Abstract:Diagnostic classification schemas and clinical features of depression may influence sleep EEG findings, but gender may be a more important consideration.
“…The pathophysiology of the illness, metabolic changes, or the effect of medications may all be causes of variations in sleep architecture 60,62 that may alter the expected patterns described in patients with MD. 17,19,20 In this respect it is also interesting to note that SWS was higher in patients on dialysis compared to predialysis or transplanted patients. 53,56 These results may indicate that the modality of the renal replacement therapy or the kidney disease itself may affect SWS and the regulation of non-rapid eye movement (NREM) sleep in some yet undefined way.…”
Section: 64mentioning
confidence: 94%
“…In fact, increased stage 2 sleep is not a characteristic feature of the sleep architecture of patients in whom MD was diagnosed. [19][20][21] However, in a randomized placebo-controlled trial a significant improvement of low mood in olanzapine-treated participants was associated with changes mainly in sleep continuity measures and also the duration of stage 2 sleep, but not with the change of SWS.…”
Study Objectives: Both depression and sleep complaints are very prevalent among kidney transplant (kTx) recipients. However, details of the complex relationship between sleep and depression in this population are not well documented. Thus, we investigated the association between depressive symptoms and sleep macrostructure parameters among prevalent kTx recipients. Methods: Ninety-five kTx recipients participated in the study (54 males, mean ± standard devation age 51 ± 13 years, body mass index 26 ± 4 kg/m 2 , estimated glomerular filtration rate 53 ± 19 ml/min/1.73 m 2 ). Symptoms of depression were assessed by the Center for Epidemiologic Studies -Depression Scale (CES-D). After 1-night polysomnography each recording was visually scored and sleep macrostructure was analyzed. Results: The CES-D score was significantly associated with the amount of stage 2 sleep (r = 0.20, P < .05), rapid eye movement (REM) latency (r = 0.21, P < .05) and REM percentage (r = −0.24, P < .05), but not with the amount of slow wave sleep (r = −0.12, P > .05). In multivariable linear regression models the CES-D score was independently associated with the amount of stage 2 sleep (β: 0.205; confidence interval: 0.001-0.409; P = .05) and REM latency (β: 0.234; confidence interval: 0.001-0.468; P = .05) after adjustment for potential confounders.
I NTRO DUCTI O NDepression is one of the most prevalent mental health conditions in patients with chronic kidney disease (CKD) [1][2][3][4] ; furthermore, it is an important determinant of impaired quality of life. 5,6 Among kidney transplant (kTx) recipients, depression is associated with reduced adherence and also with increased morbidity, graft loss, and mortality. [7][8][9][10][11][12][13] Poor sleep and various sleep problems are also frequent complaints among kTx recipients.14,15 Earlier we reported that chronic insomnia was independently associated with the presence of depression in kTx recipients. 16 In the general population there is a strong and bidirectional relationship between depression and sleep.17 This is also reflected in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition definition of major depression (MD), 18 as sleep complaints are core symptoms of MD. Several objective sleep parameters are different in patients with MD than in healthy control patients. Patients with MD have decreased amounts of slow wave sleep (SWS) and shortened rapid eye movement (REM) latency with increased amounts of REM sleep. The exact mechanisms and factors that may link depression to poor clinical outcomes among kTx recipients are not yet well defined. In a recent review focusing on kTx and depression, 23 sleep is not mentioned. This may be due to the complete lack of polysomnography (PSG) studies that assess the association between sleep and depression in this population. The frequent co-occurrence of subjective sleep complaints and depression among kTx recipients 16 suggests that the relationship between the two conditions may be similar to the association described in the g...
“…The pathophysiology of the illness, metabolic changes, or the effect of medications may all be causes of variations in sleep architecture 60,62 that may alter the expected patterns described in patients with MD. 17,19,20 In this respect it is also interesting to note that SWS was higher in patients on dialysis compared to predialysis or transplanted patients. 53,56 These results may indicate that the modality of the renal replacement therapy or the kidney disease itself may affect SWS and the regulation of non-rapid eye movement (NREM) sleep in some yet undefined way.…”
Section: 64mentioning
confidence: 94%
“…In fact, increased stage 2 sleep is not a characteristic feature of the sleep architecture of patients in whom MD was diagnosed. [19][20][21] However, in a randomized placebo-controlled trial a significant improvement of low mood in olanzapine-treated participants was associated with changes mainly in sleep continuity measures and also the duration of stage 2 sleep, but not with the change of SWS.…”
Study Objectives: Both depression and sleep complaints are very prevalent among kidney transplant (kTx) recipients. However, details of the complex relationship between sleep and depression in this population are not well documented. Thus, we investigated the association between depressive symptoms and sleep macrostructure parameters among prevalent kTx recipients. Methods: Ninety-five kTx recipients participated in the study (54 males, mean ± standard devation age 51 ± 13 years, body mass index 26 ± 4 kg/m 2 , estimated glomerular filtration rate 53 ± 19 ml/min/1.73 m 2 ). Symptoms of depression were assessed by the Center for Epidemiologic Studies -Depression Scale (CES-D). After 1-night polysomnography each recording was visually scored and sleep macrostructure was analyzed. Results: The CES-D score was significantly associated with the amount of stage 2 sleep (r = 0.20, P < .05), rapid eye movement (REM) latency (r = 0.21, P < .05) and REM percentage (r = −0.24, P < .05), but not with the amount of slow wave sleep (r = −0.12, P > .05). In multivariable linear regression models the CES-D score was independently associated with the amount of stage 2 sleep (β: 0.205; confidence interval: 0.001-0.409; P = .05) and REM latency (β: 0.234; confidence interval: 0.001-0.468; P = .05) after adjustment for potential confounders.
