Journal of Neuro-Ophthalmology, December 1993, Volume 13, Issue 4

Recovery of vision in a 47-year-old man with fulminant giant cell arteritis.

Giant cell arteritis is a systemic necrotizing vasculitis that often causes profound and irreversible visual loss in elderly individuals. We describe a 47-year-old man with fulminant giant cell arteritis whose clinical picture included severe visual loss and several unusual or previously unreported findings. Aggressive treatment with intravenous corticosteroids resulted in a dramatic improvement in the patient's vision. Although no firm conclusions can be drawn from the outcome in a single case, we believe that, in some patients with arteritic ischemic optic neuropathy, aggressive treatment with intravenous corticosteroids may be associated with a better visual prognosis than treatment by the oral route.

Journal of Clinical Neuro-ophthalmology 13(4): 262-270, 1993. © 1993 Raven Press, Ltd" New York Recovery of Vision in a 47-Year-Old Man with Fulminant Giant Cell Arteritis Eric A. Postel, M.D. and Stephen C. Pollock, M.D. Giant cell arteritis is a systemic necrotizing vasculitis that often causes profound and irreversible visual loss in el­derly individuals. We describe a 47-year-old man with fulminant giant cell arteritis whose clinical picture in­cluded severe visual loss and several unusual or previ­ously unreported findings. Aggressive treatment with intravenous corticosteroids resulted in a dramatic im­provement in the patient's vision. Although no firm con­clusions can be drawn from the outcome in a single case, we believe that, in some patients with arteritic ischemic optic neuropathy, aggressive treatment with intrave­nous corticosteroids may be associated with a better vi­sual prognosis than treatment by the oral route. Key Words: Giant cell arteritis-Recovery-Orbital isch­emic syndrome. From the Neuro-ophthalmology Service, Duke University Eye Center, Durham, North Carolina, U.S.A. Address correspondence and reprint requests to Dr. Stephen C. Pollock, Duke University Eye Center, Box 3802, Durham, NC 27710, U.S.A. 262 Giant cell arteritis is a systemic necrotizing vas­culitis that primarily affects the branches of the aortic arch. Involvement of the ophthalmic circu­lation is common, resulting in permanent visual loss in up to 50% of patients (1). It typically strikes older Caucasians living in northern climates, and affects both sexes equally (1,2). The incidence of giant cell arteritis increases with advancing age. The mean age of onset is about 70 years (1) and the disease rarely develops before age 60, though cases of patients under 50 years old have been re­ported (3-7). The clinical presentation of giant cell arteritis is variable. Most affected individuals experience nonspecific constitutional symptoms, in many in­stances accompanied by headache, scalp tender­ness, myalgias, and jaw claudication. Of the seri­ous complications of giant cell arteritis, the most common is visual loss from ischemic infarction of the distal optic nerve. Central retinal artery occlu­sion and ischemic injury of the retrobulbar portion of the optic nerve also occur but are less common. Typically, the erythrocyte sedimentation rate (ESR) is markedly elevated. Pathologic examina­tion of affected arteries discloses inflammation and thickening of the vessel wall, fragmentation of the internal elastic lamina, and giant cells. Among patients with visual loss from giant cell arteritis, the prognosis for recovery of vision is generally poor (1,8,9,14,15). While corticosteroids promptly alleviate systemic symptoms and mark­edly decrease the risk of further visual loss, they usually have no effect on existing visual deficits. We recently evaluated a young man with fulmi­nant giant cell arteritis, profound visual loss, and a remarkable constellation of rare or previously un­reported findings. After treatment with intrave­nous corticosteroids, the patient recovered excel­lent visual acuity. RECOVERY OF VISION IN 47-YEAR-OLD MAN WITH GCA 263 CASE PRESENTAnON A 47-year-old Caucasian man was in his usual