Specifying the Neuropsychology of Affective Disorders: Clinical, Demographic and Neurobiological Factors

Abstract

Neuropsychological research in patients with affective disorders shows heterogeneous results with regard to the severity and profile of cognitive impairments. In this paper we hypothesize that the investigation of clinical (subtypes, comorbidity, traumatization, personality, severity, diurnal swings, course, duration, age of onset, biased processing, rumination, motivation, experience of failure, sleep, suicidal tendencies, computer attitudes), demographic (age, education, gender) and neurobiological factors (structural and functional brain changes, glucocorticoids, medication, ECT) that are related to cognitive performance has specified the understanding of severity and profile of neuropsychological impairments. We reviewed the literature pertaining to clinical, demographic and neurobiological factors following Pubmed and PsychInfo databases using different combinations of general key-terms including "Affective Disorder," "Depression," "Mania," "Neuropsychological," "Neurobiological," "Moderator," and "Review" as well as more specific demographic, clinical and neurobiological search terms. Findings from the literature show that the consideration of these factors has improved knowledge about the severity of neuropsychological impairments in patients with affective disorders whereas the neuropsychological profile is still poorly understood. Despite limited understanding, however, the existent results provide promising suggestions for the development of treatment programs.

Rumination in bipolar disorder: a systematic review

“…In patients with BD, the main areas showing functional abnormalities are those responsible for controlling emotion and executive functions, namely, areas of the prefrontal cortex (medial, dorsolateral, anterior cingulate, and orbital regions) and amygdala. 25 All these areas have shown abnormalities in studies investigating associations between rumination and neuroimaging findings 4,30 in other disorders, in line with the hypothesis that executive dysfunction may underlie the tendency to ruminate in patients with BD. 13,16 Moreover, several studies have confirmed that rumination has negative impacts on cognitive function in mood disorders, particularly on autobiographical memories, inhibition, cognitive flexibility, problem solving, working memory, and attentional bias towards negative -There was no correlation between rumination, sex, and IQ.…”

“…According to those authors, evidence shows the same association in patients with major depression when compared with healthy controls. Taken together with the results of another article, 30 these findings underscore the difficulty in changing the focus of attention and performing new tasks among patients who engage in ruminative thoughts vs. those who do not. 25 These findings, however, are preliminary and need to be replicated.…”

“…Depending on genetic load, environmental characteristics (holding, learned behavior), intelligence, and resilience, patients faced with a ruminative thought after a stressful life event may have as an outcome either the resolution of the situation, with tolerance to its external and internal effects, or the development of phobic, anxious, obsessive, depressive, manic, escapist (binge eating/drinking, self-mutilation), and psychotic symptoms. We hypothesize that an association may exist between rumination and reduced hippocampal volume and high cortisol levels (altered cortisol cascade), possibly as a result of genetic load, based on the reported association between stress and rumination 35,38 and between stress/anxiety/depressive symptoms and increased cortisol levels 30 (Figure 2). …”

“…30 It has been suggested that patients with BD may ruminate because they face difficulties inhibiting their persistent self-focusing behavior 11 -a process that may have been initiated in response to both positive and negative affect, 12 and needs extensive research. Rumination has also been associated with changes in memory processing 8 and prefrontal activity.…”

“…32 Preliminary evidence has pointed to reduced hippocampal volume and abnormalities in cognitive function primarily in the dorsolateral prefrontal cortex of patients with depression and BD. 30 Nolen-Hoeksema et al suggested that rumination could be a mediator between the BDNF gene and depressive symptoms. 4 Another study involving 200 female adolescents and their mothers found that the Val/Val genotype of BDNF was associated with more frequent rumination and childhood-onset depression when compared with the Val/Met genotype; in mothers with adult-onset depression, in turn, Val/Met was more strongly associated with depressive symptoms.…”