Are Depression and Cognitive Performance Related in Temporal Lobe Epilepsy?

PURPOSE: The degree to which depression interacts with the cognitive deficits of epilepsy to alter cognitive skill and general functioning is unknown. Depression has significant negative effects on adaptive functioning including cognitive skills. Temporal lobe epilepsy (TLE) patients are known to possess cognitive dysfunction. Thus, TLE patients who are depressed may suffer a double burden of cognitive deficits. METHODS: We examined whether depressed patients show increased cognitive deficits relative to nondepressed TLE patients (n = 59). We then sought to determine if this effect varied for left versus right TLE patients utilizing preoperative depression and neuropsychological data. To accurately study the lateralization of any observed effects, we selected only patients with definitive evidence of unilateral pathology and seizure focus and utilized a two-year seizure-free postsurgical outcome to capture this. RESULTS: The data suggested that cognitive performance was not related to depression, and that depression did not reliably mediate the cognitive presentation of either our left or right TL patients. The notion of a double burden on cognition did not receive support from our data. The data did produce the expected advantage on verbal memory measures for right TLE patients. CONCLUSIONS: The reasons for the limited statistical effects are discussed and issues in unraveling the causal relationships between depression, cognition, and TLE are considered. We discussed the potential role depression may play in the cognitive skills of TLE patients, but the major implication is that depression and neurocognitive performance appear to bear a limited relationship in the context of TLE.     

The relationship between cognitive ability and depression: a longitudinal data analysis

Purpose

There is literature indicating cognitive ability and depression are related, but few studies have examined the direction of the relationship. This study examined the relationship between depression levels and cognitive abilities from adolescence to early adulthood.

Methods

Using the National Longitudinal Study of Adolescent Health (n = 14,322), this study used path modeling to investigate the relationship between depression and cognitive ability at baseline and again 8 years later.

Results

After controlling for initial levels of depression, cognitive ability, and other covariates, depressive symptoms in adolescence are related to cognitive ability in early adulthood, but adolescent cognitive ability is not related to adult depression levels. Moreover, after controlling for adolescent levels of depression and cognitive ability, the cognitive ability–depression relationship disappears in adulthood.

Conclusions

The cognitive ability–depression relationship appears early in life, and it is likely that the presence of depressive symptoms leads to lower cognitive ability. Thus, intervening at early signs of depression not only can help alleviate depression, but will likely have an effect of cognitive ability as well.     

Mood disorders in multiple sclerosis and the effects on cognition

BACKGROUND: Depression and cognitive dysfunction are common in patients with multiple sclerosis. However, it is unclear whether depression may cause or exacerbate cognitive problems as data remain equivocal. The current review attempts to clarify the relationship between these behavioral disorders. METHOD: The literature pertaining to the influence of depression on cognition in MS patients has been reviewed. RESULTS: Early studies consistently failed to find an association and concluded that cognitive dysfunction in MS patients occurred independently of depression. A more recent literature has found fault with this, citing numerous methodological flaws in the studies undertaken. Newer data now suggests that core symptoms of depression reduce cognitive capacity, in particular exerting an adverse effect on the executive function component of working memory. CONCLUSIONS: Depression may exacerbate cognitive dysfunction in MS patients. Whether treating depression will lead to cognitive improvement is not yet known, but warrants further exploration.     

Cognitive variables and depressed mood in adults with intellectual disability

Background Cognitive theory forms the foundation for cognitive therapy. There has been little research on cognitive theories and cognitive variables associated with depression in individuals with intellectual disability (ID). The current study examined cognitive variables of automatic thoughts, cognitive triad, hopelessness, attributions and self-esteem associated with two cognitive theories of depression: Beck's Cognitive Triad theory and the Hopelessness theory of depression. Methods Seventy-three adults with ID screened for adequate receptive vocabulary were interviewed as part of a larger study. They reported on cognitive constructs relating to depressed mood. In addition, comparisons were made between 12 adults with ID and diagnosed major depression and a matched group of 12 adults with ID and no psychiatric diagnoses in order to determine if these groups differed on the cognitive constructs associated with the two cognitive theories of depression. Results The cognitive variables examined were all significantly correlated with depressed mood in the direction predicted by their respective cognitive theory. Internal consistencies were good or excellent for most instruments, with the exception of those measuring hopelessness and attributions. In addition, significant differences were obtained between groups of individuals with and without co-morbid major depression on all variables except for hopelessness. Conclusions The results indicate that adults with ID screened for adequate receptive vocabulary are capable of reporting on subjective feelings of depressed mood and associated cognition constructs. The instruments used may be suitable for this population as they generally possessed sound internal consistencies. The results support the further examination of cognitive theories of depression among individuals with ID in order to assess the appropriateness of cognitive therapies for this population. Discrepant findings regarding hopelessness are discussed.     

