Many older patients who recover from an episode of major depression continue to suffer from depressed mood, anxiety, and sleep problems. Our study assesses the impact of these residual symptoms on the risk of recurrence during maintenance treatment of late-life depression.
We analyzed data from a randomized clinical trial of maintenance treatment in patients with unipolar depression aged > or =70, 116 of whom remitted and remained stable during open pharmacotherapy and interpersonal psychotherapy (IPT) and were randomized to clinical management/pharmacotherapy; clinical management/placebo; monthly maintenance IPT/ pharmacotherapy; or monthly maintenance IPT/placebo. We assessed the impact of overall residual symptoms (based on the Hamilton Depression Rating Scale (HAM-D) total score) and of specific residual symptom clusters - mood symptoms (depressed mood, guilt, suicidality, energy/interests), sleep disturbance (early, middle, late insomnia), and anxiety (agitation, psychic and somatic anxiety, hypochondriasis) measured at randomization. Sleep disturbance was also assessed with the Pittsburgh Sleep Quality Index (PSQI). We used Cox proportional hazards regression models controlling for assignment to antidepressant medication versus placebo to identify predictors of recurrence.
Residual anxiety and residual sleep disturbance (as measured by the PSQI but not the HAM-D) independently predicted early recurrence.
Use of HAM-D clusters to define residual symptoms; analysis limited to completers of acute and continuation treatment.
In patients with late-life depression who have remitted with pharmacotherapy and psychotherapy, the deleterious effect of residual symptoms is due to persisting anxiety and, possibly, residual sleep disturbance.
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"rks may offer a novel perspective on recurrence and relapse of MD . There is evidence that not only the number of symptoms predicts relapse , but that particular symptoms play an especially important role . Residual anxiety and sleep prob - lems independently predicted earlier MD recurrence in patients who had previously remitted from depression ( Dombrovski et al . , 2007 ) , and understanding the causal mechanisms that underlie residual symptoms may allow for developing prevention strate - gies that specifically target populations at high risk for recurrence ."
[Show abstract][Hide abstract] ABSTRACT: Major depression (MD) is a highly heterogeneous diagnostic category. Diverse symptoms such as sad mood, anhedonia, and fatigue are routinely added to an unweighted sum-score, and cutoffs are used to distinguish between depressed participants and healthy controls. Researchers then investigate outcome variables like MD risk factors, biomarkers, and treatment response in such samples. These practices presuppose that (1) depression is a discrete condition, and that (2) symptoms are interchangeable indicators of this latent disorder. Here I review these two assumptions, elucidate their historical roots, show how deeply engrained they are in psychological and psychiatric research, and document that they contrast with evidence. Depression is not a consistent syndrome with clearly demarcated boundaries, and depression symptoms are not interchangeable indicators of an underlying disorder. Current research practices lump individuals with very different problems into one category, which has contributed to the remarkably slow progress in key research domains such as the development of efficacious antidepressants or the identification of biomarkers for depression. The recently proposed network framework offers an alternative to the problematic assumptions. MD is not understood as a distinct condition, but as heterogeneous symptom cluster that substantially overlaps with other syndromes such as anxiety disorders. MD is not framed as an underlying disease with a number of equivalent indicators, but as a network of symptoms that have direct causal influence on each other: insomnia can cause fatigue which then triggers concentration and psychomotor problems. This approach offers new opportunities for constructing an empirically based classification system and has broad implications for future research.
Frontiers in Psychology 03/2015; 6(306):1-11. DOI:10.3389/fpsyg.2015.00309 · 2.80 Impact Factor
"Of note, data from the Drug Abuse Warning Network (DAWN) show that drugs used to treat anxiety and sleeplessness were involved in 38.8% of drug-related suicide attempts, of which benzodiazepines were the most common (Offi ce of Applied Studies 2006). In addition, residual anxiety symptoms can reduce the likelihood of remission (McIntyre et al. 2007; Kurian et al. 2009) and, following initial therapy, can increase rates of recurrence (Ramana et al. 1995; Flint and Rifat 1997; Dombrovski et al. 2007). Anxiety may, in fact, be a differentiating factor in treatment response to several treatments (Baghai et al. 2011; Vieta and Colom 2011). "
[Show abstract][Hide abstract] ABSTRACT: Abstract Objectives. To evaluate quetiapine XR in patients with anxious depression, as defined by HAM-A total and HAM-D anxiety/somatisation factor scores. Methods. Post hoc analyses of pooled data from two 6-week, double-blind, randomised, placebo-controlled studies of adjunctive quetiapine XR (150 or 300 mg/day) in patients with MDD and inadequate response to antidepressants. Patients were stratified in a primary analysis using HAM-A (HAM-A total score at baseline ≥ 20 ["high"] or < 20 ["low"]) and a secondary analysis using HAM-D (anxious depression defined as HAM-D anxiety/somatisation factor score ≥ 7). Outcomes included change in MADRS total score. Results. In patients with high anxiety levels (HAM-A total score ≥ 20), reductions in MADRS total score were -15.20 (P = 0.122) and -15.92 (P < 0.05) for quetiapine XR 150 and 300 mg/day, respectively, vs. placebo (-13.49). In patients with low levels of anxiety (HAM-A total score < 20), both quetiapine XR doses (P < 0.001) improved MADRS total scores vs. placebo. In the secondary analysis, quetiapine XR 150 (P < 0.01) and 300 mg/day (P < 0.001) improved MADRS total score vs. placebo in patients with HAM-D anxiety/somatisation factor score ≥ 7. Conclusions. Adjunct quetiapine XR demonstrates efficacy in patients with anxious and non-anxious depression, assessed using HAM-A total score, and anxious depression assessed using HAM-D anxiety/somatisation factor score.
The World Journal of Biological Psychiatry 02/2014; 15(2):155-66. DOI:10.3109/15622975.2013.842654 · 4.18 Impact Factor
"Sleep and major depressive disorder (MDD) are intricately related. Sleep disturbance is a core feature of MDD cross-sectionally , as a diagnostic criterion for the disorder (American Psychiatric Association, 2000), and longitudinally, as a risk factor for both incident depression (Baglioni et al., 2011) and depressive relapse after remission (Dombrovski et al., 2007; Karp et al., 2004; Paykel et al., 1995). In addition, polysomnographic abnormalities of sleep continuity, rapid eye movement (REM) sleep, and slow wave sleep (SWS) are robust, but non-specific, biological markers in MDD (Benca et al., 1992; Steiger and Kimura, 2010). "
[Show abstract][Hide abstract] ABSTRACT: Prior investigations have suggested sleep homeostasis is altered in major depressive disorder (MDD). Low frequency activity (LFA) in the electroencephalogram during waking has been correlated with sleep slow wave activity (SWA), suggesting that waking LFA reflects sleep homeostasis in healthy individuals. This study investigated whether the overnight change in waking LFA and its relationship with sleep SWA are altered in MDD.
256-channel high-density electroencephalography (hdEEG) recordings during waking (pre- and post-sleep) and during sleep were collected in 14 unmedicated, unipolar MDD subjects (9 women) and age- and sex-matched healthy controls (HC).
Waking LFA (3.25-6.25Hz) declined significantly overnight in the HC group, but not in the group of MDD subjects. Overnight decline of waking LFA correlated with sleep SWA in frontal brain regions in HC, but a comparable relationship was not found in MDD.
This study is not able to definitely segregate overnight changes in the waking EEG that may occur due to homeostatic and/or circadian factors.
MDD involves altered overnight modulation of waking low frequency EEG activity that may reflect altered sleep homeostasis in the disorder. Future research is required to determine the functional significance and clinical implications of these findings.