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

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 (p_vertex < .01, p_cluster <.05), and decreases in rsFC with each of these four prefrontal regions (p_vertex < .01, p_cluster < .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.

SUBMITTER: Han K

PROVIDER: S-EPMC6055759 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Novel and non-routine tasks often require information processing and behavior to adapt from moment to moment depending on task requirements and current performance. This ability to adapt is an executive function that is referred to as cognitive control. Patients with moderate-to-severe traumatic brain injury (TBI) have been reported to exhibit impairments in cognitive control and functional magnetic resonance imaging (fMRI) has provided evidence for TBI-related alterations in brain activation using various fMRI cognitive control paradigms. There is some support for greater and more extensive cognitive control-related brain activation in patients with moderate-to-severe TBI, relative to comparison subjects without TBI. In addition, some studies have reported a correlation between these activation increases and measures of injury severity. Explanations that have been proposed for increased activation within structures that are thought to be directly involved in cognitive control, as well as the extension of this over-activation into other brain structures, have included compensatory mechanisms, increased demand upon normal processes required to maintain adequate performance, less efficient utilization of neural resources, and greater vulnerability to cognitive fatigue. Recent findings are also consistent with the possibility that activation increases within some structures, such as the posterior cingulate gyrus, may reflect a failure to deactivate components of the default mode network (DMN) and that some cognitive control impairment may result from ineffective coordination between the DMN and components of the salience network. Functional neuroimaging studies examining cognitive control-related activation following mild TBI (mTBI) have yielded more variable results, with reports of increases, decreases, and no significant change. These discrepancies may reflect differences among the various mTBI samples under study, recovery of function in some patients, different task characteristics, and the presence of comorbid conditions such as depression and posttraumatic stress disorder that also alter brain activation. There may be mTBI populations with activation changes that overlap with those found following more severe injuries, including symptomatic mTBI patients and those with acute injuries, but future research to address such dysfunction will require well-defined samples with adequate controls for injury characteristics, comorbid disorders, and severity of post-concussive symptoms.

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

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