Neural correlates of reduced depressive symptoms following cognitive training for chronic traumatic brain injury

Kihwan Han, David Martinez, Sandra B Chapman, Daniel C Krawczyk, Kihwan Han, David Martinez, Sandra B Chapman, Daniel C Krawczyk

Abstract

Depression is the most frequent comorbid psychiatric condition among individuals with traumatic brain injury (TBI). Yet, little is known about changes in the brain associated with reduced depressive symptoms following rehabilitation for TBI. We identified whether cognitive training alleviates comorbid depressive symptoms in chronic TBI (>6 months post-injury) as a secondary effect. Further, we elucidated neural correlates of alleviated depressive symptoms following cognitive training. A total of seventy-nine individuals with chronic TBI (53 depressed and 26 non-depressed individuals, measured using the Beck Depressive Inventory [BDI]), underwent either strategy- or information-based cognitive training in a small group for 8 weeks. We measured psychological functioning scores, cortical thickness, and resting-state functional connectivity (rsFC) for these individuals before training, immediately post-training, and 3 months post-training. After confirming that changes in BDI scores were independent of training group affiliation, we identified that the depressive-symptoms group showed reductions in BDI scores over time relative to the non-depressed TBI controls (p < .01). Within the depressive-symptoms group, reduced BDI scores was associated with improvements in scores for post-traumatic stress disorder, TBI symptom awareness, and functional status (p < .00625), increases in cortical thickness in four regions within the right prefrontal cortex (pvertex < .01, pcluster <.05), and decreases in rsFC with each of these four prefrontal regions (pvertex < .01, pcluster < .0125). Overall, these findings suggest that cognitive training can reduce depressive symptoms in TBI even when the training does not directly target psychiatric symptoms. Importantly, cortical thickness and brain connectivity may offer promising neuroimaging markers of training-induced improvement in mental health status in TBI.

Keywords: depression; intervention; mental health; neural marker; neuroplasticity.

© 2018 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc.

Figures

Figure 1
Figure 1
Temporal changes in depressive symptoms severity. (a) Changes according to the presence of depressive symptoms. (b) Changes according to the types of intervention program. (c) Percentage of participants with resolved depressive symptoms following intervention. (d) The number of participants with resolved depressive symptoms following training, according to the types of intervention program. BDI–II, Beck Depression Inventory‐Second Edition; TBI + BDI, TBI‐plus‐depressive symptoms group (BDI–II of 14–63 prior to intervention); TBI only, TBI with minimal depressive symptoms group (BDI–II of 0–13 prior to intervention) [Color figure can be viewed at http://wileyonlinelibrary.com]
Figure 2
Figure 2
Trajectories of BDI‐II total scores versus psychological functioning scores. (a and b): BDI–II versus scores for PTSD symptoms from the PCL‐S. (c and d): BDI–II versus TBI awareness. (e and f): BDI‐II versus FSE. Each colored line represents the trajectory of each individual, and the black line represents group‐averaged trajectory. PCL‐S = posttraumatic stress disorder check‐list stressor‐specific; FSE = functional status examination [Color figure can be viewed at http://wileyonlinelibrary.com]
Figure 3
Figure 3
Associations between depressive symptoms and cortical thickness. Colormaps represent statistically significant associations of reduced BDI–II total scores with increased cortical thickness over time (pvertex < .01, pcluster < .05). R = right; VLPFC = ventrolateral prefrontal cortex; APFC = anterior prefrontal cortex; DPFC = dorsal prefrontal cortex [Color figure can be viewed at http://wileyonlinelibrary.com]
Figure 4
Figure 4
Associations between depressive symptoms and connectivity. Colormaps represent statistically significant associations of reduced BDI–II total scores (left) and Buckley cognitive factor scores of depressive symptoms (right) with reduced connectivity in R VLPFC, R APFC, R DPFC1, and R DPFC2 within the TBI‐plus‐depressive symptoms group, respectively (pvertex < .01, pcluster < .0125(=.05/4)). There were no statistically significant associations of reduced Buckley affective and somatic scores with increased connectivity. R = right; VLPFC = ventrolateral prefrontal cortex; APFC = anterior prefrontal cortex; DPFC = dorsal prefrontal cortex [Color figure can be viewed at http://wileyonlinelibrary.com]
Figure 5
Figure 5
Effect sizes for associations between changes in cortical thickness and reductions in depressive symptoms. Colormaps represent increases or decreases in cortical thickness per reductions in BDI–II total scores by 10. R = right; VLPFC = ventrolateral prefrontal cortex; APFC = anterior prefrontal cortex; DPFC = dorsal prefrontal cortex [Color figure can be viewed at http://wileyonlinelibrary.com]
Figure 6
Figure 6
Effect sizes for associations between changes in functional connectivity and reductions in depressive symptoms. Colormaps represent increases or decreases in functional connectivity per reductions in BDI–II total scores by 10 (left) and Buckley cognitive factor scores of depressive symptoms by 4 (right). R = right; VLPFC = ventrolateral prefrontal cortex; APFC = anterior prefrontal cortex; DPFC = dorsal prefrontal cortex [Color figure can be viewed at http://wileyonlinelibrary.com]

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Source: PubMed

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