state of good health until June 28, 1992 when he experienced the rapid onset of chills, sweats, an­orexia, and loss of energy. He was evaluated by his local family physician who felt that he had sinusitis and an "ear infection," and treated him with oral guiafed and phenylpropanolamine. Shortly there­after, he began to lose weight and had one episode of vomiting. On July 1, he awoke with bilateral periorbital swelling, binocular diplopia, photosensitivity, and a headache that was associated with extreme ten­derness of both temples. The latter resolved over several days. He was again evaluated by his local physician and started on Nafazair A eye drops for a presumed "allergy." On July 5, he noticed par­esthesias and weakness of the thumb and first two fingers of his right hand. On July 7, 10 days after the onset of his initial symptoms, the patient experienced sudden loss of vision in his right eye and sought ophthalmologic care. An examination by a local ophthalmologist revealed a visual acuity of hand motion 00 and 20/50 as, nearly complete loss of the nasal hemi­field in the left eye (Fig. 1), a right afferent pupil­lary defect, and limited motility of the right eye. The fundus examination reportedly showed rou­leaux formation in the retinal vessels of both eyes. The patient was referred to the Duke Neuro­ophthalmology Service that day for an emergency evaluation. En route, he experienced two episodes of transient visual loss in his left eye. In each in­stance, the vision blacked out completely for 15-20 seconds and then gradually returned from the cen­ter outward over about 45 seconds. He denied other neurologic symptoms, jaw claudication, or proximal myalgias. The examination at Duke revealed a thin, 47­year- old man in no distress. Physical examination was normal except for his ocular examination, which revealed a visual acuity of hand motion 00 and 20/20-1 as. The results of color vision testing with the Hardy-Rand-Rittler plates were normal in the left eye. Confrontation visual fields revealed small central and temporal islands of preserved hand motion vision 00. Although the patient was able to count fingers briskly in all quadrants of his left eye, there was slight subjective desatura­tion of a red test object nasal to the vertical merid­ian. The right pupil was 7 mm and nonreactive to direct stimulation while the left pupil constricted from 5.5 mm to 3.5 mm slightly sluggishly. There was a pronounced right afferent pupillary defect. A 6-degree right hypotropia was present in the primary position and was associated with a mod­erate limitation of elevation and abduction on that side. External examination revealed markedly en­larged, nodular, and pulseless superficial temporal arteries. Carotid upstrokes were normal. Slit lamp examination showed moderate dilation of the epi­scleral vessels in both eyes, but otherwise quiet anterior segments. Intraocular pressures were 5 mmHgOU. Nomen: Dotum; FIG. 1. Goldmann visual field of the left eye obtained shortly after onset of visual loss. Note loss of most of the nasal hemifield. The 14 isopter re­spects the vertical meridian. mm [ 4 , odeblllldebull Et 1:"11U==o:==I] o ,V v 45 Cannella OS 00 _"he , I RlIlrocUo bO.50 3 II 1 e O,e3 2 111 4 d 0.80 1 IV 16 n 1.00 0 V B4 J Gin Neuro-ophtiullmol, Vol. 13. No.4, 1993 264 E. A. POSTEL AND S. C. POLLOCK Fundus examination of the right eye revealed pallid swelling of the optic disc (Fig. 2A), venous dilation, and slowly moving rouleaux in both the arterial and venous circulations. A pale intravas­cular plug was observed within the superotempo­ral branch retinal arteriole and was noted to move peripherally in a slow, pulsatile manner. The mac­ula was normal. In the left eye, the optic disc and retinal arterioles appeared normal (Fig. 2B), but the retinal venules were dilated and contained rouleaux. A presumptive diagnosis of giant cell arteritis was made and the patient was admitted to the Duke University Eye Center. Treatment with methylprednisolone 250 mg every 6 hours was started immediately. Laboratory studies obtained on the night