Depression among older people with cognitive impairment: prevalence and detection

BACKGROUND: Past research has demonstrated that there is a high level of depression among older people, particularly for those with cognitive impairment and those in residential care. The current study was designed to determine the prevalence of depression among older people in hostels with cognitive impairment using a structured diagnostic interview. A further aim was to determine an appropriate screening instrument to detect depression within this population. It was also designed to evaluate the extent to which depression among these older people had previously been detected. METHOD: Five commonly used depression scales were administered and compared to the results of the diagnostic interview. RESULTS: The results demonstrated that 38.9% of older people were diagnosed with depression, but that only 50% of these people had been previously diagnosed with this disorder. All scales showed some level of validity to detect depression. CONCLUSIONS: The implications of these findings for our understanding of depression among older people with cognitive impairment are discussed.     

An evaluation of Beck's cognitive theory of depression in adults with intellectual disability

Background The theories supporting cognitive treatment for depression among individuals with intellectual disability (ID) have not been formally tested with this population. The current study evaluated Beck’s cognitive theory of depression to determine its appropriateness for adults with ID. Methods Forty‐eight adults with primarily mild or moderate ID participated in semi‐structured interviews, twice approximately 16 weeks apart, as did an additional 12 adults diagnosed with depression. Participants reported on depressed mood, the cognitive triad, as measured by views of the self, the world and the future, hopelessness and self‐esteem. Results The Cognitive Triad Inventory for Children (CTI‐C) displayed adequate psychometric properties in this sample. In addition, it was correlated with depressed mood, and individuals diagnosed with depression had significantly higher scores on the CTI‐C than those with no psychiatric diagnoses. Contrary to hypotheses, a negative cognitive triad did not predict depressed mood 4 months later, but the inverse relationship where depressed mood predicted a later negative cognitive triad approached statistical significance. Conclusions The findings indicate that the cognitive triad can be measured among individuals with mild or moderate ID and is related to depression and depressed mood. However, the role of the cognitive triad in the development of depression is still unknown. The findings provide some support for Beck’s cognitive theory of depression among individuals with ID and provide suggestions for further testing the theory. Implications for the treatment of depression among individuals with ID are discussed.     

Executive functioning in unipolar depression: a review

While several neuropsychological studies have demonstrated that cognitive deficits are seen across a broad range of cognitive domains, executive deficits associated with frontal lobe dysfunction may be prominent in depression. Executive function refers to cognitive processes that control and integrate other cognitive activities such as episodic memory. These executive functions involve a set of cognitive behaviors which include: dealing with novelty, selecting strategies, inhibiting incorrect responses, monitoring performance and using feedback to adjust future responding. The measurement of executive function relies mainly on the use of neuropsychological tests known to be sensitive to frontal lobe damage such as the Wisconsin and California Card Sorting Tests, verbal fluency tests, Stroop-test, Tower of London Task and Trail Making Test. The present review focuses on studies investigating executive functions in primary unipolar depression with these neuropsychological tasks. Unipolar depressed patients mainly exhibit cognitive inhibition deficits, problem-solving impairments and planning deficits. Cognitive inhibition deficits in depressed patients have been related to a reduction of cognitive resources and psychomotor retardation. Inhibition disturbance could lead depressed patients to process irrelevant information and consequently reduce their capacity to control transient mood changes. Several studies have found evidence of problem solving impairments in depressed patients. Depressed subjects show with card sorting tests difficulties in hypothesis testing with a loss of spontaneous and reactive cognitive flexibility. The cognitive rigidity and hypothesis-testing associated with dorsolateral prefrontal dysfunction in depression may prevent patients to cope with life events and lead to a perpetuation of depressed mood by a continuation of stress exposure. Planning tasks, such as the Tower of London Test, also demonstrate that depressed patients fail to use negative feedback as a motivational boost to improve their performance. Both trait and state factors influence the executive level of depressed patients. Executive deficits have been reported in more severely depressed subjects with melancholic or psychotic features. Executive functioning also might predict a poorer outcome in depression. Thus initiation and perseveration scores - a measure of cognitive flexibility - is associated with relapse and recurrence of depression and residual depressive symptoms. Brain imaging studies show that reduced blood flow, particularly in medial prefrontal cortex and dorsal anterior cingulate cortex subserve executive impairments in depression. However neuroimaging studies underscore the importance of mood-cognitive interactions in depression. A recent working model of depression (Mayberg et al., 1999) implicates failure of the coordinated interactions of distributed cortical-limbic pathways in the neuropsychopathology of depression. According to this model, neocortical (prefrontal and parietal regions) and superior limbic elements (dorsal anterior cingulate) are postulated to mediate impaired attention and executive function, whereas ventral limbic regions (ventral anterior cingulate, subcortical structures) are postulated to mediate circadian and vegetative aspects of depression. Further studies are needed to validate this model at the neuropsychological level as well as the brain level and to elucidate the complex interactions between mood, cognitive resources and executive function in depression.     

