Cortical and subcortical functional specificity associated with response inhibition.

Is motor response inhibition supported by a specialised neuronal inhibitory control mechanism, or by a more general system of action updating? This pre-registered study employed a context-cueing paradigm requiring both inhibitory and non-inhibitory action updating in combination with functional magnetic resonance imaging to test the specificity of responses under different updating conditions, including the cancellation of actions. Cortical regions of activity were found to be common to multiple forms of action updating. However, functional specificity during response inhibition was observed in the anterior right inferior frontal gyrus. In addition, fronto-subcortical activity was explored using a novel contrast method. These exploratory results indicate that the specificity for response inhibition observed in right prefrontal cortex continued downstream and was observed in right hemisphere subcortical activity, while left hemisphere activity was associated with right-hand response execution. Overall, our findings reveal both common and distinct correlates of response inhibition in prefrontal cortex, with exploratory analyses supporting putative models of subcortical pathways and extending them through the demonstration of lateralisation.

Impairment of manual but not saccadic response inhibition following acute alcohol intoxication.

BACKGROUND: Alcohol impairs response inhibition; however, it remains contested whether such impairments affect a general inhibition system, or whether affected inhibition systems are embedded in, and specific to, each response modality. Further, alcohol-induced impairments have not been disambiguated between proactive and reactive inhibition mechanisms, and nor have the contributions of action-updating impairments to behavioural 'inhibition' deficits been investigated. METHODS: Forty Participants (25 female) completed both a manual and a saccadic stop-signal reaction time (SSRT) task before and after a 0.8g/kg dose of alcohol and, on a separate day, before and after a placebo. Blocks in which participants were required to ignore the signal to stop or make an additional 'dual' response were included to obtain measures of proactive inhibition as well as updating of attention and action. RESULTS: Alcohol increased manual but not saccadic SSRT. Proactive inhibition was weakly reduced by alcohol, but increases in the reaction times used to baseline this contrast prevent clear conclusions regarding response caution. Finally, alcohol also increased secondary dual response times of the dual task uniformly as a function of the delay between tasks, indicating an effect of alcohol on action-updating or execution. CONCLUSIONS: The modality-specific effects of alcohol favour the theory that response inhibition systems are embedded within response modalities, rather than there existing a general inhibition system. Concerning alcohol, saccadic control appears relatively more immune to disruption than manual control, even though alcohol affects saccadic latency and velocity. Within the manual domain, alcohol affects multiple types of action updating, not just inhibition.

Enhanced awareness followed reversible inhibition of human visual cortex: a combined TMS, MRS and MEG study.

This series of experiments investigated the neural basis of conscious vision in humans using a form of transcranial magnetic stimulation (TMS) known as continuous theta burst stimulation (cTBS). Previous studies have shown that occipital TMS, when time-locked to the onset of visual stimuli, can induce a phenomenon analogous to blindsight in which conscious detection is impaired while the ability to discriminate 'unseen' stimuli is preserved above chance. Here we sought to reproduce this phenomenon using offline occipital cTBS, which has been shown to induce an inhibitory cortical aftereffect lasting 45-60 minutes. Contrary to expectations, our first experiment revealed the opposite effect: cTBS enhanced conscious vision relative to a sham control. We then sought to replicate this cTBS-induced potentiation of consciousness in conjunction with magnetoencephalography (MEG) and undertook additional experiments to assess its relationship to visual cortical excitability and levels of the inhibitory neurotransmitter γ-aminobutyric acid (GABA; via magnetic resonance spectroscopy, MRS). Occipital cTBS decreased cortical excitability and increased regional GABA concentration. No significant effects of cTBS on MEG measures were observed, although the results provided weak evidence for potentiation of event related desynchronisation in the ß band. Collectively these experiments suggest that, through the suppression of noise, cTBS can increase the signal-to-noise ratio of neural activity underlying conscious vision. We speculate that gating-by-inhibition in the visual cortex may provide a key foundation of consciousness.

The timing and neuroanatomy of conscious vision as revealed by TMS-induced blindsight.

Following damage to the primary visual cortex, some patients exhibit "blindsight," where they report a loss of awareness while retaining the ability to discriminate visual stimuli above chance. Transient disruption of occipital regions with TMS can produce a similar dissociation, known as TMS-induced blindsight. The neural basis of this residual vision is controversial, with some studies attributing it to the retinotectal pathway via the superior colliculus whereas others implicate spared projections that originate predominantly from the LGN. Here we contrasted these accounts by combining TMS with visual stimuli that either activate or bypass the retinotectal and magnocellular (R/M) pathways. We found that the residual capacity of TMS-induced blindsight occurs for stimuli that bypass the R/M pathways, indicating that such pathways, which include those to the superior colliculus, are not critical. We also found that the modulation of conscious vision was time and pathway dependent. TMS applied either early (0-40 msec) or late (280-320 msec) after stimulus onset modulated detection of stimuli that did not bypass R/M pathways, whereas during an intermediate period (90-130 msec) the effect was pathway independent. Our findings thus suggest a prominent role for the R/M pathways in supporting both the preparatory and later stages of conscious vision. This may help resolve apparent conflict in previous literature by demonstrating that the roles of the retinotectal and geniculate pathways are likely to be more nuanced than simply corresponding to the unconscious/conscious dichotomy.

Comparative incidence rates of mild adverse effects to transcranial magnetic stimulation.

OBJECTIVES: Past research has largely neglected to investigate mild adverse effects (MAEs) to transcranial magnetic stimulation (TMS), including headache and nausea. Here we explored the relationship between MAEs, participant characteristics (age and gender) and protocol parameters, including mode of application, coil geometry, stimulated brain region, TMS frequency, TMS intensity, and active vs. sham stimulation. METHODS: Data from 1270 standard post-monitoring forms was obtained from 113 healthy participants. Analyses aimed to identify the risk factors associated with MAE reports and specific symptoms. RESULTS: The overall rate of MAEs across TMS sessions was ∼5%, with ∼78% of symptoms occurring post-session. Initial TMS sessions were followed by a higher MAE incidence rate relative to later testing sessions. No associations between participant characteristics, TMS frequency, or intensity were observed. CONCLUSIONS: TMS-related MAEs are relatively common and may be exacerbated by initial expectations or anxieties of participants. A significant proportion of MAEs may reflect reporting of coincidental phenomena that are unrelated to TMS. Recommendations for future safety studies are proposed and monitoring documentation is provided. SIGNIFICANCE: Our findings illustrate the importance of standardized monitoring of MAEs. Such research aids our understanding of how MAEs arise and may lead to interventions for reducing their incidence.

Is delayed foveal feedback critical for extra-foveal perception?

Recent neuroimaging evidence suggests that visual inputs arising beyond the fovea can be 'fed back' to foveal visual cortex to construct a new retinotopic representation. However, whether these representations are critical for extra-foveal perception remains unclear. Using transcranial magnetic stimulation we found that relatively late (350-400 msec) disruption of foveal retinotopic cortex impaired perceptual discrimination of objects in the periphery. These results are consistent with the hypothesis that feedback to the foveal retinotopic cortex is crucial for extra-foveal perception, and provide additional evidence for 'constructive' feedback in human vision.