S1 Excitability Research Articles

Spared ulnar nerve injury results in increased layer III–VI excitability in the pig somatosensory cortex

This study describes cortical recordings in a large animal nerve injury model. We investigated differences in primary somatosensory cortex (S1) hyperexcitability when stimulating injured and uninjured nerves and how different cortical layers contribute to S1 hyperexcitability after spared ulnar nerve injury. We used a multielectrode array to record single-neuron activity in the S1 of ten female Danish landrace pigs. Electrical stimulation of the injured and uninjured nerve evoked brain activity up to 3 h after injury. The peak amplitude and latency of early and late peristimulus time histogram responses were extracted for statistical analysis. Histological investigations determined the layer of the cortex in which each electrode contact was placed. Nerve injury increased the early peak amplitude compared with that of the control group. This difference was significant immediately after nerve injury when the uninjured nerve was stimulated, while it was delayed for the injured nerve. The amplitude of the early peak was increased in layers III–VI after nerve injury compared with the control. In layer III, S1 excitability was also increased compared with preinjury for the early peak. Furthermore, the late peak was significantly larger in layer III than in the other layers in the intervention and control group before and after injury. Thus, the most prominent increase in excitability occurred in layer III, which is responsible for the gain modulation of cortical output through layer V. Therefore, layer III neurons seem to have an important role in altered brain excitability after nerve injury.

Bilateral median nerve stimulation and High-Frequency Oscillations unveil interhemispheric inhibition of primary sensory cortex

ObjectiveThis study aimed at investigating the effect of median nerve stimulation on ipsilateral cortical potentials evoked by contralateral median nerve electrical stimulation. MethodsWe recorded somatosensory-evoked potentials (SEPs) from the left parietal cortex in 15 right-handed, healthy subjects. We administered bilateral median nerve stimulation, with the ipsilateral stimulation preceding the stimulation on the contralateral by intervals of 5, 10, 20, or 40 ms. We adjusted these intervals based on each individual’s N20 latency. As a measure of S1 excitability, the amplitude of the N20 and the area of the High Frequency Oscillation (HFO) burst were analyzed for each condition. ResultsThe results revealed significant inhibition of N20 amplitude by ipsilateral median nerve stimulation at interstimulus intervals (ISIs) between 5 and 40 ms. Late HFO burst was suppressed at short ISIs of 5 and 10 ms, pointing to a transcallosal inhibitory effect on S1 intracortical circuits. ConclusionsFindings suggest interhemispheric interaction between the primary somatosensory areas, supporting the existence of transcallosal transfer of tactile information. SignificanceThis study provides valuable insights into the interhemispheric connections between primary sensory areas and underscore the potential role of interhemispheric interactions in somatosensory processing.

Facilitation of Early and Middle Latency SEP after tDCS of M1: No Evidence of Primary Somatosensory Homeostatic Plasticity

Homeostatic plasticity is a mechanism that stabilizes cortical excitability within a physiological range. Most homeostatic plasticity protocols have primed and tested the homeostatic response of the primary motor cortex (M1). This study investigated if a homeostatic response could be recorded from the primary sensory cortex (S1) after inducing homeostatic plasticity in M1. In 31 healthy participants, homeostatic plasticity was induced over M1 with a priming and testing block of transcranial direct current stimulation (tDCS) in two different sessions (anodal and cathodal). S1 excitability was assessed by early (N20, P25) and middle-latency (N33-P45) somatosensory evoked potentials (SEP) extracted from 4 electrodes (CP5, CP3, P5, P3). Baseline and post-measures (post-priming, 0-min, 10-min, and 20-min after homeostatic induction) were taken. Anodal M1 homeostatic plasticity induction significantly facilitated the N20-P25, P45 peak, and N33-P45 early SEP components up to 20-min post-induction, without any indication of a homeostatic response (i.e., reduced SEP). Cathodal homeostatic induction did not induce any significant effect on early or middle latency SEPs. M1 homeostatic plasticity induction by anodal stimulation protocol to the primary motor cortex did not induce a homeostatic response in SEPs.

Modulation of Motor Cortical Inhibition and Facilitation by Touch Sensation from the Glabrous Skin of the Human Hand.

