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Show journal of Neuw- Ophthalmohgy 160): 182- 184, 1996. © 1996 Lippincott- Raven Publishers, Philadelphia Bilateral Optic Neuropathy Associated with Influenza Vaccination Cheryl L. Ray, D. O., and Ivy J. Dreizin, M. D. Wo report a 61- year- old vvoninn with bilateral optic neu- The relatively abrupt onset of bilateral loss of litis and loss of vision following influenza vaccination. vision is alarming both to the patient and physi- The patient had good recovery of vision following ste- dan W e d e s c r i b e a w o m a n w h o had optic neuritis roid treatment. ~ , r ,, . ,. Key Words: Optic neuritis- Influenza vaccination - occurring 3 weeks following an influenza vaccina- Prednisone Blindness. tion; with treatment, she experienced good recovery of vision. CASE REPORT A 61- year- old white woman developed progressive visual loss in both eyes 3 weeks following influenza vaccination. On arising November 4, 1993, the patient noted blurring of both eyes, the right more than the left. 1 ler vision gradually decreased over 1 week. There was no history of ocular pain, cephalgia, jaw claudication, or any preceding illness. Her past medical history was negative, and she was on no medications, did not smoke or drink alcohol, and had no allergies. There was no history of cat bite or exposure to cats. There was no family history of impaired vision. On October 15, 1993, she had received an influenza vaccination consisting of Flu-ogen, which included split virus subvirion vaccine, 15 | xg of A/ Texas/ 36/ 91 MINI, 15 p, g of A/ Beijing/ 32/ 92 H3N2, and 15 jxg of B/ Panama/ 45/ 90. Computed tomography ( CT) brain scan and lumbar puncture were normal. Neuro- ophthalmological examination revealed an alert, afebrile woman with a blood pressure of 130/ 100. 1 ler visual acuity with correction was 20/ 200 OD and 20/ 40 OS. Pupils were 8 mm OU and minimally reactive to light. There was an equivocal right relative afferent pupillary defect. The extraoc-ular movements were full. Visual field testing re- Manuscripi received May 22, 1995; accented July 10, 19%. , , . , , , . . . . ° . Prom the Department of Neurosdences ( C. L. R.), Dean Med- v e a l e d a n u P P e r n a s a l l s l a n d o f v l s l o n remaining in ical Center, and the Department of Neurology ( I. J. D.), Physi- the right eye and an upper temporal island remain-dans Plus, Madison, Wisconsin, U. S. A in„- j n t n e | e r L T n e o p t j c c | j s c s w c r e s w o H e n 2- 3 Address correspondence and reprint requests to Dr. Cheryl ,. , , , . .,, , , P. Kay, Dean Medical Cenler, NeuLriences, 1313 Pish Hatch- diopters and had p e r i p a p i l l a r y h e m o r r h a g es ery Road, Madison, WI 53715, U. S. A. ( Fig. 1). The remainder of the complete neuro- 782 FLU VACCINE AND OPTIC NEUROPATHY 183 HG. 1. Fundus photographs taken 1 week after vision was affected. A: Left. B: Right. Both optic discs are swollen and have peripapillary hemorrhages. ophthalmologic and neurologic examination was normal. The patient was admitted for i. v. Solu- Medrol treatment. The following tests were performed and were negative or normal: bilateral temporal artery biopsy, magnetic resonance imaging ( MRI) of brain and orbits with and without gadolinium, electrolytes, blood urea nitrogen, serum creatine ( CR), alkaline phosphatase, LDH, serum glutamic-oxaloacetic transaminase, GGT, GPT, erythrocyte sedimentation rate, which was 15 mm/ hr, complete blood cell count, platelets, PT and PTT, lupus anticoagulant, Lyme titer, B12, folate, glucose, Leber's marker ( including 14,484 mitochondrial mutations), VDRL, RPR, angiotensin- converting enzyme, and a cholesterol panel. Lumbar puncture was performed and cerebrospinal fluid ( CSF) glucose, protein, WBC, RBC, VDRL, IgG, electrophoresis, and cytology were normal. The opening pressure was 155 mm Hg. Anticardiolipin antibody IgG was 34.4 ( on November 10, 1993) and 31.1 two weeks later ( mid-positive range, 22.6- 100). The initial ANA titer was 1: 40 and repeat ANA 2 weeks later was 1: 160 with a speckled pattern. A third ANA titer was 1: 40 with a speckled pattern, and the ANA profile was negative ( RNP, SM, SS- A/ RO, SS- B/ LA, SCL- 70, PM- 1, and antibodies to DNA). A heavy metal serum screen showed mercury elevated at 13.2 ( normal, < 5.0), and arsenic and lead were negative. The patient developed flushing, hives, and pruritus during the 500- mg preservative- free Solu- Medrol bolus. This was considered a true allergic reaction to Solu- Medrol, and she was switched to i. v. Decadron. When both temporal artery biopsies were negative, the Decadron was discontinued on day 3. The patient's vision continued to decline over the next 2 weeks. When vision reached hand motion OD and bare light perception OS, a left optic nerve sheath fenestration ( ONSF) was performed and prednisone, 60 mg orally, was instituted. The resected optic nerve sheath was negative for pathological changes. On postoperative day 1, the patient's visual acuity had improved to 20/ 800 OD and hand motion OS. The patient's visual acuity gradually improved; 