Paravascular inner retinal cleavage in a highly myopic eye.

cal syndrome characterized by abrupt visual loss, optic nerve swelling, and a macular star exudate. It is usually unilateral. Originally referred to as “Leber’s idiopathic stellate neuroretinitis,” it is now known that this syndrome is caused by a variety of infectious causes. Since the advent of accurate serologic testing it has become recognized that B henselae, the causative agent of catscratch disease, is the most common cause of neuroretinitis. In the setting of B henselae infection, neuroretinitis with peripapillary serous retinal detachment has previously been described, as well as bilateral neuroretinitis. To our knowledge, ours is the first report of bilateral neuroretinitis with bilateral peripapillary retinal detachments. This is also the first reported case of serous retinal detachment in neuroretinitis caused by an infectious agent other than B henselae. Serous retinal detachments in neuroretinitis are not specific to B henselae infection, but likely represent the severe form of a disease that can be caused by many different organisms. Human immunodeficiency virus microangiopathy, characterized by retinal hemorrhages, cottonwool spots, and microaneurysms, is the most common ophthalmic finding in HIV-positive patients. Hepatitis B virus has been listed as a suspected cause of neuroretinitis. In 1986 Farthing et al described a case of bilateral neuroretinitis in a homosexual patient with acute HBV infection who tested positive for HIV 1 year after the initial examination. It is possible that this patient was HIV-positive at the time of the initial examination, but serum testing for HIV (or human T-lymphocyte virus type III/lymphadenopathy– associated virus, as it was known then) at that time was not sensitive enough to detect the virus in the early stages of disease. Concurrent hepatitis C infection has been shown to have an additive effect on HIV retinal microangiopathy. We propose a similar synergistic effect between HIV and HBV in this case, mediated either through a coinfection mechanism or HIV-induced immunosuppression leading to enhanced HBV effect. That our patient’s condition resolved with treatment of HIV and HBV further supports this hypothesis.