Electrical Stimulation Of Median Nerve Research Articles

Effects of Isolated Hyperinsulinaemia on Sensory Function in Healthy Adults

Gastrointestinal symptoms such as pain, bloating, nausea and vomiting are more frequent in pre-diabetic states as well as established diabetes, compared to healthy individuals. The mechanisms behind these symptoms are multi-factorial and complex. Furthermore, the effect of isolated hyperinsulinaemia on visceral and peripheral sensory function is poorly understood. Thus, the current study aimed to evaluate effects of acute hyperinsulinaemia on sensory function in healthy adults. The sensitivity to electrical oesophageal and median nerve stimulation was assessed in 15 healthy volunteers together with recording of evoked brain potentials. All subjects were studied both fasting and using a euglycaemic hyperinsulinaemic clamp. There was on average a 15% increased sensitivity to oesophageal electrical stimulation during hyperinsulinaemia compared to fasting state (P<0.05), but the sensation after median nerve stimulation remained stable (P=0.58). No significant changes in latencies and amplitudes of evoked brain potentials were observed after oesophageal or median nerve stimulation (all P>0.05). This study suggests that acute isolated hyperinsulinaemia increases visceral sensitivity, but does not influence the somatic sensory function. The lack of changes in the evoked brain potentials may indicate that hyperinsulinaemia affects the visceral sensory system at a peripheral level. Our result suggests distinct functions of insulin in the various parts of the nervous system, and yields further clues to the significance of insulin as a satiety signal.

Homeostatic Modulation of Stimulation-Dependent Plasticity in Human Motor Cortex

Since recently, it is possible, using noninvasive cortical stimulation, such as the protocol of paired associative stimulation (PAS), to induce the plastic changes in the motor cortex, in humans that mimic Hebb's model of learning. Application of TMS conjugated with peripheral electrical stimulation at strictly coherent temporal manner lead to convergence of inputs in the sensory-motor cortex, with the consequent synaptic potentiation or weakening, if applied repetitively. However, when optimal interstimulus interval (ISI) for induction of LTP-like effects is applied as a single pair, Motor evoked potential (MEP) amplitude inhibition is observed, the paradigm known as short-latency afferent inhibition (SLAI). Aiming to resolve this paradox, PAS protocols were applied, with 200 repetitions of TMS pulses paired with median nerve electrical stimulation, at ISI equal to individual latencies of evoked response of somatosensory cortex (N(20)) (PAS(LTP)), and at ISI of N(20) shortened for 5 msec (PAS(LTD)) - protocols that mimic LTP-like changes in the human motor cortex. MEP amplitudes before, during and after interventions were measured as an indicator based on output signals originating from the motor system. Post-intervention MEP amplitudes following the TMS protocols of PAS(LTP) and PAS(LTD) were facilitated and depressed, respectively, contrary to MEP amplitudes during intervention. During PAS(LTP) MEP amplitudes were significantly decreased in case of PAS(LTP), while in the case of PAS(LTD) an upward trend was observed. In conclusions, a possible explanation for the seemingly paradoxical effect of PAS can be found in the mechanism of homeostatic modulation of plasticity. Those findings indicate the existence of complex relationships in the development of plasticity induced by stimulation, depending on the level of the previous motor cortex excitability.

Sympathetic skin response in electrical burn injury

BackgroundElectrical burn has been reported to be highly associated with peripheral neuropathy. This study was designed to evaluate the sympathetic skin response (SSR) of electrical burn patients to determine whether the sympathetic nervous system is involved in these patients. Materials and methodsThe sympathetic skin response of 28 patients, suffering from electrical burn injury (divided into two groups of high voltage and low voltage exposure) was compared with that of 28 matched subjects, who had never experienced electrical burn. Bilateral palmar and plantar latency and amplitude of SSR were recorded in response to Median and Tibial nerve electrical stimulation. ResultsSSR in all recording sites of the electrical burn patients compared showed significantly more prolonged latencies and reduced amplitudes, with their counterparts in the control group with no significant difference between the high voltage and low voltage electrical burns. There was no significant difference in SSR latency, between the entry and exit sites of the electrical current. The SSR amplitude however, showed more reduction in right hand than the left one, in whom the electrical current had entered the body from the right hand. The time lapse between the electrical burn and the SSR study was shown to play no role in the results. DiscussionIncreased SSR latency in electrical burn injury may be a sign of autonomic nervous system involvement, through systemic responses to electrical burn.

