this investigation includes a series of blood investigations and imaging ; when these investigations found no evidence for a demyelinating disorder ( through mri features principally ) , systemic autoimmune condition ( e.g. , antinuclear antibodies , dna , aquaporin-4 , and myelin oligodendrocyte glycoprotein antibodies ) , or infectious or metabolic causes , a granulomatous cause was considered , and further investigations were undertaken . those in whom systemic features of sarcoidosis were identified during investigation and those already known to have active systemic sarcoidosis , in whom the diagnosis of a granulomatous optic neuropathy was considered by the authors to be highly probable , were recorded prospectively and included in the study . the records were kept according to data protection regulations in the neuroophthalmology departments and collated by 2 of us ( b.j.b . and d.p.k . ) . criteria for the diagnosis of sarcoidosis involved histologic proof ( in 40 cases ) of a granulomatous disorder currently active or requiring continuing treatment or ( in 12 cases ) adequate proof on clinical grounds that no alternative explanation existed for the systemic disorder in the minds of the treating physicians : for example , clear radiologic evidence for lung and mediastinal involvement together with clear evidence for another characteristic feature of the disease , such as hypercalcemia , raised serum angiotensin - converting enzyme ( ace ) or other tissue involvement , associated with a typical pattern of isotope uptake using gallium scintigraphy or pet . ethical approval for the study was obtained , and patients gave informed consent to be included . ethical approval for the study was obtained , and patients gave informed consent to be included . twenty - four were caucasian , 24 african or caribbean , and 4 were from south asia . the diagnosis of systemic sarcoidosis was made concurrently in 33 patients and in one subsequently . the remaining 18 had already been diagnosed , between 6 months and 20 years before the onset of the optic neuropathy . a histologic diagnosis was made from respiratory tissue ( transbronchial or mediastinal lymph gland biopsy ) in 28 cases , lymph gland biopsy in 3 , liver biopsy in 1 , orbital biopsy in 3 , and neurologic tissue in 5 . all fulfilled the criteria for the  highly probable  diagnosis of the wasog ( world association of sarcoidosis and other granulomatous diseases ) sarcoidosis organ assessment instrument . in 12 cases , the diagnosis had been deemed secure on clinical grounds by the treating respiratory physicians , with clear evidence on clinical grounds for a multisystem disorder typical of sarcoidosis as noted in the methods section above ; these were all patients presenting with an optic neuropathy already diagnosed with systemic sarcoidosis . the predominate systemic clinical syndrome was respiratory in 38 cases , the orbit and lacrimal glands in 6 , cervical lymph glands in 4 , the skin in 3 , the nose and sinuses in 3 , and the liver and joints in 1 each . the serum ace was elevated in 24 ( 57% ) of available data at the time of onset of the optic neuropathy ; the median serum ace was 111 ( 18205 ) u / l ( normal range 850 gallium scans were undertaken in 10 instances , in which 1 was normal , 6 showed a panda  pattern of uptake in the lacrimal and parotid glands , 1 a  lambda  pattern of mediastinal uptake , and 2 a combination of both patterns . all patients presented with symptoms and signs of an optic neuropathy , defined as a reduction in central visual acuity and color vision , reduction in the visual field , and when seen , an abnormality of the pupillary response . patients with a subacute optic neuropathy that evolved over days were considered separately from those with a more progressive clinical course , in which the symptoms evolved over weeks . the former were considered to show an optic neuritis syndrome , the latter a progressive syndrome . forty - three cases showed an optic neuritis syndrome , of which 27 were unilateral . twelve of the bilateral cases showed a sequential optic neuropathy with a range of latency between the 2 episodes of 1 to 60 months . the median ( range ) acuity at presentation was 0.05 ( 01.0 ) in unilateral cases and 0.13 ( 01.0 ) in bilateral involvement . mri showing ( a ) swelling and high signal within the nerve , and ( b ) enhancement in a patient who presented with a painless subacute optic neuropathy to no perception of light over 5 days . with oral corticosteroid treatment ( c ) t1-weighted axial mri showing swelling and enhancement of the anterior half of the left optic nerve . ( d , e ) t1-weighted coronal mri showing 2 other cases in which the nerve is seen to be swollen and enhancing following administration of contrast . a wide range of visual field defects was noted ; most had central or centrocecal scotomas , but hemianopic and altitudinal defects were also seen . clinical characteristics and ocular findings