Somatosensory Cortical Activity Research Articles

Direct contribution of the sensory cortex to the judgment of stimulus duration

Decision making frequently depends on monitoring the duration of sensory events. To determine whether, and how, the perception of elapsed time derives from the neuronal representation of the stimulus itself, we recorded and optogenetically modulated vibrissal somatosensory cortical activity as male rats judged vibration duration. Perceived duration was dilated by optogenetic excitation. A second set of rats judged vibration intensity; here, optogenetic excitation amplified the intensity percept, demonstrating sensory cortex to be the common gateway both to time and to stimulus feature processing. A model beginning with the membrane currents evoked by vibrissal and optogenetic drive and culminating in the representation of perceived time successfully replicated rats’ choices. Time perception is thus as deeply intermeshed within the sensory processing pathway as is the sense of touch itself, suggesting that the experience of time may be further investigated with the toolbox of sensory coding.

Neural Substrates of Body Ownership and Agency during Voluntary Movement.

Body ownership and the sense of agency are two central aspects of bodily self-consciousness. While multiple neuroimaging studies have investigated the neural correlates of body ownership and agency separately, few studies have investigated the relationship between these two aspects during voluntary movement when such experiences naturally combine. By eliciting the moving rubber hand illusion with active or passive finger movements during functional magnetic resonance imaging, we isolated activations reflecting the sense of body ownership and agency, respectively, as well as their interaction, and assessed their overlap and anatomic segregation. We found that perceived hand ownership was associated with activity in premotor, posterior parietal, and cerebellar regions, whereas the sense of agency over the movements of the hand was related to activity in the dorsal premotor cortex and superior temporal cortex. Moreover, one section of the dorsal premotor cortex showed overlapping activity for ownership and agency, and somatosensory cortical activity reflected the interaction of ownership and agency with higher activity when both agency and ownership were experienced. We further found that activations previously attributed to agency in the left insular cortex and right temporoparietal junction reflected the synchrony or asynchrony of visuoproprioceptive stimuli rather than agency. Collectively, these results reveal the neural bases of agency and ownership during voluntary movement. Although the neural representations of these two experiences are largely distinct, there are interactions and functional neuroanatomical overlap during their combination, which has bearing on theories on bodily self-consciousness.SIGNIFICANCE STATEMENT How does the brain generate the sense of being in control of bodily movement (agency) and the sense that body parts belong to one's body (body ownership)? Using fMRI and a bodily illusion triggered by movement, we found that agency is associated with activity in premotor cortex and temporal cortex, and body ownership with activity in premotor, posterior parietal, and cerebellar regions. The activations reflecting the two sensations were largely distinct, but there was overlap in premotor cortex and an interaction in somatosensory cortex. These findings advance our understanding of the neural bases of and interplay between agency and body ownership during voluntary movement, which has implications for the development of advanced controllable prosthetic limbs that feel like real limbs.

Youth with Cerebral Palsy Display Abnormal Somatosensory Cortical Activity During a Haptic Exploration Task

There are numerous clinical reports that youth with cerebral palsy (CP) have proprioceptive, stereognosis and tactile discrimination deficits. The growing consensus is that the altered perceptions in this population are attributable to aberrant somatosensory cortical activity seen during stimulus processing. It has been inferred from these results that youth with CP likely do not adequately process ongoing sensory feedback during motor performance. However, this conjecture has not been tested. Herein, we address this knowledge gap using magnetoencephalographic (MEG) brain imaging by applying electrical stimulation to the median nerve of youth with CP (N = 15, Age = 15.8 ± 0.83 yrs, Males = 12, MACS levels I-III) and neurotypical (NT) controls (N = 18, Age = 14.1 ± 2.4 yrs, Males = 9) while at rest (i.e., passive) and during a haptic exploration task. The results illustrated that the somatosensory cortical activity was reduced in the group with CP compared to controls during the passive and haptic conditions. Furthermore, the strength of the somatosensory cortical responses during the passive condition were positively associated with the strength of somatosensory cortical responses during the haptic condition (r = 0.75, P = 0.004). This indicates that the aberrant somatosensory cortical responses seen in youth with CP during rest are a good predictor of the extent of somatosensory cortical dysfunction during the performance of motor actions. These data provide novel evidence that aberrations in somatosensory cortical function in youth with CP likely contribute to the difficulties in sensorimotor integration and the ability to effectively plan and execute motor actions.