Habituation within the somatosensory processing hierarchy

Habituation is a basic process of learning evident in a decrement in neuronal/behavioral responses to repeated sensory stimulation. It is generally accepted that habituation affects all sensory systems in the human brain, including the somatosensory network. However, it is not clear where habituation originates within this hierarchically organized network. In this study, we examined whether habituation effects increase relatively uniformly along the processing hierarchy or rather distinctly at a particular processing stage. We addressed these questions by performing functional magnetic resonance imaging (fMRI) on 43 healthy subjects during unilateral electrical median nerve stimulation using a block design. We found a time-dependent decrease in the positive BOLD response (indicative of habituation) in all areas of the somatosensory network with the exception of Brodmann area (BA) 3b. The increase in habituation within the presumed processing stream was most pronounced between subareas of the primary somatosensory cortex (BA3b, BA1, BA2), and no further increase in habituation effects was observed in the subsequent processing stages within either the secondary somatosensory cortex or the insula. Moreover, we found a relatively strong habituation effect within the thalamus. These findings indicate that the increase in habituation along the processing hierarchy is measurable primarily between subareas of the primary somatosensory cortex, and we hypothesize that this increase originates in thalamocortical interactions early in the processing stream.

Effect of median-nerve electrical stimulation on BOLD activity in acute ischemic stroke patients

Objective To investigate blood oxygenation level-dependent (BOLD) activation during somatosensory electrical stimulation of the median nerve in acute stroke patients and to determine its correlation with ischemic damage and clinical recovery over time. Methods Fourteen acute stroke patients underwent functional magnetic resonance imaging (fMRI) during contralesional median-nerve electrical stimulation 12–48 h after stroke. Findings were then validated by diffusion tensor imaging (DTI) and motor evoked potential by transcranial magnetic stimulation (TMS). Results Poor clinical recovery at three months was noted in four patients with no activation in the early days after stroke, whereas good clinical recovery was observed in eight patients with a normal activation pattern in the primary sensory motor area in the acute phase. In two patients BOLD activation correlated weakly with clinical recovery. Findings from TMS and DTI partially correlated with clinical recovery and functional scores. Conclusions Clinically relevant insights into the “functional reserve” of stroke patients gained with peripheral nerve stimulation during fMRI may carry prognostic value already in the acute period of a cerebrovascular accident. Significance BOLD activation maps could provide insights into the functional organization of the residual systems and could contribute to medical decision making in neurological and rehabilitative treatment.

Motor cortical plasticity is impaired in Unverricht–Lundborg disease

Patients with Unverricht-Lundborg disease, also referred to as progressive myoclonus epilepsy type 1, exhibit widespread motor symptoms and signs in addition to epileptic seizures, which suggest abnormal excitability of the primary motor pathways. To explore the plasticity of the sensory-motor cortex, we employed a modern neurophysiological method, the paired associative stimulation protocol, which resembles the concept of long-term potentiation of experimental studies. Seven patients with genetically verified Unverricht-Lundborg disease and 13 healthy control subjects were enrolled in the study to characterize cortical sensory-motor plasticity. In the study protocol, peripheral electric median nerve stimulation preceded navigated transcranial magnetic stimulation targeted to the representation area of thenar musculature on the contralateral primary motor cortex. The protocol consisted of 132 transcranial magnetic stimulation trials at 0.2 Hz, preceded by peripheral sensory stimulation at 25 ms. Motor-evoked potential amplitudes were analyzed at baseline and after the paired associative stimulation protocol at an intensity of 130% of the individual motor threshold. The patients with Unverricht-Lundborg disease exhibited an average decrease of 15% in motor-evoked potential amplitudes 30 minutes after paired associative stimulation, whereas in the control subjects, a significant increase (101%) was observed (P < .05), as expected. The results indicate a lack of normal cortical plasticity in Unverricht-Lundborg disease, which stresses the role of abnormal motor cortical functions or sensorimotor integration as possible pathophysiological contributors to the motor symptoms. The impaired cortical plasticity may be associated with the previously reported structural and physiological abnormalities of the primary motor cortex.

