ABSTRACT
BACKGROUND: This brief report aims to report a case of bilateral macular ischemia as a cause of sudden decreased vision in a patient with acquired immune deficiency syndrome (AIDS). FINDINGS: A 26-year-old male with disseminated cryptococcal meningitis, Candida thrush, Pneumocystis jiroveci pneumonia, and positive human immunodeficiency virus (HIV) infection with CD4 count of 4 cells/µl complained of sudden blurred vision in both eyes while on treatment with systemic antiviral, antifungal, and antibiotic medications. Ocular examination revealed HIV retinopathy changes with significant macular ischemia in both eyes, which was confirmed by fluorescein angiography. One dose of intravitreal foscarnet (1.2 mg/0.1 cc) was injected in both eyes. Laboratory work-up of serum and vitreous samples showed negative cytomegalovirus (CMV) titers. At 2 weeks of follow-up, he was started on treatment with atripla, a combination anti-retroviral therapy for AIDS. At 6 weeks of follow-up, there was an improvement in visual acuity and clinical findings. CONCLUSIONS: Noninfectious HIV retinopathy in AIDS is common, but bilateral macular ischemia is a rare presentation. It is important to rule out CMV retinitis as it is a major cause of visual morbidity among AIDS patients.
ABSTRACT
Two dramatic phenomena of human adolescence are sexual maturation and a steep decline in the delta EEG of non-rapid eye movement (NREM) sleep. It has long been speculated that these developmental changes are causally related. Here, we present the first longitudinal data on this issue. Cohorts of 9- and 12-year-old children (n = 31, 38) were studied with in-home sleep EEG recordings at 6-mo intervals over 2 years. Pubertal (Tanner) stage, height, and weight were obtained at each time point. NREM delta power density (DPD) did not change significantly over ages 9-11 years, and its level did not differ in boys and girls. DPD declined by 25% between ages 12 and 14 years. This decline was parallel in the two sexes, but levels were lower in girls, suggesting that their DPD decline began earlier. Mixed effect analyses demonstrated that DPD was strongly related to age with Tanner stage, height, weight and body mass index controlled but that none of these measures of physical and sexual development was related to DPD with age controlled. NREM delta is the sleep EEG component homeostatically related to prior waking duration and the intensity of waking brain activity. We hypothesize that the DPD decline is caused by age-programmed synaptic pruning that decreases waking brain metabolic rate. This reduced rate would decrease the "substrate" for delta homeostasis. Whether or not this interpretation proves correct, these longitudinal data demonstrate that the delta decline in adolescence reflects brain processes that are not predicted by physical growth or sexual maturation.
