During the antidepressant treatment phase, we found 1) the OSA group performed significantly worse on the SRT delayed recall at week 16 compared to the non-OSA group, and the results remained significant after controlling for baseline performance, age, gender, and education; 2) the OSA group had a greater microvascular burden, including DWMHs, PVHs, and SCGs, as well as grade 2 and 3 lesions in DWM, PVH, and SCG, 3) between groups, the differences in the hippocampal and entorhinal cortex volumes were not statistically different, and the results do not change after controlling for intracranial volume.
In ANCOVA analysis, the OSA group performed significantly worse than the non-OSA group on the SRT-delayed recall (p=0.000) only after antidepressant …show more content…
The OSA group had significantly more microvascular burden (e.g., MRI signal hyperintensities) compared to the non-OSA group (see Table 3). In logistic regression analyses, the combined effects of each baseline cognitive performance and each C-SVD measure improve predictive accuracy of having OSA. However, only the volume of white matter hyperintensities significantly contributes to the prediction. The odds of having OSA are 3.6 times greater as white matter hyperintensities increase (odds ratio, 3.62, 95% CI, 1.12-11.75, p< 0.20) while the OSA group did not (SRT delayed recall: ∆=-1.0, p=0.16; Trial A: ∆=-2.4, p=0.54) (see Figure 1 and Figure 2). It leaves open the question of whether antidepressants influence OSA, which may indirectly affect memory functions. Several studies examined the effectiveness of antidepressants as medication treatment option for OSA. The rationale was that serotonin plays a critical role in maintaining upper airway patency during sleep[74-76] and antidepressants might increase the upper airway dilator muscle tone thus reducing the collapsibility during sleep in patients with OSA.[77] Antidepressants, such as protriptyline (non-sedating TCA), paroxetine and fluoxetine (SSRI), and mirtazapine (mixed antagonist and agonist acting on serotonin …show more content…
Leave OSA untreated may cause continuing cognitive decline and increase the risk for conversion to dementia. The vascular contributions to cognitive impairment in DEP-CI patients with OSA suggest a mixture of microvascular and AD
In ANCOVA analysis, the OSA group performed significantly worse than the non-OSA group on the SRT-delayed recall (p=0.000) only after antidepressant …show more content…
The OSA group had significantly more microvascular burden (e.g., MRI signal hyperintensities) compared to the non-OSA group (see Table 3). In logistic regression analyses, the combined effects of each baseline cognitive performance and each C-SVD measure improve predictive accuracy of having OSA. However, only the volume of white matter hyperintensities significantly contributes to the prediction. The odds of having OSA are 3.6 times greater as white matter hyperintensities increase (odds ratio, 3.62, 95% CI, 1.12-11.75, p< 0.20) while the OSA group did not (SRT delayed recall: ∆=-1.0, p=0.16; Trial A: ∆=-2.4, p=0.54) (see Figure 1 and Figure 2). It leaves open the question of whether antidepressants influence OSA, which may indirectly affect memory functions. Several studies examined the effectiveness of antidepressants as medication treatment option for OSA. The rationale was that serotonin plays a critical role in maintaining upper airway patency during sleep[74-76] and antidepressants might increase the upper airway dilator muscle tone thus reducing the collapsibility during sleep in patients with OSA.[77] Antidepressants, such as protriptyline (non-sedating TCA), paroxetine and fluoxetine (SSRI), and mirtazapine (mixed antagonist and agonist acting on serotonin …show more content…
Leave OSA untreated may cause continuing cognitive decline and increase the risk for conversion to dementia. The vascular contributions to cognitive impairment in DEP-CI patients with OSA suggest a mixture of microvascular and AD