Interhemispheric Interactions between the Human Primary Somatosensory Cortices

In the somatosensory domain it is still unclear at which processing stage information reaches the opposite hemispheres. Due to dense transcallosal connections, the secondary somatosensory cortex (S2) has been proposed to be the key candidate for interhemispheric information transfer. However, recent animal studies showed that the primary somatosensory cortex (S1) might as well account for interhemispheric information transfer. Using paired median nerve somatosensory evoked potential recordings in humans we tested the hypothesis that interhemispheric inhibitory interactions in the somatosensory system occur already in an early cortical processing stage such as S1. Conditioning right S1 by electrical median nerve (MN) stimulation of the left MN (CS) resulted in a significant reduction of the N20 response in the target (left) S1 relative to a test stimulus (TS) to the right MN alone when the interstimulus interval between CS and TS was between 20 and 25 ms. No such changes were observed for later cortical components such as the N20/P25, N30, P40 and N60 amplitude. Additionally, the subcortically generated P14 response in left S1 was also not affected. These results document the existence of interhemispheric inhibitory interactions between S1 in human subjects in the critical time interval of 20–25 ms after median nerve stimulation.

Influences of negative BOLD responses on positive BOLD responses

Understanding possible interactions between blood oxygenation level-dependent (BOLD) responses is critical for model-based analyses and the interpretation of experiments that deal with stimuli presented close together in time. Such interactions are well documented in the case of successive positive BOLD responses. However, the influence that a stimulus-induced, negative BOLD response exerts on a subsequent positive BOLD response has yet to be investigated and is the focus of the current study. We performed functional magnetic resonance imaging on 10 healthy subjects during bilateral electrical median nerve stimulation using five different time intervals between left- and right-sided stimuli. We found an acute interruption of the ongoing negative BOLD response at the onset of the positive BOLD response. Different parameters characterizing the positive BOLD response were estimated. There was no impact of the preceding negative BOLD response on the parameters describing the subsequent positive BOLD response. These findings indicate that the underlying mechanisms for negative and positive BOLD responses do not engage parallel processes. We hypothesize that the negative BOLD response is caused by a decreased release of the same vasodilatative agents that evoke the positive BOLD response. Additionally, our results demonstrate that there is no need to adjust the model of a positive BOLD response due to a preceding negative BOLD response in the same brain area.

Functional deactivations: Multiple ipsilateral brain areas engaged in the processing of somatosensory information

Somatosensory signals modulate activity throughout a widespread network in both of the brain hemispheres: the contralateral as well as the ipsilateral side of the brain relative to the stimulated limb. To analyze the ipsilateral somatosensory brain areas that are engaged during limb stimulation, we performed functional magnetic resonance imaging (fMRI) in 12 healthy subjects during electrical median nerve stimulation using both a block- and an event-related fMRI design. Data were analyzed through the use of model-dependent (SPM) and model-independent (ICA) approaches. Beyond the well-known positive blood oxygenation level-dependent (BOLD) responses, negative deflections of the BOLD response were found consistently in several ipsilateral brain areas, including the primary somatosensory cortex, the supplementary motor area, the insula, the dorsal part of the posterior cingulate cortex, and the contralateral cerebellum. Compared to their positive counterparts, the negative hemodynamic responses showed a different time course, with an onset time delay of 2.4 s and a peak delay of 0.7 s. This characteristic delay was observed in all investigated areas and verified by a second (purely tactile) event-related paradigm, suggesting a systematic difference for brain areas involved in the processing of somatosensory information. These findings may indicate that the physiological basis of these deactivations differs from that of the positive BOLD responses. Therefore, an altered model for the negative BOLD response may be beneficial to further model-dependent fMRI analyses.

