Pathogenesis of cerebral Small-Vessel disease in obstructive sleep apnea Chapter uri icon


MeSH Major

  • Alzheimer Disease
  • Cognition
  • Cytidine Diphosphate Choline
  • Dementia, Vascular
  • Nootropic Agents
  • Stroke


  • © Cambridge University Press 2013.Introduction Elderly women affected by obstructive sleep apnea (OSA) develop cognitive deficits [1] compared to age-matched controls with normal sleep. Yaffe and her colleagues [1] concluded that the cognitive decline correlated with hypoxemia rather than with the fragmentation of the sleep architecture resulting from apneas and hypopneas. A similar deleterious effect of OSA on cognitive function has been demonstrated in patients referred to the Alzheimer and dementia clinic of the Methodist Neurological Institute in Houston, TX (Román, unpublished data). Moreover, in the latter patients, magnetic resonance imaging (MRI) of the brain showed that OSA was accompanied by varying degrees of cerebral small-vessel disease, in particular periventricular hyperintensities of the white matter and lacunar strokes, explaining the clinical picture of subcortical prefrontal dysfunction observed in these patients, in isolation or mixed with features of Alzheimer’s disease. In this chapter, the postulated pathogenesis of cerebral small-vessel disease in subjects with OSA is reviewed. Cognitive and vascular consequences of sleep apnea Sound sleep is critical for cognitive function, in particular because of its effects on synaptic plasticity and consolidation of memory [2]. Therefore, disruption of sleep and fragmentation of the sleep architecture are detrimental for memory. Moreover, sleep is a vital ancestral need and prolonged sleep deprivation leads to death in several species[2], including humans with fatal familial insomnia, a prion disease[3]. The deleterious effects of OSA on the vascular and circulatory systems are well recognized and include development of hypertension, coronary artery disease, heart failure, myocardial infarction, pulmonary hypertension, atrial fibrillation, stroke, ruptured aortic aneurysms, and sudden cardiac death[4].

publication date

  • January 2010



  • Book Chapter


Digital Object Identifier (DOI)

  • 10.1017/CBO9781139061056.010

Additional Document Info

start page

  • 97

end page

  • 103