Many patients with idiopathic NR have been managed conservatively, others treated with steroids. Most experience excellent recovery of vision with or without intervention, with a final acuity of 20/40 or better in 90% of reported cases. There appears to be a subset of patients, however, with a somewhat different clinical picture, in whom the visual prognosis is more guarded. Of the 12 patients with NR described by Maitland and Miller (7), 3 failed to experience excellent recovery. Two of the patients in the series of Dreyer et al (6) had disc-related field defects and a large RAPD, and in both of these cases, the visual outcome was poor. The authors suggested that these patients had a virus-induced occlusive vasculitis involving prelaminar arterioles, which led to disc infarction.
One recent report documented the results of treatment with intravitreal steroids plus bevacizumab in a patient with idiopathic NR (92). In this single case report, the diagnosis was made 10 days after onset of visual loss, treatment was given 3 days later, and at 1-week follow-up, visual acuity had returned to normal and macular edema resolved. One month later, optic disc edema had resolved as well. The significance of this report is difficult to evaluate, in part because the natural history of NR is usually favorable and also because 2 different forms of treatment were given. Furthermore, in cases of NR with poor visual outcome, the limiting factor for visual recovery appears to be residual optic nerve damage rather than maculopathy. Since the intravitreal treatment in this report did not hasten resolution of disc edema, it is not clear that it would improve the outcome in such cases.
The most common form of infectious NR is due to CSD. A number of single case reports and small case series have described the clinical features of NR secondary to CSD. We reviewed a total of 65 reported cases, 4 of which were bilateral (69 eyes) (see Table, Supplemental Digital Content 1, http://links.lww.com/WNO/A14). From the data available, the average age at onset was 24.5 years (median: 21 years) with a range of 4 to 64 years. There was a female to male predominance of 1.8:1, and both eyes were affected equally. Systemic symptoms were reported in 47 (73%) of 64 cases and eye pain in 4 (7.7%) of 52 cases.
Initial Snellen acuity was 20/40 or better in 14.5% of eyes, between 20/50 and 20/200 in 33.3%, and worse than 20/200 in 52.2%. Final acuity was available for 58 eyes and was much improved in almost all cases: 93% had vision of 20/40 or better and none was worse than 20/200. The average number of lines gained was 7.7. The pattern of visual field loss was available for 27 eyes and usually consisted of a central defect (88%). A RAPD was present in 25 eyes (67.5%) and was variable in magnitude. There were 7 eyes with count fingers vision in which a RAPD was absent. This would suggest that much or all of the visual loss in these cases of NR secondary to CSD was due to serous detachment of the macula rather than optic nerve dysfunction. In these 7 eyes, visual acuity returned to 20/40 or better. In addition to optic disc edema and macular star formation, focal areas of chorioretinitis may be seen with CSD-NR (Fig. 3). In rare cases, visual recovery has been limited by macular hole formation (93,94)
A retrospective study found that antibiotic treatment shortened the course of the systemic disease in moderate to severe CSD (95). In this study, the following oral medications were most effective: rifampin (87% of cases), ciprofloxacin (84%), and trimethoprim-sulfamethoxazole (58%). In our literature review of NR due to CSD, 14 patients received no treatment, 37 patients received antibiotics only, 10 received steroids plus antibiotics, and 3 were given steroids alone. In small case series, patients have been reported to do well with a combination of doxycycline and rifampin (28) and ciprofloxacin (24). Because of the high degree of spontaneous visual recovery in NR due to CSD, no conclusions can be made from these data regarding the possible efficacy of treatment for this condition. It should be noted that ciprofloxacin is not recommended for use in children or during pregnancy. Azithromycin is a good alternative treatment for CSD and can be used in both children and adults.
The majority of reported cases of recurrent NR are idiopathic. With the exception of toxoplasmosis, most infectious agents do not cause recurrent attacks. Two of the patients in the series of idiopathic cases reported by Maitland and Miller (7) had evidence of a previous attack in the fellow eye, and an additional case was reported by Vaphiades et al (46). A patient with recurrent NR and inflammatory bowel disease has been described (80). The designation of recurrent idiopathic NR as an identifiable syndrome was based on a case series of 7 patients (96). An additional 6 cases were subsequently added in an article (97) focusing on the results of immunosuppressive therapy for this syndrome.