A Val66Met polymorphism is associated with weaker somatosensory cortical activity in individuals with cerebral palsy

BackgroundThe brain-derived neurotrophic factor (BDNF) protein plays a prominent role in the capacity for neuroplastic change. However, a single nucleotide polymorphism at codon 66 of the BDNF gene results in significant reductions in neuroplastic change. Potentially, this polymorphism also contributes to the weaker somatosensory cortical activity that has been extensively reported in the neuroimaging literature on cerebral palsy (CP). AimsThe primary objective of this study was to use magnetoencephalography (MEG) to probe if BDNF genotype affects the strength of the somatosensory-evoked cortical activity seen within individuals with CP. Methods and proceduresand Procedures: Twenty individuals with CP and eighteen neurotypical controls participated. Standardized low resolution brain electromagnetic tomography (sLORETA) was used to image the somatosensory cortical activity evoked by stimulation of the tibial nerve. BDNF genotypes were determined from saliva samples. Outcomes and resultsThe somatosensory cortical activity was weaker in individuals with CP compared to healthy controls (P = 0.04). The individuals with a Val66Met or Met66Met BDNF polymorphism also showed a reduced response compared to the individuals without the polymorphism (P = 0.03), had higher GMFCS levels (P = 0.04), and decreased walking velocity (P = 0.05). Conclusions and implicationsThese results convey that BDNF genotype influences the strength of the somatosensory activity and mobility in individuals with CP. What this paper addsPrevious literature has extensively documented altered sensorimotor cortical activity in individuals with CP, which ultimately contributes to the clinical deficits in sensorimotor processing documented in this population. While some individuals with CP see vast improvements in their sensorimotor functioning following therapeutic intervention, others are clear non-responders. The underlying basis for this discrepancy is not well understood. Our study is the first to identify that a polymorphism at the gene that codes for brain derived neurotrophic factor (BDNF), a protein well-known to be involved in the capacity for neuroplastic change, may influence the altered sensorimotor cortical activity within this population. Potentially, individuals with CP that have a polymorphism at the BDNF gene may reflect those that have difficulties in achieving beneficial outcomes following intervention. Thus, these individuals may require different therapeutic approaches in order to stimulate neuroplastic change and get similar benefits from therapy as their neurotypical peers.

Aberrant movement-related somatosensory cortical activity mediates the extent of the mobility impairments in persons with cerebral palsy.

There are numerous clinical reports showing that persons with cerebral palsy (CP) have proprioceptive, stereognosis, and tactile discrimination deficits. The current consensus is that these altered perceptions are attributable to aberrant somatosensory cortical activity. It has been inferred from these data that persons with CP do not adequately process ongoing sensory feedback during motor actions, which accentuates the extent of their mobility impairments. However, this hypothesis has yet to be directly tested. We used magnetoencephalographic brain imaging to address this knowledge gap by quantifying the somatosensory dynamics evoked by applying electrical stimulation to the tibial nerve in 22 persons with CP and 25 neurotypical controls at rest and during an ankle plantarflexion isometric force motor task. We also quantified the spatiotemporal gait biomechanics of participants outside the scanner. Consistent with the literature, our results confirmed that the strength of somatosensory cortical activity was weaker in the persons with CP compared to the neurotypical controls. Our results also showed that the strength of the somatosensory cortical responses were significantly weaker during the isometric ankle force task than at rest. Most importantly, our results showed that the strength of somatosensory cortical activity during the ankle plantarflexion force production task mediated the relationship between somatosensory cortical activity at rest and both walking velocity and step length. These results suggest that youth with CP have aberrant somatosensory cortical activity during isometric force generation, which ultimately contributes to the extent of mobility impairments seen in this patient population. KEY POINTS: Persons with cerebral palsy have reduced somatosensory cortical responses at rest and during movement. The somatosensory cortical responses during movement mediate the relationship between the somatosensory cortical responses at rest and mobility. Persons with cerebral palsy may have altered sensorimotor feedback that ultimately contributes to impaired mobility.

