Global volumetric reductions across amygdala nuclei in chronic TBI
Presentation Type
Poster
Faculty Advisor
Joshua Sandry
Access Type
Event
Start Date
26-4-2023 1:44 PM
End Date
26-4-2023 2:45 PM
Description
BACKGROUND: Traumatic brain injury (TBI) may increase susceptibility to neurodegenerative diseases later in life, that is, the accelerated aging hypothesis. This is supported by recent research demonstrating subcortical gray matter atrophy patterns in chronic TBI (M=9 years post-injury) that are similar to some neurodegenerative diseases. Atrophy appears to be global across hippocampal subfields and selective across thalamic nuclei. There have been no investigations into differential atrophy patterns across amygdalar nuclei in chronic TBI. OBJECTIVE: Given the close proximity between the amygdala and hippocampus, and amygdala atrophy implicated in some neurodegenerative conditions, the aims of the present investigation are to determine 1) whether the pattern of amygdala atrophy in chronic TBI follows a global or selective pattern and 2) whether time since injury predicts specific nuclei atrophy. METHOD: 40 TBI and 33 non-TBI participants completed T1 weighted 3T magnetic resonance imaging scans. Amygdalae were segmented into 10 nuclei using freesurfer, summed bilaterally and adjusted for estimated intracranial volume and sex. Unpaired t-tests (alpha Holm adjusted) and Cohen’s D were used to compare groups. Partial correlations (adjusting for age) were used to test the relationship between nuclei and time since injury. RESULTS: Amygdala volumes were smaller in the TBI group than the non-TBI group and this pattern was consistent across all 10 amygdala nuclei suggesting a global pattern. No correlations between amygdala nuclei and time since injury were significant. CONCLUSION: Global changes across amygdala nuclei is evident in chronic TBI. This is similar to the global pattern of atrophy observed across hippocampal subfields and in contrast to selective thalamic atrophy that is evident in these same individuals. Lack of a relationship between nuclei and time since injury does not support the accelerated
Global volumetric reductions across amygdala nuclei in chronic TBI
BACKGROUND: Traumatic brain injury (TBI) may increase susceptibility to neurodegenerative diseases later in life, that is, the accelerated aging hypothesis. This is supported by recent research demonstrating subcortical gray matter atrophy patterns in chronic TBI (M=9 years post-injury) that are similar to some neurodegenerative diseases. Atrophy appears to be global across hippocampal subfields and selective across thalamic nuclei. There have been no investigations into differential atrophy patterns across amygdalar nuclei in chronic TBI. OBJECTIVE: Given the close proximity between the amygdala and hippocampus, and amygdala atrophy implicated in some neurodegenerative conditions, the aims of the present investigation are to determine 1) whether the pattern of amygdala atrophy in chronic TBI follows a global or selective pattern and 2) whether time since injury predicts specific nuclei atrophy. METHOD: 40 TBI and 33 non-TBI participants completed T1 weighted 3T magnetic resonance imaging scans. Amygdalae were segmented into 10 nuclei using freesurfer, summed bilaterally and adjusted for estimated intracranial volume and sex. Unpaired t-tests (alpha Holm adjusted) and Cohen’s D were used to compare groups. Partial correlations (adjusting for age) were used to test the relationship between nuclei and time since injury. RESULTS: Amygdala volumes were smaller in the TBI group than the non-TBI group and this pattern was consistent across all 10 amygdala nuclei suggesting a global pattern. No correlations between amygdala nuclei and time since injury were significant. CONCLUSION: Global changes across amygdala nuclei is evident in chronic TBI. This is similar to the global pattern of atrophy observed across hippocampal subfields and in contrast to selective thalamic atrophy that is evident in these same individuals. Lack of a relationship between nuclei and time since injury does not support the accelerated