OSA Model

OSA causes nocturnal intermittent hypoxemia and sleep fragmentation (arousals) in response to oxygen desaturation. There is emerging evidence that OSA, vascular depression, and cognitive impairment/dementia are linked to several pathological processes in the cerebral microvascular and neurovascular systems. We present a model describing the key pathophysiological mechanisms that underlie those associations for which intermittent hypoxia plays a critical role, including hypoperfusion, endothelial dysfunction, and neuroinflammation (see Figure 2).
I. Hypoperfusion
OSA
In OSA, there are profound changes in nocturnal intracranial hemodynamics and oxygen saturation. During an apneic episode, cerebral blood flow velocity increases progressively, …show more content…
Because more markedly decrease in hemoglobin levels from baseline during rapid eye movement (REM) sleep than non-REM (NREM) sleep, an increased CBF to meet the demand of oxygen may not be able to compensate for oxygen desaturation during REM sleep in patients with severe OSA.[6, 7] The evidence of myocardial infarction happens during early morning hours is more often seen in patients with OSA compared to those with no OSA,[8, 9] demonstrating the significance of hypoxemia involvement in infarction.[7] Chronic nocturnal hypoxemia accelerates the development and progression of C-SVD,[10] resulting in lacunar infarcts, white matter and/or gray matter lesions, and white matter integrity abnormalities.[2, 5] Such microvascular damage results in abnormal myelin and axonal integrity.[11] Anatomically, certain regions of the brain are especially vulnerable to prolonged hypoxic-ischemic injury, such as the prefrontal and frontal lobes,[12, 13] basal ganglia,[14] and hippocampus.[15, 16] Damage to these brain regions is associated with an aberrant neural function, resulting in mood disturbance and cognitive deficits in patients with OSA.[17-19] There is strong …show more content…
CRP), and adhesion molecules (e.g., ICAM).[50, 51] OSA induces a chronic inflammatory state at the BBB, leading to exacerbate microvessel permeability through changes in BBB transports, tight junctions of BBB, and vascular pores during angiogenesis.[52] In some patients with OSA, a chronic inflammatory state may lead to cognitive impairment by causing persistent microglial activation and altering synaptic plasticity.[52] In summary, chronic BBB dysfunction leads to BBB hyperpermeability and neuroinflammation, resulting in the development or progression of vascular depression, mild cognitive impairment, and

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