Transcranial Magnetic Stimulation in Different Current Directions Activates Separate Cortical Circuits

Transcranial magnetic stimulation (TMS) to the primary motor cortex (M1) produces a series of corticospinal descending waves, with a direct (D) wave followed by several indirect (I) waves. TMS inducing posterior-anterior (PA) current in the brain predominantly recruits the early I1-wave, whereas anterior-posterior (AP) directed current preferentially recruits the late I3-wave. However, it is not known whether I-waves elicited by different current directions are mediated by the same neuronal populations. We studied the neuronal mechanisms mediating I-waves by examining the influence of short-latency afferent inhibition (SAI) on various I-waves. SAI was tested with electrical median nerve stimulation at the wrist followed by TMS to the contralateral M1 at different current directions. Surface electromyograms and single motor units were recorded from the first dorsal interosseous muscle. SAI was weaker for the AP compared with that for the PA current direction. With increasing median nerve stimulation intensities, SAI increased for the PA direction but showed a U-shaped relationship for the AP direction. SAI produced more inhibition of late I-waves generated by PA than those generated by AP current direction. We conclude that late I-waves generated by PA and AP current directions are mediated by different neuronal mechanisms.

Neurovascular coupling in the human somatosensory cortex

Oscillations in the higher frequency range are closely related to regional brain hemodynamic changes. Here we investigated this neurovascular coupling in humans in response to electrical stimulation of the right median nerve. In a single-trial study, we simultaneously recorded hemodynamic fluctuations in the somatosensory cortex by near infrared spectroscopy and brain neuronal oscillations by whole-head magnetoencephalography (MEG). The results from six volunteers showed that neural fluctuations at β or γ-band power were correlated with hemodynamic fluctuation during stimulus conditions. These correlations were prominent with a time delay of 5-7 s. This study provides new direct evidence that hemodynamic onset lags specific neural oscillations in the order of seconds in human awake conditions using noninvasive methods.

Source localization of sensory gating: A combined EEG and fMRI study in healthy volunteers

Reduced sensory gating appears to be among the core features in schizophrenia. The sources of sensory gating however are largely unknown. The aim of the current study was to identify these sources, with concurrent EEG and fMRI methodology. Twenty healthy male volunteers were tested with identical P50 suppression paradigms in two separate sessions: an EEG setting, and an EEG concurrent with fMRI setting. The stimuli in the P50 paradigm consisted of weak electrical stimulation of the left median nerve. The stimuli were presented in pairs with either 500ms or 1000ms interstimulus intervals (ISI). No difference was found between the EEG setting and the concurrent EEG and fMRI setting. P50 suppression was, in both settings, found only in the 500ms trials, not in the 1000ms trials. EEG-dipole modeling resulted in 4 sources located in the medial frontal gyrus, the insula, the hippocampus, and primary somatosensory cortex. These sources corresponded to significant fMRI clusters located in the medial frontal gyrus, the insula, the claustrum, and the hippocampus. Activity in the hippocampus and the claustrum was higher in the trials with suppression, suggesting that these brain areas are involved in the inhibitory processes of P50 suppression. The opposite was found for activity in the medial frontal gyrus and the insula, suggesting that these brain areas are involved in the generation of the P50 amplitude. To our knowledge, this is the first study demonstrating that P50 suppression can be reliably assessed inside an MRI scanner.

