Age: 16.0
Sex: F
Vaccine: HPVX
Symptoms: White blood cell count normal
Clinical narrative: This case was reported in a literature article and described the occurrence of bilateral vision loss in a 16-year-old female subject who was vaccinated with HPV vaccine (manufacturer unspecified). No family history of demyelinating disease, collagen-vascular disease or rheumatological disorders. On an unspecified date, the subject received 2nd dose of HPV vaccine (administration site and route unknown, batch number not provided). 8 days after vaccination with HPV vaccine, the subject experienced an acute onset of vision loss. Initially, the visual loss was noted in the right eye accompanied by a left side headache. These symptoms worsened over the next 24 hours. Her examination disclosed a visual acuity of only counting fingers bilaterally with mild left side weakness accompanied by sensory loss to pinprick in the left arm. This case was assessed as medically serious by GSK. There was a left afferent pupillary defect and normal fundoscopic examination. Her visual ability deteriorated further to inconsistently identifying light and movement from the left eye only. She complained of no other symptoms and denied antecedent trauma or prodromal illness. The magnetic resonance imaging brain showed swollen enhancement within the chiasm extending into both retrobulbar optic nerves and a right occipitoparietal lobe mass (later disclosed as tumefactive demyelination) with a large zone of surrounding vasogenic edema. Complete spine magnetic resonance imaging was normal. Biopsy of the hemispheric mass was performed and histology revealed demyelination. Subsequent cultures for aerobic and anaerobic bacteria, fungus, acid fast bacilli and examination for parasites were negative as were serum immunoglobulin G and immunoglobulin M titers for Toxoplasma gondii. The subject was treated with steroid and plasma. 3 months after the onset, the subject still had not regained any visual function, her weakness and sensory deficit recovered completely however. A repeat magnetic resonance imaging of brain revealed resolution of the hemispheric and chiasmal lesions. At 6 months, her fundoscopic examination disclosed bilateral optic disc pallor. A repeat magnetic resonance imaging at this time demonstrated no new lesions and continued resolution of the previously identified chiasmal enhancement and tumefactive lesion. Again complete spine magnetic resonance imaging was normal. Cerebrospinal fluid obtained 6 months after initial symptom onset was negative for malignancy. Additional studies revealed a clear and colorless fluid with 3 white blood cells and 0 red blood cells per microliter. At 18 months after the onset of her symptoms, her examination remained stable with no further neurological complaints, persistent profound visual impairment, inconsistently identifying light and movement from the left eye only. A magnetic resonance imaging of the brain was performed and was unchanged compared with the previous one done at 6 months. An acute demyelinating encephalomyelitis was likely to explain the multifocal deficits. There was no supportive clinical or laboratory evidence for systemic lupus erythematous, Sjogren syndrome or Lyme infection. Other viral studies were unrevealing or negative. The radiological resolution of the chiasmal lesion preceded the occipito-parietal lesion by months. This dissociation of the clinico-radiographic evolution might suggest a clinical feature in favor of acute demyelinating encephalomyelitis. According the authors, it was possible that human papilloma virus was the precipitant for the demyelinating event in the subject. It was tempting to speculate whether there might be a specific immune mechanism initiated with human papilloma virus not yet identified which resulted in not only acute demyelinating encephalomyelitis but also in an unusual clinical course that resulted in persistent visual loss.