Cognitive Dysfunction in Major Depressive Disorder: Assessment, Impact, and Management

Abstract

Cognitive dysfunction is increasingly being recognized as an important clinical dimension in major depressive disorder. This review summarizes the existing data on the epidemiology, assessment, and treatment of cognitive dysfunction among nonelderly adults with the disorder. Overall, cognitive dysfunction is prevalent, persists through periods of symptom remission, and may be independently associated with functional outcomes. However, although the evidence increasingly suggests that clinicians should be heedful of their patients' cognitive functioning, there is as yet no consensus on how best to monitor cognition clinically. In addition, although most studies have reported improved cognition with antidepressant medications, psychotherapy, and neuromodulation, the clinical significance of these improvements is unclear, and high-level evidence to guide decision making is limited. Nonetheless, given the important functional implications, clinicians should assess and monitor cognition and optimize both medication and psychological treatments to mitigate cognitive dysfunction among patients with major depressive disorder.

Figure 1.

Proposed Network Model of Cognitive Dysfunction in Major Depressive Disorder^{a a} Abnormal recruitment and connectivity of the SN (consisting of dACC and AI), CEN (consisting of dlPFC and PPC), and DMN (consisting of PCC and vmPFC) contribute to hot (emotion dependent, indicated with dashed arrow) and cold (emotion independent, indicated with dotted arrow) cognitive dysfunction in major depressive disorder. The SN, responsible for detecting and filtering relevant information, is disproportionately affected by negative stimuli and emotional perception. The SN in major depressive disorder is also less efficient in mediating the anticorrelated activation of the CEN and DMN during cognitive tasks. Subsequent DMN overactivity results in increased negative self-referential processing and rumination that distracts from task-relevant stimuli, and the underactive CEN is less able to provide top-down inhibitory control. The net result is less efficient recruitment of networks involved in attention, working memory, and higher-order processes necessary for successful completion of cognitive tasks. SN, salience network; dACC, dorsal anterior cingulate cortex; AI, anterior insula; CEN, central executive network; dlPFC, dorsolateral prefrontal cortex; PPC, posterior parietal cortex; DMN, default mode network; PCC, posterior cingulate cortex; vmPFC, ventromedial prefrontal cortex. Adapted from Hamilton et al. (77) and Menon (74).