Behavioral and Neurophysiological Effects of Repetitive Transcranial Magnetic Stimulation on the Minimally Conscious State

Background. In 2007, Schiff et al reported a patient in a minimally conscious state (MCS) who responded to deep brain stimulation (DBS), but clinicians cannot predict which patients might respond prior to the implantation of electrodes. Methods. A patient in a MCS for 5 years participated in an ABA design alternating between repetitive transcranial magnetic stimulation (rTMS) and peripheral nerve stimulation. rTMS (condition A) involved the delivery of 10 trains of 100 stimuli at 20 Hz using a stimulator with a 70-mm figure-of-eight coil to elicit a contraction of the abductor pollicis brevis. Condition B used median nerve electrical stimulation. Results. After peripheral stimulation, the patient did not exhibit clinical, behavioral, or electroencephalographic (EEG) changes. The frequency of specific and meaningful behaviors increased after rTMS, along with the absolute and relative power of the EEG δ, β, and α bands. Conclusion. These results suggest that rTMS may improve awareness and arousal in MCS. If these results are reproducible, rTMS may identify subgroups of MCS patients who might benefit from DBS.

Pharmacological Functional MRI Assessment of the Effect of Ibuprofen-Arginine in Painful Conditions

Pharmacological functional magnetic resonance imaging (phMRI) is a valuable tool for the investigation of pharmacological effects of a drug on pain processing. We hypothesized that the ibuprofen-arginine combination, in line with its characteristic analgesic properties, may influence the phMRI response at the central level, as compared to placebo. Ten healthy subjects underwent a double-blind, placebo-controlled, randomized, cross-over phFMRI study with somatosensory painful stimulation of the right median nerve. We measured the blood oxygen level dependent (BOLD) signal variations induced in conditions of pain after oral administration of either ibuprofen-arginine or placebo formulations. Independent component analysis (ICA) was used for the analysis of the fMRI data, without assuming a specific hemodynamic response function (HRF), which may be altered by drug administration. Median nerve electrical painful stimulation mainly activated the primary contralateral and the secondary somatosensory cortices, the insula, the supplementary motor area, and the middle frontal gyrus. Placebo and ibuprofen-arginine administration induced activation bilaterally in the premotor cortex, and an overall reduction in the other pain-related areas, which was more prominent in the left hemisphere. A task-related increase of BOLD signal between drug and placebo was observed bilaterally in the primary somatosensory area and the middle frontal gyrus without any changes in subjective pain scores. Overall, our findings show that ibuprofen-arginine, in line with the characteristic analgesic properties of ibuprofen, influences the BOLD response in specific pain-related brain areas with respect to placebo, with a vasoactive effect possibly due to arginine.

Somatosensory evoked potentials and high frequency oscillations are differently modulated by theta burst stimulation over primary somatosensory cortex in humans

Objective The effects of theta burst stimulation (TBS) have been extensively investigated in primary motor cortex, where it leads to long-lasting LTP/LTD-like effects on synaptic plasticity. This study aimed to extend these observations to sensory cortex. Methods Fourteen healthy subjects participated in the study. Conditioning 600-pulse intermittent TBS (iTBS) and continuous TBS (cTBS) were delivered to left somatosensory cortex (S1) with an intensity of 80% active motor threshold. Somatosensory evoked potentials (SEPs) were evoked by median nerve electrical stimulation at right wrist. High frequency oscillations (HFOs) were obtained by digital filtering of original SEPs and divided into early and late subcomponents, relative to N20 peak latency. Results Repeated-measures ANOVA showed that iTBS facilitated N20 onset–N20 peak at 15 min and N20 peak–P25 at 15 and 30 min after conditioning, whereas cTBS did not. iTBS left the early and late HFOs unchanged. Conversely, cTBS facilitated the early HFOs, whereas it inhibited the late HFOs at 15 min after conditioning. Conclusions S1-iTBS facilitated SEPs without changes in HFOs whereas cTBS modulated early and late HFOs without changes in SEPs. Significance S1-TBS produces lasting changes in the excitability of intracortical circuits generating SEPs and HFOs differentially through mechanisms of LTP/LTD-like synaptic plasticity.

