Non-invasive induction of plasticity in the human cortex: uses and limitations

The last couple of decades have seen the development of a number of non-invasive brain stimulation (NIBS) techniques that are capable of inducing short-lasting plasticity in the human cortex. Importantly, the induction of lasting plastic changes can, under some conditions, reversibly modify behaviour and interact with learning. These techniques have provided novel opportunities to study human cortical plasticity and examine the role of cortical regions in behaviour. In this review we briefly summarise current NIBS techniques, outline approaches to characterise and quantify cortical plastic change, and describe mechanisms that are implicated in the induced plastic changes. We then outline the areas in which these techniques might be useful, namely, investigating the mechanisms of human cortical plasticity, the characterisation of influences on plasticity, and the investigation of the role of cortical regions in behaviour. Finally, we conclude by highlighting some current limitations of the techniques and suggest that further development of the current NIBS paradigms and more focussed targeting should further enhance the utility of these powerful non-invasive techniques for the investigation of the cortical plasticity and pathophysiology

Non-invasive induction of plasticity in the human cortex: uses and limitations

The last couple of decades have seen the development of a number of non-invasive brain stimulation (NIBS) techniques that are capable of inducing short-lasting plasticity in the human cortex. Importantly, the induction of lasting plastic changes can, under some conditions, reversibly modify behaviour and interact with learning. These techniques have provided novel opportunities to study human cortical plasticity and examine the role of cortical regions in behaviour. In this review we briefly summarise current NIBS techniques, outline approaches to characterise and quantify cortical plastic change, and describe mechanisms that are implicated in the induced plastic changes. We then outline the areas in which these techniques might be useful, namely, investigating the mechanisms of human cortical plasticity, the characterisation of influences on plasticity, and the investigation of the role of cortical regions in behaviour. Finally, we conclude by highlighting some current limitations of the techniques and suggest that further development of the current NIBS paradigms and more focussed targeting should further enhance the utility of these powerful non-invasive techniques for the investigation of the cortical plasticity and pathophysiology

A comparison of neuroplastic responses to non-invasive brain stimulation protocols and motor learning in healthy adults

Non-invasive brain stimulation (NBS) techniques can induce neuroplastic changes similar to those associated with motor learning and there is evidence for the involvement of common mechanisms. Whether there are correlations between the changes induced by NBS and those associated with motor learning remains unclear. We investigated whether there was any relationship between an individual's neuroplastic responses to several different NBS protocols (continuous theta-burst stimulation (cTBS); intermittent theta-burst stimulation (iTBS); facilitatory paired associative stimulation (PAS: inter-stimulus interval 25ms)) and whether these responses correlated with the neuroplastic response associated with a motor training (MT) task involving repeated fast-as-possible thumb abductions. Changes in motor evoked potential (MEP) amplitude were used to assess the neuroplastic response to each protocol. MEP amplitude decreased significantly following cTBS, however there was no significant change in MEP amplitude following iTBS, PAS or MT. There were no significant correlations between individuals' neuroplastic responses to any of the NBS protocols tested or between individuals' neuroplastic responses to the NBS protocols and motor learning. These results provide no support for an association between individuals' neuroplastic responses to several plasticity-inducing protocols. Although there is evidence for involvement of common mechanisms in the neuroplastic changes induced by NBS and motor learning, the results of this study suggest (1) the mechanisms mediating TBS-, PAS-, and MT-induced plasticity may only partially overlap, and (2) additional factors, including large intra and inter-subject response variability, may make the demonstration of associations between neuroplastic responses to the various protocols difficult

Investigating the impact of feedback update interval on the efficacy of restorative brain–computer interfaces