at presentation in the 52 patients studied intraocular inflammation was seen at the same time as the optic neuropathy in 19 cases ( 36% ) : a granulomatous anterior uveitis was seen in 10 cases , an isolated vitritis in 1 , a panuveitis in 1 , isolated choroidal involvement in 1 , features of a retinal vasculitis in 2 , cotton wool spots in 2 , macular exudates in 1 , and episcleritis in 1 . in no case was the intraocular disease longstanding and associated with chronic glaucoma or retinal ischaemia . one patient underwent ct ; the remainder had mri studies of the orbits and brain , of which 13 were adjudged to be normal . twenty patients had abnormalities restricted to the optic nerve or sheath , of whom 14 showed enhancement of the optic nerve and sheath ( figure 1 ) with intrinsic lesions of one or both optic nerves , while the remainder showed high signal within the nerve without enhancement . in addition , 3 cases ( and the one who had ct ) showed intrinsic lesions within the nerve and thickening of the adjacent optic nerve sheath complex . the chiasmal lesion was associated with enhancement of the chiasm extending forward into one of the nerves . both patients with a perineuritis showed features of this , i.e. , the predominate feature was of enhancement and thickening of the sheath , not the whole complex ( figure 2 ) . ( b , c ) optic perineuritis : t1-weighted axial and coronal mri showing enlargement of and enhancement of the optic nerve and its sheath throughout its entire length . this was the presenting feature of the disease , which was diagnosed subsequently on histologic analysis of a cervical lymph node . a minority of patients whose clinical syndrome was one of a subacute optic neuropathy resembling an optic neuritis showed additional imaging features of more widespread involvement of the nervous system by the disease : 8 patients with unilateral optic neuropathies and 2 with bilateral involvement showed high signal within the nerves , enhancement of the complex , which also involved the orbital apex ( 5 cases ) ( figure 3a ) , the floor of the middle cranial fossa ( 4 cases ) ( figure 3b ) , and the frontal lobes ( 1 case ) . ( a , b ) orbital apex mass with a progressive painful optic neuropathy and sarcoidosis of the lungs , mediastinum , and heart . ( c , d ) two cases of progressive optic neuropathy with striking meningeal enhancement and swelling to form mass lesions . despite intensive treatment with corticosteroids and immunosuppression , in general , the initial acuity was better in those with normal imaging and no enhancement than in those in whom enhancement was seen ( figure 4 ) . histogram showing the relationships between mri features at onset / diagnosis ( abscissa ) and initial ( nadir ) visual acuity then best acuity after treatment ( ordinate ) . those whose clinical syndrome was of a progressive optic neuropathy ( 6 cases ) all showed meningeal enhancing lesions that had formed masses , in each case at the intracranial portion of the orbital apex ( figure 3 ) . csf results were available in 33 cases , including 2 with mass lesions and one with perineuritis . seven ( 21% ) showed csf protein levels greater than 0.6 g / dl ( median 0.95 g / dl , range 0.791.92 ) . five ( 15% ) showed a leukocyte pleocytosis ( > 5 cells / cm ) ( median 19 , range 670 ) . twenty - eight ( 85% ) had no oligoclonal bands , and 5 showed matched bands in both csf and serum . patients were treated in an individual way in 3 different hospitals so there was a wide range of medications , dosage regimens , and treatment durations . forty - nine were treated with corticosteroids , of whom 14 commenced with iv methylprednisolone followed by oral prednisolone , while the remainder received treatment with oral steroids from the outset . the daily dose of prednisolone varied between 30 and 80 mg per day . the duration of treatment varied greatly ( 4320 weeks ) . the median ( range ) length of follow - up was 8 ( 020 ) years . the median ( range ) change in visual acuity ( defined as the best acuity following treatment , even after relapse ) was + 0.46 ( 0.01 to + 1.22 ) in bilateral cases and + 0.175 ( 0.05 to + 1.25 ) in unilateral cases . the median final acuity in these 2 groups was 0.7 ( 01.25 ) and 0.5 ( 01.25 ) . those with a subacute syndrome showed a median improvement of + 0.225 ( range 0.01 to + 1.22 ) . those in the progressive subgroup showed no improvement in visual acuity with treatment although in each case there was resolution of meningeal enhancement over time . while there was a suggestion that mri abnormalities at onset ( figure 4 ) correlated with nadir acuity and an improvement following treatment , this was not significant ( p > 0.3 ) . considering treatment in those without a progressive disease course or perineuritis , 12 were treated with iv then oral steroids ; median ( range ) acuity was 0.02 ( 01 ) and increased to 0.75 ( 0.021 ) , median change + 0.3 , and those treated with oral