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Show Journal of Neuro- Ophthalmotogy 18( 1): 56- 59, 1998. © 1998 Lippincott- Raven Publishers, Philadelphia Bilateral Anterior Ischemic Optic Neuropathy Following Influenza Vaccination Aki Kawasaki, M. D., Valerie A. Purvin, M. D., and Rosa Tang, M. D., M. PH. Optic neuritis is an occasional complication of vaccination. Visual loss can be unilateral or bilateral, and most patients recover substantially without treatment. The presumptive mechanism is an immune- mediated demyelinating injury of the optic nerve. We report two patients who had permanent visual loss following influenza vaccination. Their pattern of visual loss, segmental optic disc changes, and failure of visual recovery were atypical for demyelinating optic neuritis and reminiscent of a primary ischemic injury to the optic nerve. We speculate that an immune complex- mediated vasculopathy following vaccination can cause anterior ischemic optic neuropathy. Clinicians should be aware of this entity because of the less favorable prognosis for visual recovery in these cases. Key Words: Optic neuritis- Optic neuropathy- Vaccination. Optic neuritis is an occasional complication of vaccination. Visual loss can be unilateral or bilateral. Optic disc edema may or may not be present acutely. The presumptive mechanism is an immune- mediated demyelinating injury of the optic nerve, and most patients are believed to recover substantially without treatment. We report two patients with bilateral optic disc edema following influenza vaccination whose clinical features suggested an ischemic mechanism of injury. CASE REPORTS Case 1 This 47- year- old woman with mild strabismic amblyopia in her right eye ( OD) noted decreased vision OD at 1 week after influenza vaccination ( October 1994, Indianapolis, IN). This was associated with transient eye pain. Five days later, she developed blurriness in her left eye ( OS). She was otherwise healthy and taking no medications. Manuscript accepted 9/ 2/ 97 From the Midwest Eye Institute ( A. K., V. A. P.), Methodist Hospitals of Indiana; and Departments of Ophthalmology and Neurology ( A. K., V. A. P.), Indiana University Medical Center, Indianapolis, Indiana; and Department of Ophthalmology ( R. T.), University of Texas Medical Branch, Galveston, Texas, U. S. A. Address correspondence and reprint requests to Dr. A. Kawasaki, Midwest Eye Institute, 201 Pennsylvania Parkway, Indianapolis, IN 46280, U. S. A. On examination, her visual acuity was 20/ 20 in both eyes, but Goldmann perimetry showed a superior arcuate defect OD and an inferior altitudinal defect OS ( Fig. 1). There was no relative afferent pupillary defect. Both optic discs were moderately edematous with splinter hemorrhages and cotton- wool spots ( Fig. 2). The results of a complete blood count, metabolic screen, urinalysis, fluorescent treponemal antibody test, vitamin B12, glucose, and folate levels were normal. Serum protein electrophoresis with immunofixation showed a nonspecific polyclonal hypergammaglobulinemia. A Westergren test indicated that the sedimentation rate was mildly elevated at 44 mm/ h, but specific vasculitis serologies ( antinuclear antibodies, anti- DNA antibodies, rheumatoid factor, complement level, cryoglobulins, antineutrophilic cytoplasmic antibodies, and an-ticardiolipin antibodies) revealed no abnormalities. Cranial magnetic resonance imaging and lumbar puncture with opening pressure and cerebrospinal fluid analysis were normal. She was treated with intravenous methylprednisolone 250 mg every 6 h for 3 days and then oral prednisone for 14 days. The visual field defects in either eye did not improve and, eventually, segmental disc atrophy appeared. The results of her examination remained unchanged at 1 year ( Fig. 3). Case 2 This 51- year- old woman became febrile with chills and myalgias the day after influenza vaccination ( October 1994, Houston, TX). These symptoms resolved over 3 weeks. Four weeks later, she had ear pain, headache, and blurry vision first in her right eye then in her left eye. Examination revealed acuities of 25/ 50 OD