I NTRO DUCTI O NDepression is one of the most prevalent mental health conditions in patients with chronic kidney disease (CKD) [1][2][3][4] ; furthermore, it is an important determinant of impaired quality of life. 5,6 Among kidney transplant (kTx) recipients, depression is associated with reduced adherence and also with increased morbidity, graft loss, and mortality. [7][8][9][10][11][12][13] Poor sleep and various sleep problems are also frequent complaints among kTx recipients.14,15 Earlier we reported that chronic insomnia was independently associated with the presence of depression in kTx recipients. 16 In the general population there is a strong and bidirectional relationship between depression and sleep.17 This is also reflected in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition definition of major depression (MD), 18 as sleep complaints are core symptoms of MD. Several objective sleep parameters are different in patients with MD than in healthy control patients. Patients with MD have decreased amounts of slow wave sleep (SWS) and shortened rapid eye movement (REM) latency with increased amounts of REM sleep. The exact mechanisms and factors that may link depression to poor clinical outcomes among kTx recipients are not yet well defined. In a recent review focusing on kTx and depression, 23 sleep is not mentioned. This may be due to the complete lack of polysomnography (PSG) studies that assess the association between sleep and depression in this population. The frequent co-occurrence of subjective sleep complaints and depression among kTx recipients 16 suggests that the relationship between the two conditions may be similar to the association described in the g...
“…Eighty percent of depression patients report insomnia, whereas 15%-35% complain of hypersomnia. 12,13 The characteristic sleep EEG changes (Figure 1) in depressed patients consist of: 1) impaired sleep continuity (increase of sleep latency, elevated number of intermittent awakenings, early morning awakening); 2) disinhibited REM sleep: shortened REM latency, or sleep onset REM period (SOREMP; REM latency 0-20 minutes), prolonged first REM period, and elevated REM density (a measure of the amount of REM), particularly during the first REM period; and 3) changes of non-REM sleep (decreases of SWS, SWA, and N2; in younger patients, SWS and SWA shift from the first to the second non-REM period). 14,15 Sleep EEG is influenced by age and sex in normal subjects and also in patients with depression.…”
Section: Sleep Eeg In Patients With Depressionmentioning
Abstract:The sleep electroencephalogram (EEG) provides biomarkers of depression, which may help with diagnosis, prediction of therapy response, and prognosis in the treatment of depression. In patients with depression, characteristic sleep EEG changes include impaired sleep continuity, disinhibition of rapid-eye-movement (REM) sleep, and impaired non-REM sleep. Most antidepressants suppress REM sleep in depressed patients, healthy volunteers, and in animal models. REM suppression appears to be an important, but not an absolute requirement, for antidepressive effects of a substance. Enhanced REM density, a measure for frequency of REM, characterizes high-risk probands for affective disorders. REM-sleep changes were also found in animal models of depression. Sleep-EEG variables were shown to predict the response to treatment with antidepressants. Furthermore, certain clusters of sleep EEG variables predicted the course of the disorder for several years. Some of the predicted sleep EEG markers appear to be related to hypothalamic-pituitary-adrenal system activity.
“…Hyperarousal is a state of abnormally high alertness in the sleep environment characterized by the failure to appropriately modulate the metabolic activity of the prefrontal cortex (Nofzinger et al 2004) and the brain's electrical activity during sleep (Krystal et al 2002;Merica et al 1998;Perlis et al 2001), by the sympathetic cardiovascular response (Bonnet and Arand 1997), hypercortisolemia (Rodenbeck et al 2002;Vgontzas et al 2001), and increased systemic metabolism (Bonnet and Arand 1995). Hyperarousal and, more broadly, disruption of the circadian cycle, appears to play a particularly important role in depressed women (Armitage 2007); it may interfere with mood regulation and thus precipitate new depressive episodes in these patients.…”
Section: Effects Of Persistent Insomnia On Moodmentioning
Background-Even low levels of residual symptoms are known to increase the risk of relapse and early recurrence of major depression. It is not known if ongoing psychotherapy lessens this risk. We therefore examined the impact of persistent symptoms, including mood, insomnia, and anxiety symptoms, on time to recurrence in women receiving maintenance interpersonal psychotherapy (IPT-M) for recurrent depression.
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