steroids at onset 0.1 ( 01 ) increasing to 0.75 ( 01.25 ) , and median change + 0.5 ( p = 0.77 ) . for the most part , this occurred early on ; for example , patients treated with 60 mg prednisolone developed recurrence of symptoms and signs at 40 to 20 mg , and the signs settled with an escalation of treatment . immunosuppressive agents were added in 7 cases  azathioprine in 4 and mycophenolate and methotrexate in one each . the patient treated with methotrexate had had repeated relapses , which stopped on the immunosuppressive drug . one patient had an intracranial relapse of neurosarcoidosis and her optic neuropathy worsened ; she was treated with cyclophosphamide then infliximab . in those who relapsed , the improvement in acuity following treatment was + 0.25 ( 0.15 to + 1.2 ) , and relapse did not appear to influence the outcome in any way . we have seen 6 additional patients who presented with an optic neuritis and were found during investigation to have a raised serum ace ( median 100 [ range 80178 ] u / l ) . the clinical syndrome was not different from the others described above ; half were caribbean , half caucasian , and half were bilateral . the median ( range ) acuity in each eye was 0.1 ( 01.0 ) . in each case , the affected discs were seen to be swollen . imaging was normal in 3 and showed high signal within the affected nerve in the other 3 . csf in 4 cases showed normal protein and negative oligoclonal bands in 3 ; in the other case , matched serum and csf bands were found . in this case one was considered to have a disc granuloma and was watched without treatment ; he improved over 2 years . these cases have been followed and none has developed further or recurrent neurologic or systemic symptoms . they appear to have neither sarcoidosis nor multiple sclerosis . twenty - four were caucasian , 24 african or caribbean , and 4 were from south asia . the diagnosis of systemic sarcoidosis was made concurrently in 33 patients and in one subsequently . the remaining 18 had already been diagnosed , between 6 months and 20 years before the onset of the optic neuropathy . a histologic diagnosis was made from respiratory tissue ( transbronchial or mediastinal lymph gland biopsy ) in 28 cases , lymph gland biopsy in 3 , liver biopsy in 1 , orbital biopsy in 3 , and neurologic tissue in 5 . all fulfilled the criteria for the  highly probable  diagnosis of the wasog ( world association of sarcoidosis and other granulomatous diseases ) sarcoidosis organ assessment instrument . in 12 cases , the diagnosis had been deemed secure on clinical grounds by the treating respiratory physicians , with clear evidence on clinical grounds for a multisystem disorder typical of sarcoidosis as noted in the methods section above ; these were all patients presenting with an optic neuropathy already diagnosed with systemic sarcoidosis . the predominate systemic clinical syndrome was respiratory in 38 cases , the orbit and lacrimal glands in 6 , cervical lymph glands in 4 , the skin in 3 , the nose and sinuses in 3 , and the liver and joints in 1 each . the serum ace was elevated in 24 ( 57% ) of available data at the time of onset of the optic neuropathy ; the median serum ace was 111 ( 18205 ) u / l ( normal range 850 gallium scans were undertaken in 10 instances , in which 1 was normal , 6 showed a  panda pattern of uptake in the lacrimal and parotid glands , 1 a  lambda  pattern of mediastinal uptake , and 2 a combination of both patterns . all patients presented with symptoms and signs of an optic neuropathy , defined as a reduction in central visual acuity and color vision , reduction in the visual field , and when seen , an abnormality of the pupillary response . patients with a subacute optic neuropathy that evolved over days were considered separately from those with a more progressive clinical course , in which the symptoms evolved over weeks . the former were considered to show an optic neuritis syndrome , the latter a progressive syndrome . forty - three cases showed an optic neuritis syndrome , of which 27 were unilateral . twelve of the bilateral cases showed a sequential optic neuropathy with a range of latency between the 2 episodes of 1 to 60 months . the median ( range ) acuity at presentation was 0.05 ( 01.0 ) in unilateral cases and 0.13 ( 01.0 ) in bilateral involvement . mri showing ( a ) swelling and high signal within the nerve , and ( b ) enhancement in a patient who presented with a painless subacute optic neuropathy to no perception of light over 5 days . with oral corticosteroid treatment ( c ) t1-weighted axial mri showing swelling and enhancement of the anterior half of the left optic nerve . ( d , e ) t1-weighted coronal mri showing 2 other cases in which the nerve is seen to be swollen and enhancing following administration of contrast . a wide range of visual field defects was noted ; most had central or centrocecal scotomas , but hemianopic and altitudinal defects were also seen . intraocular