We further expanded this series in a recent review of 41 patients including clinical features and results of treatment (86). Median age at onset was 28 years with a range of 10 to 54 years. Average follow-up was 67 months. Overall, 147 episodes were documented in 75 eyes with an average of 3.6 attacks per patient and an average interval between attacks of 3 years (range, 1 month to 16 years). Most were not preceded by systemic symptoms, and eye pain was uncommon. Patterns of visual field loss consisted primarily of a central scotoma plus nerve fiber bundle defects, and loss was cumulative with repeated episodes. Some eyes sustained extensive field loss, despite preservation of visual acuity. In this series, only 36% of eyes were left with 20/40 or better acuity and retained more than two thirds of their visual field. The fundus features in recurrent NR were similar to other cases of NR but with repeated episodes, exudates may not form a macular star (Fig. 4).
We performed an additional analysis of a subgroup of these patients, looking only at features of the acute event in a previously unaffected eye. We analyzed data from 23 eyes of 21 patients and found several differences when compared to our CSD and idiopathic cases. Visual acuity was similar at onset in all 3 groups, but the pattern and magnitude of visual field loss were different in recurrent cases. Whereas visual field loss was confined to the central field in the majority of CSD and idiopathic cases, this pattern was uncommon in recurrent NR. Rather, one half of the recurrent cases demonstrated a combination of central and nerve fiber bundle defects. This difference in visual field involvement may be due to the fact that in idiopathic and CSD cases, visual loss in large part reflects macular dysfunction, whereas in recurrent idiopathic cases, visual loss is due to optic disc vasculitis leading to optic neuropathy. In addition, the severity of field loss was significantly greater in recurrent cases, and recovery of both acuity and field was less substantial. This lesser degree of recovery also manifest as a smaller percentage of patients who showed improvement in the magnitude of the RAPD at follow-up (11% vs 59% and 50% of CSD and idiopathic cases, respectively). The fundus features at onset were similar in all 3 groups, except for the presence of chorioretinal white spots (Fig. 3), which were more common in CSD patients and rare in idiopathic NR. The presence of such white spots has been taken as evidence of a hematogenously spread organism in cases of CSD-NR, and likewise their absence in idiopathic cases favors a different mechanism. In cases of recurrent NR, hard exudates often become less prominent and more localized during subsequent attacks (Fig. 4).
OCT is a sensitive method for detecting serous retinal detachment, particularly in the early stages of NR before the appearance of a macular star. In occasional cases of optic disc edema secondary to CSD, peripapillary serous detachment occurs but a macular star never develops (98,99). In such cases, OCT may help establish the diagnosis. FA is not usually necessary for diagnosis but may furnish additional information. FA typically demonstrates diffuse disc edema and peripapillary dye staining during the midvenous and late phases of the angiogram. This staining may be segmental and is occasionally present in the fellow eye even when visual loss is unilateral. Fundus autofluorescence may also be helpful for demonstrating macular exudates (100).
Initial interest in the MRI findings in NR focused on the detection of periventricular white matter changes as seen in MS. The consistent absence of these changes and the failure to develop clinical MS on long-term follow-up (87) have put this issue to rest. Dedicated MRI of the orbit with fat suppression and intravenous contrast has emerged as the more sensitive sequence for the evaluation of optic neuropathies, but there are relatively few reports using this technique in patients with NR. Schmalfuss et al (101) evaluated the MRI findings in 82 patients with various optic neuropathies, including 9 with CSD. Of these 9 cases, 5 had macular exudates, and in 4 of these, MRI showed enhancement of the optic disc extending up to 4 mm posteriorly along the optic nerve. The authors suggested that this “short segment enhancement” is highly specific for CSD-NR. Two additional cases with similar findings have been reported (46,102). However, other authors have found other neuroimaging results in patients with NR. Wals et al (103) reported a patient with idiopathic NR in whom MRI showed enhancement confined to the optic nerve sheath. A combination of optic nerve and sheath enhancement was seen on CT in 1 case of idiopathic NR (104) and on MRI in 1 patient with recurrent idiopathic NR (46).
We reviewed the orbital MRI scans in 36 of our cases, looking particularly for features that might differentiate subtypes of NR. In the CSD-NR group, 2 of 4 scans were abnormal, both showing enhancement confined to the optic disc. In patients with idiopathic NR, 2 of 6 scans were abnormal, one showing disc enhancement and the other enhancement of the disc with slight posterior extension, similar to what has been described in CSD-NR (101). In patients with recurrent NR, 3 showed enhancement confined to the disc (Fig. 5) and 1 showed retrobulbar optic nerve enhancement; scans in the remaining 22 were normal. Based on these findings, it seems likely that the MRI findings described by Schmalfuss et al (101) are indeed characteristic of NR but not specific for NR due to CSD. Additional MRI studies in NR are needed to clarify this issue.