of admission included an ESR (West­ergren) of 69 mm/h, a hemoglobin of 16 gldl, and a white blood cell count of 14,000/1J.1. Fluorescein angiography, performed in both eyes, showed delayed appearance of dye in the retinal arterioles of both eyes, aD > as, and a prolonged arteriovenous transit time; absent fluo­rescence of the right optic disc; markedly delayed choroidal filling and nonperfusion of the temporal hemichoroid au (Fig. 3); and late reconstitution of choroidal flow around the fovea in the left eye. A magnetic resonance imaging (MRI) of the brain and orbits obtained 1 day after admission revealed no intracranial pathology and patent in­tracavernous carotid arteries. However, orbital im­ages showed pronounced, bilateral loss of ana­tomic definition in the retrobulbar space, slight en­largement of all extraocular muscles, and diffuse soft tissue enhancement, findings consistent with ischemic necrosis and swelling of the orbital con­tents (Fig. 4). One day after the initiation of steroid therapy, a , elin Neuro-ophthalmol. Vol. 13, No.4. 1993 FIG. 2. Fifteen-degree fundus photo­graphs obtained at the time of initial presentation. A: Mild pallid swelling of the right optic disc. B: Normal ap­pearance of the left optic disc. RECOVERY OF VISION IN 47-YEAR-OLD MAN WITH GCA 265 A 9 FIG. 3. Fluorescein angiography. early arteriovenous phase. A: Right eye at 40.1 seconds. There is com­plete nonperfusion of the temporal choroid and absence of fluorescence of the optic disc. B: Left eye at 23.8 seconds. There is complete nonper­fusion of the temporal choroid. 4-cm segment of the right superficial temporal ar­tery was biopsied and submitted for pathologic ex­amination. This revealed transmural inflamma­tion, scattered giant cells, disruption of the inter­nal elastic lamina, and thrombosis of the lumen (Fig. 5). The findings were interpreted as pathog­nomonic for giant cell arteritis. Additional studies obtained included an ele­vated fibrinogen of 405 mg/dl (normal = 152-344 mg/dl), a CHso of 59 units/ml (normal = 25-51 units/ml), a protein C of 153% (normal = 60­108%), and a serum protein electrophoretic pattern consistent with inflammation. The following tests were normal or negative: serum electrolytes, FTA, hepatitis serology, antineutrophil cytoplasmic an­tibody (ANCA), disseminated intravascular coag­ulation (DIC) screen, lupus anticoagulant, creatine kinase, serum cryoglobulins, thrombosis panel (excluding protein C), urine electrophoresis, and chest radiograph. Urinalysis initially revealed mi­crohematuria (10-15 RBClHPF) without casts or protein. However, a repeat urinalysis obtained the following day was found to be normal. During his 4-day hospitalization, the patient was maintained on methylprednisolone 250 mg Lv. ev­ery 6 hours. The vision in his right eye fluctuated 1Clin Neuro-ophthalmol, Vol. 13, No.4, 1993 266 A E. A. POSTEL AND 5. C. POLLOCK FIG. 4. Magnetic resonance scan of the orbits, employing fat suppression technique and gadolinium. A: Coronal view, showing homogenization of signal and blurring of anatomic boundaries along with diffuse gadolinium enhancement. B: Normal scan for comparison. between light perception (LP) and hand motion, while that in his left eye remained stable at 20/15, with normal color vision and very mild constric­tion of the nasal visual field. His constitutional symptoms abated within 12 hours of his receiving the initial dose of steroids, and the ESR dropped from 69 to 40 and then to 12. Nerve conduction studies of the right median nerve were normal. The patient was discharged on prednisone 60 mg per day, one coated aspirin daily, and Zantac. One week later his vision was unchanged, ex-traocular movements had normalized, and intraoc­ular pressures were 13 OU. The diffuse conjuncti­val injection had disappeared, though mild epi­scleral venous dilation was still present. Fundus examination of the right eye revealed persistent pallid swelling of the optic disc and no intravascu­lar rouleaux. The left fundus appeared normal. One month later, visual acuity in the right eye had improved to 20/300. The right optic disc was markedly pale, and discrete geographic areas of pigment epithelial mottling consistent with prior JGin Neuro-ophthalmol. Vol. 13. No.4. 