Touch sensation from the glabrous skin of the hand is essential for precisely controlling dexterous movements, yet the neural mechanisms by which tactile inputs influence motor circuits remain largely unexplored. By pairing air-puff tactile stimulation on the hand's glabrous skin with transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), we examined the effects of tactile stimuli from single or multiple fingers on corticospinal excitability and M1's intracortical circuits. Our results showed that when we targeted the hand's first dorsal interosseous (FDI) muscle with TMS, homotopic (index finger) tactile stimulation, regardless of its point (fingertip or base), reduced corticospinal excitability. Conversely, heterotopic (ring finger) tactile stimulation had no such effect. Notably, stimulating all five fingers simultaneously led to a more pronounced decrease in corticospinal excitability than stimulating individual fingers. Furthermore, tactile stimulation significantly increased intracortical facilitation (ICF) and decreased long-interval intracortical inhibition (LICI) but did not affect short-interval intracortical inhibition (SICI). Considering the significant role of the primary somatosensory cortex (S1) in tactile processing, we also examined the effects of downregulating S1 excitability via continuous theta burst stimulation (cTBS) on tactile-motor interactions. Following cTBS, the inhibitory influence of tactile inputs on corticospinal excitability was diminished. Our findings highlight the spatial specificity of tactile inputs in influencing corticospinal excitability. Moreover, we suggest that tactile inputs distinctly modulate M1's excitatory and inhibitory pathways, with S1 being crucial in facilitating tactile-motor integration.

Sensory and motor cortical excitability changes induced by rTMS and sensory stimulation in stroke: A randomized clinical trial.

The ability to produce coordinated movement is dependent on dynamic interactions through transcallosal fibers between the two cerebral hemispheres of the brain. Although typically unilateral, stroke induces changes in functional and effective connectivity across hemispheres, which are related to sensorimotor impairment and stroke recovery. Previous studies have focused almost exclusively on interhemispheric interactions in the primary motor cortex (M1). To identify the presence of interhemispheric asymmetry (ASY) of somatosensory cortex (S1) excitability and to investigate whether S1 repetitive transcranial magnetic stimulation (rTMS) combined with sensory stimulation (SS) changes excitability in S1 and M1, as well as S1 ASY, in individuals with subacute stroke. A randomized clinical trial. Participants with a single episode of stroke, in the subacute phase, between 35 and 75 years old, were allocated, randomly and equally balanced, to four groups: rTMS/sham SS, sham rTMS/SS, rTMS/SS, and sham rTMS/Sham SS. Participants underwent 10 sessions of S1 rTMS of the lesioned hemisphere (10 Hz, 1,500 pulses) followed by SS. SS was applied to the paretic upper limb (UL) (active SS) or non-paretic UL (sham SS). TMS-induced motor evoked potentials (MEPs) of the paretic UL and somatosensory evoked potential (SSEP) of both ULs assessed M1 and S1 cortical excitability, respectively. The S1 ASY index was measured before and after intervention. Evaluator, participants and the statistician were blinded. Thirty-six participants divided equally into groups (nine participants per group). Seven patients were excluded from MEP analysis because of failure to produce consistent MEP. One participant was excluded in the SSEP analysis because no SSEP was detected. All somatosensory stimulation groups had decreased S1 ASY except for the sham rTMS/Sham SS group. When compared with baseline, M1 excitability increased only in the rTMS/SS group. S1 rTMS and SS alone or in combination changed S1 excitability and decreased ASY, but it was only their combination that increased M1 excitability. clinicaltrials.gov, identifier (NCT03329807).

Modified ischaemic nerve block of the forearm: use for the induction of cortical plasticity in distal hand muscles.

