ArticleNeurobiology of stress2021
Neural activity during response inhibition in mild traumatic brain injury and posttraumatic stress disorder.
Article in Neurobiology of stress, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Posttraumatic stress symptomatology rather than mild traumatic brain injury is related to atypical early neural processing during cognitive control.Neuropsychology · 2025Article
- The Stress Phenotyping Framework: A multidisciplinary biobehavioral approach for assessing and therapeutically targeting maladaptive stress physiology.Stress (Amsterdam, Netherlands) · 2024Review
- A comparison of the functional connectome in mild traumatic brain injury and post-traumatic stress disorder.Human brain mapping · 2023Article
- Stress amelioration and anti-inflammatory potential of Shiikuwasha (Citrus depressa Hayata) essential oil, limonene, and γ-terpinene.Journal of food and drug analysis · 2022Article
- Sex differences in cognitive flexibility are driven by the estrous cycle and stress-dependent.Frontiers in behavioral neuroscience · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mild traumatic brain injury (mTBI) is often characterized by deficits in response inhibition, which can contribute to marked social and occupational dysfunction. mTBI often occurs in the context of psychologically traumatic events. This can cause posttraumatic stress disorder (PTSD), which also impedes response inhibition. The overlap or distinction in these inhibitory deficits in mTBI and PTSD is unclear. This study aimed to assess behavioral, neurophysiological, and neuroimaging indices of response inhibition in mTBI by also assessing these parameters in healthy controls (HC) and PTSD participants. Participants with mTBI (without PTSD) (n = 46), PTSD (without mTBI) (n = 41), and HC (n = 40) were assessed during a response inhibition task (the Go/NoGo task) during neuropsychological testing and separate functional magnetic imaging and event-related potentials sessions. PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale. Both mTBI and PTSD participants performed more omission errors on the Go/NoGo task and were associated with greater N2 amplitude, greater left inferior parietal activation and reduced connectivity of the left inferior parietal cluster and left angular gyrus compared to HC. There were no differences between mTBI and PTSD on any of these measures. These findings highlight that both mTBI and PTSD contribute to neural dysfunction during response inhibition, and arguably these occur due to distinct mechanisms. In the context of the common comorbidity between these two conditions, strategies to address response inhibition deficits in mTBI may need to consider causative factors underpinning neurological insult of mTBI and psychological effects associated with PTSD.
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