Cognitive disinhibition and socioemotional functioning in Alzheimer's disease.

Individuals with Alzheimer's disease (AD) experience difficulties with socioemotional functioning, and it has been proposed that cognitive disinhibition may be one potential mechanism that contributes to difficulties in this area. To test this possibility, twenty individuals with AD and 20 demographically matched controls were administered self-report measures of depression, emotion regulation and empathy, in addition to a behavioral measure that has proven to be very sensitive to inhibitory failures (the Hayling Sentence Completion Test). Relative to controls AD participants exhibited increased inhibitory failures on the Hayling, and self-reported significantly reduced cognitive empathy, but did not differ with respect to affective empathy, depression or perceived capacity for emotion regulation. Controlling for general cognitive status, in the AD (but not the control) group, reduced cognitive inhibition was associated with lower levels of depression. The theoretical and practical implications of these results are discussed.     

The influence of lifetime depression on self-reported memory and cognitive problems: results from the National Comorbidity Survey-Replication

The current study investigated the association between lifetime major depressive disorder (MDD) and self-reported memory and cognitive problems in a general population sample. The study was based on data from the National Comorbidity Survey-Replication (n = 5692). The relationship between lifetime MDD and self-reported memory and cognitive problems was examined while controlling for other 1-year and lifetime psychiatric disorders. We found a lifetime history of depression, but no other lifetime psychiatric disorder, to be associated with self-reported memory and cognitive problems. We review the results in relation to theories regarding the comorbidity of depression and cognitive problems. A history of depression increases the likelihood that individuals will make negative evaluations of their memory and cognitive functioning. Though depression is highly comorbid with other disorders, our results are unique in demonstrating the specificity of depression in its association with self-reported memory and cognitive problems. The observed association between depression and self-reported memory and cognitive problems may reflect that depression increases the risk for cognitive decline or may reflect that individuals with a history of depression tend to rate their memory as poor, or both.     

Cognitive impairments and depression in Parkinson''s disease: a follow up study.

The presence of depression and cognitive impairments was examined in seventy patients with Parkinson's disease (PD). Forty nine patients of this original cohort were re-examined between three and four years after the first evaluation. While both depressed and non-depressed patients showed a significant decline in cognitive function during the follow up period, intellectual decline was significantly more severe for the depressed group. Depressed patients also showed a faster rate of progression of motor signs (mainly tremor) than the non-depressed group. Patients that died during the follow up period showed significantly more cognitive impairments than patients who were alive at follow up. These findings suggest that either there may be two forms of PD: one with depression and rapid cognitive decline and one without depression and a gradual cognitive decline; or that the mechanisms of cognitive impairment in PD and depression may interact to produce a more rapid evolution in cognitive impairment among PD patients with a previous depression than among patients without a previous depression.     

Association between change in brain gray matter volume,cognition, and depression severity: Pre- and post- antidepressant pharmacotherapy for late-life depression

Late-life depression (LLD) is associated with cognitive impairments and reduced gray matter volume (GMV); however the mechanisms underlying this association are not well understood. The goal of this study was to characterize changes in depression severity, cognitive function, and brain structure associated with pharmacologic antidepressant treatment for LLD. We administered a detailed neurocognitive battery and conducted structural magnetic resonance imaging (MRI) on 26 individuals with LLD, pre-/post-a 12-week treatment trial with venlafaxine. After calculating changes in cognitive performance, GMV, and depression severity, we calculated Pearson's correlations, performed permutation testing, and false discovery rate correction. We found that loss of GMV over 12 weeks in the superior orbital frontal gyrus was associated with less improvement in depression severity and that increased GMV in the same was associated with greater improvement in depression severity. We detected no associations between changes in cognitive performance and improvements in either depressive symptoms or changes in GMV.     

