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This chapter reviews the association between sleep-related breathing disorders (SRBDs) and cognitive functioning, depression, and anxiety. Obstructive sleep apnea (OSA) patients complain of various neuropsychiatric symptoms. Approximately 80% of OSA patients complain of both excessive daytime sleepiness and cognitive impairments, and half report personality changes. The pathogenesis of cognitive deficits in OSA is controversial and most likely multifactorial. Many studies have examined cognitive functioning after treatment for OSA has been initiated. Depression is the most commonly encountered affective disorder associated with OSA. As with cognitive impairment, sleep fragmentation and hypoxemia during sleep are suspected to be responsible for depressive symptoms in OSA. There is a growing literature suggesting that the links between depressive symptoms and OSA may be associated with obesity and the metabolic syndrome. Clinicians should suspect OSA particularly in depressed patients who present with symptoms such as snoring and excessive daytime fatigue.
Background: A growing body of literature suggests that caregiving burden is associated with impaired immune system functioning, which may contribute to elevated morbidity and mortality risk among dementia caregivers. However, potential mechanisms linking these relationships are not well understood. The purpose of this study was to investigate whether stress-related experience of depressive symptoms and reductions in personal mastery were related to alterations in ß2-adrenergic receptor sensitivity.
Methods: Spousal Alzheimer's caregivers (N = 106) completed measures assessing the extent to which they felt overloaded by their caregiving responsibilities, experienced depressive symptoms, and believed their life circumstances were under their control. We hypothesized that caregivers reporting elevated stress would report increased depressive symptoms and reduced mastery, which in turn would be associated with reduced ß2- adrenergic receptor sensitivity on peripheral blood mononuclear cells (PBMC), as assessed by in vitro isoproterenol stimulation.
Results: Regression analyses indicated that overload was negatively associated with mastery (β = −0.36, p = 0.001) and receptor sensitivity (β = −0.24, p = 0.030), whereas mastery was positively associated with receptor sensitivity (β = 0.29, p = 0.005). Finally, the relationship between overload and receptor sensitivity diminshed upon simultaneous entry of mastery. Sobel's test confirmed that mastery significantly mediated some of the relationship between overload and receptor sensitivity (z = −2.02, p = 0.044).
Conclusions: These results suggest that a reduced sense of mastery may help explain the association between caregiving burden and reduced immune cell ß2-receptor sensitivity.
Baroreflex (BR) testing with phenylephrine (PE)
and amyl nitrite (AN) provided an opportunity to evaluate
the ability of impedance cardiography (IC) to track the
rapid hemodynamic (HD) changes elicited by these drugs.
The AN response was measured after inhalation and the PE
response was measured after a bolus injection in 19 subjects
on two occasions. High reliability was observed for all
of the HD measures. Blood pressure (BP), peripheral resistance
(PR), and preejection period (PEP) decreased significantly
after administration of AN, whereas heart rate (HR) and
cardiac output (dotted Q) increased. BP and total PR increased
significantly after administration of PE; HR and dotted Q decreased
and PEP did not change significantly. Stroke volume did
not change significantly with either drug. The BR slope
was reliably elicited with AN and PE. The IC and Finapres
BP consistently detected short-term changes in HD responses
to AN and PE. The pharmacological interventions demonstrated
that IC measures followed the course predicted by the actions
of the drugs. Change in PEP and dZ/dt reflected increased
contractility. The BR sensitivity was also reproducible.
While studies from diverse fields of research suggest a relationship between problems expressing anger and cardiovascular illness, few studies have provided a potential pathophysiological link of such a relationship. Forty-five males were classified according to one of three anger expression categories: those who did not suppress their anger (N = 13), those who partially suppressed their anger (N = 19), and those who definitely suppressed their anger (N = 13). For each, we determined lymphocyte β-adrenergic receptor function and blood pressure responsiveness to a standardized mathematics stressor. Those subjects who routinely suppressed their expression of anger had increased β-adrenergic receptor sensitivity (P = 0·01) (isoproterenol-stimulated cyclic AMP production) and a greater systolic blood pressure response to the stressor (P = 0·001). Anger suppression was unrelated to the subject's age, weight, or socioeconomic status. These findings may be germane to prior clinical and epidemiologic observations relating anger expression and cardiovascular illness.
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