Contralateral Sensorimotor Cortex Research Articles

P24-S Abnormal patterns of corticomuscular and intermuscular coherence in acquired and idiopathic/genetic childhood dystonias

Background Sensorimotor processing is abnormal in Idiopathic/Genetic dystonias but remains unstudied in Acquired dystonias. We test the hypothesis that sensory modulation of Beta-Corticomuscular coherence (CMC) and Intermuscular coherence (IMC) differs with dystonia aetiology. Methods Participants: 11 children with Acquired dystonia, 5 with Genetic/Idiopathic dystonia and 13 typically-developing-children (TDC) (12–18 yrs). The child grasped a ruler between thumb and index finger. Mechanical perturbations were provided by an electromechanical tapper. Surface EMG (first dorsal interosseous and forearm extensors) and bipolar EEG over contralateral sensorimotor cortex were recorded in 5-s epochs (200×). Signals were amplified, bandpass filtered (EEG 0.5–100 Hz; EMG 5–250 Hz) and digitised (1024 Hz). CMC and IMC were computed using a 512-point short-time Fourier transform and 95% confidence levels were derived. The analysis window moved across the epoch to assess change in CMC/IMC over time. Results Beta-CMC (14–36 Hz) was identified in 13/13 TDCs, 3/5 children with Idiopathic/Genetic and 9/11 with Acquired dystonia. Beta-CMC magnitude increased significantly from baseline to early post-stimulus in TDCs and Acquired dystonia (Wilcoxon signed rank test p = 0.001 and p = 0.004 respectively), but not in Idiopathic/Genetic dystonia (p = 0.959). Post-stimulus beta-CMC magnitude was significantly higher in TDCs than Idiopathic/Genetic dystonia (Mann Whitney p = 0.002) and in Acquired than Idiopathic/Genetic dystonia (p = 0.038). Beta-IMC was similar across groups. Prominent low frequency (4–8 Hz) IMC was seen in all dystonia patients, but not in TDCs, and correlated with severity (BFMDRS-m). Conclusion Idiopathic/Genetic and Acquired dystonia share an abnormal low-frequency IMC but patterns of beta-CMC sensory modulation are distinct, indicating different sensorimotor processing abnormalities between these groups.

O-08 Brain connectivity modulation after exoskeleton gait in chronic stroke survivors: a pilot study

Background Restoration of independent gait after stroke is a principal goal of survivors. Exoskeleton overground gait training provides trunk support and inter-limb coordination based on fine-tuning of the robot control parameters. The aim of our study was to identify short-term plasticity based on electroencephalography (EEG) data induced by a single trial of exoskeleton gait training in unilateral hemiplegic stroke survivors. Material and methods 64-channel EEG was recorded before gait (T0), after overground walking (T1) and after overground exoskeleton (EksoGT) gait training (T2) in 9 stroke survivors. Relative power and coherence were estimated for alpha1 (8–10 Hz), alpha2 (10.5–12.5 Hz) and beta (13–30 Hz) frequency ranges. Graph analysis assessed network model properties: node strength (S) and betweenness centrality (BC). Results Left-hemisphere stroke subjects showed S decrease over anterior and posterior cortex in alpha1, alpha2 and beta at T1 and T2. BC decreased at vertex at T1 and T2 in alpha2 and beta. Right-hemisphere stroke subjects displayed power decrease after exoskeleton walking in alpha2 over CPZ and CP2, and in beta over left contralateral sensorimotor cortex (cSM) and right ipsilateral prefrontal cortex (iPFC). S increased in alpha1 and alpha2 over cSM and iPFC at T2; BC decreased in alpha2 over iPFC at T2 compared to T1. Conclusions A single session of tailored exoskeleton training provides short-term neuroplastic modulation in chronic stroke. Right-hemisphere stroke subjects re-establish a more physiological activation network; a similar reorganization does not take place in left-hemisphere stroke subjects, supporting the role of lateralization in limb control and stroke recovery.

