title: A two-part preliminary investigation of encoding-related activation changes after moderate to severe traumatic brain injury: hyperactivation, repetition suppression, and the role of the prefrontal cortex.
abstract: Traumatic brain injury (TBI) survivors typically exhibit significant learning and memory deficits and also frequently demonstrate hyperactivation during functional magnetic resonance imaging (fMRI) tasks involving working memory encoding and maintenance. However, it remains unclear whether the hyperactivation observed during such working memory tasks is also present during long-term memory encoding. The preliminary experiments presented here were designed to examine this question. In Experiment 1, 7 healthy controls (HC) and 7 patients with moderate to severe TBI encoded ecologically relevant object location associations (OLA) while undergoing fMRI and then completed a memory test outside of the fMRI environment. fMRI data analysis included only the correctly encoded trials and revealed hyperactivation in the TBI relative to HC group in regions critical for OLA encoding, including bilateral dorsal and ventral visual processing areas, bilateral frontoparietal working memory network regions, and the left medial temporal lobe. There was also an incidental finding that this hyperactivation persisted after multiple exposures to the same stimulus, which may indicate an attenuated repetition suppression effect that could ultimately contribute to cognitive fatigue and inefficient memory encoding after TBI. Experiment 2 directly assessed repetition suppression in some of the same HC and TBI participants. During early encoding trials, the TBI group showed large areas of hyperactivation in the right prefrontal cortex and bilateral posterior parietal cortices relative to the HC. Following additional exposure to these stimuli, the TBI group showed repetition suppression in visual and spatial processing regions, but continued to show hyperactivation in the right dorsolateral prefrontal cortex. Findings from these preliminary studies may reflect that increased reliance on cognitive control mechanisms following TBI extends to memory encoding.
authors.affiliation: Department of Rehabilitation Medicine, Emory University School of Medicine, Center for Rehabilitation Medicine, 1441 Clifton Road NE, Atlanta, GA, 30322, USA.
authors.forename: M Meredith
authors.initials: MM
authors.lastname: Gillis
authors.affiliation: Rehabilitation R&D Center of Excellence, Atlanta VAMC, 1670 Clairmont Road (151R), Decatur, GA, 30033, USA. bhampste@med.umich.edu.|Department of Rehabilitation Medicine, Emory University School of Medicine, Center for Rehabilitation Medicine, 1441 Clifton Road NE, Atlanta, GA, 30322, USA. bhampste@med.umich.edu.|Neuropsychology Section, Department of Psychiatry, University of Michigan, 2101 Commonwealth Blvd Suite C, Ann Arbor, MI, 48105, USA. bhampste@med.umich.edu.
authors.forename: Benjamin M
authors.initials: BM
authors.lastname: Hampstead
mesh_terms: D000293:Adolescent; D000328:Adult; D001245:Association Learning / Q000502:physiology; D001930:Brain Injuries / Q000503:physiopathology* / Q000523:psychology*; D001931:Brain Mapping; D002908:Chronic Disease; D006801:Humans; D008279:Magnetic Resonance Imaging; D008568:Memory / Q000502:physiology*; D008875:Middle Aged; D009483:Neuropsychological Tests; D017397:Prefrontal Cortex / Q000503:physiopathology*; D012720:Severity of Illness Index; D014796:Visual Perception / Q000502:physiology; D055815:Young Adult
keywords: Encoding; Functional neuroimaging; Memory; Repetition suppression; Traumatic brain injury; Working memory