OSA Group Case Study

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The main findings of this study include: 1), the OSA group performed significantly worse on the SRT delayed recall compared to the non-OSA group only after antidepressant treatment at week 16, and the results remained significant after controlling for the baseline performance; 2), compared to the non-OSA group, the OSA group had a greater microvascular burden with the evidence of more severe MRI signal hyperintensities of DWM, PVH, and SCG, as well as higher percentages of patients with advanced lesions (e.g., grade 2 and 3) of DWM, PVH, and SCG; and 3), between the groups, the differences in the hippocampal and entorhinal cortex volumes were not statistically different, and the results did not change after controlling for intracranial volume. …show more content…
After 16 weeks of antidepressant treatment, only the SRT delayed recall (effect size=0.45, p=0.000) discriminated best between the OSA group and the non-OSA group whereas the SRT immediate recalls (adjusted effect size=0.45, p=0.07) and recognition (adjusted effect size=-0.06, p=0.51) did not. (See Table 2 and Figure 1). Our findings are consistent with the results from two meta-analysis studies investigated memory function in OSA compared to age-matched norms, showing that OSA most frequently affects verbal episodic memory compared to other cognitive domains, in particular, verbal delayed recall (effect sizes d= 0.44-0.52).[11, 52] These data suggests that OSA predominantly affects memory retrieval process and that encoding process may not be the primary resource of episodic memory impairment in …show more content…
Disruption of white matter integrity (fiber tracts) connecting frontal and temporal cortex and frontal-subcortical structures are associated with vascular depression[24, 53, 54] and cognitive impairment,[55-59] including episodic memory impairment.[60-62] OSA is an independent risk factor for C-SVD. White matter hyperintensities on MRI and low fractional anisotropy (FA) on Diffusion Tensor Imaging (DTI) have found in patients with moderate to severe OSA as a consequence of repetitive ischemic-hypoxic insults to the brain,[63-67] resulting in abnormal myelin and axonal integrity over time.[68] Several longitudinal studies reported that C-SVD was associated with cognitive decline in patients with untreated moderate to severe OSA.[64, 69, 70] Therefore, when OSA causes damages to the deep and subcortical white matter and white matter fiber tracts, patients may experience vascular depression, executive dysfunction, and amnestic

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