Local-to-distant development of the cerebrocerebellar sensorimotor network in the typically developing human brain: a functional and diffusion MRI study

Sensorimotor function is a fundamental brain function in humans, and the cerebrocerebellar circuit is essential to this function. In this study, we demonstrate how the cerebrocerebellar circuit develops both functionally and anatomically from childhood to adulthood in the typically developing human brain. We measured brain activity using functional magnetic resonance imaging while a total of 57 right-handed, blindfolded, healthy children (aged 8–11 years), adolescents (aged 12–15 years), and young adults (aged 18–23 years) (n = 19 per group) performed alternating extension–flexion movements of their right wrists in precise synchronization with 1-Hz audio tones. We also collected their diffusion MR images to examine the extent of fiber maturity in cerebrocerebellar afferent and efferent tracts by evaluating the anisotropy-sensitive index of hindrance modulated orientational anisotropy (HMOA). During the motor task, although the ipsilateral cerebellum and the contralateral primary sensorimotor cortices were consistently activated across all age groups, the functional connectivity between these two distant regions was stronger in adults than in children and adolescents, whereas connectivity within the local cerebellum was stronger in children and adolescents than in adults. The HMOA values in cerebrocerebellar afferent and efferent tracts were higher in adults than in children (some were also higher than in adolescents). The results indicate that adult-like cerebrocerebellar functional coupling is not completely achieved during childhood and adolescence, even for fundamental sensorimotor brain function, probably due to anatomical immaturity of cerebrocerebellar tracts. This study clearly demonstrated the principle of “local-to-distant” development of functional brain networks in the human cerebrocerebellar sensorimotor network.

Preparing to Stop Action Increases Beta Band Power in Contralateral Sensorimotor Cortex.

How do we prepare to stop ourselves in the future? Here, we used scalp EEG to test the hypothesis that people prepare to stop by putting parts of their motor system (specifically, here, sensorimotor cortex) into a suppressed state ahead of time. On each trial, participants were cued to prepare to stop one hand and then initiated a bimanual movement. On a minority of trials, participants were instructed to stop the cued hand while continuing quickly with the other. We used a guided multivariate source separation method to examine oscillatory power changes in presumed sensorimotor cortical areas. We observed that, when people prepare to stop a hand, there were above-baseline beta band power increases (12-24 Hz) in contralateral cortex up to a second earlier. This increase in beta band power in the proactive period was functionally relevant because it predicted, trial by trial, the degree of selectivity with which participants subsequently stopped a response but did not relate to movement per se. Thus, preparing to stop particular response channels corresponds to increased beta power from contralateral (sensorimotor) cortex, and this relates specifically to subsequent stopping. These results provide a high temporal resolution and frequency-specific electrophysiological signature of the preparing-to-stop state that is pertinent to future studies of mitigating provocation, including in clinical disorders. The results also highlight the utility of guided multivariate source separation for revealing the cortical dynamics underlying both movement and response suppression.

Functional plasticity of the ipsilateral primary sensorimotor cortex in an elite long jumper with below-knee amputation.

Functional plasticity of the sensorimotor cortex occurs following motor practice, as well as after limb amputation. However, the joint effect of limb amputation and intensive, long-term motor practice on cortical plasticity remains unclear. Here, we recorded brain activity during unilateral contraction of the hip, knee, and ankle joint muscles from a long jump Paralympic gold medalist with a unilateral below-knee amputation (Amputee Long Jumper, ALJ). He used the amputated leg with a prosthesis for take-off. Under similar conditions to the ALJ, we also recorded brain activity from healthy long jumpers (HLJ) and non-athletes with a below-knee amputation. During a rhythmic isometric contraction of knee extensor muscles with the take-off/prosthetic leg, the ALJ activated not only the contralateral primary sensorimotor cortex (M1/S1), but also the ipsilateral M1/S1. In addition, this ipsilateral M1/S1 activation was significantly greater than that seen in the HLJ. However, we did not find any significant differences between the ALJ and HLJ in M1/S1 activation during knee muscle contraction in the non-take-off/intact leg, nor during hip muscle contraction on either side. Region of interest analysis revealed that the ALJ exhibited a greater difference in M1/S1 activity and activated areas ipsilateral to the movement side between the take-off/prosthetic and non-take-off/intact legs during knee muscle contraction compared with the other two groups. However, difference in activity in M1/S1 contralateral to the movement side did not differ across groups. These results suggest that a combination of below-knee amputation and intensive, prolonged long jump training using a prosthesis (i.e. fine knee joint control) induced an expansion of the functional representation of the take-off/prosthetic leg in the ipsilateral M1/S1 in a muscle-specific manner. These results provide novel insights into the potential for substantial cortical plasticity with an extensive motor rehabilitation program.