It is possible that recurrent NR is more common than would appear from the literature. Because the characteristic macular star is not present at the time of visual loss, the diagnosis may be missed if a careful repeat fundus examination is not performed at least 2 weeks after onset. In the absence of a macular star, such cases might be termed “recurrent optic neuritis” or “papillitis” rather than NR. Increased recognition of the syndrome of recurrent NR may lead to the diagnosis of more cases and greater accuracy of its frequency.
From informal communication with colleagues, we have the impression that recurrent NR is more common in the Midwestern United States and rare in other parts of the country. One way to examine this issue would be a survey of the membership of the North American Neuro-Ophthalmology Society (NANOS). Collection of this information could be helpful in determining incidence as well as possible geographic clustering of cases. Another approach to the question of geographic distribution would be the examination of the database from a large tertiary referral base, such as Mayo Clinic, which draws from a large geographic area and tends to see a large number of such complex and rare disorders.
If recurrent NR cases have a particular geographic distribution, this might be a clue as to etiology. For example, the Midwest has a higher incidence of presumed ocular histoplasmosis syndrome (POHS), and we have considered this as a potential cause of recurrent NR. Our patients do not have a high frequency of fundus changes typical of POHS, but since serologic testing for this condition is not available, it remains a possibility. If recurrent NR is in fact an autoimmune disorder, progress in testing for other autoantibodies may reveal a marker for the disease, as we have seen for neuromyelitis optica.
Continued technical advances in retinal imaging, particularly the ability to correlate different imaging modalities, should further our understanding of these disorders. The work of Kitamei et al (5) is an example of the value of such correlation. These authors documented an isolated leakage from a single vessel in a case of idiopathic NR, in contrast to previous reports, which have described a more diffuse leakiness of disc capillaries. This focal leakage was more easily appreciated with indocyanine green than with FA, and it is not clear whether these findings are typical of NR or represent an unusual occurrence. Perhaps, the pathophysiology is different in the various subgroups of NR. Further application of these techniques should further our understanding of the pathophysiology in NR.
As the typical clinical findings in NR are better characterized, atypical “outlier” cases will be easier to identify. For example, pain is an uncommon feature in all 3 forms, described by about one fourth of all our patients with a similar frequency in all 3 groups (unpublished data). When present, pain is mild. The presence of severe pain, especially with eye movement, should suggest an alternative diagnosis. In our series of patients initially diagnosed as NR, 3 cases were subsequently reclassified as having idiopathic posterior scleritis based on characteristic findings on ultrasonography. Each of these patients had recurrent attacks with severe pain that was steroid responsive. Extensive enhancement of the retrobulbar optic nerve (beyond 4 mm behind the globe) is suggestive of idiopathic NR, particularly the recurrent variety and, to our knowledge, has not been described in CSD-NR.
The optic disc edema in NR is self-limited. In cases with protracted disc edema, alternative diagnoses should be considered, such as disc tumor or chronic inflammatory disorders including sarcoidosis, diffuse subacute nematode syndrome (DUSN), or IRVAN.
Bilateral simultaneous NR is uncommon and should suggest the more likely possibility of malignant hypertension or increased ICP. When NR does present with bilateral involvement, it may also be due to a specific infectious etiology. For example, bilaterality occurred in only 2 of 27 patients in series of Dreyer et al (6) and in 2 of 12 in that of Maitland and Miller (7). In contrast, bilateral NR has been reported in patients with Bartonella infection (31,45), Lyme disease (63), mumps (65), secondary syphilis (59), toxoplasmosis (57), rabies vaccine (77), chikungunya fever (72,73), and dengue (74).
Cases that are strongly suspicious for CSD but with negative serologies should be retested 6 weeks later to look for rising IgG titers. A rise in convalescent IgG titers may be diagnostic, even in the absence of elevated IgM antibodies. In addition to a history of cat exposure, features that would be considered “suspicious” for CSD include young age (younger than 16 years), preceding systemic symptoms, and poor visual acuity but with small or no RAPD. In contrast, features that suggest a low likelihood of CSD and a high risk of recurrence are no systemic symptoms, visual field defect outside the central field, preserved acuity with a large RAPD, poor recovery, and evidence of a previous episode in either eye. In cases with the latter features, steroid treatment should be considered. Simultaneous bilateral involvement is suggestive of an underlying infectious etiology, although not specifically CSD. In most cases seen acutely, treatment with a broad-spectrum antibiotic is reasonable while serologic tests are pending, especially in cases with findings suggestive of an infectious cause. In patients with recurrence, long-term immunosuppressive treatment should be considered.
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