Ischaemic nerve block (INB) of the forearm rapidly reduces somatosensory input to a part of the body, which leads to the functional reorganization of the temporarily deafferented primary motor cortex (M1). We applied a novel modified INB (mINB) to the forearm, maintaining mean blood pressure, to assess cortical plasticity in the primary somatosensory cortex (S1) and the M1 regions associated with small hand muscles. S1 excitability was measured by median nerve somatosensory-evoked potentials (SEPs), while M1 excitability was evaluated by motor-evoked potentials (MEPS), using transcranial magnetic stimulation. The finding that S1 excitability increased and M1 excitability decreased after the mINB was removed reflects the differential short-term cortical plasticity of the S1 and M1 regions. These opposite effects observed for the S1 and M1 regions following the mINB may indicate a possible intra-hemispheric interaction between the S1 and M1 regions. Ischaemic nerve block (INB) causes short-term sensory deprivation, leading to functional reorganization in the deafferented motor cortex (M1). We used a modified INB (mINB) to evaluate cortical plasticity in the somatosensory cortex (S1) and M1 region associated with small hand muscles, because INB strongly inhibits muscles distal to the tourniquet. Thirty-three healthy adults participated in different combinations of four experiments. A pneumatic tourniquet was placed just below the right elbow and inflated to induce a mINB. We recorded the median nerve somatosensory- and motor-evoked potentials (SEPs and MEPs) before, during and after mINB placement and assessed spinal cord excitability using F-wave measurements. SEPs at Erb's point (N9) were abolished during the mINB; those at cortical N20 were suppressed. After removing the mINB, N20 amplitudes increased significantly, while those at N9 did not fully recover. P14 amplitudes after tourniquet deflation immediately recovered to baseline levels. M1-MEP amplitudes decreased during the mINB, and Erb-MEPs were suppressed. After the mINB was removed, M1-MEPs remained suppressed, while Erb-MEPs fully recovered. F-waves were not affected by the intervention. Therefore, sensory, but not motor, nerve function was affected by the mINB. S1 excitability was enhanced after the mINB was removed, indicating that S1 and M1 excitability were modulated in opposing directions after deflation. These after-effects may reflect isolated effects or interactions between the S1 and M1 regions. Our findings may facilitate improved understanding of the sensorimotor modulations that occur distal to the tourniquet due to temporal deafferentation and lead to development of novel neuromodulation protocols.

Repetitive Passive Finger Movement Modulates Primary Somatosensory Cortex Excitability.

Somatosensory inputs induced by repetitive passive movement (RPM) modulate primary motor cortex (M1) excitability; however, it is unclear whether RPM affects primary somatosensory cortex (S1) excitability. In this study, we investigated whether RPM affects somatosensory evoked potentials (SEPs) and resting state brain oscillation, including alpha and beta bands, depend on RPM frequency. Nineteen healthy subjects participated in this study, and SEPs elicited by peripheral nerve electrical stimulation were recorded from the C3’ area in order to assess S1 excitability (Exp. 1: n = 15). We focused on prominent SEP components such as N20, P25 and P45-reflecting S1 activities. In addition, resting electroencephalograms (EEGs) were recorded from C3’ area to assess the internal state of the brain network at rest (Exp. 2: n = 15). Passive abduction/adduction of the right index finger was applied for 10 min at frequencies of 0.5, 1.0, 3.0, and 5.0 Hz in Exp. 1, and 1.0, 3.0, and 5.0 Hz in Exp. 2. No changes in N20 or P25 components were observed following RPM. The 3.0 Hz-RPM decreased the P45 component for 20 min (p < 0.05), but otherwise did not affect the P45 component. There was no difference in the alpha and beta bands before and after any RPM; however, a negative correlation was observed between the rate of change of beta power and P45 component at 3.0 Hz-RPM. Our findings indicated that the P45 component changes depending on the RPM frequency, suggesting that somatosensory inputs induced by RPM influences S1 excitability. Additionally, beta power enhancement appears to contribute to the P45 component depression in 3.0 Hz-RPM.

Primary sensory and motor cortex function in response to acute muscle pain: A systematic review and meta-analysis.