The relationship of current depressive symptoms and past depression with cognitive impairment and instrumental activities of daily living in an elderly population: the Sydney Memory and Ageing Study

Depressive symptoms are common in the elderly and they have been associated with cognitive and functional impairment. However, relatively less is known about the relationship of a lifetime history of depression to cognitive impairment and functional status. The aim of this cross-sectional study was to assess whether current depressive symptoms and past depression are associated with cognitive or functional impairment in a community-based sample representative of east Sydney, Australia. We also examined whether there was an interaction between current and past depression in their effects on cognitive performance. Eight hundred non-demented aged participants received a neuropsychological assessment, a past psychiatric history interview and the 15-item Geriatric Depression Scale. The Bayer-Activities of Daily Living scale was completed by an informant to determine functional ability. Clinically relevant depressive symptoms were present in 6.1% of the sample and 16.6% reported a history of depression. Participants with current depression had significantly higher levels of psychological distress and anxiety, and lower life satisfaction and performed worse on memory and executive function compared to participants without current depression. After controlling for anxiety the effect on executive function was no longer significant while the effect on memory remained significant. A history of depression was associated with worse executive function, higher levels of psychological distress and anxiety, and lower life satisfaction. After controlling for psychological distress the effect of past depression on executive function was no longer significant. There were no significant interactions between current and past depression in their effects on cognitive performance. There were no differences between participants with or without current depression and with or without past depression on functional abilities. These results support the view that current and past depressive episodes are associated with poorer cognitive performance but not with functional abilities.     

A model of risk for major depression: effects of life stress and cognitive style vary by age

Empirical studies increasingly attribute risk for depression to adverse life events, cognitive style, and possibly to the interaction between cognitive style and event type. We present an evidence-based model, developed with independent samples of adults and elderly adults, indicating that risk for major depression associated with these factors varies with age. According to the model, adverse events and need for control, the cognitive style that is a key feature of Beck's concept of autonomy, are significant risk factors for depression in younger adults but not in elderly adults. The cognitive style of sociotropy, characterized by a high need for relatedness and concern about disapproval, is a stable risk factor, independent of age, in posing a risk for depression. The effects of the interactions of adverse event type (achievement events and interpersonal events) and cognitive style in predicting depression each appear to vary with age, expanding prior work, which suggests that adverse events affecting one's personal vulnerability are likely to precipitate depression. Age-specific approaches to reducing risk for major depression are clinically important, and the model presented here suggests that the use of an age-specific perspective would advance research in stress-diathesis models for risk of depression.     

Relationship between coping,cognitive dysfunction and depression in multiple sclerosis

Given its relatively high prevalence, one possible source of stress for patients with multiple sclerosis (MS) is cognitive dysfunction. The authors' study was guided by a new theoretical model suggesting that cognitive dysfunction in MS may be most likely to lead to depression when patients use high levels of avoidance coping and/or low levels of active coping. To test this model, 55 patients with definite MS were administered a neuropsychological battery and measures of depression and coping. Consistent with predictions, regression analyses showed that coping significantly moderated the relationship between cognitive dysfunction and depression. Specifically, cognitive dysfunction was most likely to be associated with depression when patients used either high levels of avoidance or low levels of active coping. Implications of these data for clinical applications and for our theoretical conceptualization are discussed and limitations of the model explored.     