Dependence of the negative BOLD response on somatosensory stimulus intensity

The primary somatosensory cortex (SI) has been shown to encode the intensity of a stimulus applied to the contralateral side of the body. Recent studies have demonstrated that ipsilateral SI is also involved in the processing of somatosensory information. In this study, we investigated the dependence of the negative BOLD response in ipsilateral SI on the intensity of somatosensory stimulation. Functional MRI was performed in 12 healthy subjects during electrical median nerve stimulation at four different intensities. A monotonic relationship between stimulus intensity and the strength of the negative BOLD response in ipsilateral SI was found. Additionally, a psychophysiological experiment revealed tight coupling between the stimulus intensity applied to one hand and increased perceptual threshold of the other hand. These findings indicate a stimulus intensity-dependent inhibition of ipsilateral SI.

Early expression of injury-induced neuropeptide Y in primary sensory neurons and the cuneate nucleus in diabetic rats with median nerve transection

In this study we examined the temporal changes in neuropeptide Y (NPY) expression in dorsal root ganglion (DRG) neurons and cuneate nucleus (CN) in streptozotocin (STZ)-induced diabetic rats with or without median nerve transection (MNT). Numerous NPY-like immunoreactive (NPY-LI) neurons and fibers were detected in the DRG and CN of the diabetic MNT (DMNT) rats respectively, but not in those with diabetes-alone. Following MNT, the time-course of NPY expression pattern in the diabetic DRG and CN was similar and both peaked at 2 weeks, which was earlier than those in the non-diabetic MNT rats. Consequently, the expression of neurotrophin-3 (NT-3) immunoreactivity in DRG neurons was coincidentally decreased and reached the nadir at 2 weeks in the diabetic MNT rats, which was also earlier than that in the non-diabetic MNT rats. Following electrical stimulation of the injured nerves, the number of NPY-LI fibers became attenuated and the induced c-Fos-LI cells concurrently appeared in the ipsilateral CN. In the diabetic CN, the number of c-Fos-LI cells also peaked at 2 weeks after MNT, which was consistent with the temporal pattern of changes in NPY expression. The results suggest that in diabetes, MNT induced NPY expression via the reduction of NT-3, and electrical stimulation of the injured median nerve evoked the release of NPY and accordingly more c-Fos-LI cells were identified in the CN. Furthermore, this study demonstrated early NPY and c-Fos expression in the diabetic rats after MNT, suggesting that the development of neuropathic signs may be advanced in hyperglycemic rats.

Individual head-casts for MEG

Event Abstract Back to Event Individual head-casts for MEG David Bradbury1*, Paul Hammond1 and Gareth Barnes1 1 UCL, United Kingdom The objective of this work is accurate, repeatable head positioning and co-registration for MEG. Methods:By placing the subject’s head in a helmet-shaped duplicate of the measurement dewar and filling the surrounding space with silicon composite we were able to make subject-specific head casts. These head-casts were moulded to the subjects head internally yet externally located precisely into the measurement dewar. To test the relocation accuracy we used a median nerve electrical stimulation paradigm (motor-twitch threshold, 4Hz, 500 trials) lasting for approximately 2 minutes per-recording run. After each run the subject was removed from the dewar and given a two minute break to allow free movement of the head. This was repeated nine times, without removing the head-cast from the subject. Initial results (based on nasion coil location) suggest that the head could be located to within an error of rms error 1.7mm. Within-run head movement was consistently less than 1mm. We are currently testing different head-cast materials and the incorporation of fiducial markers within the cast for MRI visibility. Conclusions:The MEG head cast means that high SNR can be achieved through multiple independent recording sessions. Ultimately the use of individual MEG head casts promises reduced subject movement, precise subject relocation and high co-registration accuracy. Conference: Biomag 2010 - 17th International Conference on Biomagnetism , Dubrovnik, Croatia, 28 Mar - 1 Apr, 2010. Presentation Type: Poster Presentation Topic: Instrumentation and Multi-modal Integrations: MEG, Low-field MRI,EEG, fMRI,TMS,NIRS Citation: Bradbury D, Hammond P and Barnes G (2010). Individual head-casts for MEG. Front. Neurosci. Conference Abstract: Biomag 2010 - 17th International Conference on Biomagnetism . doi: 10.3389/conf.fnins.2010.06.00031 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 19 Mar 2010; Published Online: 19 Mar 2010. * Correspondence: David Bradbury, UCL, London, United Kingdom, d.bradbury@fil.ion.ucl.ac.uk Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers David Bradbury Paul Hammond Gareth Barnes Google David Bradbury Paul Hammond Gareth Barnes Google Scholar David Bradbury Paul Hammond Gareth Barnes PubMed David Bradbury Paul Hammond Gareth Barnes Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Motor cortex plasticity induced by paired associative stimulation is enhanced in physically active individuals