Acute muscle pain has both motor and sensory consequences, yet the effect of muscle pain on the primary sensory (S1) and motor (M1) cortices has yet to be systematically evaluated. Here we aimed to determine the strength of the evidence for (1) altered activation of S1/M1 during and after pain, (2) the temporal profile of any change in activation and (3) the relationship between S1/M1 activity and the symptoms of pain. In September 2015, five electronic databases were systematically searched for neuroimaging and electrophysiological studies investigating the effect of acute experimental muscle pain on S1/M1 in healthy volunteers. Demographic data, methodological characteristics and primary outcomes for each study were extracted for critical appraisal. Meta-analyses were performed where appropriate. Twenty-five studies satisfied the inclusion criteria. There was consistent evidence from fMRI for increased S1 activation in the contralateral hemisphere during pain, but insufficient evidence to determine the effect at M1. Meta-analyses of TMS and EEG data revealed moderate to strong evidence of reduced S1 and corticomotor excitability during and following the resolution of muscle pain. A comprehensive understanding of the temporal profile of altered activity in S1/M1, and the relationship to symptoms of pain, is hampered by differences in methodological design, pain modality and pain severity between studies. Overall, the findings of this review indicate reduced S1 and corticomotor activity during and after resolution of acute muscle pain, mechanisms that could plausibly underpin altered sensorimotor function in pain. WHAT DOES THIS REVIEW ADD?: We provide the first systematic evaluation of the primary sensory (S1) and motor (M1) cortex response to acute experimental muscle pain in healthy volunteers. We present evidence from a range of methodologies to provide a comprehensive understanding of the effect of pain on S1/M1. Through meta-analyses we evaluate the strength of evidence concerning the direction and temporal profile of the S1/M1 response to acute muscle pain.

Differential effects of cathodal transcranial direct current stimulation of prefrontal, motor and somatosensory cortices on cortical excitability and pain perception - a double-blind randomised sham-controlled study.

The primary aim of this study was to assess the effects of cathodal transcranial direct current stimulation (c-tDCS) over cortical regions of the pain neuromatrix, including the primary motor (M1), sensory (S1) and dorsolateral prefrontal (DLPFC) cortices on M1/S1 excitability, sensory (STh), and pain thresholds (PTh) in healthy adults. The secondary aim was to evaluate the placebo effects of c-tDCS on induced cortical and behavioural changes. Before, immediately after and 30min after c-tDCS the amplitude of N20-P25 components of somatosensory evoked potentials (SEPs) and peak-to-peak amplitudes of motor evoked potentials (MEPs) were measured under four different experimental conditions. STh and PTh for peripheral electrical and mechanical stimulation were also evaluated. c-tDCS of 0.3mA was applied for 20min. A blinded assessor evaluated all outcome measures. c-tDCS of M1, S1 and DLPFC significantly decreased the corticospinal excitability of M1 (P<0.05) for at least 30min. Following the application of c-tDCS over S1, M1 and DLPFC, the amplitude of the N20-P25 component of SEPs decreased for at least 30min (P<0.05). Compared with baseline values, significant STh and PTh increases were observed after c-tDCS of these three sites. Decreasing the level of S1 and M1 excitability, following S1, M1 and DLPFC stimulation, confirmed the functional connectivities between these cortical sites involved in pain processing. Furthermore, increasing the level of STh/PTh after c-tDCS of these sites indicated that stimulation of not only M1 but also S1 and DLPFC could be considered a technique to decrease the level of pain in patients.

Effects of cathodal transcranial direct current stimulation to primary somatosensory cortex on short-latency afferent inhibition.

The aim of this study was to investigate the effects of cathodal transcranial direct current stimulation (tDCS) applied over the primary somatosensory cortex (S1) on short-interval afferent inhibition (SAI). Thirteen healthy individuals participated in this study. Cathodal tDCS was applied for 15 min at 1 mA over the left S1. Motor-evoked potentials (MEPs) were measured from the right first dorsal interosseous muscle in response to transcranial magnetic stimulation (TMS) of the left motor cortex before tDCS (pre), immediately after tDCS (immediately), and 15 min after tDCS (post-15 min). SAI was evaluated by measuring MEPs in response to TMS pulses applied 40 ms after peripheral electrical stimulation of the index finger. For each measurement period (pre, immediately, and post-15 min), MEP amplitude was significantly smaller when TMS followed index finger stimulation (SAI condition) than when TMS was delivered alone (single TMS) (P<0.01), indicating expression of SAI. The MEP ratio (MEP of SAI/MEP of single TMS) at post-15 min was significantly larger than that of pre (P<0.05), indicating suppression of SAI. However, no significant difference was observed between pre and immediately, and immediately and post-15 min. These results suggest that cathodal tDCS applied over the S1 causes a decrease in S1 excitability following peripheral electrical stimulation and cathodal tDCS applied over the S1 decreased the inhibitory effects of SAI.

Brain Plasticity Effects of Neuromodulation Against Multiple Sclerosis Fatigue.