Restorative brain-computer interfaces (BCIs) have been proposed to enhance stroke rehabilitation. Restorative BCIs are able to close the sensorimotor loop by rewarding motor imagery (MI) with sensory feedback. Despite the promising results from early studies, reaching clinically significant outcomes in a timely fashion is yet to be achieved. This lack of efficacy may be due to suboptimal feedback provision. To the best of our knowledge, the optimal feedback update interval (FUI) during MI remains unexplored. There is evidence that sensory feedback disinhibits the motor cortex. Thus, in this study, we explore how shorter than usual FUIs affect behavioural and neurophysiological measures following BCI training for stroke patients using a single-case proof-of-principle study design. The action research arm test was used as the primary behavioural measure and showed a clinically significant increase (36%) over the course of training. The neurophysiological measures including motor evoked potentials and maximum voluntary contraction showed distinctive changes in early and late phases of BCI training. Thus, this preliminary study may pave the way for running larger studies to further investigate the effect of FUI magnitude on the efficacy of restorative BCIs. It may also elucidate the role of early and late phases of motor learning along the course of BCI training

Obesity is associated with reduced plasticity of the human motor cortex

Obesity is characterised by excessive body fat and is associated with several detrimental health conditions, including cardiovascular disease and diabetes. There is some evidence that people who are obese have structural and functional brain alterations and cognitive deficits. It may be that these neurophysiological and behavioural consequences are underpinned by altered plasticity. This study investigated the relationship between obesity and plasticity of the motor cortex in people who were considered obese (n = 14, nine males, aged 35.4 ± 14.3 years) or healthy weight (n = 16, seven males, aged 26.3 ± 8.5 years). A brain stimulation protocol known as continuous theta burst transcranial magnetic stimulation was applied to the motor cortex to induce a brief suppression of cortical excitability. The suppression of cortical excitability was quantified using single-pulse transcranial magnetic stimulation to record and measure the amplitude of the motor evoked potential in a peripheral hand muscle. Therefore, the magnitude of suppression of the motor evoked potential by continuous theta burst stimulation was used as a measure of the capacity for plasticity of the motor cortex. Our results demonstrate that the healthy-weight group had a significant suppression of cortical excitability following continuous theta burst stimulation (cTBS), but there was no change in excitability for the obese group. Comparing the response to cTBS between groups demonstrated that there was an impaired plasticity response for the obese group when compared to the healthy-weight group. This might suggest that the capacity for plasticity is reduced in people who are obese. Given the importance of plasticity for human behaviour, our results add further emphasis to the potentially detrimental health effects of obesity.Sophia X. Sui, Michael C. Ridding and Brenton Hordacr

Proprioceptive feedback facilitates motor imagery-related operant learning of sensorimotor β-band modulation

Motor imagery (MI) activates the sensorimotor system independent of actual movements and might be facilitated by neurofeedback. Knowledge on the interaction between feedback modality and the involved frequency bands during MI-related brain self-regulation is still scarce. Previous studies compared the cortical activity during the MI task with concurrent feedback (MI with feedback condition) to cortical activity during the relaxation task where no feedback was provided (relaxation without feedback condition). The observed differences might, therefore, be related to either the task or the feedback. A proper comparison would necessitate studying a relaxation condition with feedback and a MI task condition without feedback as well. Right-handed healthy subjects performed two tasks, i.e., MI and relaxation, in alternating order. Each of the tasks (MI vs. relaxation) was studied with and without feedback. The respective event-driven oscillatory activity, i.e., sensorimotor desynchronization (during MI) or synchronization (during relaxation), was rewarded with contingent feedback. Importantly, feedback onset was delayed to study the task-related cortical activity in the absence of feedback provision during the delay period. The reward modality was alternated every 15 trials between proprioceptive and visual feedback. Proprioceptive input was superior to visual input to increase the range of task-related spectral perturbations in the α- and β-band, and was necessary to consistently achieve MI-related sensorimotor desynchronization (ERD) significantly below baseline. These effects occurred in task periods without feedback as well. The increased accuracy and duration of learned brain self-regulation achieved in the proprioceptive condition was specific to the β-band. MI-related operant learning of brain self-regulation is facilitated by proprioceptive feedback and mediated in the sensorimotor β-band