Ipsilateral finger representations in the sensorimotor cortex are driven by active movement processes, not passive sensory input.

Hand and finger movements are mostly controlled through crossed corticospinal projections from the contralateral hemisphere. During unimanual movements, activity in the contralateral hemisphere is increased while the ipsilateral hemisphere is suppressed below resting baseline. Despite this suppression, unimanual movements can be decoded from ipsilateral activity alone. This indicates that ipsilateral activity patterns represent parameters of ongoing movement, but the origin and functional relevance of these representations is unclear. In this study, we asked whether ipsilateral representations are caused by active movement or whether they are driven by sensory input. Participants alternated between performing single finger presses and having fingers passively stimulated while we recorded brain activity using high-field (7T) functional imaging. We contrasted active and passive finger representations in sensorimotor areas of ipsilateral and contralateral hemispheres. Finger representations in the contralateral hemisphere were equally strong under passive and active conditions, highlighting the importance of sensory information in feedback control. In contrast, ipsilateral finger representations in the sensorimotor cortex were stronger during active presses. Furthermore, the spatial distribution of finger representations differed between hemispheres: the contralateral hemisphere showed the strongest finger representations in Brodmann areas 3a and 3b, whereas the ipsilateral hemisphere exhibited stronger representations in premotor and parietal areas. Altogether, our results suggest that finger representations in the two hemispheres have different origins: contralateral representations are driven by both active movement and sensory stimulation, whereas ipsilateral representations are mainly engaged during active movement. NEW & NOTEWORTHY Movements of the human body are mostly controlled by contralateral cortical regions. The function of ipsilateral activity during movements remains elusive. Using high-field neuroimaging, we investigated how human contralateral and ipsilateral hemispheres represent active and passive finger presses. We found that representations in contralateral sensorimotor cortex are equally strong during both conditions. Ipsilateral representations were mostly present during active movement, suggesting that sensorimotor areas do not receive direct sensory input from the ipsilateral hand.

Brain Functional Connectivity Plasticity Within and Beyond the Sensorimotor Network in Lower-Limb Amputees.

Cerebral neuroplasticity after amputation has been elucidated by functional neuroimaging. However, little is known concerning how brain network-level functional reorganization of the sensorimotor system evolves following lower-limb amputation. We studied 32 unilateral lower-limb amputees (LLAs) and 32 matched healthy controls (HCs) using resting-state functional magnetic resonance imaging (rs-fMRI). A regions of interest (ROI)-wise connectivity analysis was performed with ROIs in eight brain regions in the sensorimotor network to investigate intra-network changes, and seed-based whole-brain functional connectivity (FC) with a seed in the contralateral primary sensorimotor cortex (S1M1) was used to study the FC reorganization between the sensorimotor region (S1M1) and other parts of the brain in the LLAs. The ROI-wise connectivity analysis showed that the LLAs had decreased FC, mainly between the subcortical nuclei and the contralateral S1M1 (p < 0.05, FDR corrected). Seed-based whole-brain FC analysis revealed that brain regions with decreased FC with the contralateral S1M1 extended beyond the sensorimotor network to the prefrontal and visual cortices (p < 0.05, FDR corrected). Moreover, correlation analysis showed that decreased FC between the subcortical and the cortical regions in the sensorimotor network progressively increased in relation to the time since amputation. These findings indicated a cascade of cortical reorganization at a more extensive network level following lower-limb amputation, and also showed promise for the development of a possible neurobiological marker of changes in FC related to motor function recovery in LLAs.