We recently reported on the efficacy of a personalized transcranial direct current stimulation (tDCS) treatment in reducing multiple sclerosis (MS) fatigue. The result supports the notion that interventions targeted at modifying abnormal excitability within the sensorimotor network could represent valid non-pharmacological treatments. The present work aimed at assessing whether the mentioned intervention also induces changes in the excitability of sensorimotor cortical areas. Two separate groups of fatigued MS patients were given a 5-day tDCS treatments targeting, respectively, the whole body somatosensory areas (S1wb) and the hand sensorimotor areas (SM1hand). The study had a double blind, sham-controlled, randomized, cross-over (Real vs. Sham) design. Before and after each treatment, we measured fatigue levels (by the modified fatigue impact scale, mFIS), motor evoked potentials (MEPs) in response to transcranial magnetic stimulation and somatosensory evoked potentials (SEPs) in response to median nerve stimulation. We took MEPs and SEPs as measures of the excitability of the primary motor area (M1) and the primary somatosensory area (S1), respectively. The Real S1wb treatment produced a 27% reduction of the mFIS baseline level, while the SM1hand treatment showed no difference between Real and Sham stimulations. M1 excitability increased on average 6% of the baseline in the S1wb group and 40% in the SM1hand group. Observed SEP changes were not significant and we found no association between M1 excitability changes and mFIS decrease. The tDCS treatment was more effective against MS fatigue when the electrode was focused on the bilateral whole body somatosensory area. Changes in S1 and M1 excitability did not correlate with symptoms amelioration. The neuromodulation treatment that proved effective against MS fatigue induced only minor variations of the motor cortex excitability, not enough to explain the beneficial effects of the intervention.

How does anodal transcranial direct current stimulation of the pain neuromatrix affect brain excitability and pain perception? A randomised, double-blind, sham-control study.

BackgroundIntegration of information between multiple cortical regions of the pain neuromatrix is thought to underpin pain modulation. Although altered processing in the primary motor (M1) and sensory (S1) cortices is implicated in separate studies, the simultaneous changes in and the relationship between these regions are unknown yet. The primary aim was to assess the effects of anodal transcranial direct current stimulation (a-tDCS) over superficial regions of the pain neuromatrix on M1 and S1 excitability. The secondary aim was to investigate how M1 and S1 excitability changes affect sensory (STh) and pain thresholds (PTh).MethodsTwelve healthy participants received 20 min a-tDCS under five different conditions including a-tDCS of M1, a-tDCS of S1, a-tDCS of DLPFC, sham a-tDCS, and no-tDCS. Excitability of dominant M1 and S1 were measured before, immediately, and 30 minutes after intervention respectively. Moreover, STh and PTh to peripheral electrical and mechanical stimulation were evaluated. All outcome measures were assessed at three time-points of measurement by a blind rater.ResultsA-tDCS of M1 and dorsolateral prefrontal cortex (DLPFC) significantly increased brain excitability in M1 (p < 0.05) for at least 30 min. Following application of a-tDCS over the S1, the amplitude of the N20-P25 component of SEPs increased immediately after the stimulation (p < 0.05), whilst M1 stimulation decreased it. Compared to baseline values, significant STh and PTh increase was observed after a-tDCS of all three stimulated areas. Except in M1 stimulation, there was significant PTh difference between a-tDCS and sham tDCS.Conclusiona-tDCS of M1 is the best spots to enhance brain excitability than a-tDCS of S1 and DLPFC. Surprisingly, a-tDCS of M1 and S1 has diverse effects on S1 and M1 excitability. A-tDCS of M1, S1, and DLPFC increased STh and PTh levels. Given the placebo effects of a-tDCS of M1 in pain perception, our results should be interpreted with caution, particularly with respect to the behavioural aspects of pain modulation.Trial RegistrationAustralian New Zealand Clinical Trials, ACTRN12614000817640, http://www.anzctr.org.au/.