Reproducibility of neuroplastic responses induced by continuous theta-burst stimulation

See Attache

Physiological evidence consistent with reduced neuroplasticity in human adolescents born preterm

Preterm-born children commonly experience motor, cognitive, and learning difficulties that may be accompanied by altered brain microstructure, connectivity, and neurochemistry. However, the mechanisms linking the altered neurophysiology with the behavioral outcomes are unknown. Here we provide the first physiological evidence that human adolescents born preterm at or before 37 weeks of completed gestation have a significantly reduced capacity for cortical neuroplasticity, the key overall mechanism underlying learning and memory. We examined motor cortex neuroplasticity in three groups of adolescents who were born after gestations of ≤32 completed weeks (early preterm), 33–37 weeks (late preterm), and 38–41 weeks (term) using a noninvasive transcranial magnetic brain stimulation technique to induce long-term depression (LTD)-like neuroplasticity. Compared with term-born adolescents, both early and late preterm adolescents had reduced LTD-like neuroplasticity in response to brain stimulation that was also associated with low salivary cortisol levels. We also compared neuroplasticity in term-born adolescents with that in term-born young adults, finding that the motor cortex retains a relatively enhanced neuroplastic capacity in adolescence. These findings provide a possible mechanistic link between the altered brain physiology of preterm birth and the subsequent associated behavioral deficits, particularly in learning and memory. They also suggest that altered hypothalamic–pituitary–adrenal axis function due to preterm birth may be a significant modulator of this altered neuroplasticity. This latter finding may offer options in the development of possible therapeutic interventions

Characterising activity and diet compositions for dementia prevention: protocol for the ACTIVate prospective longitudinal cohort study

Introduction Approximately 40% of late-life dementia may be prevented by addressing modifiable risk factors, including physical activity and diet. Yet, it is currently unknown how multiple lifestyle factors interact to influence cognition. The ACTIVate Study aims to (1) explore associations between 24-hour time-use and diet compositions with changes in cognition and brain function; and (2) identify duration of time-use behaviours and the dietary compositions to optimise cognition and brain function.Methods and analysis This 3-year prospective longitudinal cohort study will recruit 448 adults aged 60-70 years across Adelaide and Newcastle, Australia. Time-use data will be collected through wrist-worn activity monitors and the Multimedia Activity Recall for Children and Adults. Dietary intake will be assessed using the Australian Eating Survey food frequency questionnaire. The primary outcome will be cognitive function, assessed using the Addenbrooke's Cognitive Examination-III. Secondary outcomes include structural and functional brain measures using MRI, cerebral arterial pulse measured with diffuse optical tomography, neuroplasticity using simultaneous transcranial magnetic stimulation and electroencephalography, and electrophysiological markers of cognitive control using event-related potential and time frequency analyses. Compositional data analysis, testing for interactions between time point and compositions, will assess longitudinal associations between dependent (cognition, brain function) and independent (time-use and diet compositions) variables. Conclusions The ACTIVate Study will be the first to examine associations between time-use and diet compositions, cognition and brain function. Our findings will inform new avenues for multidomain interventions that may more effectively account for the co-dependence between activity and diet behaviours for dementia prevention. Ethics and dissemination Ethics approval has been obtained from the University of South Australia's Human Research Ethics committee (202639). Findings will be disseminated through peer-reviewed manuscripts, conference presentations, targeted media releases and community engagement events. Trial registration number >Australia New Zealand Clinical Trials Registry (ACTRN12619001659190).Ashleigh E Smith, Alexandra T Wade, Timothy Olds, Dorothea Dumuid, Michael J Breakspear, Kate Laver ... et al

Cortico-cortical connections in man

SIGLEAvailable from British Library Document Supply Centre-DSC:DXN008951 / BLDSC - British Library Document Supply CentreGBUnited Kingdo