Power training alters somatosensory cortical activity of youth with cerebral palsy.

ObjectiveOur prior magnetoencephalographic (MEG) investigations demonstrate that persons with cerebral palsy (CP) have weaker somatosensory cortical activity than neurotypical (NT) controls, which is associated with reduced muscular strength and mobility. Power training can improve lower extremity isokinetic strength, muscular power, and walking performance of youth with CP. Potentially, these clinically relevant improvements are partially driven by changes in somatosensory processing. The objective of this investigation was to determine if power training has complementary changes in muscular function and somatosensory cortical activity in youth with CP.MethodsA cohort of youth with CP (N = 11; age = 15.90 ± 1.1 years) and NT controls (N = 10; Age = 15.93 ± 2.48 years) participated in this investigation. Youth with CP underwent 24 power training sessions. Pre‐post bilateral leg press 1‐repetition maximum (1RM), peak power production, 10‐m walking speed, and distance walked 1‐min were used as outcome measures. MEG neuroimaging assessed the changes in somatosensory cortical activity while at rest. NT controls only underwent a baseline MEG assessment.ResultsYouth with CP had a 56% increase in 1RM (p < 0.001), a 33% increase in peak power production (p = 0.019), and a 4% improvement in 1‐min walk (p = 0.029). Notably, there was a 46% increase in somatosensory cortical activity (p = 0.02).InterpretationThese results are the first to show that power training is associated with improvements in muscular function, walking performance, and the resting somatosensory cortical activity in individuals with CP. This treatment approach might be advantageous due to the potential to promote cortical and muscular plasticity, which appear to have carryover effects for improved walking performance.

Youth with Cerebral Palsy Display Abnormal Somatosensory Cortical Activity During a Haptic Exploration Task

Youth with Cerebral Palsy Display Abnormal Somatosensory Cortical Activity During a Haptic Exploration Task

Altered Somatosensory Cortical Activity Is Associated with Cortical Thickness in Adults with Cerebral Palsy: Multimodal Evidence from MEG/sMRI.

Somatosensory cortical activity is altered in individuals with cerebral palsy (CP). However, previous studies have focused on the lower extremities in children with CP and have given less attention to structural changes that may contribute to these alterations. We used a multimodal neuroimaging approach to investigate the relationship between somatosensory cortical activity and cortical thickness in 17 adults with CP (age = 32.8 ± 9.3years) and 18 healthy adult controls (age = 30.7 ± 9.8years). Participants performed a median nerve paired-pulse stimulation paradigm while undergoing magnetoencephalography (MEG) to investigate somatosensory cortical activity and sensory gating. Participants also underwent magnetic resonance imaging to evaluate cortical thickness within the area of the somatosensory cortex that generated the MEG response. We found that the somatosensory responses were attenuated in the adults with CP (P = 0.004). The adults with CP also hypergated the second stimulation (P = 0.030) and had decreased cortical thickness in the somatosensory cortex (P = 0.015). Finally, the strength of the somatosensory response was significantly correlated with the cortical thickness (P = 0.023). These findings demonstrate that the aberrant somatosensory cortical activity in adults with CP extends to the upper extremities and appears to be related to cortical thickness.

The somatosensory cortical activity in individuals with cerebral palsy displays an aberrant developmental trajectory.