and 20/ 25 OS with an inferonasal visual field defect OD and a supernasal defect OS. Both optic discs were edematous, worse segmentally superiorly OD and inferiorly OS. Despite intravenous methylprednisolone, her vision progressively worsened over several weeks to count- fingers OD and 20/ 100 OS. The results of head and orbit magnetic resonance imaging, lumbar puncture with immunologic cerebrospinal fluid analysis, complete blood count, Westergren sedimentation rate, fluorescent treponemal antibody test, Rochalimaea antibody test, and tests for antinuclear an- 56 BILATERAL ANTERIOR ISCHEMIC OPTIC NEUROPATHY 57 mm. 105 90 75 60 120 105 90 76 MH WW 1 0,0) 11 3 0.100 1 0.311 • 1.00 * 0.40 * O. M c 0J1 * 0* 3 • 1.00 d l It to 1 0 4 1 I 1 0 V0\ ** « mm- 0 '•. 1 II 1 III 4 IV 1 « V M FIG. 1. Goldmann visual field of the right and left eyes. The right visual field ( right) shows a superior arcuate scotoma, and the left visual field shows an inferior altitudinal defect. tibodies, antineutrophilic antibodies, anticardiolipin antibodies, and angiotensin- converting enzyme were normal. Fluorescein angiography showed late optic disc staining consistent with disc edema. Her visual function was unchanged at 2 months, and bilateral optic disc atrophy had developed. COMMENT The influenza vaccine contains either inactivated whole virus or split viral antigens. The viruses are grown in chick- embryo allantoic fluid and then killed with formalin and purified. Adults receive a trivalent whole virus vaccine, which is a vaccine containing three different viral strains anticipated to be prevalent in the upcoming season/ year. It has been speculated that whole, killed virus vaccines such as trivalent influenza or swine influenza vaccination may share similar antigens ( molecular mimicry) with CNS proteins. The viral antigens are believed to stimulate an allergic reaction that produces CNS inflammation and demyelination. This immunologic demyelinating response to a vaccine may present clinically as an acute neurologic deficit with good spontaneous recovery. There are three well- described cases of influenza-vaccine- associated optic neuritis with good visual recovery in the English literature ( 1- 3). Two of the patients FiG. 1. runaus photograph of tne right and left optic discs 2 weeks following influenza vaccination. Both discs are edematous and hyperemic with peripapillary splinter hemorrhages and cotton- wool spots. J Neuro- Ophthalmol, Vol. 18, No. 1, 1998 58 A. KAWASAKI ET AL. FIG. 3. Fundus photograph of the right and left optic discs 1 year after onset of visual loss following influenza vaccination. The right optic disc ( left) has diffuse atrophy with superimposed inferior segmental pallor, and the left optic disc ( right) has significant superior segmental atrophy. had bilateral disc edema and visual loss. The third patient had a unilateral retrobulbar optic neuritis. All three patients had received steroids in some form, and all eyes recovered fully. In contrast, influenza vaccine- associated optic neuritis with poor visual recovery has been reported in two cases ( 4,5). Two possible pathogenic mechanisms can be postulated for the lack of visual recovery. One possibility is that an allergic cross- reaction to viral antigens stimulated optic nerve inflammation and demyelination severe enough to cause direct axonal injury. Another possible mechanism of injury is an immune- mediated vasculitis causing ischemic optic neuropathy. No pathologic examination of vaccination- associated optic neuritis cur- TABLE 1. Clinical characteristics of patients with optic neuritis following influenza vaccination Author Bicnfang ct al Perry et al Ray et al Cangemi et al Macoul et al Kawasaki et al Kawasaki el al Year 1977 1979 1996 1980 1982 1997 1997 Patient age/ sex 27 M 58 M 61 F 38 M 31 M 47 F 51 F Systemic symptoms myalgias, arthralgias, fever frontal headache none none none eye pain fever, myalgias, headaches Time to systemic symptoms* 11 days 4 days 7 days 1 day Time to onset of visual loss* 3 weeks OS ~ 1 week OD - 2- 3 weeks OS 3 weeks OU then progressive decline 3 weeks OD 3 weeks OU 7 days 