Impairment In Late-life Depression Research Articles

The pattern and course of cognitive impairment in late-life depression

Cognitive deficits persist despite clinical recovery in subjects with late-life depression, but more needs to be known about their longer-term outcome and factors affecting their course. To investigate this, we followed the pattern of cognitive impairments over time and examined the effects of current mood, remission status, age of depression onset and antidepressant (AD) treatment on these deficits. Sixty-seven subjects aged > or = 60 years with DSM-IV major depressive disorder and 36 healthy comparison subjects underwent tests of global cognition, memory, executive functioning and processing speed at baseline, 6 and 18 months, with some subjects tested again after 4 years. z scores were compared between groups, with analyses of clinical factors that may have influenced cognitive performance in depressed subjects. Half of the patients exhibited a generalized cognitive impairment (GCI) that persisted after 18 months. Patients performed worse across all cognitive domains at all time points, without substantial variability due to current mood, remission status or AD treatment. Late age of onset was associated significantly with decline in memory and executive functioning. Impaired processing speed may be a partial mediator of some deficits, but was insufficient to explain differences between patients and controls. Four-year follow-up data suggest impairments persist, but do not further decline. Cognitive deficits in late-life depression persist up to 4 years, affect multiple domains and are related to trait rather than state effects. Differences in severity and course between early and late onset depression suggest different pathogenic processes.

Late life depression with cognitive impairment: Evaluation and treatment

Older adults with depression often present with signs and symptoms indicative of functional or cognitive impairment. These somatic symptoms make evaluating and treating depression in older adults more complex. Late life depression (LLD), depression in adults over the age of 65, is more frequently associated with cognitive changes. Cognitive impairment in LLD may be a result of the depressive disorder or an underlying dementing condition. Memory complaints are also common in older adults with depression. There is a wide range of cognitive impairment in LLD including decreased central processing speed, executive dysfunction, and impaired short-term memory. The etiology of cognitive impairment in LLD may include cerebrovascular disease, a significant risk factor for LLD, which likely interrupts key pathways between frontal white matter and subcortical structures important in mood regulation. Because depressive symptoms often coexist with dementia, it is important to determine the temporal relationship between depressive symptoms and cognitive change. If depressive symptoms pre-date the cognitive impairment and cognitive symptoms are mild and temporary, LLD is the likely etiology of the cognitive impairment. If cognitive changes appear prior to depressive symptoms and persist after LLD is successfully treated, an underlying dementia is more likely. Clinicians should be exclude common conditions such as thyroid disease which can contribute to depressive symptoms and cognitive impairment prior to treating LLD. Both antidepressants and psychotherapy can be effective in treating LLD. Subsequent evaluations following treatment should also reassess cognition.

A comparison of neurocognitive impairment in younger and older adults with major depression

Neurocognitive impairment is a well-recognized feature of depression that has been reported in younger and older adults. Similar deficits occur with ageing and it is unclear whether the greater deficits in late-life depression are an ageing-related phenomenon or due to a difference in the nature of late-life depression itself. We hypothesized that ageing alone would not fully explain the increased neurocognitive impairment in late-life depression but that differences in the illness explain the greater decrements in memory and executive function. Comparison of the neuropsychological performance of younger (<60 years) and older (60 years) adults with major depressive disorder (MDD) and healthy comparison subjects. Scores for each depression group were normalized against their respective age-matched control group and the primary comparisons were on four neurocognitive domains: (i) attention and executive function; (ii) verbal learning and memory; (iii) visuospatial learning and memory; and (iv) motor speed. We recruited 75 subjects with MDD [<60 years (n=44), 60 years (n=31)] and 82 psychiatrically healthy comparison subjects [<60 years (n=42), 60 years (n=40)]. The late-life depression group had greater impairment in verbal learning and memory and motor speed but not in executive function. The two depressed groups did not differ in depression severity, global cognitive function, intelligence or education. Late-life depression is associated with more severe impairment in verbal learning and memory and motor speed than depression in earlier adult life and this is not due to ageing alone.

P2-236: Odor identification test as a predictor of mild cognitive impairment in late-life depression

P2-236: Odor identification test as a predictor of mild cognitive impairment in late-life depression

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

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.

Residual cognitive impairment in late-life depression after a 12-month period follow-up.

This study investigated cognitive impairment in late-life depression in a follow-up design. The main objective was to assess the most important cognitive domains implicated in late-life depression, in patients who underwent pharmacological treatment, in the acute phase and twelve months after. Neuropsychological and clinical data were used from the baseline of patients and controls, to determine the cognitive impairment in the acute phase. Patients repeated the neuropsychological assessment at twelve months. There were significant differences between patients and controls at baseline. But in the patients there was no change over twelve months. There were no differences between remitted and non-remitted patients on neuropsychological scores. The cognitive impairment seen in the elderly depressed patients seems to be a trait characteristic of this mental disease, even when the depressive episode has remitted.

Mortality, symptoms, and functional impairment in late-life depression.

To determine whether depressive symptoms measured at baseline are associated with mortality and to describe the course of depressive symptoms and their relation to physical decline in patients over a 6-year period. Prospective cohort study conducted from 1990 through 1996. Urban academic primary care group practice. A cohort of 3,767 patients aged 60 years and older screened for depressive symptoms during routine office visits using the Centers for Epidemiologic Studies Depression Scale (CES-D) participated in the mortality study. A subsample of 300 patients with CES-D scores 16 or above and a subsample of 100 patients with CES-D scores less than 16 participated in the study of the course of depressive symptoms and physical decline. Mortality by December 1995 was measured for all screened patients; reinterviewed patients completed the CES-D and the Sickness Impact Profile (SIP). The mean follow-up period was 45 months (+/- SD 12.2 months); 561 (14.9%) of the patients died by December 1995. In proportional hazards models, age, gender, race, history of smoking, serum albumin value, and an ideal body weight in the lowest 10% were significant correlates of time to death, but the baseline CES-D was not. Patients with depressive symptoms had significantly worse physical and psychosocial functioning scores on the SIP than did patients without depressive symptoms. Using the generalized estimating equation method, the strongest predictor of the current CES-D score was the patient's prior CES-D score. However, worsening physical functioning score on the SIP was also independently correlated with worse CES-D scores p < or = .001). Symptoms of depression were not associated with mortality in this cohort of older adults. However, patients with depressive symptoms reported greater functional impairment than did those without depressive symptoms. Moreover, decline in physical functioning was independently correlated with a concurrent increase in depressive symptoms.

Cognitive Impairment in late-life depression: Clinical correlates and treatment implications

Elderly depressed inpatients with high vs. low scores on a quantitative mental status examination (the Mini-Mental State (MMS)) were compared with regard to demographic and clinical characteristics, treatment and short-term response, and functional status at 2-year follow-up. Low-MMS patients were less well educated and more likely to be delusional, anxious, and globally impaired than high-MMS patients. The two groups responded equally well to treatment, but the low-MMS group required a lengthier hospital stay and greater use of neuroleptic medications. The two groups also had similar long-term outcomes, although greater attrition was observed among cognitively impaired subjects.