Individuals with cerebral palsy (CP) have a reduced somatosensory cortical response Somatosensory cortical response strength decreases from adolescence to early adulthood Somatosensory cortical responses in youth with CP are similar to adult controls Individuals with CP may have aberrant maturation of the somatosensory system ABSTRACT: Numerous studies have documented tactile and proprioceptive deficits in children with cerebral palsy (CP) and linked these with weaker somatosensory cortical activity. However, whether such aberrations in somatosensory processing extend and/or progress into adulthood remains poorly understood. In the current study, we used magnetoencephalography (MEG) to investigate the primary somatosensory responses in a sample of individuals with CP (N=42; age=9-28years) and a cohort of healthy controls (N=23; age range=11-23years). Briefly, transient electrical stimulation was applied to the right tibial nerve, and standardized low-resolution brain electromagnetic tomography (sLORETA) was used to image the dynamic somatosensory cortical response. We found that the strength of somatosensory cortical activity within the 112-252ms time window was significantly reduced in the individuals with CP compared with the healthy controls (HC=286.53±30.51, 95% CI [226.74, 346.32]; CP=208.30±19.66,CI [169.77, 246.83], P=0.0126). These results corroborate previous findings of aberrant somatosensory cortical activity in individuals with CP. Our results also suggest that the somatosensory cortical activity tends to become weaker with age, with a similar rate of neurophysiological change in individuals with CP and healthy controls (P=0.8790). Visualization of regression models fitted to the data imply that youth with CP may have somatosensory cortical activity similar to adult controls. These findings suggest that some individuals with CP exhibit an aberrant developmental trajectory of their somatosensory system.

Effect of mild traumatic brain injury on spontaneous activity of rat primary somatosensory cortex and its responsivity to vibrotactile stimulation

While it has been previously demonstrated that concussion severity can be assessed using sensory tests of cortical functionality, the underlying neural mechanisms affected by concussion are still poorly understood. By using an animal model, it is possible to directly observe the neurophysiological effects of concussion, and thus shed light on the underlying changes in cortical functionality. In order to assess the effects of a single concussion, we recorded spike discharge activity of neurons in the rat primary somatosensory cortex prior to as well as 6-12hr and 78-86hr after a mild weight-drop impact-acceleration closed-head trauma. During the 6-12hr post-impact period, cortical spontaneous activity was elevated by 40% compared to the healthy control state, but its responsivity to vibrotactile stimulation was not significantly affected. However, the responsivity to vibrotactile stimulation did decline in the 78-86hr post-impact period. Also during this period, spontaneous activity in the middle and upper cortical layers was reduced by 35% below the healthy control state, but it remained high in the deep layers. We also recorded somatosensory cortical activity 6-12hr after delivering a second head trauma, identical to the one delivered 72hr prior. Although the two impacts mechanically were the same, the neurophysiological effect of the second impact was very different from that observed after the first impact: both the stimulus-evoked response and spontaneous activity were significantly reduced as compared to the same time period after the first impact. These findings demonstrate that mTBI alters the functional state of the somatosensory cortex in a post-injury time-dependent manner.

Gamma somatosensory cortical oscillations are attenuated during the stance phase of human walking

It is well appreciated that processing of peripheral feedback by the somatosensory cortices plays a prominent role in the control of human motor actions like walking. However, very few studies have actually quantified the somatosensory cortical activity during walking. In this investigation, we used electroencephalography (EEG) and beamforming source reconstruction methods to quantify the frequency specific neural oscillations that are induced by an electrical stimulation that is applied to the right tibial nerve under the following experimental conditions: 1) sitting, 2) standing in place, and 3) treadmill walking. Our experimental results revealed that the peripheral stimulation induced a transient increase in theta-alpha (4−12 Hz; 50−350 ms) and gamma (40−80 Hz; 40−100 ms) activity in the leg region of the contralateral somatosensory cortices. The strength of the gamma oscillations were similar while sitting and standing, but were markedly attenuated while walking. Conversely, the strength of the theta-alpha oscillations were not different across the respective experimental conditions. Prior research suggests the afferent feedback from the Ia sensory fibers are likely attenuated during walking, while afferent feedback from the β polysynaptic sensory fibers are not. We suggest that the attenuated gamma oscillations seen during walking reflect the gating of the Ia afferents, while the similarity of theta-alpha oscillations across the experimental conditions is associated with the afferent information from the type II (Aα and β) polysynaptic sensory fibers.

The metabotropic glutamate receptor subtype 1 regulates development and maintenance of lemniscal synaptic connectivity in the somatosensory thalamus.

