TY - JOUR
T1 - Aberrant modulation of brain activity underlies impaired working memory following traumatic brain injury
AU - Taing, Abbie S.
AU - Mundy, Matthew E.
AU - Ponsford, Jennie L.
AU - Spitz, Gershon
N1 - Funding Information:
GS was funded by a National Health and Medical Research Council Early Career Fellowship (APP1104692) and the Brain Foundation.
Funding Information:
This work was supported by the Multi-modal Australian ScienceS Imaging and Visualisation Environment (MASSIVE) HPC facility (www.massive.org.au). The authors would like to thank Olivia McConchie at the Monash Epworth Rehabilitation Research Centre and the staff at the Acquired Brain Injury Ward at Epworth Hospital (Richmond) for their help with recruitment. The authors would also like to thank the staff at Bridge Road Imaging and Monash Biomedical Imaging for their assistance with data collection. Lastly, the authors would like to thank the participants who participated in the study.
Publisher Copyright:
© 2021 The Author(s)
PY - 2021/1
Y1 - 2021/1
N2 - Impaired working memory is a common and disabling consequence of traumatic brain injury (TBI) that is caused by aberrant brain processing. However, little is known about the extent to which deficits are perpetuated by specific working memory subprocesses. Using a combined functional magnetic resonance imaging (fMRI) and working memory paradigm, we tested the hypothesis that the pattern of brain activation subserving working memory following TBI would interact with both task demands and specific working memory subcomponents: encoding, maintenance, and retrieval. Forty-three patients with moderate-severe TBI, of whom 25 were in the acute phase of recovery (M = 2.16 months, SD = 1.48 months, range = 0.69 – 6.64 months) and 18 in the chronic phase of recovery (M = 23.44 months, SD = 6.76 months, range = 13.35 – 34.82 months), were compared with 38 demographically similar healthy controls. Behaviourally, we found that working memory deficits were confined to the high cognitive load trials in both acute (P = 0.006) and chronic (P = 0.024) cohorts. Furthermore, results for a subset of the sample (18 chronic TBI and 17 healthy controls) who underwent fMRI revealed that the TBI group showed reduced brain activation when simply averaged across all task trials (regardless of cognitive load or subcomponent). However, interrogation of the subcomponents of working memory revealed a more nuanced pattern of activation. When examined more closely, patterns of brain activity following TBI were found to interact with both task demands and the working memory subcomponent: increased activation was observed during encoding in the left inferior occipital gyrus whereas decreased activation was apparent during maintenance in the bilateral cerebellum and left calcarine sulcus. Taken together, findings indicate an inability to appropriately modulate brain activity according to task demand that is specific to working memory encoding and maintenance.
AB - Impaired working memory is a common and disabling consequence of traumatic brain injury (TBI) that is caused by aberrant brain processing. However, little is known about the extent to which deficits are perpetuated by specific working memory subprocesses. Using a combined functional magnetic resonance imaging (fMRI) and working memory paradigm, we tested the hypothesis that the pattern of brain activation subserving working memory following TBI would interact with both task demands and specific working memory subcomponents: encoding, maintenance, and retrieval. Forty-three patients with moderate-severe TBI, of whom 25 were in the acute phase of recovery (M = 2.16 months, SD = 1.48 months, range = 0.69 – 6.64 months) and 18 in the chronic phase of recovery (M = 23.44 months, SD = 6.76 months, range = 13.35 – 34.82 months), were compared with 38 demographically similar healthy controls. Behaviourally, we found that working memory deficits were confined to the high cognitive load trials in both acute (P = 0.006) and chronic (P = 0.024) cohorts. Furthermore, results for a subset of the sample (18 chronic TBI and 17 healthy controls) who underwent fMRI revealed that the TBI group showed reduced brain activation when simply averaged across all task trials (regardless of cognitive load or subcomponent). However, interrogation of the subcomponents of working memory revealed a more nuanced pattern of activation. When examined more closely, patterns of brain activity following TBI were found to interact with both task demands and the working memory subcomponent: increased activation was observed during encoding in the left inferior occipital gyrus whereas decreased activation was apparent during maintenance in the bilateral cerebellum and left calcarine sulcus. Taken together, findings indicate an inability to appropriately modulate brain activity according to task demand that is specific to working memory encoding and maintenance.
KW - Encoding
KW - Maintenance
KW - MRI
KW - Traumatic brain injury
KW - Working memory
UR - http://www.scopus.com/inward/record.url?scp=85111481385&partnerID=8YFLogxK
U2 - 10.1016/j.nicl.2021.102777
DO - 10.1016/j.nicl.2021.102777
M3 - Article
C2 - 34343728
AN - SCOPUS:85111481385
VL - 31
JO - NeuroImage: Clinical
JF - NeuroImage: Clinical
SN - 2213-1582
M1 - 102777
ER -