T154. Functional Connectivity of the Anterior Cingulate Cortex in Veterans With Mild Traumatic Brain Injury

2019 ◽  
Vol 85 (10) ◽  
pp. S188-S189
Author(s):  
Chandni Sheth ◽  
Jadwiga Rogowska ◽  
Margaret Legarreta ◽  
Erin McGlade ◽  
Deborah Yurgelun-Todd
2021 ◽  
Vol 396 ◽  
pp. 112882 ◽  
Author(s):  
Chandni Sheth ◽  
Jadwiga Rogowska ◽  
Margaret Legarreta ◽  
Erin McGlade ◽  
Deborah Yurgelun-Todd

2020 ◽  
Vol 123 (5) ◽  
pp. 1619-1629
Author(s):  
Chandni Sheth ◽  
Andrew P. Prescot ◽  
Margaret Legarreta ◽  
Perry F. Renshaw ◽  
Erin McGlade ◽  
...  

In this study of veterans, we used a state-of-the-art neuroimaging tool to probe the neurometabolic profile of the anterior cingulate cortex in veterans with traumatic brain injury (TBI). We report significantly elevated myoinositol levels in veterans with TBI compared with those without TBI.


2020 ◽  
Author(s):  
Xuan Niu ◽  
Lijun Bai ◽  
Yingxiang Sun ◽  
Yuan Wang ◽  
Guanghui Bai ◽  
...  

Abstract Background:Mild traumatic brain injury (mTBI) is higher prevalence (more than 50%) to develop chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. However, the underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who finally developing CPTH at follow-up.Methods:77 mTBI patients initially underwent neuropsychological measurements, 9-plex panel of serum cytokines and MRI scans within 7 days post-injury (T-1) and 54 (70.1%) of patients follow-up at 3-month (T-2). 42 matched healthy controls completed the same protocol at T-1 once. Results:MTBI patients with APTH presented significantly increased GM volume mainly in the right dorsal anterior cingulate cortex (dACC) and dorsal posterior cingulate cortex (dPCC), of which the dPCC volume can predict much worse impact of headache on patients’ lives by HIT-6 (β = 0.389, P = 0.007). Serum levels of C-C motif chemokine ligand 2 (CCL2) were also elevated in these patients, and its effect on the impact of headache on quality of life was partially mediated by the dPCC volume (mean [SE] indirect effect, 0.088 [0.0462], 95% CI, 0.01-0.164). Longitudinal analysis showed that the dACC and dPCC volumes as well as CCL2 levels persistently increased in patients developing CPTH 3 month postinjury. Conclusion:The findings suggested that structural remodelling of DMN brain regions were involved in the progression from acute to chronic PTH following mTBI, which also mediated the effect of inflammation processes on pain modulation.Trial registration: ClinicalTrial.gov ID: NCT02868684; registered 16 August 2016.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Xuan Niu ◽  
Lijun Bai ◽  
Yingxiang Sun ◽  
Yuan Wang ◽  
Guanghui Bai ◽  
...  

Abstract Background Mild traumatic brain injury (mTBI) has a higher prevalence (more than 50%) of developing chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. However, the underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who finally developed CPTH at follow-up. Methods Seventy-seven mTBI patients initially underwent neuropsychological measurements, 9-plex panel of serum cytokines and MRI scans within 7 days post-injury (T-1) and 54 (70.1%) of patients completed the same protocol at a 3-month follow-up (T-2). Forty-two matched healthy controls completed the same protocol at T-1 once. Results At baseline, mTBI patients with APTH presented significantly increased GM volume mainly in the right dorsal anterior cingulate cortex (dACC) and dorsal posterior cingulate cortex (dPCC), of which the dPCC volume can predict much worse impact of headache on patients’ lives by HIT-6 (β = 0.389, P = 0.007) in acute stage. Serum levels of C-C motif chemokine ligand 2 (CCL2) were also elevated in these patients, and its effect on the impact of headache on quality of life was partially mediated by the dPCC volume (mean [SE] indirect effect, 0.088 [0.0462], 95% CI, 0.01–0.164). Longitudinal analysis showed that the dACC and dPCC volumes as well as CCL2 levels had persistently increased in patients developing CPTH 3 months postinjury. Conclusion The findings suggested that structural remodelling of DMN brain regions were involved in the progression from acute to chronic PTH following mTBI, which also mediated the effect of inflammation processes on pain modulation. Trial registration ClinicalTrial.gov ID: NCT02868684; registered 16 August 2016.