1993 FIG. 5. Right temporal artery biopsy demonstrating inflammation and thickening of the vessel wall, throm­bosis and obliteration of the lumen, and a giant cell (arrow) (hematoxylin and eosin; X40). RECOVERY OF VISION IN 47-YEAR-OLD MAN WITH GCA 267 choroidal ischemia were evident in both eyes. The dose of prednisone was tapered slowly over suc­ceeding months. Two months after discharge, visual acuity in the patient's right eye was 20/30. Formal perimetry disclosed marked irregular constriction of the field in that eye, albeit with preservation of a small paracentral island of 12 sensitivity. The field in the left eye was essentially normal (Fig. 6). By Decem­ber 1992, five months after the onset of ipsilateral blindness, an acuity of 20/25+ 2 OD was docu­mented. The patient remains otherwise asymp­tomatic, and repeat sedimentation rates have con­sistently been less than 6 mm/h. DISCUSSION Age Giant cell arteritis typically affects older individ­uals, with a mean age of onset of about 70 years (1). Although the disease rarely strikes before age 60, reports of giant cell arteritis in younger indi­viduals have occasionally appeared in the litera­ture (3-7,10-12). Some of these reports included patients who were less than 50 years old when symptoms developed (3-7,13). In several cases, however, the diagnosis of giant cell arteritis was not confirmed by biopsy (7,10), and it seems likely that at least some of these patients suffered from other illnesses. A careful review of the remaining "biopsy­proven" cases reveals that most of the patients in these reports had symptoms and signs that were highly atypical for giant cell arteritis. Shah (13) de­scribed a 41-year-old woman with left-sided scalp and periorbital pain, a normal ocular examination, and an ESR of 10. Bethenfalvey and Nusynowitz (3) described a 35-year-old man with constitutional symptoms and temporal headaches who had no visual complaints and was found to have a normal ESR. Bugg and colleagues (5) described 3 young patients with an "acute hand syndrome," and at­tributed the condition to giant cell arteritis in each case. None of these individuals had any visual symptoms, and all were cured by excision of the involved peripheral vessel. Kent and Arnold's re­port (6) of a 35-year-old man with aneurysmal di­latation of the aorta is particularly suspect. Appar­ently, a number of known causes of acquired weakening of the aortic wall were not fully inves­tigated. We are aware of only one prior case of classic, biopsy-proven giant cell arteritis in a patient under the age of 50 (4). That patient was 48 years old when symptoms developed. Our patient, a 47­year- old man with well-documented, fulminant disease, is the youngest reported to date. Prognosis In patients with loss of vision complicating giant cell arteritis, the prognosis for visual recovery is poor (1,8,9,14,15), particularly if associated with ischemic optic neuropathy. Nevertheless, im­provement in vision following treatment with sys­temic steroids has been reported (9,14-21). We reviewed reports of improvement in visual acuity with steroid treatment for ischemic optic neuropathy related to giant cell arteritis (15-18,21). In one patient, treatment was initiated long before ___ ~MJ I-om',i 2'0:100"'110 .... 3 ~CI.3I.-. . ';;"" ~ >~.:o. ~;. ~.~ :.:::~ ;.. ~ ;'o..u -:2.--. :~~:: J; .~~:: ' ... 