The metabotropic glutamate receptor subtype 1 (mGluR1) is a major subtype of group I mGluRs, which contributes to the development and plasticity of synapses in the brain. In the sensory thalamus, the thalamocortical neuron receives sensory afferents and massive feedback input from corticothalamic (CT) fibers. Notably, mGluR1 is more concentrated in CT synapses in the sensory thalamus. In the visual thalamus, mGluR1 maintains mature afferent synaptic connectivity. However, it is unknown whether mGluR1 contributes to strengthening of immature synapses or weakening of excess synapses during development and whether mGluR1 at CT synapses heterosynaptically regulates the development or refinement of afferent synapses. Here we investigated the effects of knocking out the gene encoding mGluR1 or pharmacologically blocking cortical activity on the development and maintenance of lemniscal synapses, i.e., the somatosensory afferent synapses, in the ventral posteromedial somatosensory thalamus. mGluR1-knockout (KO) mice exhibited delayed developmental strengthening as well as incomplete elimination and remodeling after maturation of lemniscal synapses. Similar to the phenotypes exhibited by mGluR1-KO mice, pharmacological blockade of somatosensory cortical activity from P12 or P21 for 1 week in wild-type mice perturbed elimination or maintenance of lemniscal synapses, respectively. The same manipulation in mGluR1-KO mice failed to induce additional abnormalities in lemniscal synaptic connectivity. These results suggest that activation of mGluR1, driven by CT input, regulates multiple stages of the development of lemniscal synapses, including strengthening, refinement, and maintenance in the somatosensory thalamus.

Somatosensory cortical representation of the body size.

The knowledge of the size of our own body parts is essential for accurately moving in space and efficiently interact with objects. A distorted perceptual representation of the body size often represents a core diagnostic criterion for some psychopathological conditions. The metric representation of the body was shown to depend on somatosensory afferences: local deafferentation indeed causes a perceptual distortion of the size of the anesthetized body part. A specular effect can be induced by altering the cortical map of body parts in the primary somatosensory cortex. Indeed, the present study demonstrates, in healthy adult participants, that repetitive Transcranial Magnetic Stimulation to the somatosensory cortical map of the hand in both hemispheres causes a perceptual distortion (i.e., an overestimation) of the size of the participants' own hand (Experiments 1-3), which does not involve other body parts (i.e., the foot, Experiment 2). Instead, the stimulation of the inferior parietal lobule of both hemispheres does not affect the perception of the own body size (Experiment 4). These results highlight the role of the primary somatosensory cortex in the building up and updating of the metric of body parts: somatosensory cortical activity not only shapes our somatosensation, it also affects how we perceive the dimension of our body.

Functional neural mechanisms of sensory phenomena in obsessive-compulsive disorder

Sensory phenomena (SP) are aversive or uncomfortable sensations that accompany and/or drive repetitive behaviors in obsessive-compulsive disorder (OCD). Although SP are associated with significant distress and may respond less well to standard treatments than harm-related obsessions, little is known about their underlying neurobiology. The present study used functional magnetic resonance imaging (fMRI) to measure brain functioning related to severity of SP during a “body-focused” videos task designed to elicit activation in sensorimotor brain regions. Regression analysis examined the relationship between severity of SP and activation during task using permutation analysis, cluster-level corrected for multiple comparisons (family-wise error rate p < 0.05). The distribution of SP severity was not significantly different from normal, with both high- and low-severity scores represented in the OCD sample. Severity of SP was not correlated with other clinical symptoms in OCD including general anxiety, depression, or harm avoidance. When viewing body-focused videos, patients with greater severity of SP showed increased activity in the mid-posterior insula, a relationship that remained significant when controlling for other clinical symptoms, medication status, and comorbidities. At uncorrected thresholds, SP severity was also positively related to somatosensory, mid orbitofrontal, and lateral prefrontal cortical activity. These data suggest that SP in OCD are dissociable from other symptoms in the disorder and related to hyperactivation of the insula. Future work examining neural mechanisms of SP across different disorders (tics, trichotillomania) as well as with other imaging modalities will be needed to further understand the neurobiology of these impairing symptoms.

Neuroplastic changes in anterior cruciate ligament reconstruction patients from neuromechanical decoupling.