inflammation was seen at the same time as the optic neuropathy in 19 cases ( 36% ) : a granulomatous anterior uveitis was seen in 10 cases , an isolated vitritis in 1 , a panuveitis in 1 , isolated choroidal involvement in 1 , features of a retinal vasculitis in 2 , cotton wool spots in 2 , macular exudates in 1 , and episcleritis in 1 . in no case was the intraocular disease longstanding and associated with chronic glaucoma or retinal ischaemia . one patient underwent ct ; the remainder had mri studies of the orbits and brain , of which 13 were adjudged to be normal . twenty patients had abnormalities restricted to the optic nerve or sheath , of whom 14 showed enhancement of the optic nerve and sheath ( figure 1 ) with intrinsic lesions of one or both optic nerves , while the remainder showed high signal within the nerve without enhancement . in addition , 3 cases ( and the one who had ct ) showed intrinsic lesions within the nerve and thickening of the adjacent optic nerve sheath complex . the chiasmal lesion was associated with enhancement of the chiasm extending forward into one of the nerves . both patients with a perineuritis showed features of this , i.e. , the predominate feature was of enhancement and thickening of the sheath , not the whole complex ( figure 2 ) . the lesion was biopsied and granulomatous inflammation identified . the optic neuropathy improved with steroids . ( b , c ) optic perineuritis : t1-weighted axial and coronal mri showing enlargement of and enhancement of the optic nerve and its sheath throughout its entire length . this was the presenting feature of the disease , which was diagnosed subsequently on histologic analysis of a cervical lymph node . a minority of patients whose clinical syndrome was one of a subacute optic neuropathy resembling an optic neuritis showed additional imaging features of more widespread involvement of the nervous system by the disease : 8 patients with unilateral optic neuropathies and 2 with bilateral involvement showed high signal within the nerves , enhancement of the complex , which also involved the orbital apex ( 5 cases ) ( figure 3a ) , the floor of the middle cranial fossa ( 4 cases ) ( figure 3b ) , and the frontal lobes ( 1 case ) . ( a , b ) orbital apex mass with a progressive painful optic neuropathy and sarcoidosis of the lungs , mediastinum , and heart . ( c , d ) two cases of progressive optic neuropathy with striking meningeal enhancement and swelling to form mass lesions . despite intensive treatment with corticosteroids and immunosuppression , neither case showed a meaningful improvement in visual acuity . in general , the initial acuity was better in those with normal imaging and no enhancement than in those in whom enhancement was seen ( figure 4 ) . histogram showing the relationships between mri features at onset / diagnosis ( abscissa ) and initial ( nadir ) visual acuity then best acuity after treatment ( ordinate ) . those whose clinical syndrome was of a progressive optic neuropathy ( 6 cases ) all showed meningeal enhancing lesions that had formed masses , in each case at the intracranial portion of the orbital apex ( figure 3 ) . csf results were available in 33 cases , including 2 with mass lesions and one with perineuritis . seven ( 21% ) showed csf protein levels greater than 0.6 g / dl ( median 0.95 g / dl , range 0.791.92 ) . five ( 15% ) showed a leukocyte pleocytosis ( > 5 cells / cm ) ( median 19 , range 670 ) . twenty - eight ( 85% ) had no oligoclonal bands , and 5 showed matched bands in both csf and serum . patients were treated in an individual way in 3 different hospitals so there was a wide range of medications , dosage regimens , and treatment durations . forty - nine were treated with corticosteroids , of whom 14 commenced with iv methylprednisolone followed by oral prednisolone , while the remainder received treatment with oral steroids from the outset . the daily dose of prednisolone varied between 30 and 80 mg per day . the duration of treatment varied greatly ( 4320 weeks ) . the median ( range ) length of follow - up was 8 ( 020 ) years . the median ( range ) change in visual acuity ( defined as the best acuity following treatment , even after relapse ) was + 0.46 ( 0.01 to + 1.22 ) in bilateral cases and + 0.175 ( 0.05 to + 1.25 ) in unilateral cases . the median final acuity in these 2 groups was 0.7 ( 01.25 ) and 0.5 ( 01.25 ) . those with a subacute syndrome showed a median improvement of + 0.225 ( range 0.01 to + 1.22 ) . those in the progressive subgroup showed no improvement in visual acuity with treatment although in each case there was resolution of meningeal enhancement over time . while there was a suggestion that mri abnormalities at onset ( figure 4 ) correlated with nadir acuity and an improvement following treatment , this was not significant ( p > 0.3 ) . considering treatment in those without a progressive disease course or perineuritis , 12 were treated with iv then oral steroids ; median ( range ) acuity was 0.02 ( 01 ) and increased to 0.75 ( 0.021 ) , median change + 0.3 , and those treated with oral steroids at onset 0.1 ( 01 ) increasing to 0.75 ( 01.25 ) , and median change + 0.5 ( p = 0.77 ) . for the most part , this occurred early on ; for example , patients treated with 60 mg prednisolone developed recurrence of symptoms and signs at 40 to 20 mg , and the signs settled with an escalation of treatment . immunosuppressive agents were added in 7 cases  azathioprine in 4 and mycophenolate and methotrexate in one each . the patient treated with methotrexate had had repeated relapses , which stopped on the immunosuppressive drug . one patient had an intracranial relapse of neurosarcoidosis and her optic neuropathy worsened ; she was treated with cyclophosphamide then infliximab . in those who relapsed , the improvement in acuity following treatment was + 0.25 ( 0.15 to + 1.2 ) , and relapse did not appear to influence the outcome in any way . we have seen 6 additional patients who presented with an optic neuritis and were found during investigation to have a raised serum ace ( median 100 [ range 80178 ] the clinical syndrome was not different from the others described above ; half were caribbean , half caucasian , and half were bilateral . the median ( range ) acuity in each eye was 0.1 ( 01.0 ) . in each case , the affected discs were seen to be swollen . imaging was normal in 3 and showed high signal within the affected nerve in the other 3 . csf in 4 cases showed normal protein and negative oligoclonal bands in 3 ; in the other case , matched serum and csf bands were found . in this case one was considered to have a disc granuloma and was watched without treatment ; he improved over 2 years . these cases have been followed and none has developed further or recurrent neurologic or systemic symptoms . this work forms the largest series of patients with optic neuropathy in sarcoidosis identified and each has been followed prospectively . the age range was wide but the condition was more prevalent in the first half of life . the majority of patients were women and there were equal numbers in caucasian and african or caribbean ethnic groups . according to the epidemiologic findings in access , the ethnic subgroups in london are 60% caucasian , 14% african and caribbean , and 18% south asian , and our results therefore suggest a greater prevalence of the disease in african and caribbean people who live in london . in general , the clinical syndrome resembled an optic neuritis , although in some , the disease course was more slowly progressive . pain was a less prevalent feature than is seen in demyelinating optic neuritis , and the median visual acuity at nadir was equivalent , although more were no perception of light ( table 2 ) . sixty - four percent had a unilateral involvement , 28% presented at a later time with involvement of the second eye , while synchronous bilateral involvement was less common ( 9% ) . it is noteworthy that there was evidence for concurrent intraocular inflammation in only a minority of cases . predominately this was mild ( although more severe cases had been excluded because of the uncertainty of the pathogenesis of the optic neuropathy ) . indeed , in 64% of patients , there was no history of ocular involvement at any stage of the disease to date . imaging showed clear abnormalities , which accounted for the clinical features in 75% of cases . comparison of clinical features with results of the onsg spontaneous improvement occurred ( as has been noted previously ) , although the majority of patients were treated with steroids . following this , an often substantial improvement in vision took place , even after several weeks without treatment . relapse occurred in 25% of cases , necessitating recommencement or an escalation of treatment , and in the majority , this occurred early , as steroids were withdrawn . six cases ( 11% ) had a more progressive disease course and were shown to have a more widespread neurologic involvement , each showing evidence for adjacent meningeal inflammation . visual outcome in this subgroup was poor , even though the disease process required , in general , a higher and more prolonged dose of steroids , concurrent immunosuppression , and in 2 cases , a requirement for biological agents with refractory disease . evidence for neurosarcoidosis defined as the presence of intracranial meningeal enhancement arose in 16 cases overall  all of those with a progressive course and 10 with a subacute course . involvement of the optic nerve in sarcoidosis may arise through a variety of mechanisms : inflammation of the nerve itself , compression or infiltration by an inflammatory mass adjacent to the anterior visual pathway ( e.g. , the orbital apex or pituitary gland ) , secondary involvement through ischemic complications of retinal and choroidal inflammation and glaucoma , granulomas within the disc itself , meningeal inflammation within the optic nerve