2011 ◽  
Vol 1 ◽  
Author(s):  
Fabienne Cazalis ◽  
Talin Babikian ◽  
Christopher Giza ◽  
Sarah Copeland ◽  
David Hovda ◽  
...  

2020 ◽  
Author(s):  
Xuan Niu ◽  
Lijun Bai ◽  
Yingxiang Sun ◽  
Yuan Wang ◽  
Guanghui Bai ◽  
...  

Abstract Background:Mild traumatic brain injury (mTBI) has a higher prevalence (more than 50%) of developing chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. However, the underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who finally developed CPTH at follow-up.Methods:77 mTBI patients initially underwent neuropsychological measurements, 9-plex panel of serum cytokines and MRI scans within 7 days post-injury (T-1) and 54(70.1%) of patients completed the same protocol at a 3-month follow-up (T-2). 42 matched healthy controls completed the same protocol at T-1 once. Results:At baseline, mTBI patients with APTH presented significantly increased GM volume mainly in the right dorsal anterior cingulate cortex (dACC) and dorsal posterior cingulate cortex (dPCC), of which the dPCC volume can predict much worse impact of headache on patients’ lives by HIT-6 (β = 0.389, P = 0.007) in acute stage. Serum levels of C-C motif chemokine ligand 2 (CCL2) were also elevated in these patients, and its effect on the impact of headache on quality of life was partially mediated by the dPCC volume (mean [SE] indirect effect, 0.088 [0.0462], 95% CI, 0.01-0.164). Longitudinal analysis showed that the dACC and dPCC volumes as well as CCL2 levels had persistently increased in patients developing CPTH 3 months postinjury. Conclusion:The findings suggested that structural remodelling of DMN brain regions were involved in the progression from acute to chronic PTH following mTBI, which also mediated the effect of inflammation processes on pain modulation.Trial registration: ClinicalTrial.gov ID: NCT02868684; registered 16 August 2016.


2020 ◽  
Author(s):  
Xuan Niu ◽  
Lijun Bai ◽  
Yingxiang Sun ◽  
Yuan Wang ◽  
Guanghui Bai ◽  
...  

Abstract Background:Mild traumatic brain injury (mTBI) has a higher prevalence (more than 50%) of developing chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. However, the underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who finally developed CPTH at follow-up.Methods:77 mTBI patients initially underwent neuropsychological measurements, 9-plex panel of serum cytokines and MRI scans within 7 days post-injury (T-1) and 54(70.1%) of patients completed the same protocol at a 3-month follow-up (T-2). 42 matched healthy controls completed the same protocol at T-1 once. Results:At baseline, mTBI patients with APTH presented significantly increased GM volume mainly in the right dorsal anterior cingulate cortex (dACC) and dorsal posterior cingulate cortex (dPCC), of which the dPCC volume can predict much worse impact of headache on patients’ lives by HIT-6 (β = 0.389, P = 0.007) in acute stage. Serum levels of C-C motif chemokine ligand 2 (CCL2) were also elevated in these patients, and its effect on the impact of headache on quality of life was partially mediated by the dPCC volume (mean [SE] indirect effect, 0.088 [0.0462], 95% CI, 0.01-0.164). Longitudinal analysis showed that the dACC and dPCC volumes as well as CCL2 levels had persistently increased in patients developing CPTH 3 months postinjury. Conclusion:The findings suggested that structural remodelling of DMN brain regions were involved in the progression from acute to chronic PTH following mTBI, which also mediated the effect of inflammation processes on pain modulation.Trial registration: ClinicalTrial.gov ID: NCT02868684; registered 16 August 2016.


2014 ◽  
Vol 111 (4) ◽  
pp. 787-803 ◽  
Author(s):  
Michael J. Koval ◽  
R. Matthew Hutchison ◽  
Stephen G. Lomber ◽  
Stefan Everling

The dorsolateral prefrontal cortex (dlPFC) and anterior cingulate cortex (ACC) have both been implicated in the cognitive control of saccadic eye movements by single neuron recording studies in nonhuman primates and functional imaging studies in humans, but their relative roles remain unclear. Here, we reversibly deactivated either dlPFC or ACC subregions in macaque monkeys while the animals performed randomly interleaved pro- and antisaccades. In addition, we explored the whole-brain functional connectivity of these two regions by applying a seed-based resting-state functional MRI analysis in a separate cohort of monkeys. We found that unilateral dlPFC deactivation had stronger behavioral effects on saccades than unilateral ACC deactivation, and that the dlPFC displayed stronger functional connectivity with frontoparietal areas than the ACC. We suggest that the dlPFC plays a more prominent role in the preparation of pro- and antisaccades than the ACC.


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