80............." .. z.;I.,hI•• _~"r....,." I I I ' .....n.. '__ lo~,,,,,,,,,,,.MUfl...,, I I I ." :; -" ~"': .pllO _ .. Iyl-•- FIG. 6. Goldmann visual field obtained 2 months after onset of visual loss. JClin Neuro-ophthalmol, Vol. 13, No.4, 1993 268 E. A. POSTEL AND S. C. POLLOCK visual loss occurred (18), while the lowest recorded visual acuity in another patient was 20/200 (17). Siatkowski and coworkers (21), however, recorded an improvement in visual acuity from counting fin­gers 00 and 6 feet/200 OS to 20/40 OU after treat­ment with corticosteroids. Aiello and associates (15) also noted visual improvement in 5 of 34 pa­tients with giant cell arteritis, three of whom had ischemic optic neuropathy. However, the worst acuity recorded prior to treatment was 20/200. Matzkin and coworkers (9) described two pa­tients with giant cell arteritis and profound visual loss caused by central retinal artery occlusion, both of whom were initially treated with high-dose IV corticosteroids. These patients experienced a re­markable recovery of vision, though neither suf­fered from ischemic optic neuropathy. Most physicians who treat patients with giant cell arteritis routinely employ oral corticosteroids to control the disease process and to prevent the development or progression of visual compromise. Our patient was treated promptly with high-dose intravenous corticosteroids shortly after the onset of severe visual loss and subsequently experienced dramatic relief of systemic symptoms, disappear­ance of objective signs of acute ocular ischemia, and substantial improvement in visual acuity. Al­though no firm conclusions should be drawn from the outcome in a single case, the remarkable recov­ery of visual function in our patient leads us to believe that, in some patients with arteritic isch­emic optic neuropathy, aggressive treatment with intravenous corticosteroids may be associated with a better visual prognosis than is treatment with oral steroids. Clinical Findings Enlargement of the superficial temporal arteries and pallid swelling of the optic disc are common features of giant cell arteritis, and it is not surpris­ing that both contributed to the clinical picture in the case presented. More noteworthy, however, is the remarkable number of unusual clinical findings that were simultaneously observed in this patient. Some of these have not been previously described. Choroidal Perfusion Patterns Abnormalities in choroidal filling have been re­ported to occur in patients with giant cell arteritis (21-24). Mack and colleagues (22) noted that pro­longed choroidal filling time is common in patients with arteritic anterior ischemic optic neuropathy but not among patients with the nonarteritic form. J Clin Neuro-ophthalmoI, Vol. 13, No.4, 1993 Siatkowski and colleagues (21) reviewed fluores­cein angiograms from 16 patients with arteritic an­terior ischemic optic neuropathy and compared them with angiograms from 19 patients with non­arteritic anterior ischemic optic neuropathy. They found statistically significant delays in the choroi­dal dye appearance time and in choroidal filling time in the group of patients with arteritic disease. They also noted delayed appearance of dye in the retinal arterioles in the arteritic group. Spolaore and coworkers (24) described two pa­tients with "Horton's disease" who had angio­graphic evidence of selective hypoperfusion of the temporal choroid and who eventually developed triangular pigment epithelial scars. Slavin (23) sug­gested that visual loss in patients with giant cell arteritis may be caused by choroidal ischemia. Our patient demonstrated profoundly delayed choroi­dal dye appearance in his more severely affected eye, and persistent temporal hemichoroidal non­perfusion in both eyes (Fig. 3A,B). Geographic scars consistent with choroidal infarction eventu­ally developed at the level of the pigment epithe­lium. Visual Field Defects The patterns of field loss seen in patients with giant cell arteritis include altitudinal and combined altitudinal and central defects. Other optic nerve­related defects also occur. Rarely, bitemporal and homonymous hemianopias caused by ischemic damage to the chiasm or retrochiasmal pathways, respectively, may complicate GCA (1). Initially, our patient was found to have nearly complete loss of the nasal half of the visual field in his left eye. In the context of monocular blindness on the right, there was concern about the possibil­ity that the hemifield defect represented a right homonymous hemianopia, presumably from ar­teritic infarction of the left cerebral cortex. How­ever, the MRI revealed no intracranial