Temporal association between changes in primary sensory cortex and corticomotor output during muscle pain

BackgroundIntegration of information between multiple cortical regions is thought to underpin the experience of pain. Yet studies tend to focus on pain related changes in discrete cortical regions. Although altered processing in the primary motor (M1) and sensory cortex (S1) is implicated in pain, the temporal relationship between these regions is unknown and may provide insight into the interaction between them. MethodsWe used recordings of somatosensory-evoked potentials (SEPs) and transcranial magnetic stimulation to investigate the temporal relationship between altered excitability of the primary sensory cortex and corticomotor output during and after muscle pain induced by hypertonic saline infusion into the right first dorsal interosseous. SEPs and motor-evoked potentials (MEPs) were recorded in 12 healthy individuals. ResultsParticipants reported an average pain intensity of 5.4 (0.5) on a 10-cm visual analogue scale. The area of the N20–P25–N33 complex of the SEP was reduced during and after pain, but MEP amplitudes were suppressed only after pain had resolved. ConclusionsOur data show that pain reduces sensory processing before motor output is altered. This temporal dispersion, coupled with the lack of correlation between pain-induced changes in S1 and M1 excitability, imply either that independent processes are involved, or that reduced excitability of S1 during acute experimental muscle pain mediates latent reductions in motor output via processes that are non-linear and potentially involve activation of a wider brain network.

Primary Sensory and Motor Cortex Excitability Are Co-Modulated in Response to Peripheral Electrical Nerve Stimulation

Peripheral electrical stimulation (PES) is a common clinical technique known to induce changes in corticomotor excitability; PES applied to induce a tetanic motor contraction increases, and PES at sub-motor threshold (sensory) intensities decreases, corticomotor excitability. Understanding of the mechanisms underlying these opposite changes in corticomotor excitability remains elusive. Modulation of primary sensory cortex (S1) excitability could underlie altered corticomotor excitability with PES. Here we examined whether changes in primary sensory (S1) and motor (M1) cortex excitability follow the same time-course when PES is applied using identical stimulus parameters. Corticomotor excitability was measured using transcranial magnetic stimulation (TMS) and sensory cortex excitability using somatosensory evoked potentials (SEPs) before and after 30 min of PES to right abductor pollicis brevis (APB). Two PES paradigms were tested in separate sessions; PES sufficient to induce a tetanic motor contraction (30–50 Hz; strong motor intensity) and PES at sub motor-threshold intensity (100 Hz). PES applied to induce strong activation of APB increased the size of the N20-P25 component, thought to reflect sensory processing at cortical level, and increased corticomotor excitability. PES at sensory intensity decreased the size of the P25-N33 component and reduced corticomotor excitability. A positive correlation was observed between the changes in amplitude of the cortical SEP components and corticomotor excitability following sensory and motor PES. Sensory PES also increased the sub-cortical P14-N20 SEP component. These findings provide evidence that PES results in co-modulation of S1 and M1 excitability, possibly due to cortico-cortical projections between S1 and M1. This mechanism may underpin changes in corticomotor excitability in response to afferent input generated by PES.

Association of Activity Changes in the Primary Sensory Cortex With Successful Motor Rehabilitation of the Hand Following Stroke

Background. Previous studies demonstrated a posterior shift of activation toward the primary sensory cortex (S1) following stroke; however, any relationship between this posterior shift and clinical outcome measures for the affected hand function were unclear. Objective. The authors investigated the possible role of S1 in motor recovery. Methods. Assuming that previous studies examined inhomogeneous groups of patients, the authors selected participants with chronic stroke who had moderate hand paresis, normal sensory examination and somatosensory-evoked potentials, and no lesion within the S1, thalamus, or brain stem. Constraint-induced movement therapy (CIMT) was used to train the impaired hand. To relate fMRI (functional MRI) activation changes from baseline to post-CIMT, a correlation analysis was performed with changes of the Wolf Motor Function Test (WMFT) as a test for the hand function. Results. A close relationship was found between increases in hand function and peak changes in activation within the ipsilesional S1. With a better outcome, greater increases in activation within the S1 were evident (P < .03; r = 0.73). Conclusion. In selected patients, the sensory network influences training-induced motor gains. This predictive knowledge of plasticity when applying CIMT may suggest strategies to enhance the effect of therapy, such as the addition of electrical stimulation to enhance S1 excitability.

