¡¡¡¡Optic perineuritis occurs occasionally as a manifestation of giant cell arteritis [10]. Although clinical findings were suggestive of associated anterior ischaemic optic neuropathy but magnetic resonance images suggested optic perineuritis in this case. Thus this case is unique as optic perineuritis is not a common association of giant cell arteritis. Optic perineuritis describes inflammation involving the optic nerve sheath evidenced by the characteristic pattern of enhancement around the optic nerve ("tramtrack" on axial views and "doughnut" on coronal views) in MRI scan [10].

¡¡¡¡A temporal artery biopsy is generally considered to be the gold standard for diagnosing GCA. Our patient has a high index suspicion of GCA clinically even though the temporal artery biopsy was negative. The negative biopsy in our patient is most probably due to resolution of the inflammatory infiltrates as the biopsy was performed two weeks after initiation of steroids. Moreover reported skip lesions about 5% to 9% in this procedure carries a significant false negative rate due to giant cell arteritis presentation may affects vessels focally and segmentally[1, 11]. Thus the need for multiple histological sections examination is important to confirm the diagnosis [11]. Patients with a high clinical suspicion of temporal arteritis may require a contralateral biopsy if the initial one is negative. The number of patients diagnosed histologically as having GCA increased by 10% by performing bilateral temporal artery biopsy in a prospective study [11].

¡¡¡¡The patient has fulfilled the American College of Rheuª²matology traditional format classification for GCA evidenced by the age more than 50 years, scalp tenderness, new onset of headache and ESR greater than 50mm in the first hour [12]. Erythrocyte sedimentation rate (ESR) and Cª²reactive protein (CRP) in this patient were elevated, 67mm/h and 42mg/L respectively. The CRP is superior to the ESR in establishing the diagnosis of GCA [2].

¡¡¡¡There are three fundamental aims of treatment in ocular giant cell arteritis. These are prevention of further visual loss and involvement of the fellow eye, restoration of vision, and suppression of disease activity [13]. Systemic corticosteroid should be started as soon as GCA becomes a viable diagnostic possibility [2]. It is important because the greatest risk for visual deterioration would be the first 6 days [14]. The estimated risk of bilateral ocular involvement in GCA is at 10%ª²50%. It depends on whether steroids have been given, and the interval between involvements of the two eyes is measured in days or weeks [12]. According to the resolution of systemic symptoms and reduction of ESR and CRP, tapering of the dose of the steroids should be done [12]. Steroid sparing agents is used to decrease the duration and total dose of corticosteroid therapy to avoid complications of steroids [2]. Jover et al[15] found that combination of methotrexate plus corticosteroid is a safe alternative to corticosteroid therapy alone in patients with giant cell arteritis and is more effective in controlling disease.

¡¡¡¡Temporal arteritis is a relatively rare condition. Sufficient information from clinical grounds and an ESR enable us to make the diagnosis of temporal arteritis with confidence[1]. The patient¬ðs history and clinical presentation should alert the attending clinicians of the diagnosis. A clinical diagnosis of temporal arteritis does not require a positive biopsy. Optic perineuritis, although being a rare association should be considered when dealing with giant cell arteritis. The clinical sequelae, particularly unilateral blindness requires prompt diagnosis and urgent initiation of corticosteroid for a satisfactory outcome in GCA and to prevent blindness in the fellow eye.

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  ¡¡¡¡1 Davies C, Frost B, Eshan O, McLain AD, Shandall A. Temporal artery biops. Temporal artery biopsy... who needs one? Postgrad Med J 2006;82(969):476ª²478

¡¡¡¡2 Daneshª²Meyer HV, Savino PJ. Giant cell arteritis. Curr Opin Ophthalmol 2007;18(6):443ª²449

¡¡¡¡3 Cullen JF, Chan CM, Chuah KL. Giant cell arteritis (temporal arteritis, cranial arteritis) and a case from Singapore. Singapore Med J 2003;44(6):306ª²308

¡¡¡¡4 Su GW, Foroozan R. Update on giant cell arteritis. Curr Opin Ophthalmol 2003;14(6):332ª²338

¡¡¡¡5 Levine SM, Hellmann DB. Giant cell arteritis. Curr Opin Rheumatol 2002;14(1):3ª²10

¡¡¡¡6 Miller NR. Visual manifestations of temporal arteritis. Rheum Dis Clin North Am 2001;27(4):781ª²797

¡¡¡¡7 Ahmad I, Zaman M. Bilateral internuclear ophthalmoplegia: an initial presenting sign of giant cell arteritis. J Am Geriatr Soc 1999;47(6):734ª²736

¡¡¡¡8 Purvin V, Kawasaki A. Giant cell arteritis with spontaneous remission. Clin Exp Ophthalmol 2007;35(1):59ª²61

¡¡¡¡9 Killer HE, Holtz DJ, Kaiser HJ, Laeng RH. Diplopia, ptosis, and hepatitis as presenting signs and symptoms of giant cell arteritis. Br J Ophthalmol 2000;84(11):1319ª²1320

¡¡¡¡10 Purvin V, Kawasaki A, Jacobson DM. Optic perineuritis: clinical and radiographic features. Ach Ophthalmol 2001;119(9):1299ª²1306

¡¡¡¡11 Miguel A. Gonzalezª²Gay, Carlos Garciaª²Porrua, Jose A. Mirandaª²Filloy, Javier Martin. Giant cell arteritis and polymyalgia rheumatica pathophysiology and management. Drugs aging 2006;23(8):627ª²649

¡¡¡¡12 Riordanª²Eva P, Landau K, O¬ðDay J. Temporal artery biopsy in the management of giant cell arteritis with neuroª²ophthalmic complications. Br J Ophthalmol 2001;85(10):1248ª²1251

¡¡¡¡13 Chan CC, Paine M, O¬ðDay J. Steroid management in giant cell arteritis. Br J Ophthalmol 2001;85(9):1061ª²1064

¡¡¡¡14 Daneshª²Meyer H, Savino PJ, Gamble GG. Poor prognosis of visual outcome after visual loss from giant cell arteritis. Ophthalmology 2005;112(6):1098ª²1103

¡¡¡¡15 Jover JA, Hern¢~ndezª²Garc¨ªa C, Morado IC, Vargas E, Ba ares A, Fern¢~ndezª²Guti¨¦rrez B. Combined treatment of giantª²cell arteritis with methotrexate and prednisone. A randomized, doubleª²blind, placeboª²controlled trial. Ann Intern Med 2001;134(2):106ª²114

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