Dr Patrick Skippen

Objective: It remains unclear to what extent Transcranial Magnetic Stimulation-evoked potentials (TEPs) reflect sensory (auditory and somatosensory) potentials as opposed to cortical excitability. The present study aimed to determine; a) the extent to which sensory potentials contaminate TEPs using a spatially-matched sham condition, and b) whether sensory potentials reflect auditory or somatosensory potentials alone, or a combination of the two. Methods: Twenty healthy participants received active or sham stimulation, with the latter consisting a sham coil click combined with scalp electrical stimulation. Two additional conditions i) electrical stimulation and ii) auditory stimulation alone, were included in a subset of 13 participants. Results: Signals from active and sham stimulation were correlated in spatial and temporal domains > 55 ms post-stimulation. Relative to auditory or electrical stimulation alone, sham stimulation resulted in a) larger potentials, b) stronger correlations with active stimulation and c) a signal that was not a linear sum of electrical and auditory stimulation alone. Conclusions: Sensory potentials can confound interpretations of TEPs at timepoints > 55 ms post-stimulation. Furthermore, TEP contamination cannot be explained by auditory or somatosensory potentials alone, but instead reflects a non-linear interaction between both. Significance: Future studies may benefit from controlling for sensory contamination using spatially-matched sham conditions, and which consist of combined auditory and somatosensory stimulation.

Determining the mechanistic causes of complex biopsychosocial health conditions such as low back pain (LBP) is challenging, and research is scarce. Cross-sectional studies demonstrate altered excitability and organization of the somatosensory and motor cortex in people with acute and chronic LBP, however, no study has explored these mechanisms longitudinally or attempted to draw causal inferences. Using sensory evoked potential area measurements and transcranial magnetic stimulation derived map volume we analyzed somatosensory and motor cortex excitability in 120 adults experiencing acute LBP. Following multivariable regression modelling with adjustment for confounding, we identified lower primary (OR = 2.08, 95% CI = 1.22¿3.57) and secondary (OR = 2.56, 95% CI = 1.37¿4.76) somatosensory cortex excitability significantly increased the odds of developing chronic pain at 6-month follow-up. Corticomotor excitability in the acute stage of LBP was associated with higher pain intensity at 6-month follow-up (B = -0.15, 95% CI: -0.28 to -0.02) but this association did not remain after confounder adjustment. These data provide evidence that low somatosensory cortex excitability in the acute stage of LBP is a cause of chronic pain. Perspective: This prospective longitudinal cohort study design identified low sensorimotor cortex excitability during the acute stage of LBP in people who developed chronic pain. Interventions that target this proposed mechanism may be relevant to the prevention of chronic pain.

During task-switching paradigms, both event-related potentials and time-frequency analyses show switch and mixing effects at frontal and parietal sites. Switch and mixing effects are associated with increased power in broad frontoparietal networks, typically stronger in the theta band (~4¿8¿Hz). However, it is not yet known whether mixing and switch costs rely upon common or distinct networks. In this study, we examine proactive and reactive control networks linked to task switching and mixing effects, and whether strength of connectivity in these networks is associated with behavioural outcomes. Participants (n¿= 197) completed a cued-trials task-switching paradigm with concurrent electroencephalography, after substantial task practice to establish strong cue-stimulus¿response representations. We used inter-site phase clustering, a measure of functional connectivity across electrode sites, to establish cross-site connectivity from a frontal and a parietal seed. Distinct theta networks were activated during proactive and reactive control periods. During the preparation interval, mixing effects were associated with connectivity from the frontal seed to parietal sites, and switch effects with connectivity from the parietal seed to occipital sites. Lateralised occipital connectivity was common to both switch and mixing effects. After target onset, frontal and parietal seeds showed a similar pattern of connectivity across trial types. These findings are consistent with distinct and common proactive control networks and common reactive networks in highly practised task-switching performers.

Investigations into the neurophysiological underpinnings of control suggest that frontal theta activity is increased with the need for control. However, these studies typically show this link by reporting associations between increased theta and RT slowing ¿ a process that is contemporaneous with cognitive control but does not strictly reflect the specific use of control. In this study, we assessed frontal theta responses that underpinned the switch cost in task switching ¿ a specific index of cognitive control that does not rely exclusively on RT slowing. Here, we utilised a single-trial regression approach to assess 1) how cognitive control demands beyond simple RT slowing were linked to midfrontal theta and 2) whether midfrontal theta effects remained stable over time. In a large cohort that included a longitudinal subsample, we found that midfrontal theta was modulated by switch costs, with enhanced theta power when preparing to switch vs. repeating a task. These effects were reliable after a two-year interval (Cronbach's a.39-0.74). In contrast, we found that trial-by-trial modulations of midfrontal theta power predicted the size of the switch cost ¿ so that switch trials with increased theta produced smaller switch costs. Interestingly, these relationships between theta and behaviour were less stable over time (Cronbach's a 0-0.61), with participants first using both delta and theta bands to influence behaviour whereas after two years only theta associations with behaviour remained. Together, these findings suggest midfrontal theta supports the need for control beyond simple RT slowing and reveal that midfrontal theta effects remain relatively stable over time.

The ability to control behaviour is thought to rely at least partly on adequately suppressing impulsive responses to external stimuli. However, the evidence for a relationship between response inhibition ability and impulse control is weak and inconsistent. This study investigates the relationship between response inhibition and both self-report and behavioural measures of impulsivity as well as engagement in risky behaviours in a large community sample (N = 174) of healthy adolescents and young adults (15¿35 years). Using a stop-signal paradigm with a number parity go task, we implemented a novel hierarchical Bayesian model of response inhibition that estimates stop-signal reaction time (SSRT) as a distribution and also accounts for failures to react to the stop-signal (i.e., "trigger failure"), and failure to react to the choice stimulus (i.e., "go failure" or omission errors). In line with previous studies, the model reduced estimates of SSRT by approximately 100 ms compared with traditional non-parametric SSRT estimation techniques. We found significant relationships between behavioural and self-report measures of impulsivity and traditionally estimated SSRT, that did not hold for the model-based SSRT estimates. Instead, behavioural impulsivity measures were correlated with rate of trigger failure. The relationship between trigger failure and impulsivity suggests that the former may index a higher order inhibition process, whereas SSRT may index a more automatic inhibition process. We suggest that the existence of distinct response inhibition processes that may be associated with different levels of cognitive control.