Midbrain lesions and third-nerve palsy.
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Biomedical subjects
Publications and source records attributed to M Strominger.
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BACKGROUND: Sarcoidosis is frequently overlooked as a cause of optic neuropathy. A cascade of immune interactions has been cited in the pathogenesis. Optic nerve involvement can be the initial manifestation of systemic disease, making the diagnosis even more elusive. Compatible clinicoradiographic and abnormal laboratory findings along with histologic evidence of noncaseating granuloma are necessary to secure the diagnosis of sarcoidosis. METHODS: A case report is presented of a 41-year-old patient with severe papillitis and a junctional scotoma as the first declaration heralding neurosarcoidosis (NS). Co-management with a neuroophthalmologist at an academic teaching hospital prompted the necessary diagnostic studies to preserve vision. RESULTS: Sarcoidosis was diagnosed on the basis of the patient's clinical presentation of rapid vision loss, enlarging mass in the anterior visual pathway revealed by CT and MRI, as well as increased uptake of gallium in the lungs and lacrimal glands. Also considered in the differential diagnosis were glioblastoma, lymphoma, and demyelinating disease. CONCLUSIONS: This case represents an example of triage referral involving optometry and academic ophthalmology. Rapid intervention with intravenous corticosteroids should be considered in the face of atypical optic neuritis with a suspected inflammatory etiology.
BACKGROUND: Systemic lupus erythematosus (SLE) is a multisystemic inflammatory disease of unknown etiology. Physiopathology includes small vessel occlusion and auto-antibody production. Neuro-ophthalmic complications can be detected in 10-30% of SLE cases. Further, some patients can present with neuro-ophthalmic complications prior to diagnosis of SLE. PATIENTS AND METHODS: We report seven cases of neuro-ophthalmic complications of SLE demonstrating lesions from the retina to the brain. The other possible manifestations of SLE will be reviewed. RESULTS: Two cases were not yet diagnosed with SLE when neuro-ophthalmic disease occurred. Anti-double stranded DNA antibodies were detected at a very high titer, suggesting SLE, later confirmed by rheumatologists. CONCLUSIONS: Ophthalmologists should be aware of the unusual patient presenting with a neuroophthalmic disorder prior to the diagnosis of SLE. In such cases, autoantibodies should be sought. Antinuclear antibodies are very sensitive but non specific for SLE. Anti-double stranded DNA antibodies are specific for SLE and elevated titer should raise the suspicion of undiagnosed SLE.