Combining Movement-Related Cortical Potentials and Event-Related Desynchronization to Study Movement Preparation and Execution

This study applied a comprehensive electroencephalography (EEG) analysis for movement-related cortical potentials (MRCPs) and event-related desynchronization (ERD) in order to understand movement-related brain activity changes during movement preparation and execution stage of unilateral wrist extension. Thirty-four healthy subjects completed two event-related potential tests in the same sequence. Unilateral wrist extension was involved in both tests as the movement task. Instruction Response Movement (IRM) was a brisk movement response task with visual “go” signal, while Cued Instruction Response Movement (CIRM) added a visual cue contenting the direction information to create a prolonged motor preparation stage. Recorded EEG data were segmented and averaged to show time domain changes and then transformed into time-frequency mapping to show the time-frequency changes. All components were calculated and compared among C3, Cz, and C4 locations. The motor potential appeared bilaterally in both tests' movement execution stages, and Cz had the largest peak value among the investigated locations (p < 0.01). In CIRM, a contingent negative variation (CNV) component presented bilaterally during the movement preparation stage with the largest amplitude at Cz. ERD of the mu rhythm (mu ERD) presented bilateral sensorimotor cortices during movement execution stages in both tests and was the smallest at Cz among the investigated locations. In the movement preparation stage of CIRM, mu ERD presented mainly in the contralateral sensory motor cortex area (C3 and C4 for right and left wrist movements, respectively) and showed significant differences between different locations. EEG changes in the time and time-frequency domains showed different topographical features. Movement execution was controlled bilaterally, while movement preparation was controlled mainly by contralateral sensorimotor cortices. Mu ERD was found to have stronger contra-lateralization features in the movement preparation stage and might be a better indicator for detecting movement intentions. This information could be helpful and might provide comprehensive information for studying movement disorders (such as those in post-stroke hemiplegic patients) or for facilitating the development of neuro-rehabilitation engineering technology such as brain computer interface.

High-frequency peripheral vibration decreases completion time on a number of motor tasks.

A recent theoretical account of motor control proposes that modulation of afferent information plays a role in affecting how readily we can move. Increasing the estimate of uncertainty surrounding the afferent input is a necessary step in being able to move. It has been proposed that an inability to modulate the gain of this sensory information underlies the cardinal symptoms of Parkinson's disease (PD). We aimed to test this theory by modulating the uncertainty of the proprioceptive signal using high‐frequency peripheral vibration, to determine the subsequent effect on motor performance. We investigated if this peripheral stimulus might modulate oscillatory activity over the sensorimotor cortex in order to understand the mechanism by which peripheral vibration can change motor performance. We found that 80 Hz peripheral vibration applied to the right wrist of a total of 54 healthy human participants reproducibly improved performance across four separate randomised experiments on a number of motor control tasks (nine‐hole peg task, box and block test, reaction time task and finger tapping). Improved performance on all motor tasks (except the amplitude of finger tapping) was also seen for a sample of 18PD patients ON medication. EEG data investigating the effect of vibration on oscillatory activity revealed a significant decrease in beta power (15–30 Hz) over the contralateral sensorimotor cortex at the onset and offset of 80 Hz vibration. This finding is consistent with a novel theoretical account of motor initiation, namely that modulating uncertainty of the proprioceptive afferent signal improves motor performance potentially by gating the incoming sensory signal and allowing for top‐down proprioceptive predictions.

Primary Sensorimotor Cortex Drives the Common Cortical Network for Gamma Synchronization in Voluntary Hand Movements.

Background: Gamma synchronization (GS) may promote the processing between functionally related cortico-subcortical neural populations. Our aim was to identify the sources of GS and to analyze the direction of information flow in cerebral networks at the beginning of phasic movements, and during medium-strength isometric contraction of the hand.Methods: We measured 64-channel electroencephalography in 11 healthy volunteers (age: 25 ± 8 years; four females); surface electromyography detected the movements of the dominant hand. In Task 1, subjects kept a constant medium-strength contraction of the first dorsal interosseus muscle, and performed a superimposed repetitive voluntary self-paced brisk squeeze of an object. In Task 2, brisk, and in Task 3, constant contractions were performed. Time-frequency analysis of the EEG signal was performed with the multitaper method. GS sources were identified in five frequency bands (30–49, 51–75, 76–99, 101–125, and 126–149 Hz) with beamformer inverse solution dynamic imaging of coherent sources. The direction of information flow was estimated by renormalized partial directed coherence for each frequency band. The data-driven surrogate test, and the time reversal technique were performed to identify significant connections.Results: In all tasks, we depicted the first three common sources for the studied frequency bands that were as follows: contralateral primary sensorimotor cortex (S1M1), dorsolateral prefrontal cortex (dPFC) and supplementary motor cortex (SMA). GS was detected in narrower low- (∼30–60 Hz) and high-frequency bands (>51–60 Hz) in the contralateral thalamus and ipsilateral cerebellum in all three tasks. The contralateral posterior parietal cortex was activated only in Task 1. In every task, S1M1 had efferent information flow to the SMA and the dPFC while dPFC had no detected afferent connections to the network in the gamma range. Cortical-subcortical information flow captured by the GS was dynamically variable in the narrower frequency bands for the studied movements.Conclusion: A distinct cortical network was identified for GS in voluntary hand movement tasks. Our study revealed that S1M1 modulated the activity of interconnected cortical areas through GS, while subcortical structures modulated the motor network dynamically, and specifically for the studied movement program.