sheath leading to an optic perineuritis , and finally as a consequence of hydrocephalus . it was seen in 5% of one series of 202 patients with ocular disease in sarcoidosis , but only one in a series of 649 patients with systemic sarcoidosis and none in another of 285 . in the literature before 2000 , 57 cases had been published , of which 35 involved the optic nerve itself , 9 compression due to an intracerebral lesion , 6 due to hydrocephalus , and 6 due to the complications of uveitis . many noted that bilateral involvement occurred and that imaging showed enlargement of the optic nerve others noted that the acuity was lower than that seen in a demyelinating optic neuritis . one study described 24 cases with optic neuropathy : 71% had not been known previously to have systemic sarcoidosis and 42% showed previous or current intraocular inflammation . another showed that 14 of 67 patients known to have neurologic sarcoidosis had some form of optic neuropathy . we have identified a small subgroup of patients in whom the serum ace is elevated at presentation and then subsequently normalizes without relapse . on further investigation , these patients do not have sarcoidosis and on follow - up show no sign of transformation into a more widespread disease . the serum ace appears to increase in a nonspecific way and appears not to indicate a systemic granulomatous disease . it is important to identify this subgroup , which requires no additional treatment , merely close follow - up and observation . this large series of patients with optic neuropathy in conjunction with sarcoidosis has shown that more than half are not previously diagnosed with sarcoidosis , only a third have concurrent intraocular inflammation , and the clinical characteristics and in most cases the imaging features are not substantially different from that seen in a regular demyelinating optic neuritis . however , patients should be identified early because the response to treatment may lessen with time , and the identification of more widespread disease , particularly within the nervous system , will require prolonged , often high - dose treatment with steroids , immunosuppressive drugs , and modern biological therapies . modern imaging investigations including pet may make identification of these cases easier , but a high index of clinical suspicion is still important , particularly in non - caucasian patients presenting with a painless optic neuritis . once identified , we recommend that patients be treated with high - dose ( oral or iv ) corticosteroids , followed by a slow taper watching carefully for relapse as the dose is reduced . repeated relapses , particularly preventing steroid dose reduction , should be treated with an additional immunosuppressive agent . the presence of neurosarcoidosis requires more prolonged higher - dose treatment with steroids and immunosuppression from the outset , with early recourse to biological agents should the clinical and radiologic features of the disorder fail to improve quickly . further study is required to identify precisely which treatments are best and over what period of time . dr . kidd was responsible for the study design , data acquisition , analysis and interpretation , and writing the manuscript . burton served on the scientific advisory board for bayer , novartis , received travel funding from novartis , bayer , is subeditor for eastern european journal of neurology , received research support from novartis alcon .
objective : to identify and follow a series of 52 patients with optic neuropathy related to sarcoidosis.methods:prospective observational cohort study.results:the disorder was more common in women and affected a wide age range . 
 it was proportionately more common in african and caribbean ethnic groups . 
 two clinical subtypes were identified : the more common was a subacute optic neuropathy resembling optic neuritis ; a more slowly progressive optic neuropathy arose in the remaining 17% . 
 sixteen ( 31% ) were bilateral . 
 concurrent intraocular inflammation was seen in 36% . 
 pain arose in only 27% of cases . 
 an optic perineuritis was seen in 2 cases , and predominate involvement of the chiasm in one . 
 mri findings showed optic nerve involvement in 75% of cases , with adjacent and more widespread inflammation in 31% . 
 treatment with corticosteroids was helpful in those with an inflammatory optic neuropathy , but not those with mass lesions 
 . relapse of visual signs arose in 25% of cases , necessitating an increase or escalation of treatment , but relapse was not a poor prognostic factor.conclusions:this is a large prospective study of the clinical characteristics and outcome of treatment in optic neuropathy associated with sarcoidosis . 
 patients who experience an inflammatory optic neuropathy respond to treatment but may relapse . 
 those with infiltrative or progressive optic neuropathies improve less well even though the inflammatory disorder responds to therapy .