accommodation, convergence, and pupillary constriction. The ratio of convergence to accommodation may increase with anticholinergics due to partial block of accommodation. To see a near target in the setting of blocked accommodation, children would increase accommodative effort, resulting in increased convergence. Too much convergence may cause esotropia. Nonetheless, the mechanism by which benztropine mesylate might cause esotropia remains unclear. The preserved ocular versions during the period of esotropia suggest that it was neither paralytic nor restrictive in origin. Furthermore, decompensation of a preexisting, well-compensated esotropia by benztropine mesylate seems unlikely because the patient never had a history of esotropia and showed orthophoria after discontinuing the medication. Increased intracranial pressure ( ICP) may produce divergence paralysis without evidence of a sixth cranial nerve palsy ( 6). However, our patient showed no symptoms or signs of increased ICP and had full ductions and versions. One possibility is that the esotropia in our patient was due to a temporary disruption of binocular function. The mydriasis in our patient is also interesting. Whereas systemically administered anticholinergics do not alter pupillary diameter in dogs ( 7), they may cause mydriasis in men ( 7). Failure of 0.1% and 1% pilocarpine drops to contract the pupils of our patient indicates that the iris sphincter had been blocked by an anticholinergic agent. The reason for the rare occurrence of esotropia in patients using anticholinergics remains unknown. The reduced fusional divergence amplitude, found after the resolution of mydriasis and esotropia in our patient, may be a prerequisite for development of esotropia when anticholinergics are used. Alternatively, because strabismus ( esotropia) is common in children with developmental disabilities, including mental retardation and cerebral palsy ( 8), the combination of Tourette syndrome and pseudohypoparathyroidism with mental retardation may have contributed to the occurrence of the ophthalmic manifestations in our patient. Sun- Young Oh, MD Byoung- Soo Shin, MD Department of Neurology Chonbuk National University Jeonju, Korea FIG. 2. Pupils are dilated in bright light ( left) and do not constrict after application of 1% pilocarpine ( right). Yeon- Hee Lee, MD Department of Ophthalmology Chungnam National University Daejeon, Korea Ae Young Lee, MD Chungnam National University Daejeon, Korea Ji Soo Kim, MD Seoul National University Seoul, Korea jisookim@ snu. ac. kr REFERENCES 1. Thaler JS. Effects of benztropine mesylate ( Cogentin) on accommodation in normal volunteers. Am J Optom Physiol Opt 1982; 59: 918- 9. 2. Isawa S, Murasaki M, Miura S, et al. Pharmacokinetic and pharmacodynamic interactions among haloperidol, carteolol hydrochloride and biperiden hydrochloride. Nihon Shinkei Seishin Yakurigaku Zasshi 1999; 19: 111- 8. 3. Hadjikoutis S, Morgan JE, Wild JM, et al. Ocular complications of neurological therapy. Eur J Neurol 2005; 12: 499- 507. 4. Christoferson KW, Ogle KN. The effect of homatropine on the accommodation- convergence association. AMA Arch Ophthalmol 1956; 55: 779- 791. 5. Good Wy Crain LS. Esotropia in a child treated with a scopolamine patch for drooling. Pediatrics 1996; 9"': 126- 7'. 6. Schanzer B, Bordaberry M, Jeffery AR, et al. The child with divergence paresis. Surv Ophthalmol 1998; 42: 571- 6. 7. Frischmeyer KJ, Miller PE, Bellay Y, et al. Parenteral anticholinergics in dogs with normal and elevated intraocular pressure. Vet Surg 1993; 22: 230^. 8. Feinberg M. The problems of anticholinergic adverse effects in older patients. Drugs Aging 1993; 3: 335^ 8. Idiopathic Intracranial Hypertension in a Transgender Man We report a case of idiopathic intracranial hypertension ( IIH) in a transgender man. To our knowledge, no such case has been described previously. A 3 3- year- old man presented to the neuro- ophthal-mology clinic at the University of Florida in January 2007. He was complaining of headaches and blurred vision. IIH had been diagnosed 8 months earlier, and he was treated 313 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Letters to the Editor FIG. 1. Optic disc edema is present in both eyes. with 1,500 mg/ day acetazolamide. He reported being a transgender woman- to- man who had undergone bilateral mastectomies and testosterone