Longitudinal brain activation changes related to electrophysiological findings in patients with cervical spondylotic myelopathy before and after spinal cord decompression: an fMRI study.

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction, potentially leading to severe disability. Abnormal cervical spine magnetic resonance imaging (MRI) and motor evoked potentials (MEPs) are independent predictors of disease progression. Abnormal MRI is accompanied by various activation changes in functional brain MRI (fMRI), whereas preoperative and postoperative fMRI adaptations associated with abnormal preoperative MEP remain unknown. Twenty patients (9 males, average age 56.6) with evidence of spinal cord compression on MRI and clinical signs of mild CSM were included. Participants were classified according to their preoperative MEP and underwent three brain fMRI examinations: before surgery, 6, and 12months after surgery while performing repeated extension-flexion of each wrist. Functional MRI activation was compared between two subsets of patients, with normal and clearly abnormal MEP (right wrist: 8 vs. 8; left wrist: 7 vs. 9). At baseline, abnormal MEPs were associated with hyperactivation in the cerebellum. At the first follow-up, further hyperactivations emerged in the contralateral sensorimotor cortices and persisted for 1year. In normal baseline MEP, activation mostly decreased in the ipsilateral sensorimotor cortex postoperatively. The ipsilateral sensorimotor activation after 1-year follow-up correlated with baseline MEP. Abnormal corticospinal MEP findings in cervical spondylotic myelopathy were associated with differences in brain activation, which further increased after spinal cord decompression and did not resolve within 12-month follow-up. In summary, surgery may come too late for those patients with abnormal MEP to recover completely despite their mild clinical signs and symptoms.

Brain remodeling after chronic median nerve compression in a rat model.

Carpal tunnel syndrome is the most common compressive neuropathy, presenting with sensorimotor dysfunction. In carpal tunnel syndrome patients, irregular afferent signals on functional magnetic resonance imaging are associated with changes in neural plasticity during peripheral nerve injury. However, it is difficult to obtain multi-point neuroimaging data of the brain in the clinic. In the present study, a rat model of median nerve compression was established by median nerve ligation, i.e., carpal tunnel syndrome model. Sensory cortex remodeling was determined by functional magnetic resonance imaging between normal rats and carpal tunnel syndrome models at 2 weeks and 2 months after operation. Stimulation of bilateral paws by electricity for 30 seconds, alternating with 30 seconds of rest period (repeatedly 3 times), resulted in activation of the contralateral sensorimotor cortex in normal rats. When carpal tunnel syndrome rats received this stimulation, the contralateral cerebral hemisphere was markedly activated at 2 weeks after operation, including the primary motor cortex, cerebellum, and thalamus. Moreover, this activation was not visible at 2 months after operation. These findings suggest that significant remodeling of the cerebral cortex appears at 2 weeks and 2 months after median nerve compression.

Anodal Transcranial Direct Current Stimulation Increases Bilateral Directed Brain Connectivity during Motor-Imagery Based Brain-Computer Interface Control.