3 weeks postoperatively she was able to read 20/ 30 + 1 OD and 20/ 70 - 1 OS. The prednisone was slowly tapered over 2 months. One year later, visual acuity was 20/ 25 OD and 20/ 30 OS. She still has a + 2 left relative pupillary defect and bilaterally pale optic nerves. The optic nerve edema and peripapillary hemorrhage have resolved. Her visual fields have also improved, with resolution of the constricted field; however, the enlarged blind spot remains OS. DISCUSSION In bilateral optic neuropathy, one must consider the more common causes in a 61- year- old woman, such as temporal arteritis. The patient had no jaw claudication, headaches, fevers, myalgias, or arthralgias. Two separate sedimentation rates were normal ( at 15 and 12), and both temporal artery biopsies were negative. Therefore, temporal arteritis is highly unlikely. Other ischemic causes such as small vessel disease associated with hypertensive disease were considered; however, these rarely occur in both eyes simultaneously, and the / Neuro- Ophtlmluiol, Vol. 16, No. 3, 1996 184 C. L. RAY AND 1. ]. DREIZIN patient was healthy. In addition the visual loss would not have been reversible by steroids and optic nerve sheath fenestration. A compressive mass or infiltrative tumor was excluded by the normal findings of the MRI scan and the normal histopathology of the optic nerve sheath. The CSF studies also excluded meningeal carcinomatosis. Normal laboratory testing excluded sarcoid, Lyme disease, and Leber's optic neuropathy ( including 14,484 mitochondrial mutation). There was a mildly positive speckled- pattern ANA titer and a normal ANA profile. Therefore, the ANA titer was only a marker of an autoimmune reaction and not systemic lupus. The heavy metal screen revealed a mild elevation in mercury. Mercury has been associated with peripheral neuropathies and cerebellar symptoms ( such as ataxia), but not with optic neuropathies. Optic neuropathy associated with influenza vaccination is a rare occurrence and is a diagnosis of exclusion. Five cases of optic neuropathy associated with influenza vaccination ( 1,2) and two cases associated with swine influenza vaccine ( 2) have been reported. The patient had received the influenza vaccine Fluogen, which is a subvirion vaccine that is ether-extracted. The vaccine is propagated in embryo-nated chicken eggs. Streptomycin sulfate, polysor-bate, ethyl ether, formalin, sodium bisulfate solution, phosphate buffer, and thimerosal are used during the processing of the vaccine. Concentrations of streptomycin sulfate and sodium bisulfite are reported to not be detectable in the final product ( 3). Optic neuropathy does not follow influenza vaccination as often as acute inflammatory demyelin-ating polyneuropathy ( Guillain- Barre syndrome). This case supports influenza vaccine as a cause of optic neuropathy. The patient's visual recovery appears correlated to the restarting of steroids. Was her recovery due just to time or was it from the combined use of prednisone, or from the prednisone alone? One would suspect that time was an important factor since the patient did not respond to the initial i. v. steroid bolus, plus she continued to improve slowly over the subsequent year. Perry et al. ( 1) and Bienfang et al. ( 4) described visual recovery with prednisone treatment. Our patient's recovery of vision may well have been due to the prednisone and time. Although the cases described by Perry et al. and Bienfang et al. do support the theory of visual recovery due to the prednisone, the case numbers were small. Our patient's vision improved after ONSF, which too may have played a role in her recovery. The patient's visual loss began 3 weeks after the influenza immunization, which is similar to the time onset described by other authors. Both the Perry et al. and Bienfang et al. patients had visual symptoms 2.5 weeks after immunization; this time course is consistent with viral replication and was presumed to be the explanation for the interval between immunization and visual loss. However, since the current influenza vaccine was not a live virus and was incapable of viral replication, there must be another explanation for our patient's visual loss occurring 3 weeks after immunization: 3 weeks is also the time course for an immune response. The patient's optic neuropathy may have been an immune response to the influenza vaccine. We propose that the time frame was related to a systemic immune response, as confirmed by the patient's transiently elevated ANA titer, which marks an autoimmune reaction. REFERENCES 1. Perry H, Mallen F, Grodin R, Cossari A. Reversible blindness in optic neuritis associated with influenza vaccination. Ann Ophthalmol 1979; 11: 545- 50. 2. Poser C. Neurological complications of swine influenza vaccination. Acta Neurol Scand 1982; 66: 413- 31. 3. Fluogen package insert. Morris Plains, NJ: Parke- Davis, Division of Warner- Lambert Company, 1993. 4. Bienfang DC, Kantrowitz F, Noble J, Raynor A. Ocular abnormalities after influenza immunization [ Letter]. Arch Ophthalmol 1977; 95: 1649. ] Neiiro- Ophlhalmol, Vol 16, No. 3, 2996 |
