Sleep-Disordered Breathing and Idiopathic Normal-Pressure Hydrocephalus: Recent Pathophysiological Advances.

PURPOSE OF REVIEW: Idiopathic normal-pressure hydrocephalus (iNPH) is characterized clinically by ventriculomegaly, abnormal gait, falls, incontinence, and cognitive decline. This article reviews recent advances in the pathophysiology of iNPH concerning sleep-disordered breathing (SDB) and glymphatic circulation during deep sleep. RECENT FINDINGS: The authors found iNPH frequently associated with obstructive sleep apnea (OSA). A critical factor in iNPH is intracranial venous hypertension delaying drainage of cerebrospinal fluid (CSF) into the cerebral venous sinuses. CSF-venous blood circulates in the jugular veins and finally drains into the heart. During SDB, repeated reflex attempts to breathe induce strong respiratory efforts against a closed glottis thereby increasing the negative intrathoracic pressure. This causes atrial distortion and decreases venous return to the heart resulting in retrograde intracranial venous hypertension. Additionally, repeated awakenings from OSA impede sleep-associated circulation of interstitial CSF into the glymphatic circulation contributing to hydrocephalus. Sleep has become a critical element in the cognitive changes of aging including iNPH.

Idiopathic normal-pressure hydrocephalus and obstructive sleep apnea are frequently associated: A prospective cohort study.

BACKGROUND: Idiopathic normal-pressure hydrocephalus (iNPH) is defined by ventriculomegaly, cognitive decline, urinary incontinence and gait problems. Vascular risk factors (VRF) are associated with iNPH but obstructive sleep apnea (OSA) -a well-known independent VRF- is seldom mentioned. METHODS: We investigated the presence of sleep-disordered breathing in a prospective cohort of 31 consecutive unselected patients with iNPH using sleep questionnaires and nocturnal polysomnography (PSG). RESULTS: We found OSA in 90·3% (28/31) patients with iNPH; all had undiagnosed sleep abnormalities (snoring, awakenings, nocturia) and excessive daytime sleepiness (Epworth scale = 11·4 ±â€¯6·4; normal <8). Nocturnal PSG showed moderate-to-severe OSA in 25 patients (80·6%) with mean apnea-hypopnea index (AHI) 31·6 ±â€¯23·6/h; mean respiratory distress index (RDI) 34·5/h; and, mean SaO2 desaturation at nadir, 82·2 ±â€¯7·5%. The observed OSA prevalence is statistically significant: 90·3%, 95%CI 74·3-97·5; p = 0·000007. Other VRF included overweight body-mass index (BMI >25- < 30 kg/m2) in 59%, hyperhomocysteinemia 57%, hypertension 43%, hyperlipidemia 39%, diabetes 32%, smoking 21%, coronary disease 18%, and previous stroke 10%. CONCLUSION: Abnormal sleep breathing is frequently associated with iNPH. Validation in larger series is required but we suggest including sleep evaluation in patients suspected of iNPH.