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 commo 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. These findings highlight that in addition to the clinical overlap between mTBI and PTSD, there are commonalities in neural functioning during response inhibition in both conditions. Although there have been a number of studies addressing the differential neural profiles of mTBI and PTSD ( Spadoni et al., 2017 ; Spielberg et al., 2015 ), there is a dearth of studies directly disentangling the neural processes underpinning response inhibition in the two conditions. One study that focused on behavioural responses found no differences on the Go/NoGo task between PTSD and mTBI participants ( Swick et al., 2012 ). To this end, we assessed participants with mTBI (without PTSD), PTSD (without mTBI), and healthy controls. The comparison groups were used to remove potential overlap between mTBI and PTSD, and to investigate the effects of mTBI without the confound of PTSD. There is also a Planned contrasts revealed a significant difference between the mTBI and HC group only for omission errors ( p = 0.017; mTBI > HC). There were no differences in omission errors between mTBI and PTSD, but the PTSD group also committed more omission errors than HC ( p = 0.013). There were no significant correlations between omission errors and PTSD symptom severity or time since trauma for the mTBI or PTSD group. There were no differences in commission errors or reaction time between the three groups. 3.3. EEG results We observed a significant group difference for the peak amplitude of the N2 wave with higher amplitude for mTBI relative to HC (F = 5.42, p = 0.025). Posthoc analyses on individual electrodes within this set (Fz, FCz, and Cz) found a significant difference on all three electrodes (Fz: t = 2.28, p = 0.028, FCz: t = 2.415, p = 0.021, Cz: t = 2.404, p = 0.021) (See Fig. 1 ). There were no differences between the mTBI and PTSD group on the N2 wave whereas significant differences were also observed for PTSD relative to HC, with a higher amplitude for PTSD relative to HC (F = 10.69, p = 0.002). All electrodes tested showed higher amplitude for the PTSD group relative to HC on the N2 wave (Fz: t = 2.92, p = 0.007, FCz: t = 3.32, p = 0.002, Cz: t = 3.04, p = 0.005). Fig. 1 EEG responses to NoGo trials. 1 There were no significant correlations for N2 amplitude with the CAPS score or time since trauma for the mTBI or PTSD group. There were no differences between mTBI and HC for amplitude of P3 or latency for both N2 and P3 components. 3.4. fMRI results For fMRI activation for response inhibition (NoGo vs Go), we observed significantly greater activity in the left inferior parietal cortex for the mTBI sample as compared to HC ( pFWE = 0.024; Supplementary Table S6). As with the EEG data, we did not find any significant activation differences between the mTBI and PTSD groups, but PTSD also demonstrated greater activity within this region relative to HC ( Fig. 2 , pFWE = 0.033). Fig. There were no further significant connections within or between the DMN-CCN brain networks which differentiated the mTBI group from healthy controls. Neither activation nor connectivity were significantly correlated with CAPS scores or with time since trauma for the mTBI or PTSD group. 4. Discussion This study aimed to refine our understanding of the neural processes involved in response inhibition in mTBI by also considering response inhibition patterns in PTSD. Overall, we found that both mTBI and PTSD demonstrated abnormalities in response inhibition with more omission errors during the task, greater N2 ERP amplitude, greater fMRI activation in the left inferior parietal cortex and reduced connectivity for this region relative to healthy controls. There were no differences between mTBI and PTSD. These findings indicate commonalities in neural mechanisms responsible for response inhibition difficulties in both conditions. mTBI is often followed by a range of functional, cognitive and emotional problems collectively known as postconcussive syndrome.