Transcranial direct current stimulation (tDCS) has been shown to affect motor and cognitive task performance and learning when applied to brain areas involved in the task. Targeted stimulation has also been found to alter connectivity within the stimulated hemisphere during rest. However, the connectivity effect of the interaction of endogenous task specific activity and targeted stimulation is unclear. This study examined the aftereffects of concurrent anodal high-definition tDCS over the left sensorimotor cortex with motor network connectivity during a one-dimensional EEG based sensorimotor rhythm brain-computer interface (SMR-BCI) task. Directed connectivity following anodal tDCS illustrates altered connections bilaterally between frontal and parietal regions, and these alterations occur in a task specific manner; connections between similar cortical regions are altered differentially during left and right imagination trials. During right-hand imagination following anodal tDCS, there was an increase in outflow from the left premotor cortex (PMC) to multiple regions bilaterally in the motor network and increased inflow to the stimulated sensorimotor cortex from the ipsilateral PMC and contralateral sensorimotor cortex. During left-hand imagination following anodal tDCS, there was increased outflow from the stimulated sensorimotor cortex to regions across the motor network. Significant correlations between connectivity and the behavioral measures of total correct trials and time-to-hit (TTH) correct trials were also found, specifically that the input to the left PMC correlated with decreased right hand imagination performance and that flow from the ipsilateral posterior parietal cortex (PPC) to midline sensorimotor cortex correlated with improved performance for both right and left hand imagination. These results indicate that tDCS interacts with task-specific endogenous activity to alter directed connectivity during SMR-BCI. In order to predict and maximize the targeted effect of tDCS, the interaction of stimulation with the dynamics of endogenous activity needs to be examined comprehensively and understood.

The impact of GABAergic drugs on TMS-induced brain oscillations in human motor cortex

Brain responses to transcranial magnetic stimulation (TMS) as measured with electroencephalography (EEG) have so far been assessed either by TMS-evoked EEG potentials (TEPs), mostly reflecting phase-locked neuronal activity, or time-frequency-representations (TFRs), reflecting oscillatory power arising from a mixture of both evoked (i.e., phase-locked) and induced (i.e., non-phase-locked) responses. Single-pulse TMS of the human primary motor cortex induces a specific pattern of oscillatory changes, characterized by an early (30–200 ms after TMS) synchronization in the α- and β-bands over the stimulated sensorimotor cortex and adjacent lateral frontal cortex, followed by a late (200–400 ms) α- and β-desynchronization over the stimulated and contralateral sensorimotor cortex. As GABAergic inhibition plays an important role in shaping oscillatory brain activity, we sought here to understand if GABAergic inhibition contributes to these TMS-induced oscillations. We tested single oral doses of alprazolam, diazepam, zolpidem (positive modulators of the GABAA receptor), and baclofen (specific GABAB receptor agonist). Diazepam and zolpidem enhanced, and alprazolam tended to enhance while baclofen decreased the early α-synchronization. Alprazolam and baclofen enhanced the early β-synchronization. Baclofen enhanced the late α-desynchronization, and alprazolam, diazepam and baclofen enhanced the late β-desynchronization. The observed GABAergic drug effects on TMS-induced α- and β-band oscillations were not explained by drug-induced changes on corticospinal excitability, muscle response size, or resting-state EEG power. Our results provide first insights into the pharmacological profile of TMS-induced oscillatory responses of motor cortex.

Blood Oxygenation Level-Dependent Functional Magnetic Resonance Imaging in Early Days: Correlation between Passive Activation and Motor Recovery After Unilateral Striatocapsular Cerebral Infarction

This study aimed to investigate the correlation between the functional magnetic resonance imaging (fMRI) pattern and the motor function recovery of an affected limb during the passive movement of the affected limb at an early stage of the striatocapsular infarction (SCI). A total of 17 patients with an acute stage of SCI and 3 healthy volunteers as controls were included in this study. fMRI scans of passive movement were performed on the affected limbs of stroke patients within 1 week of onset. Follow-ups were carried out for the motor functions of the affected limbs (before fMRI scan, 1 month, and 3 months after the scan). The control group showed that the activation was mainly located in the contralateral sensorimotor cortex (SMC) and the bilateral supplementary motor area (SMA). The fMRI scan region of interest for stroke patients can be divided into 3 types: type I includes mainly the affected side, bilateral SMC, and SMA with activation; type II includes SMC on the affected side and SMA with activation; type III includes only SMC on the affected side or M1 with activation. The recovery of type I patients was better and faster, while the recovery of type II patients was better but slower, but recovery of type III patients was poorer and slower. Multiple cortical activation patterns were noted during the passive movement of the affected limbs at an early stage of SCI, and a correlation was found between the different activation patterns and the clinical prognosis of patients.