The evolution of the cognitive model of depression and its neurobiological correlates

Although the cognitive model of depression has evolved appreciably since its first formulation over 40 years ago, the potential interaction of genetic, neurochemical, and cognitive factors has only recently been demonstrated. Combining findings from behavioral genetics and cognitive neuroscience with the accumulated research on the cognitive model opens new opportunities for integrated research. Drawing on advances in cognitive, personality, and social psychology as well as clinical observations, expansions of the original cognitive model have incorporated in successive stages automatic thoughts, cognitive distortions, dysfunctional beliefs, and information-processing biases. The developmental model identified early traumatic experiences and the formation of dysfunctional beliefs as predisposing events and congruent stressors in later life as precipitating factors. It is now possible to sketch out possible genetic and neurochemical pathways that interact with or are parallel to cognitive variables. A hypersensitive amygdala is associated with both a genetic polymorphism and a pattern of negative cognitive biases and dysfunctional beliefs, all of which constitute risk factors for depression. Further, the combination of a hyperactive amygdala and hypoactive prefrontal regions is associated with diminished cognitive appraisal and the occurrence of depression. Genetic polymorphisms also are involved in the overreaction to the stress and the hypercortisolemia in the development of depression--probably mediated by cognitive distortions. I suggest that comprehensive study of the psychological as well as biological correlates of depression can provide a new understanding of this debilitating disorder.     

Pathways linking late-life depression to persistent cognitive impairment and dementia

There is a strong association between late-life depression, cognitive impairment, cerebrovascular disease, and poor cognitive outcomes, including progressive dementia, especially Alzheimer's disease. While neuroimaging evidence suggests that cerebrovascular disease plays a prominent role, it seems that depression alone may also confer substantial risk for developing Alzheimer's disease. The relationships between the prominent cerebrovascular changes, other structural abnormalities, specific forms of cognitive dysfunction, and increased risk for developing Alzheimer's disease among those with late-life depression have been difficult to reconcile. The varied findings suggest that there are likely multiple pathways to poor cognitive outcomes. We present a framework outlining multiple, non-mutually exclusive etiologic links between depression, cognitive impairment, and progressive decline, including dementia. Importantly, the model is both testable and falsifiable. Going forward, using models such as this to inform research should accelerate knowledge acquisition on the depression/dementia relationship that may be useful for dementia prevention, monitoring the impact of depression treatment on clinical status and course of illness.     

How Late-Life Depression Affects Cognition: Neural Mechanisms

Late-life depression is a major health problem and a significant cause of dysfunction that warrants closer evaluation and study. In contrast to younger depressed patients, most depressed older adults suffer more severe variants of the disorder, including significant cognitive impairments. These cognitive changes add to the severity of symptoms and disability that older depressed patients face and likely reflect compromise of certain neural circuits, linking cognitive impairment to late-life depression. Studies examining clinical correlates, neuropsychological testing, and functional and anatomic imaging have yielded a clearer understanding of the neural mechanisms underlying cognitive deficits in late-life depression. This article discusses cognitive impairment in geriatric depression and how developing a better understanding of its neural correlates may lead to improved understanding and outcome of this specific disorder.     

The prevalence and recognition of major depression among low-level aged care residents with and without cognitive impairment

Previous research has demonstrated a high level of depression in nursing homes. The current study was designed to determine the prevalence of depression, using a structured diagnostic interview, among older people with and without mild-moderate cognitive impairment residing in low-level care facilities. The results demonstrated that, consistent with previous research in nursing homes, 16.9% of older people were diagnosed with major depressive disorder. Less than half of these cases had been detected or treated. Individuals with moderate cognitive impairment were more likely to be depressed, but cognitive impairment did not appear to act as a strong impediment to the detection of depression by general practitioners. A low awareness of their use of antidepressant medications was demonstrated among older people prescribed this treatment, including those with normal cognitive function. Reasons for the poor recognition of depression among older people are discussed.     

Consensual Sadomasochistic Sex (BDSM): The Roots, the Risks, and the Distinctions Between BDSM and Violence

Depression and cognitive disorders, including dementia and mild cognitive impairment, are common in the elderly. Depression is also a common feature of cognitive impairment although the symptoms of depression in cognitive impairment differ from depression without cognitive impairment. Pre-morbid depression approximately doubles the risk of subsequent dementia. There are two predominant, though not mutually exclusive, constructs linking pre-morbid depression to subsequent cognitive impairment: Alzheimer’s pathology and the vascular depression hypothesis. When evaluating a patient with depression and cognitive impairment, it is important to obtain caregiver input and to evaluate for alternative etiologies for depressive symptoms such as delirium. We recommend a sequential approach to the treatment of depression in dementia patients: (1) a period of watchful waiting for milder symptoms, (2) psychosocial treatment program, (3) a medication trial for more severe symptoms or failure of psychosocial interventions, and (4) possible ECT for refractory symptoms.