4 weeks Initial examination 20/ 15 OD with mild ititis 20/ 30 OS with paracentral scotoma and nl fundus NLPOD LP OS bilateral disc edema HM OD LP OS bilateral disc edema CFOD central scotoma disc edema CFOU nl fundus 20/ 20 OU superior arcuate defect OD inferior altitudinal defect OS 20/ 25 OU inferonasal defect OD superonasal OS Steroids oral prednisone retrobulbar methyl - prednisolone and oral prednisone intravenous decadron then ONSF OS and oral prednisone none none intravenous SoluMedrol then oral prednisone intravenous SoluMedrol Time to recovery* 6 weeks ~ 6 weeks significant recovery 6 weeks then gradual improvement over 1 year none by 3 months none by 2 years none none Final examination " nl and equal acuity" OU no optic atrophy 20/ 25 OD 20/ 20 OS enlarged blindspot and inferonasal visual field defect OS 20/ 25 OD 20/ 30 OS enlarged blindspot OS bilaterally pale optic nerves CFOD optic atrophy CFOU optic atrophy OU same as initial examination segmental optic atrophy OU CFOD 20/ 100 OS bilateral optic atrophy il = normal; M = male; F = female; NLP = no light perception; LP = light perception; ONSF = optic nerve sheath decompression. ; All lime is given from the day of influenza vaccination. J Neitro- Ophlhalmol, Vol. IS, No. I, 1998 BILATERAL ANTERIOR ISCHEMIC OPTIC NEUROPATHY 59 rently exists to help differentiate these two mechanisms of injury. The details of all five cases are summarized in Table 1. Our two patients share similar clinical features. Both patients noted visual loss in one eye with eye pain or headache within 4 weeks of an influenza vaccine in 1994. Involvement of the second eye occurred shortly thereafter. Bilateral optic disc edema and nerve fiber bundle visual field defects were acute findings in both patients. Despite steroid treatment, both failed to have any visual improvement and eventually developed optic atrophy. An immune- mediated demyelinative injury of the optic nerve that was severe enough also to cause secondary axonal injury with subsequent poor recovery would seem an unlikely mechanism in our first patient, who maintained 20/ 20 acuity at all times but developed only the permanent field defects. In our two patients, we feel that the pattern of visual field loss, segmental disc changes, and failure of visual recovery is more consistent with anterior ischemic optic neuropathy ( AION) than with demyelinative optic neuritis. Because of the close temporal relationship to influenza vaccination and the bilateral involvement, we speculate that the mechanism of AION in our two patients may be an immune complex- mediated vasculopathy. This presumptive mechanism might also account for the systemic symptoms experienced by one of the patients ( case 2) prior to visual loss and for abnormal serum markers ( elevated sedimentation rate and polyclonal hypergammaglobulinemia) in our other patient ( case 1). We remind clinicians to consider influenza vaccination as a potential etiology for patients who present with visual loss and disc edema, especially bilaterally, within several weeks of vaccination. A nerve fiber bundle pattern of visual field loss and/ or segmental disc swelling are more characteristic of ischemic rather than demyelinative injury and may be indicators for a less favorable prognosis. Acknowledgment: This research was supported by the Midwest Eye Foundation at Methodist Hospital and a Research to Prevent Blindness grant. REFERENCES 1. Bienfang DC, Kantrowitz FG, Noble JL, Raynor AM. Ocular abnormalities after influenza immunization. Arch Ophthalmol 1977; 95: 1649. 2. Perry HD, Mallen FJ, Grodin RW, Cossari AJ. Reversible blindness in optic neuritis associated with influenza vaccination. Ann Ophthalmol 1979; 11: 545- 50. 3. Ray CL, Dreizen IJ. Bilateral optic neuropathy associated with influenza vaccination. J Neuro Ophthalmol 1996; 16: 182- 4. 4. Cangemi FE, Bergen RL. Optic atrophy following swine flu vaccination. Ann Ophthalmol 1980; 12: 857- 63. 5. Macoul KL. Bilateral optic nerve atrophy and blindness following swine influenza vaccination. Ann Ophthalmol 1982; 14: 398- 399. J Neuro- Ophthalmol, Vol. IS, No. I, 1998 |