treatment that had been discontinued 18 months earlier. Our examination disclosed a patient who weighed 168 lbs with height of 5 feet 3 inches. Blood pressure was 118/ 72 mm Hg with a pulse of 84/ min. Best- corrected visual acuities were 20/ 15 in each eye. Color vision was normal by Ishihara plate testing. Ophthalmoscopy showed optic disc edema in both eyes ( Fig. 1). Humphrey visual fields showed nerve fiber bundle defects and enlarged blind spots in both eyes ( Fig. 2). Results of a CT angiogram with attention to the venous phase was normal. A lumbar puncture disclosed an opening pressure of 300 mm H20 with normal constituents. Because of side effects from acetazolamide, 80 mg/ day furosemide was substituted for acetazolamide. For headache control, he was treated with 150 mg/ day topiramate. On a follow- up 1 month later, visual field defects had improved. However, 2 months later, the visual field defects worsened, and he underwent an optic nerve fenestration in the right eye. One week postoperatively, visual field defects had improved in the left eye, but the right eye remained *:::::::: •.•.•..\.\.*:::::\ W& gEiiiii" FIG. 2. Humphrey visual fields show nasal defects and enlarged blind spots in both eyes. stable. On month later, visual field defects had improved in both eyes. IIH is found most commonly in overweight women in their reproductive years. It may also be caused by dural sinus thrombosis ( 5,6), a reduction in corticosteroid therapy, or hormonal imbalance ( 7- 10), vitamin A, anabolic corticosteroids, tetracycline, lithium, and pregnancy ( 11- 13). Our patient had prior use of testosterone. Despite the availability of transgender medicine for decades, we were unable to find a published report of IHH in patients who change gender. Clinton Sheets, MD Marc Peden, MD John Guy, MD Department of Ophthalmology University of Florida Gainesville, Florida j ohnguy @ eye . ufl. edu REFERENCES Lee AG, Brazis PW. Case studies in neuro- ophthalmology for the neurologist. Neurol Clin 2006; 24: 331^ 5. Binder DK, Horton JC, Lawton MT, et al. Idiopathic intracranial hypertension. Neurosurgery 2004; 54: 538- 51. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension. Neurology 2002; 59: 1492- 5. Banik R, Lin D, Miller NR. Prevalence of Chiari I malformation and cerebellar ectopia in patients with pseudotumor cerebri. J Neurol Sci 2006; 247: 71- 5. Friedman DI. Cerebral venous pressure, intra- abdominal pressure, and dural venous sinus stenting in idiopathic intracranial hypertension. J Neuroophthalmol 2006; 26: 61^ k Lin A, Foroozan R, Danesh- Meyer HY et al. Occurrence of cerebral venous sinus thrombosis in patients with presumed idiopathic intracranial hypertension. Ophthalmology 2006; 113: 2281^ 4. Balasubramanian S, Shivbalan S, Ganesh R. Pseudotumor cerebri following oral betamethasone for common cold. Indian J Pediatr 2005; 72: 994. Toscano Y Sancesario G, Bianchi P. Cerebrospinal fluid estrone in pseudotumor cerebri: a change in cerebral steroid hormone metabolism? J Endocrinol Invest 1991; 14: 81- 6. 314 © 2007 Lippincott Williams & Wilkins Letters to the Editor J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 9. Donaldson JO, Binstock ML. Pseudotumor cerebri in an obese woman with Turner syndrome. Neurology 1981; 31: 758- 60. 10. Stiebel- Kalish H, Kalish Y, Lusky M, et al. Puberty as arisk factor for less favorable visual outcome in idiopathic intracranial hypertension. Am J Ophthalmol 2006; 142: 279- 83. 11. Tang RA, Dorotheo EU, Schiffman JS, et al. Medical and surgical management of idiopathic intracranial hypertension in pregnancy. Curr Neurol Neurosci Rep 2004; 4: 398^ 109. 12. Lee AG, Pless M, Falardeau J, et al. The use of acetazolamide in idiopathic intracranial hypertension during pregnancy. Am J Ophthalmol 2005; 139: 855- 9. 13. Bagga R, Jain Y Das CP, et al. Choice of therapy and mode of delivery in idiopathic intracranial hypertension during pregnancy. MedGenMed 2005; 7: 42. 14. Clements- Nolle K, Marx R, Katz M. Attempted suicide among transgender persons: the influence of gender- based discrimination and victimization. JHomosex 2006; 51: 53- 69. 15. Gorton RN. Health care and insurance issues for transgender persons. Am Fam Physician 2006: 74: 2022. 