Persistence of Neuropsychologic Deficits in the Remitted State of Late-Life Depression

Department of Psychiatry, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
American Journal of Geriatric Psychiatry (Impact Factor: 4.24). 06/2006; 14(5):419-27. DOI: 10.1097/01.JGP.0000203130.45421.69
Source: PubMed


Cognitive impairment in late-life depression (LLD) is prevalent, disabling, and persists despite the remission of depressive symptoms. This article characterizes neuropsychologic functioning during remission in LLD.
The authors examined longitudinal performance on a comprehensive neuropsychologic battery in 56 nondemented subjects age 60 or older who initially presented with an episode of nonpsychotic unipolar major depression and 40 nondemented, age- and education-equated comparison subjects with no history of depression. Subjects were assessed at baseline (in a depressed state) and one year later (when remitted).
After one year, 45% of the LLD subjects were cognitively impaired despite remission of depression. Visuospatial ability, information-processing speed, and delayed memory were most frequently impaired; 94% of the patients who were impaired at baseline remained impaired one year later. Twenty-three percent of the patients who were cognitively normal while depressed developed impairment one year later.
Most older individuals who are cognitively impaired during a depressive episode remain impaired when their depression remits. In addition, a substantial proportion of older depressed individuals who are cognitively intact when depressed are likely to be impaired one year later, although their depression has remitted.

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    • "Persistent cognitive, molecular and neurochemical changes are also seen in rodents after recovery from CMS (Elizalde et al., 2008, 2010; Surget et al., 2009). Consistent with these observations, there are reports of persistent cognitive (Bhalla et al., 2006; Preiss et al., 2009) and sensory (Naudin et al., 2012) impairments, and increased responsiveness to aversive stimuli (McCabe et al., 2009), following recovery from a depressive episode . But even against this background, physiological abnormalities that represent risk factors for depression are associated with resistance to antidepressant treatment ; compared with patients who responded to treatment , nonresponders have been found to have a higher level of HPA activity (Ising et al., 2007), a smaller hippocampus (MacQueen et al., 2008) and a more active amygdala (Paillère Martinot et al., 2011; Ruhé et al., 2012). "
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    ABSTRACT: The first half of this paper briefly reviews the evidence that (i) stress precipitates depression by damaging the hippocampus, leading to changes in the activity of a distributed neural system involving, inter alia, the amygdala, the ventromedial and dorsolateral prefrontal cortex, the lateral habenula and ascending monoamine pathways, and (ii) antidepressants work by repairing the damaged hippocampus, thus restoring the normal balance of activity within that circuitry. In the second half of the paper we review the evidence that heightened vulnerability to depression, either because of a clinical history of depression or because of the presence of genetic, personality or developmental risk factors, also confers resistance to antidepressant drug treatment. Thus, although antidepressants provide an efficient means of reversing the neurotoxic effects of stress, they are much less effective in conditions where vulnerability to depression is elevated and the role of stress in precipitating depression is correspondingly lower. Consequently, the issue of vulnerability should feature much more prominently in antidepressant research. Most of the current animal models of depression are based on the induction of a depressive-like phenotype by stress, and pay scant attention to vulnerability. As antidepressants are relatively ineffective in vulnerable individuals, this in turn implies a need for the development of different clinical and preclinical methodologies, and a shift of focus away from the current preoccupation with the hippocampus as a target for antidepressant action in vulnerable patients.
    Behavioural Pharmacology 09/2014; 25(5 and 6):352-371. DOI:10.1097/FBP.0000000000000066 · 2.15 Impact Factor
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    • "Prior research indicated cognitive impairment in some but not all rLLDs (Bhalla et al., 2006), providing grounds to speculate on differences in IADL in rLLD. Compared with int-rLLDs, we found cognitive disadvantages including verbal delayed recall and processing speed in imp-rLLDs, which is consistent with the findings from the aforementioned study. "

    International Journal of Geriatric Psychiatry 01/2014; 29(1):109-10. DOI:10.1002/gps.3997 · 2.87 Impact Factor
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    • "Impairments in cognition have been found to persist beyond acute episodes of depression, and between one-third and one-half of remitted depressed patients are thought to be affected by cognitive deficits (Abas et al. 1990; Bhalla et al. 2006; Reppermund et al. 2009). Furthermore, one study revealed that 94% of patients who had cognitive impairment while depressed continued to experience deficits in cognition when remitted from depression (Bhalla et al. 2006). "
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    ABSTRACT: This review aimed to address the question of whether cognitive impairment should be considered a core feature of depression that may be a valuable target for treatment. We conducted a systematic review and meta-analysis of cognitive function, assessed with a single neuropsychological test battery, the Cambridge Neuropsychological Test Automated Battery (CANTAB), in patients with depression during symptomatic and remitted states. Inclusion of studies comparing patients remitted from depression and controls enabled us to investigate whether cognitive impairment persists beyond episodes of low mood in depression. Our meta-analysis revealed significant moderate cognitive deficits in executive function, memory and attention in patients with depression relative to controls (Cohen's d effect sizes ranging from -0.34 to -0.65). Significant moderate deficits in executive function and attention (Cohen's d ranging from -0.52 to -0.61) and non-significant small/moderate deficits in memory (Cohen's d ranging from -0.22 to -0.54) were found to persist in patients whose depressive symptoms had remitted, indicating that cognitive impairment occurs separately from episodes of low mood in depression. Both low mood and cognitive impairment are associated with poor psychosocial functioning. Therefore, we argue that remediation of cognitive impairment and alleviation of depressive symptoms each play an important role in improving outcome for patients with depression. In conclusion, this systematic review and meta-analysis demonstrates that cognitive impairment represents a core feature of depression that cannot be considered an epiphenomenon that is entirely secondary to symptoms of low mood and that may be a valuable target for future interventions.
    Psychological Medicine 10/2013; 44(10):1-12. DOI:10.1017/S0033291713002535 · 5.94 Impact Factor
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