Autonomic responses to tonic pain are more closely related to stimulus intensity than to pain intensity.

Pain serves the protection of the body by translating noxious stimulus information into a subjective percept and protective responses. Such protective responses rely on autonomic responses that allocate energy resources to protective functions. However, the precise relationship between objective stimulus intensity, subjective pain intensity, autonomic responses, and brain activity is not fully clear yet. Here, we addressed this question by continuously recording pain ratings, skin conductance, heart rate, and electroencephalography during tonic noxious heat stimulation of the hand in 39 healthy human subjects. The results confirmed that pain intensity dissociates from stimulus intensity during 10 minutes of noxious stimulation. Furthermore, skin conductance measures were significantly related to stimulus intensity but not to pain intensity. Correspondingly, skin conductance measures were significantly related to alpha and beta oscillations in contralateral sensorimotor cortex, which have been shown to encode stimulus intensity rather than pain intensity. No significant relationships were found between heart rate and stimulus intensity or pain intensity. The findings were consistent for stimulation of the left and the right hands. These results suggest that sympathetic autonomic responses to noxious stimuli in part directly result from nociceptive rather than from perceptual processes. Beyond, these observations support concepts of pain and emotions in which sensory, motor, and autonomic components are partially independent processes that together shape emotional and painful experiences.

Mapping of the brain hemodynamic responses to sensorimotor stimulation in a rodent model: A BOLD fMRI study.

Blood Oxygenation Level Dependent functional MRI (BOLD fMRI) during electrical paw stimulation has been widely used in studies aimed at the understanding of the somatosensory network in rats. However, despite the well-established anatomical connections between cortical and subcortical structures of the sensorimotor system, most of these functional studies have been concentrated on the cortical effects of sensory electrical stimulation. BOLD fMRI study of the integration of a sensorimotor input across the sensorimotor network requires an appropriate methodology to elicit functional activation in cortical and subcortical areas owing to the regional differences in both neuronal and vascular architectures between these brain regions. Here, using a combination of low level anesthesia, long pulse duration of the electrical stimulation along with improved spatial and temporal signal to noise ratios, we provide a functional description of the main cortical and subcortical structures of the sensorimotor rat brain. With this calibrated fMRI protocol, unilateral non-noxious sensorimotor electrical hindpaw stimulation resulted in robust positive activations in the contralateral sensorimotor cortex and bilaterally in the sensorimotor thalamus nuclei, whereas negative activations were observed bilaterally in the dorsolateral caudate-putamen. These results demonstrate that, once the experimental setup allowing necessary spatial and temporal signal to noise ratios is reached, hemodynamic changes related to neuronal activity, as preserved by the combination of a soft anesthesia with a soft muscle relaxation, can be measured within the sensorimotor network. Moreover, the observed responses suggest that increasing pulse duration of the electrical stimulus adds a proprioceptive component to the sensory input that activates sensorimotor network in the brain, and that these activation patterns are similar to those induced by digits paw’s movements. These findings may find application in fMRI studies of sensorimotor disorders within cortico-basal network in rodents.

Dl-3-n-butylphthalide promotes neuroplasticity and motor recovery in stroke rats

Backgrounds and aimsRacemic l-3-n-butylphthalide (dl-NBP), is able to achieve a functional recovery in animal models of cerebral ischemia, vascular dementia, and Alzheimer’s disease. In this study, we investigated the effect of dl-NBP on axonal growth, neurogenesis and behavioral performances in rats with cerebral ischemia. MethodsFocal cerebral ischemia in rats was produced by intracerebral injection of endothelin-1. Starting from postoperative day 7, the experimental rats were administered 70mg/kg dl-NBP by oral gavage for two weeks. Biotinylated dextran amine (BDA) was injected into the contralateral sensorimotor cortex on day 14 after ischemia to trace the sprouting of corticospinal tract (CST) fibers into the denervated cervical spinal cord. The expressions of Nogo-A, Nogo-R, Rho-A, and ROCK in the perilesional cortex, the expressions of BDA, PSD-95, and vGlut1 in the denervated spinal cord, 5-bromo-20-deoxyuridine (BrdU)/DCX-positive cells in the subventricular zone (SVZ) of the injured hemisphere were detected by immunofluorescence. The rats’ behavioral abilities were measured on postoperative days 30–32 in the beam-walking, cylinder and sticky label tests. Resultsdl-NBP treatment significantly increased the number and length of crossing CST fibers, enhanced significantly the expression levels of synapse-associated proteins including PSD95 and VGlut-1 in the denervated cervical spinal cord, elevated the number of BrdU+/DCX+ cells in SVZ, and reduced markedly those of Rho-A+, ROCK+, Nogo-A+ and Nogo-R+ cells in perilesional cortex. In addition, dl-NBP improved the behavioral performance of the ischemic rats. Conclusiondl-NBP enhanced the behavioral recovery after cerebral ischemia in rats, possibly by increasing axonal growth and neurogenesis.

