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This chapter highlights the significance of oxidative stress and vascular inflammation in promoting endothelial disease and atherosclerosis in sleep apnea patients, with an emphasis on the contribution of these mechanisms to the development of cardiovascular morbidity and stroke in these patients. Most studies investigating oxidative stress in patients with obstructive sleep apnea (OSA) present indirect findings by using various bodily fluid markers such as plasma, serum, or urine. The presence of IH is a key factor in initiating proatherogenic activity and a likely link for the close association between OSA and cardiovascular diseases. Increased oxidative stress, vascular inflammation, and endothelial dysfunction resulting from intermittent hypoxia (IH) can lead to high susceptibility of patients with OSA to stroke. The balance between proatherogenic and protective mechanisms may determine the predisposition of OSA patients to stroke or other cardiocerebrovascular diseases.
This chapter talks about an 83-year-old man with a 3-4-year history of progressive speech difficulty. Past medical history was remarkable for hypertension and ischemic heart disease. Psychiatric history was unremarkable. General neurological exam was remarkable for bilateral cogwheeling in the upper extremities, rigid posture, and bilateral decreased arm swing. Magnetic Resonance Imaging (MRI) of the brain showed diffuse atrophy. Single-Photon Emission Computed Tomography (SPECT) showed decreased perfusion in the left temporo-parietal region. The findings suggested a diagnosis of progressive non-fluent aphasia (PNFA). The possibility of corticobasal syndrome (CBS) was also raised. A variety of neuropathological changes have been associated with PNFA. The most common are non-Alzheimer tauopathies. Alzheimer pathology has also being identified in PNFA, with some reports showing these in up to 30% of cases. In these patients, the distribution of AD pathology may be unusual, showing a frontotemporal pattern.