abnormali­ties. Fluorescein angiography, on the other hand, demonstrated persistent temporal hemichoroidal nonperfusion in the left eye that respected the ver­tical meridian and was likely responsible for the ~ocumentednasal field loss. This appears to be the frrst report of a "pseudohomonymous hemiano­pia" in a patient with giant cell arteritis. Ocular Ischemic Syndrome Active arteritis can produce signs of global ocu­lar hypoperfusion. Radda and colleagues (25) re­ported the development of acute hypotony in el- RECOVERY OF VISION IN 47-YEAR-OLD MAN WITH GCA 269 derly patients with giant cell arteritis, and sug­gested that the reduction in intraocular pressure resulted from ciliary body ischemia and decreased aqueous production. Hamed and associates (26) additionally described four patients with biopsy­proven giant cell arteritis who manifested signs of the ocular ischemic syndrome, including corneal edema and ocular hypotony. Our patient's clinical findings included ocular injection, severe hypot­ony, dilated retinal veins, and the presence of rouleaux in the retinal arterioles and veins. All of these abnormalities resolved during the course of treatment. Orbital Ischemic Syndrome Clark and Victor (27) described an orbital cellu­litis~ like syndrome associated with giant cell arteri­tis, consisting of conjunctival injection and chemo­sis, proptosis, resistance to retropulsion, and a limitation of abduction. Laidlaw and colleagues (28) reported a 66-year-old woman with restricted ocular motility and proptosis, and attributed the findings to "orbital pseudotumor" complicating gi­ant cell arteritis. A CT scan in that case demon­strated normal-sized extraocular muscles. Chertok and colleagues (29), however, reported a discrete, tumorlike swelling of a single muscle in a patient with giant cell arteritis, and Barricks and col­leagues (30) emphasized the pathologic finding of ischemic necrosis of the extraocular muscles asso­ciated with severe cranial arteritis. More recently, Borruat and coworkers (31) reported orbital infarc­tion occurring in an 85-year-old woman with giant cell arteritis, manifested by total ophthalmoplegia, blindness, and ocular ischemia. Prior to the onset of visual loss, our patient ex­perienced marked bilateral periorbital soft tissue swelling and transient diplopia. Subsequently, he was noted to have a limitation of ocular motility that did not "map out" to a single cranial nerve. An MRI obtained during the acute phase of his illness demonstrated a remarkable homogeniza­tion of orbital signal, blurring of anatomic bound­aries, and diffuse gadolinium enhancement, find­ings thought to be consistent with generalized ischemia of the orbital contents. It appears that he suffered from what might be termed the "orbital ischemic syndrome," and thus manifested signs of compromised perfusion of both the eye and the orbit. Peripheral Neuropathic Syndromes Peripheral neuropathies occurred in 14% of 166 giant cell arteritis patients examined in one series (32). It has been proposed that nerve damage in such cases is caused by widespread arteritis and occlusion of vessels supplying the affected nerves (1,32). Treatment with steroids may result in a re­turn of nerve function (32). Median neuropathy is the most common peripheral mononeuropathy as­sociated with giant cell arteritis, occurring in 2 of the 23 affected patients in Caselli's series. An "acute hand syndrome" has also been described in patients with giant cell arteritis (5). Our patient complained of paresthesia and weakness in the distribution of the right median nerve, and a sensory examination revealed slightly decreased sensation in the same distribution. The results of EMG testing were interpreted as normal, although it should be noted that the test was per­formed after 2 days of treatment with high-dose intravenous steroids. Acknowledgments: The authors thank Charles Syd­nor, M.D., for referring the patient and for providing the initial Goldmann visual field (Fig. 1). REFERENCES 1. Miller NR. Walsh & Hoyt's clinical neuro-ophthalmology, 4th Ed. Baltimore: Williams & Wilkins, 1991;2601-27. 