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Modafinil enhances cognitive, but not emotional conflict processing via enhanced inferior frontal gyrus activation and its communication with the dorsomedial prefrontal cortex.

ABSTRACT: Cognitive control regulates cognitive and emotional systems to facilitate goal-directed behavior in the context of task-irrelevant distractors. Cognitive control deficits contribute to residual functional impairments across psychiatric disorders and represent a promising novel treatment target. Translational evidence suggests that modafinil may enhance performance in executive functions; however, differential effects on regulatory control in cognitive and emotional domains have not been examined. The present pre-registered randomized-controlled pharmacological fMRI trial examined differential effects of modafinil (single-dose, 200 mg) on cognitive and emotional conflict processing. To further separate objective cognitive enhancing effects from subjective performance perception, a metacognitive paradigm was employed. Results indicated that modafinil specifically enhanced cognitive conflict performance and concomitantly increased activation in the inferior frontal gyrus and its functional communication with the dorsomedial prefrontal cortex. Exploratory analysis further revealed modafinil-enhanced basolateral amygdala reactivity to cognitive conflict, with stronger reactivity being associated with higher cognitive conflict performance. Whereas modafinil enhanced cognitive performance in the metacognitive paradigm, confidence indices remained unaffected. Overall, the present results suggest that modafinil has the potential to enhance cognitive conflict processing while leaving emotional conflict processing unaffected. On the neural level modafinil enhanced the recruitment of a network engaged in general conflict and regulatory control processes, whereas effects on the amygdala may reflect improved arousal-mediated attention processes for conflicting information. The pattern of cognitive enhancing effects in the absence of effects on affective processing suggests a promising potential to enhance cognitive control in clinical populations.

SUBMITTER: Li J

PROVIDER: S-EPMC7162953 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundTinnitus can interfere with a patient's speech discrimination, but whether tinnitus itself or the accompanying sensorineural hearing loss (SNHL) causes this interference is still unclear. We analyzed event-related electroencephalograms (EEGs) to observe auditory-related brain function and explore the possible effects of SNHL on auditory processing in tinnitus patients.MethodsSpeech discrimination scores (SDSs) were recorded in 21 healthy control subjects, 24 tinnitus patients, 24 SNHL patients, and 27 patients with both SNHL and tinnitus. EEGs were collected under an oddball paradigm. Then, the mismatch negativity (MMN) amplitude and latency, the clustering coefficient and average path length of the whole network in the tinnitus and SNHL groups were compared with those in the control group. Additionally, we analyzed the intergroup differences in functional connectivity among the primary auditory cortex (AC), parahippocampal gyrus (PHG), and inferior frontal gyrus (IFG).ResultsSNHL patients with or without tinnitus had lower SDSs than the control subjects. Compared with control subjects, tinnitus patients with or without SNHL had decreased MMN amplitudes, and SNHL patients had longer MMN latencies. Tinnitus patients without SNHL had a smaller clustering coefficient and a longer whole-brain average path length than the control subjects. SNHL patients with or without tinnitus had a smaller clustering coefficient and a longer average path length than patients with tinnitus alone. The connectivity strength from the AC to the PHG and IFG was lower on the affected side in tinnitus patients than that in control subjects; the connectivity strength from the PHG to the IFG was also lower on the affected side in tinnitus patients than that in control subjects. However, the connectivity strength from the IFG to the AC was stronger in tinnitus patients than that in the control subjects. In SNHL patients with or without tinnitus, these changes were magnified.ConclusionChanges in auditory processing in tinnitus patients do not influence SDSs. Instead, SNHL might cause the activity of the AC, PHG and IFG to change, resulting in impaired speech recognition in tinnitus patients with SNHL.

Project description:BackgroundInhibition is a critical executive control process and an established neurobiological phenotype of PTSD, yet to our knowledge, no prospective studies have examined this using a contextual cue task that enables measurement of behavioural response and neural activation patterns across proactive and reactive inhibition.ObjectiveThe current longitudinal study utilised functional magnetic resonance imaging (fMRI) to examine whether deficits in proactive and reactive inhibition predicted PTSD symptoms six months after trauma.MethodTwenty-three (65% males) medical patients receiving emergency medical care from a level 1 trauma centre were enrolled in the study and invited for an MRI scan 1-2-months post-trauma. PTSD symptoms were measured using self-report at scan and 6-months post-trauma. A stop-signal anticipation task (SSAT) during an fMRI scan was used to test whether impaired behavioural proactive and reactive inhibition, and reduced activation in right inferior frontal gyrus (rIFG), ventromedial prefrontal cortex (vmPFC), and bilateral hippocampus, were related to PTSD symptoms. We predicted that lower activation levels of vmPFC and rIFG during reactive inhibition and lower activation of hippocampus and rIFG during proactive inhibition would relate to higher 6-month PTSD symptoms.ResultsNo significant associations were found between behavioural measures and 6-month PTSD. Separate linear regression analyses showed that reduced rIFG activation (F1,21 = 9.97, R2 = .32, p = .005) and reduced vmPFC activation (F1,21 = 5.19, R2 = .20, p = .03) significantly predicted greater 6-month PTSD symptoms; this result held for rIFG activation controlling for demographic variables and baseline PTSD symptoms (β = -.45, p = .04) and Bonferroni correction.ConclusionOur findings suggest that impaired rIFG and, to a lesser extent, vmPFC activation during response inhibition may predict the development of PTSD symptoms following acute trauma exposure. Given the small sample size, future replication studies are needed.HighlightsImpaired inhibition may be an important risk factor for the development of PTSD following trauma, with less right inferior frontal gyrus and ventromedial prefrontal cortex activation during response inhibition predicting PTSD development.

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Modafinil enhances cognitive, but not emotional conflict processing via enhanced inferior frontal gyrus activation and its communication with the dorsomedial prefrontal cortex.

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