Loss of white matter connections after severe traumatic brain injury (TBI) and its relationship to social cognition.
Adult
Aged
Brain
/ pathology
Brain Injuries
/ psychology
Brain Injuries, Traumatic
/ physiopathology
Cognition
/ physiology
Cognition Disorders
/ pathology
Connectome
Diffusion Magnetic Resonance Imaging
/ methods
Diffusion Tensor Imaging
/ methods
Female
Humans
Male
Middle Aged
Neuropsychological Tests
Social Behavior
White Matter
/ pathology
Diffuse axonal injury
Social cognition
Traumatic brain injury
White matter
Journal
Brain imaging and behavior
ISSN: 1931-7565
Titre abrégé: Brain Imaging Behav
Pays: United States
ID NLM: 101300405
Informations de publication
Date de publication:
Jun 2019
Jun 2019
Historique:
pubmed:
28
6
2018
medline:
13
11
2019
entrez:
28
6
2018
Statut:
ppublish
Résumé
Adults with severe traumatic brain injury (TBI) often suffer poor social cognition. Social cognition is complex, requiring verbal, non-verbal, auditory, visual and affective input and integration. While damage to focal temporal and frontal areas has been implicated in disorders of social cognition after TBI, the role of white matter pathology has not been examined. In this study 17 adults with chronic, severe TBI and 17 control participants underwent structural MRI scans and Diffusion Tensor Imaging. The Awareness of Social Inference Test (TASIT) was used to assess their ability to understand emotional states, thoughts, intentions and conversational meaning in everyday exchanges. Track-based spatial statistics were used to perform voxelwise analysis of Fractional Anisotropy (FA) and Mean Diffusivity (MD) of white matter tracts associated with poor social cognitive performance. FA suggested a wide range of tracts were implicated in poor TASIT performance including tracts known to mediate, auditory localisation (planum temporale) communication between nonverbal and verbal processes in general (corpus callosum) and in memory in particular (fornix) as well as tracts and structures associated with semantics and verbal recall (left temporal lobe and hippocampus), multimodal processing and integration (thalamus, external capsule, cerebellum) and with social cognition (orbitofrontal cortex, frontopolar cortex, right temporal lobe). Even when controlling for non-social cognition, the corpus callosum, fornix, bilateral thalamus, right external capsule and right temporal lobe remained significant contributors to social cognitive performance. This study highlights the importance of loss of white matter connectivity in producing complex social information processing deficits after TBI.
Identifiants
pubmed: 29948905
doi: 10.1007/s11682-018-9906-0
pii: 10.1007/s11682-018-9906-0
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
819-829Subventions
Organisme : Australian Research Council
ID : DP15010026
Organisme : National Health and Medical Research Council
ID : PG1081923