2. Cullen JF, Coleiro JA. Ophthalmic complications of giant cell arteritis. Surv OphthalmoI1976;20:247-60. 3. Bethlenfalvey NC, Nusynowitz ML. Temporal arteritis: a rarity in the young adult. Arch Intern Med 1964;114:487-9. 4. Biller J, Asconape J, Weinblatt ME, Toole JF. Temporal ar­teritis associated with a normal sedimentation rate. JAMA 1982;247:486-7. 5. Bugg El, Coonrad RW, Grim KB. Giant cell arteritis: an acute hand syndrome. J Bone Joint Surg 1963;45:1269-72. 6. Kent DC, Arnold H. Aneurysm of the aorta due to giant cell arteritis: successful surgical correction. J Thorac Cardiovasc Surg 1967;53:572-7. 7. Lie JT, Gordon LP, Titus JL. Juvenile temporal arteritis: biopsy of four cases. JAMA 1975;234:496-9. 8. Hayreh 55. Anterior ischemic optic neuropathy: treatment, prophylaxis, and differential diagnosis. Br J Ophthalmol 1974;58:981-9. 9. Malzkin DC, Siamovits TL, Sachs R, Burde RM. Visual re­covery in two patients after intravenous methylpredniso­lone treatment of central retinal artery occlusion secondary to giant-eell arteritis. Ophthalmology 1992;99:6S--71. 10. Hunder GG, Sheps SG. Intermittent claudication and poly­myalgia rheumatica: association with panarteritis. Arch In­tern Med 1967;119:63S--43. 11. MacCraig IN. Giant cell arteritis presenting with pyrexia of uncertain origin. Proc R Soc Med 1962;55:327-S. 12. McCormick HM, Neuberger KT. Giant-eell arteritis involv­ing small meningeal and intracerebral vessels. J Neuropathol Exp Neurol 1958;17:471-8. 13. Shah P, Murray PI, Harry J. An unusual case of giant cell arteritis. Am J OphthalmoI1993;115:57-63. 14. Schneider HA, Weber AA, Ballen PH. The visual prognosis in temporal arteritis. Ann Ophthalmol 1971;3:1215--30. 15. Aiello PD, Trautmann JC, McPhee TJ, et al. Visual progno­sis in giant cell arteritis. Ophthalmology 1993;100:550-5. 16. Clearkin L. Treatable blindness in temporal arteritis. Br J OphthalmoI1992;76:63-4. 17. Clearkin L, Caballero J. Recovery of visual function in an- J Gin Neuro-ophthalmol, Vol. 13, No.4, 1993 270 E. A. POSTEL AND S. C. POLLOCK terior ischemic optic neuropathy due to giant cell arteritis. Am JMed 1992;92:703-4. 18. Diamond JP. Treatable blindness in temporal arteritis. Br J OphthalmoI1991;75:432. 19. Lipton RB, Solomon S, Wertenbaker C. Gradual loss and recovery of vision in temporal arteritis. Arch Intern Med 1985;145:2252-3. 20. Model DG. Reversal of blindness in temporal arteritis with methylprednisolone. Lancet 1978;1:340. 21. Siatkowski RM, Gass JDM, Glaser JS, et al. Fluorescein an­giography in the diagnosis of giant cell arteritis. Am JOph­thalmol 1993;115:57--63. 22. Mack HG, O'Day J, Currie IN. Delayed choroidal perfusion in giant cell arteritis. JClin Neuro-ophthalmoI1991;11:221-7. 23. Slavin ML. Isolated "retrobulbar neuropathy" in the elder­ly. Presented at the North American Neuro-ophthalmology So­ciety Meeting, 1993. 24. Spolaore R, Gaudric A, Coscas G, De Mergerie J. Acute sectorial choroidal ischemia. Am J Ophthalmol 1984;98:707­16. 25. Radda TM, Bardach H, Riss B. Acute ocular hypotony: a JClin Neuro-ophthalmol, Vol. 13, No.4, 1993 rare complication of temporal arteritis. Ophthalmologica 1981;182:148-52. 26. Harned LM, Guy JR, Moster ML, Bosley T. Giant cell ar­teritis in the ocular ischemic syndrome. Am J Ophthalmol 1992;113:702-5. 27. Clark AE, Victor WHo An unusual presentation of temporal arteritis. Ann OphthalmoI1987;19:343--6. 28. Laidlaw DAH, Smith PEM, Hudgson P. Orbital pseudotu­mor secondary to giant cell arteritis: an unreported condi­tion. Br Med J 1990;300:784. 29. Chertok P, Leroux JL, LeMarchand M, et al. Orbital pseu­dotumor in temporal arteritis revealed by computerized to­mography. Clin Exp Rheumatol 1990;8:587. 30. Barricks ME, Traviesa DB, Glaser JS, Levy IS. Ophthal­moplegia in cranial arteritis. Brain 1977;100:209. 31. Borruat FX, Bogousslavsky J, Uffer S, et al. Orbital infarc­tion syndrome. Ophthalmology 1993;100:562--8. 32. Caselli R], Daube JR, Hunder GG, Whisnant JP. Peripheral neuropathic syndromes in giant cell (temporal) arteritis. Neurology 1988;38:685--9.