Recent evidence indicates that regular physical activity enhances brain plasticity (i.e. the ability to reorganise neural connections) and improves neurocognitive function. However, the effect of regular physical activity on human motor cortex function is unknown. The purpose of this study was to examine motor cortex plasticity for a small hand muscle in highly active and sedentary individuals. Electromyographic recordings were obtained from the left abductor pollicis brevis (APB) muscle of 14 active and 14 sedentary subjects (aged 18-38 yrs). The extent of physical activity was assessed by questionnaire, where the physically active subjects performed >150 min per day moderate-to-vigorous aerobic activity on at least 5 days per week, whereas the sedentary group performed <20 min per day of physical activity on no more than 3 days per week. Transcranial magnetic stimulation (TMS) of the right hemisphere was used to assess changes in APB motor-evoked potentials (MEPs), input-output curve (IO curve), short-interval intracortical inhibition (SICI) and cortical silent period (CSP). Neuroplastic changes were induced using paired-associative stimulation (PAS), which consisted of 90 paired stimuli (0.05 Hz for 30 min) of median nerve electrical stimulation at the wrist followed 25 ms later by TMS to the hand area of motor cortex. The IO curve slope was 35% steeper in individuals with increased physical activity (combined before and after PAS, P < 0.05), suggesting increased motor cortex excitability, although there was no difference in SICI or CSP between groups. PAS induced an increase in MEP amplitude in the physically active subjects (54% increase compared with before, P < 0.01), but no significant facilitation in the sedentary subjects. We conclude that participation in regular physical activity may offer global benefits to motor cortex function that enhances neuroplasticity, which could improve motor learning and neurorehabilitation in physically active individuals.

Noxious Somatosensory Stimulation Affects the Default Mode of Brain Function: Evidence from Functional MR Imaging

To investigate whether default mode network (DMN) spatial properties can be directly affected by pain, with a comparison of painful and nonpainful conditions. The authors performed a functional magnetic resonance (MR) imaging study, approved by the local institutional ethics committee, involving 10 healthy male subjects (age range, 18-45 years) who gave written informed consent. The subjects underwent two experimental sessions of median nerve electrical stimulation at painful and nonpainful levels. Independent component analysis of the functional MR imaging data was performed to determine the DMN spatiotemporal pattern. Group-level DMN connectivity maps for painful and nonpainful conditions were obtained (P < .001, corrected with false discovery rate). The contrast between the connectivity maps in the two conditions was also computed (P < .05, corrected with false discovery rate). The DMN maintained its typical temporal properties but was subject to modifications in connectivity pattern during painful stimulation, affecting the brain areas associated with pain processing. Increased connectivity in painful conditions was found mainly in the left prefrontal cortex and posterior cingulate cortex-precuneus, and decreased connectivity was found in the lateral parietal cortex. Study findings were in line with the impairments of the DMN reported in patients with chronic pain. They support the hypothesis that alteration of the DMN connectivity pattern localized in specific brain areas during acute pain, if repeated across time, might induce permanent changes that could disrupt the DMN functional architecture.