Neuroretinitis.

Abstract

Despite the growing list of agents that can present as neuroretinitis, nearly one-half remain idiopathic. However, many of the candidate etiologies are treatable conditions, and accurate diagnosis can result in visual rehabilitation. A complete workup in patients presenting with acute neuroretinitis should include a thorough history and general medical evaluation. Exposure history should be thoroughly explored, including recent travel, unpasteurized and uncooked foods, sexual experience, and animal contacts. A detailed physical examination should be performed to note hidden rashes and inoculation sites and should include routine measurements of blood pressure and heart rate. Laboratory tests should be tailored to the history and may include complete blood count; erythrocyte sedimentation rate; bacterial, fungal, and viral blood cultures; antinuclear antibody test; angiotensin-converting enzyme; anti-double-stranded DNA; and C3. Serological evaluation should look for syphilis, Lyme disease, histoplasmosis, brucellosis, chlamydia, HIV, toxoplasmosis, Epstein-Barr virus, viral hepatitis B and C, and tuberculin skin test. Neuroretinitis is a clinical entity in which there is inflammation of the retinal architecture and optic nerve. There are numerous entities that can cause a picture of neuroretinitis ranging from vascular to infectious to autoimmune. With regards to the infectious etiologies, it is interesting to note that many of these organisms are obligate intracellular pathogens. The microorganisms B. henselae, T. gondii, R. typhi, T. pallidum, Mycobacterium tuberculosis, Histoplasma capsulatum, and various viruses, such as HIV, mumps, and HSV, are known intracellular agents. Other major infectious agents, such as B. burgdorferi and Leptospirosis spp. are known to remain sequestered within the circulatory system. It is possible that in this way these agents are able to breach the delicate blood-brain barrier. The implication of such findings on the treatment and management of neuroretinitis remains to be explored. Interestingly, the vast majority of infected patients do not develop neuroretinitis or demonstrate CNS involvement. Detailed examination of this variability may provide further insight into the pathogenic properties of these infectious agents, host tissue susceptibility, and mechanisms of blood-retina barrier integrity. A detailed retinal examination can provide an unobstructed view of the CNS. Careful inspection of this delicate interface may reveal subtle findings critical for accurate and rapid diagnosis of underlying systemic pathology. The varied visual and neurological symptoms of neuroretinitis attest to the fact that this is a disease of both the retina and contiguous neuronal elements. Such involvement significantly elevates the risk to the patient and emphasizes the need for early detection and prompt treatment.