Patients with idiopathic intracranial hypertension (IIH) frequently have coexisting obstructive sleep apnea (OSA). We aimed to determine if the prevalence and severity of OSA is greater in patients with IIH than would be expected, given their other risk factors for OSA. We included 24 patients (20 women, four men) with newly-diagnosed IIH who had undergone overnight polysomnography. We calculated the expected apnea-hypopnea index (AHI) for each patient, based on their age, sex, race, body mass index (BMI), and menopausal status, using a model derived from 1,741 randomly-sampled members of the general population who had undergone overnight polysomnography. We compared the AHI values obtained from polysomnography with those predicted by the model using a paired t test. Our study had 80 % power to detect a 10-unit change in mean AHI at α = 0.05. Eight patients (33.3 %; six women, two men) had OSA by polysomnography. AHIs from polysomnography were not significantly different from those predicted by the model (mean difference 3.5, 95 % CI: -3.0-9.9, p = 0.28). We conclude that the prevalence and severity of OSA in IIH patients is no greater than would be expected for their age, sex, race, BMI, and menopausal status. It remains unclear whether the presence or treatment of OSA influences the clinical course of IIH.

Numerous lines of evidence converge in suggesting that sleep apnea may play a causal role in severe cognitive impairment, most likely Alzheimer's Disease (AD) but also including vascular dementia. Until recently, most of these studies have been based on small samples of clinic patients or population-based, descriptive studies of sleep apnea and cognition. Although randomized clinical trials have been completed for treating sleep apnea in middle-aged cognitively intact patients with sleep apnea using continuous positive airway pressure (CPAP), systematic intervention studies in well-characterized AD patients are very rare and have been published from only a single research group. Results suggest some very modest improvement in selected aspects of cognition over a very limited period of time. There is, thus, a lack of conclusive evidence that treating sleep apnea in AD is likely to have a major impact on dementia, although it may benefit daytime hypersomnolence, excessive napping, and lethargy so common in many dementia patients. In addition, anecdotal evidence suggests that in some selected cases, treatment can have relatively dramatic effects. At this point in time, the best indications for pursuing treatment for sleep apnea with nasal CPAP in AD patients would be factors promoting adherence, such as presence of a caregiver/family member invested in treatment, and a realistic appraisal of what goals of intervention should be expected (eg, increasing daytime functionality by enhancing alertness) over a reasonable window of time. Speculative factors implicating a potentially causal role for sleep apnea in dementing illness would be comorbid diseases well-established to be associated with both sleep apnea and dementia (cardiovascular disease, diabetes) and presence of the Apolipoprotein-E4 genotype. None of these factors have been shown conclusively to influence CPAP efficacy in dementia, but to the extent that they lie on a putative causal pathway for sleep apnea and dementia (either as moderators or mediators of CPAP efficacy), their presence might be expected to enhance, rather than mitigate, a more favorable response in the domain of cognition.