16. Newfield E, Hart S, Dibble S, et al. Female- to- male transgender quality of life. Qual Life Res 2006; 15: 1447- 57. Simultaneous Ischemic Optic Neuropathy and Third Cranial Nerve Palsy in Giant Cell Arteritis We report for the first time the concurrence of ischemic optic neuropathy and third cranial nerve palsy in a case of histologically proven giant cell arteritis ( GCA). An 87- year- old woman was admitted to the hospital with a 4- week history of pain on her scalp, under her chin, and in the occipital area and neck. In addition, she had jaw claudication, which gradually increased in intensity. One day earlier, the patient simultaneously developed sudden profound vision loss and ptosis of the right eye. She had lost the vision in the left eye many years earlier from direct trauma. Our examination revealed a best- corrected visual acuity of 20/ 200 in the right eye and no light perception in the left eye. The right pupil measured 5 mm in dim illumination and did not constrict to direct light. The left pupil was irregular, measured about 2.5 mm, and did not constrict to direct light. The right upper lid had 3 mm of ptosis. In the right eye, abduction was normal, but adduction, supra-duction, and infraduction were absent. Ophthalmoscopy of the right eye revealed mild optic disc swelling. Evaluation of the left eye could not be done because of the history of trauma. Pulsations of the right temporal artery were not palpable, and those of the left temporal artery were feeble. There was scalp tenderness. The erythrocyte sedimentation rate was 55 mm/ h ( normal value < 15 mm/ h), C- reactive protein ( CRP) was 8.3 mg/ L ( normal value < 6 mg/ L), and platelet count was 625,000/| JLL ( normal value 142,000- 424,000/| JLL). Brain MRI • • ' " FIG. 1. Histopathologic analysis of a temporal artery biopsy specimen shows an inflammatory infiltrate in the media and intimal fibrosis ( hematoxylin- eosin). was normal. On color duplex ultrasonography, no fluximetric alterations of carotid and vertebral arteries were seen. The following day, biopsy of the right temporal artery showed marked inflammation and intimal fibrosis ( Fig. 1). The media contained lymphocytes and giant cells. Fragmentation of the internal elastic lamina of the artery was evident. A diagnosis of giant cell arteritis was made and treatment with 50 mg oral prednisolone was started. Within a few days, the headache disappeared. The medication was continued at the same dose for 20 days, after which the dose was tapered. Three months after the corticosteroid treatment was started, the features of third cranial nerve palsy had disappeared except for a dilated unreactive pupil. The vision loss persisted. Impairment of the third, fourth, or sixth cranial nerves has been reported in only 2% of patients with GCA ( 1- 8). This case illustrates the fact that ischemic optic neuropathy and third cranial nerve palsy may be coincident manifestations of GCA. Cagatay Oncel, MD Neurology Department Pamukkale University Denizli, Turkey Ferda Bir, MD Pathology Department Pamukkale University Denizli, Turkey L. Sinan Bir, MD Neurology Department Pamukkale University Denizli, Turkey cagatayoncel@ yahoo. com 315 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Letters to the Editor REFERENCES 1. Caselli RJ, Hunder GG, Whisnant JP. Neurologic disease in biopsy- proven giant cell ( temporal) arteritis. Neurology 1988; 38: 352- 9. 2. Bondeson J, Asman P. Giant cell arteritis presenting with oculomotor nerve palsy. Scand J Rheumatol 1997; 26: 327- 8. 3. Loflredo L, Parrotto S, Violi F. Giant cell arteritis, oculomotor nerve palsy, and acute hearing loss. Scand J Rheumatol 2004 ; 33: 279- 80. 4. Day A, Malik N. Giant cell arteritis presenting as painful third nerve palsy. BrJHosp Med 2006; 67: 383. 5. Madge SN, Klys H, Twomey JM. Giant cell arteritis presenting as painful third nerve palsy with normal erythrocyte sedimentation rate. BrJHosp Med 2006; 67: 268. 6. Lazaridis C, Torabi A, Cannon S. Bilateral third nerve palsy and temporal arteritis. Arch Neurol 2005; 62: 1766- 8. 7. Polak P, Pokorny Y Stvrtina S, et al. Temporal arteritis presenting with paresis of the oculomotor nerve, and polymyalgia rheumatica, despite a low erythrocyte sedimentation rate. J Clin Rheumatol 2005; 11: 242^. 8. Lotery A, Best J, Houston S. Occult giant cell ( temporal) arteritis presenting with bilateral sixth and unilateral fourth nerve palsies. Eye 1998; 12: 1014- 6. 316 © 2007 Lippincott Williams & Wilkins [CLcataractsurgery] |