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Altered Amygdala Connectivity in Individuals with Chronic Traumatic Brain Injury and Comorbid Depressive Symptoms

View Article: PubMed Central

ABSTRACT

Depression is one of the most common psychiatric conditions in individuals with chronic traumatic brain injury (TBI). Though depression has detrimental effects in TBI and network dysfunction is a “hallmark” of TBI and depression, there have not been any prior investigations of connectivity-based neuroimaging biomarkers for comorbid depression in TBI. We utilized resting-state functional magnetic resonance imaging to identify altered amygdala connectivity in individuals with chronic TBI (8 years post-injury on average) exhibiting comorbid depressive symptoms (N = 31), relative to chronic TBI individuals having minimal depressive symptoms (N = 23). Connectivity analysis of these participant sub-groups revealed that the TBI-plus-depressive symptoms group showed relative increases in amygdala connectivity primarily in the regions that are part of the salience, somatomotor, dorsal attention, and visual networks (pvoxel < 0.01, pcluster < 0.025). Relative increases in amygdala connectivity in the TBI-plus-depressive symptoms group were also observed within areas of the limbic–cortical mood-regulating circuit (the left dorsomedial and right dorsolateral prefrontal cortices and thalamus) and the brainstem. Further analysis revealed that spatially dissociable patterns of correlation between amygdala connectivity and symptom severity according to subtypes (Cognitive and Affective) of depressive symptoms (pvoxel < 0.01, pcluster < 0.025). Taken together, these results suggest that amygdala connectivity may be a potentially effective neuroimaging biomarker for comorbid depressive symptoms in chronic TBI.

No MeSH data available.


Group comparison maps of amygdala connectivity.
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Figure 1: Group comparison maps of amygdala connectivity.

Mentions: Group analysis revealed enhanced bilateral amygdala connectivity for the TBI-plus-depressive symptoms group relative to the TBI-only group across multiple regions except left amygdala connectivity with the left superior parietal lobule (SPL), right insula and right thalamus and right amygdala connectivity with the right thalamus at pvoxel < 0.01 and pcluster < 0.025 (Figure 1). Spatial patterns of relatively enhanced amygdala connectivity of the TBI-plus-depressive symptoms group were fairly consistent over both amygdala connectivities though right amygdala connectivity showed stronger increases in the TBI-plus-depressive symptoms group over the TBI-only group. Conjunction analysis results (Figure 2) highlighted brain regions with consistently increased bilateral amygdala connectivity of the TBI-plus-depressive symptoms group over the TBI-only group. The regions showing increased connectivity for both left and right amygdala include the bilateral posterior midcingulate cortex, marginal sulcus, paracentral sulcus, precentral gyrus; the left SPL; the right dorsolateral prefrontal cortex (DLPFC), central sulcus, postcentral gyrus, and insula. Local peak coordinates of these regions and their Z-scores were listed in Table 4. Group comparison maps, including a network-based parcelation (Figure 3), revealed that alterations in amygdala connectivity of the TBI-plus-depressive symptoms group primarily occurred in the areas originally reported by Biswal et al. (118) and later labeled the somatomotor network (SMN) (119), the dorsal attention network (DAN) (112, 120), SN (35), and visual network (VN) (121). Relative increases in amygdala connectivity of the TBI group with depressive symptoms also occurred within areas of the limbic–cortical mood-regulating circuit (45), including the left DMPFC and right DLPFC and right thalamus (Figures 1–3).


Altered Amygdala Connectivity in Individuals with Chronic Traumatic Brain Injury and Comorbid Depressive Symptoms
Group comparison maps of amygdala connectivity.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4631949&req=5

Figure 1: Group comparison maps of amygdala connectivity.
Mentions: Group analysis revealed enhanced bilateral amygdala connectivity for the TBI-plus-depressive symptoms group relative to the TBI-only group across multiple regions except left amygdala connectivity with the left superior parietal lobule (SPL), right insula and right thalamus and right amygdala connectivity with the right thalamus at pvoxel < 0.01 and pcluster < 0.025 (Figure 1). Spatial patterns of relatively enhanced amygdala connectivity of the TBI-plus-depressive symptoms group were fairly consistent over both amygdala connectivities though right amygdala connectivity showed stronger increases in the TBI-plus-depressive symptoms group over the TBI-only group. Conjunction analysis results (Figure 2) highlighted brain regions with consistently increased bilateral amygdala connectivity of the TBI-plus-depressive symptoms group over the TBI-only group. The regions showing increased connectivity for both left and right amygdala include the bilateral posterior midcingulate cortex, marginal sulcus, paracentral sulcus, precentral gyrus; the left SPL; the right dorsolateral prefrontal cortex (DLPFC), central sulcus, postcentral gyrus, and insula. Local peak coordinates of these regions and their Z-scores were listed in Table 4. Group comparison maps, including a network-based parcelation (Figure 3), revealed that alterations in amygdala connectivity of the TBI-plus-depressive symptoms group primarily occurred in the areas originally reported by Biswal et al. (118) and later labeled the somatomotor network (SMN) (119), the dorsal attention network (DAN) (112, 120), SN (35), and visual network (VN) (121). Relative increases in amygdala connectivity of the TBI group with depressive symptoms also occurred within areas of the limbic–cortical mood-regulating circuit (45), including the left DMPFC and right DLPFC and right thalamus (Figures 1–3).

View Article: PubMed Central

ABSTRACT

Depression is one of the most common psychiatric conditions in individuals with chronic traumatic brain injury (TBI). Though depression has detrimental effects in TBI and network dysfunction is a &ldquo;hallmark&rdquo; of TBI and depression, there have not been any prior investigations of connectivity-based neuroimaging biomarkers for comorbid depression in TBI. We utilized resting-state functional magnetic resonance imaging to identify altered amygdala connectivity in individuals with chronic TBI (8&thinsp;years post-injury on average) exhibiting comorbid depressive symptoms (N&thinsp;=&thinsp;31), relative to chronic TBI individuals having minimal depressive symptoms (N&thinsp;=&thinsp;23). Connectivity analysis of these participant sub-groups revealed that the TBI-plus-depressive symptoms group showed relative increases in amygdala connectivity primarily in the regions that are part of the salience, somatomotor, dorsal attention, and visual networks (pvoxel&thinsp;&lt;&thinsp;0.01, pcluster&thinsp;&lt;&thinsp;0.025). Relative increases in amygdala connectivity in the TBI-plus-depressive symptoms group were also observed within areas of the limbic&ndash;cortical mood-regulating circuit (the left dorsomedial and right dorsolateral prefrontal cortices and thalamus) and the brainstem. Further analysis revealed that spatially dissociable patterns of correlation between amygdala connectivity and symptom severity according to subtypes (Cognitive and Affective) of depressive symptoms (pvoxel&thinsp;&lt;&thinsp;0.01, pcluster&thinsp;&lt;&thinsp;0.025). Taken together, these results suggest that amygdala connectivity may be a potentially effective neuroimaging biomarker for comorbid depressive symptoms in chronic TBI.

No MeSH data available.