Objective To compare clinical features, visual characteristics, and treatment of idiopathic intracranial hypertension patients with and without papilledema. Background Idiopathic intracranial hypertension does not often occur without papilledema. This study estimates the prevalence and compares the clinical characteristics of idiopathic intracranial hypertension patients with and without papilledema. Methods We performed a cross-sectional analysis of all idiopathic intracranial hypertension patients diagnosed at the University of Utah Neuro-Ophthalmology Unit between 1990 and 2003. Patient records were reviewed for presence of papilledema and other signs, symptoms, and treatment characteristics. Each patient without papilledema was matched to the patient with papilledema who was closest to his/her age and sex. McNemar’s and Wilcoxon-signed rank sum tests were used to compare characteristics between matched pairs. Results Among all patients (n = 353), the prevalence of those without papilledema was 5.7% (n = 20). Patients without papilledema reported photopsias (20%), and were found to have spontaneous venous pulsations (75%) and non-physiologic visual field constriction (20%) more often than did those with papilledema. Mean opening pressure, although above normal, was lower in patients without papilledema (mean = 309 mm cerebrospinal fluid) compared with those with papilledema (mean = 373 mm cerebrospinal fluid, P = .031). Idiopathic intracranial hypertension patients without papilledema had more frequent diagnostic lumbar punctures than did patients with papilledema. Visual acuities and treatment were similar between groups. Conclusions The clinical presentation of idiopathic intracranial hypertension without papilledema is only somewhat different from that of idiopathic intracranial hypertension with papilledema. The lower opening pressure in patients without papilledema may explain variations in symptoms and signs between the 2 groups. When there are visual field changes in idiopathic intracranial hypertension without papilledema, non-physiologic visual loss should be considered.

High levels of human immunodeficiency virus (HIV) DNA in peripheral blood mononuclear cells (PBMCs), and specifically within CD14+ blood monocytes, have been found in HIV-infected individuals with neurocognitive impairment and dementia. The failure of highly active antiretroviral therapy (HAART) to eliminate cognitive dysfunction in HIV may be secondary to persistence of HIV-infected PBMCs which cross the blood-brain barrier, leading to perivascular inflammation and neuronal injury. This study assessed brain cortical thickness relative to HIV DNA levels and identified, we believe for the first time, a neuroimaging correlate of detectable PBMC HIV DNA in subjects with undetectable HIV RNA. Cortical thickness was compared between age- and education-matched groups of older (>40 years) HIV-seropositive subjects on HAART who had detectable (N = 9) and undetectable (N = 10) PBMC HIV DNA. Statistical testing revealed highly significant (P < 0.001) cortical thinning associated with detectable HIV DNA. The largest regions affected were in bilateral insula, orbitofrontal and temporal cortices, right superior frontal cortex, and right caudal anterior cingulate. Cortical thinning correlated significantly with a measure of psychomotor speed. The areas of reduced cortical thickness are key nodes in cognitive and emotional processing networks and may be etiologically important in HIV-related neurological deficits.