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It is paramount to further unravel these processes, because the possible long\u2010term cognitive effects resulting from ongoing secondary injury in the developing brain are not known. In the current fMRI study, neural processes related to cognitive control were studied in 181 patients with pmTBI at sub\u2010acute (SA; ~1\u2009week) and early chronic (EC; ~4\u2009months) stages post\u2010injury. Additionally, a group of 162 age\u2010 and sex\u2010matched healthy controls (HC) were recruited at equivalent time points. Proactive (post\u2010cue) and reactive (post\u2010probe) cognitive control were examined using a multimodal attention fMRI paradigm for either congruent or incongruent stimuli. To study brain network function, the triple\u2010network model was used, consisting of the executive and salience networks (collectively known as the cognitive control network), and the default mode network. Additionally, whole\u2010brain voxel\u2010wise analyses were performed. Decreased deactivation was found within the default mode network at the EC stage following pmTBI during both proactive and reactive control. Voxel\u2010wise analyses revealed sub\u2010acute hypoactivation of a frontal area of the cognitive control network (left pre\u2010supplementary motor area) during proactive control, with a reversed effect at the EC stage after pmTBI. Similar effects were observed in areas outside of the triple\u2010network during reactive control. Group differences in activation during proactive control were limited to the visual domain, whereas for reactive control findings were more pronounced during the attendance of auditory stimuli. No significant correlations were present between task\u2010related activations and (persistent) post\u2010concussive symptoms. In aggregate, current results show alterations in neural functioning during cognitive control in pmTBI up to 4\u2009months post\u2010injury, regardless of clinical recovery. We propose that subacute decreases in activity reflect a general state of hypo\u2010excitability due to the injury, while early chronic hyperactivation represents a compensatory mechanism to prevent default mode interference and to retain cognitive control.<\/jats:p>","DOI":"10.1002\/hbm.26504","type":"journal-article","created":{"date-parts":[[2023,10,6]],"date-time":"2023-10-06T17:50:41Z","timestamp":1696614641000},"page":"6173-6184","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Neural correlates of cognitive control deficits in pediatric mild traumatic brain injury"],"prefix":"10.1002","volume":"44","author":[{"given":"Harm J.","family":"van der Horn","sequence":"first","affiliation":[{"name":"The Mind Research Network\/LBERI  Albuquerque New Mexico USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew B.","family":"Dodd","sequence":"additional","affiliation":[{"name":"The Mind Research 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