Magnetic resonance spectroscopy of current hand amputees reveals evidence for neuronal-level changes in former sensorimotor cortex.

Deafferentation is accompanied by large-scale functional reorganization of maps in the primary sensory and motor areas of the hemisphere contralateral to injury. Animal models of deafferentation suggest a variety of cellular-level changes including depression of neuronal metabolism and even neuronal death. Whether similar neuronal changes contribute to patterns of reorganization within the contralateral sensorimotor cortex of chronic human amputees is uncertain. We used functional MRI-guided proton magnetic resonance spectroscopy to test the hypothesis that unilateral deafferentation is associated with lower levels of N-acetylaspartate (NAA, a putative marker of neuronal integrity) in the sensorimotor hand territory located contralateral to the missing hand in chronic amputees (n = 19) compared with the analogous hand territory of age- and sex-matched healthy controls (n = 28). We also tested whether former amputees [i.e., recipients of replanted (n = 3) or transplanted (n = 2) hands] exhibit NAA levels that are indistinguishable from controls, possible evidence for reversal of the effects of deafferentation. As predicted, relative to controls, current amputees exhibited lower levels of NAA that were negatively and significantly correlated with the time after amputation. Contrary to our prediction, NAA levels in both replanted and transplanted patients fell within the range of the current amputees. We suggest that lower levels of NAA in current amputees reflects altered neuronal integrity consequent to chronic deafferentation. Thus local changes in NAA levels may provide a means of assessing neuroplastic changes in deafferented cortex. Results from former amputees suggest that these changes may not be readily reversible through reafferentation.NEW & NOTEWORTHY This study is the first to use functional magnetic resonance-guided magnetic resonance spectroscopy to examine neurochemical mechanisms underlying functional reorganization in the primary somatosensory and motor cortices consequent to upper extremity amputation and its potential reversal through hand replantation or transplantation. We provide evidence for selective alteration of cortical neuronal integrity associated with amputation-related deafferentation that may not be reversible.

The effect of physical fatigue on oscillatory dynamics of the sensorimotor cortex.

While physical fatigue is known to arise in part from supraspinal mechanisms within the brain, exactly how brain activity is modulated during fatigue is not well understood. Therefore, this study examined how typical neural oscillatory responses to voluntary muscle contractions were affected by fatigue. Eleven healthy adults (age 27±4years) completed two experimental sessions in a randomized crossover design. Both sessions first assessed baseline maximal voluntary isometric wrist-flexion force (MVFb ). Participants then performed an identical series of fourteen test contractions (2×100%MVFb , 10×40%MVFb , 2×100%MVFb ) both before and after one of two interventions: forty 12-s contractions at 55%MVFb (fatigue intervention) or 5%MVFb (control intervention). Magnetoencephalography (MEG) was used to characterize both the movement-related mu and beta decrease (MRMD and MRBD) and the post-movement beta rebound (PMBR) within the contralateral sensorimotor cortex during the 40%MVFb test contractions, while the 100%MVFb test contractions were used to monitor physical fatigue. The fatigue intervention induced a substantial physical fatigue that endured throughout the post-intervention measurements (28.9-29.5% decrease in MVF, P<0.001). Fatigue had a significant effect on both PMBR (anova, session×time-point interaction: P=0.018) and MRBD (P=0.021): the magnitude of PMBR increased following the fatigue but not the control interventions, whereas MRBD was decreased post-control but not post-fatigue. Mu oscillations were unchanged throughout both sessions. Physical fatigue resulted in an increased PMBR, and offset attenuations in MRBD associated with task habituation.