Modulation of excitability in human primary somatosensory and motor cortex by paired associative stimulation targeting the primary somatosensory cortex

Input from primary somatosensory cortex (S1) to primary motor cortex (M1) is important for high-level motor performance, motor skill learning and motor recovery after brain lesion. This study tested the effects of manipulating S1 excitability with paired associative transcranial stimulation (S1-PAS) on M1 excitability. Given the important role of S1 in sensorimotor integration, we hypothesized that changes in S1 excitability would be directly paralleled by changes in M1 excitability. We applied two established protocols (S1-PAS(LTP) and S1-PAS(LTD) ) to the left S1 to induce long-term potentiation (LTP)-like or long-term depression (LTD)-like plasticity. S1 excitability was assessed by the early cortical components (N20-P25) of the median nerve somatosensory-evoked potential. M1 excitability was assessed by motor-evoked potential amplitude and short-interval intracortical inhibition. Effects of S1-PAS(LTP) were compared with those of a PAS(LTP) protocol targeting the left M1 (M1-PAS(LTP) ). S1-PAS(LTP) and S1-PAS(LTD) did not result in significant modifications of S1 or M1 excitability at the group level due to substantial interindividual variability. The individual S1-PAS-induced changes in S1 and M1 excitability showed no correlation. Furthermore, the individual changes in S1 and M1 excitability induced by S1-PAS(LTP) did not correlate with changes in M1 excitability induced by M1-PAS(LTP) . This demonstrates that the effects of S1-PAS in S1 are variable across individuals and, within a given individual, unrelated to those induced by S1-PAS or M1-PAS in M1. Potentially, this extends the opportunities of therapeutic PAS applications because M1-PAS 'non-responders' may well respond to S1-PAS.

Modulation of motor cortical excitability by paired associative stimulation (PAS) of the primary somatosensory cortex

The primary somatosensory cortex (S1) plays a crucial role in learning and adapting of motor skills. Due to the high interconnectedness to primary motor cortex (M1), manipulation of S1 excitability offers an opportunity to alter M1 excitability function. We applied paired associative stimulation (PAS) to S1 in order to induce long-term potentiation (LTP)-like or long-term depression (LTD)-like effects in S1 and evaluated the consequences of S1-PAS on excitability in the adjacent M1.

Increased cortical plasticity in the elderly: changes in the somatosensory cortex after paired associative stimulation

A fundamental feature of the human cortex is the capability to express plastic changes that seem to be present even during physiological aging. The paired associative stimulation (PAS) protocol is a paradigm capable of inducing neuroplastic changes, possibly by mechanisms related to spike timing-dependent associative neuronal activity, and represents a suitable tool for investigating age-dependent neuroplastic modulations of the primary somatosensory cortex (S1). To examine age dependency of S1 plasticity, the amplitude changes of median nerve somatosensory evoked potential (SEP) before and after PAS intervention were investigated in young and elderly subjects. The main finding of our study is that low-frequency medial nerve stimulation paired with transcranial magnetic stimulation over the contralateral cortex enhances S1 excitability. Moreover, the S1 long term potentiation–like plasticity changes as a function of aging, with a significant increase of N20–P25 complex in the elderly compared to young subjects. These results are congruent with the hypothesis that some elderly subjects retain a high level of plasticity in specific neuronal circuits. Such plasticity could represent a compensatory mechanism, in terms of functional reserve of somatosensory cortex, used by the aging brain to counterbalance the cortical degeneration associated with aging.

Early adaptations in somatosensory cortex after focal ischemic injury to motor cortex

In response to a lesion, intact regions of cortex in both hemispheres undergo adaptive changes in network function. For example, changes in excitability and intracortical inhibition in primary motor cortex (M1) were reported after lesioning contralateral or ipsilateral brain regions. Close interactions exist between M1 and primary somatosensory cortex (S1) within one hemisphere. Therefore, we hypothesized that lasting modifications would occur in S1 excitability after lesioning ipsilateral M1. Imaging of intrinsic optical signals (IOS, at 570 nm) was used to investigate the evolution of the somatosensory cortical response evoked by contralateral median nerve stimulation during the first hour after a photothrombotic lesion to M1 (caudal motor cortex) of the rat (n=10). Control rats (n=6) received no lesion. Perfusion was monitored by Laser speckle imaging and the extent of the resulting lesion was determined histologically. Control animals did not show evidence for reduced perfusion, infarction, or changes in IOS. M1 infarction led to a significant increase in evoked response amplitude, duration, and area of activation, and a shortening of latencies. These parameters reached a plateau around 50 min after ischemia. These results indicate S1 hyperexcitability after M1 injury. Whether these adaptations contribute to functional deficits or play a role in recovery, remains to be determined.