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the patient was seen in 1996 at the age of 32 , with blurred vision in the right eye and headache .
there was mild epithelial edema of the cornea with a few keratic precipitates and no cells seen on slit - lamp examination of the right eye .
he had five episodes of pss crises over the next 14 years , with a highest iop of 60 mmhg .
anterior segment inflammation and elevated iop were controlled after few weeks of treatment with antiglaucoma medication and topical corticosteroids .
this was his treatment course after each pss event . at his first medical examination in 1996 , his cup / disc ratio was noted to be 0.4 in the right eye and 0.4 in the left eye .
1a and 1b ) . after his fifth attack , in 2010 , his uncorrected visual acuity was 1.0 in both eyes and a relative afferent papillary defect of right eye was observed .
his right optic disc was pale and the field loss in the right eye had progressed to a superior paracentral scotoma ( fig .
there was p100 delay of the right eye in the visual evoked potential test ( fig .
4 ) . there were no abnormal findings on brain magnetic resonance image ( fig .
pss is a syndrome associated with recurrent anterior segment inflammation and elevated iop . after an attack , iop and facility of aqueous outflow return to normal .
the etiology of pss is unknown , although abnormal vascular process , autonomic defect , allergic conditions , variation of developmental glaucoma , association of hla - bw54 , cytomegalovirus , and herpes simplex virus have been suggested [ 6 - 8 ] .
the presumed mechanism causing naion was decreased perfusion to the optic disc secondary to the rise in intraocular pressure .
risk factors for naion such as old age , small cup to disc ratio , and hypertension were considered when treating pss patients .
this is case of optic disc pallor in a patient with recurrent anterior segment inflammation and high intraocular pressure .
optic disc perfusion is directly proportional to mean arterial pressure and inversely proportional to iop .
we had not found something that explained optic disc pallor excluding high iop . decreased optic nerve perfusion by recurrent high iop
might induce optic disc pallor . in conclusion , pss could cause optic disc changes such as glaucomatous change and ischemic change .
thoughtful attention and aggressive iop control are required especially in pss patients with prolonged periods of high intraocular pressure and recurrent attacks .
a 32-year - old man with blurred vision in the right eye and headache presented with anterior uveitis , an intraocular pressure ( iop ) of 60 mmhg , an open angle , no visual field defects , and normal optic nerve . 
 he had a history of five previous similar attacks . in each of the previous instances , 
 his anterior uveitis and high iop were controlled with antiglaucoma medications and topical steroids . 
 however , at the fifth attack , his optic disc was pale and a superior paracentral visual field defect was shown . 
 brain magnetic resonance image studies were normal . 
 this case represents that a recurrent posner - schlossman syndrome ( pss)-induced optic disc atrophy likely due to ocular ischemia caused by a recurrent , high iop . 
 although pss is a self - limiting syndrome , we should manage high iop and prevent ischemia of the optic nerve head by treating with ocular antihypertensive medications .