The purpose of this study was to identify how the brain simultaneously perceives proprioceptive input during joint loading in anterior cruciate ligament reconstruction (ACLR) patients, when compared to healthy controls. Seventeen ACLR patients (ACLR) and seventeen controls (CONT) were tested for the somatosensory cortical activation using electroencephalography (EEG) while measuring knee laxity using a knee arthrometer. The relationship between cortical activation and joint laxity within group was also examined. The ACLR patients had increased cortical activation (36.4%±11.5%) in the somatosensory cortex during early loading (ERD1) to the injured limb compared to the CONT's matched limb (25.3%±13.2%, P=0.013) as well as compared to the noninjured limb (25.1%±14.2%, P=0.001). Higher somatosensory cortical activity during midloading (ERD2) to the ACLR knee positively correlated with knee laxity (mm) during early loading (LAX1, r=0.530), midloading (LAX2, r=0.506), total anterior loading (LAXA, r=0.543), and total antero-posterior loading (LAXT, r=0.501), while the noninjured limb revealed negative correlations between ERD1 and LAXA (r=-0.534) as well as between ERD2 and LAX2 (r=-0.565). ACLR patients demonstrate greater brain activation during joint loading in the injured knees when compared to healthy controls' matched knees as well as contralateral healthy knees, while the CONT group shows similar brain activation patterns during joint loading between limbs. These different neural activation strategies may indicate neuromechanical decoupling following an ACL reconstruction and evidence of altered sensorimotor perception and control of the knee (neuroplasticity), which may be critical to address after surgery for optimal neuromuscular control and patients' outcomes.

Children with cerebral palsy display abnormal somatosensory cortical activity during a haptic exploration task

Children with cerebral palsy display abnormal somatosensory cortical activity during a haptic exploration task

Movement-Related Somatosensory Activity Is Altered in Patients with Multiple Sclerosis.

During active movement the somatosensory cortical responses are often attenuated. This attenuation is referred to as movement-related sensory gating. It is well known that patients with multiple sclerosis (MS) have sensory processing deficits, and recent work has also suggested that these patients display impaired motor control of the ankle musculature. The primary goal of the current study was to: (1) examine the movement-related somatosensory gating in patients with MS and demographically-matched controls, and (2) identify the relationship between the sensory gating and motor control of the ankle musculature. To this end, we used magnetoencephalography brain imaging to assess the neural responses to a tibial nerve electrical stimulation that was applied at rest (passive) and during an ankle plantarflexion motor task (active condition). All participants also completed an ankle isometric motor control task that was performed outside the scanner. Our results indicated that the controls, but not patients with MS, exhibited significantly reduced somatosensory responses during the active relative to passive conditions, and that patients with MS had stronger responses compared with controls during the active condition. Additionally, control of the ankle musculature was related to the extent of movement-related sensory attenuation, with poor motor control being associated with reduced gating. Overall, these results show that patients with MS do not attenuate the somatosensory cortical activity during motor actions, and that the inability to modulate somatosensory cortical activity is partially related to the poor ankle motor control seen in these patients.

Empathic Care and Distress: Predictive Brain Markers and Dissociable Brain Systems

Encountering another's suffering can elicit both empathic distress and empathic care-the warm desire to affiliate. It remains unclear whether these two feelings can be accurately and differentially predicted from neural activity and to what extent their neural substrates can be distinguished. We developed fMRI markers predicting moment-by-moment intensity levels of care and distress intensity while participants (n= 66) listened to true biographies describing human suffering. Both markers' predictions correlated strongly with self-report in out-of-sample participants (r= 0.59 and r= 0.63, p<0.00001), and both markers predicted later trial-by-trial charitable donation amounts (p< 0.05). Empathic care was preferentially associated with nucleus accumbens and medial orbitofrontal cortex activity, whereas distress was preferentially associated with premotor and somatosensory cortical activity. In tests of marker specificity with an independent behavioral sample (n= 200), the empathic care marker was associated with a mixed-valence feeling state, whereas the empathic distress marker was specific to negative emotion.

Altered Brain Activity During Joint Loading After Anterior Cruciate Ligament Reconstruction

Following an anterior cruciate ligament rupture, many patients that undergo surgical intervention (ACLR) fail to return to pre-injury levels of physical activity due to repetitive “giving-way” episodes. This functional joint instability may result from an insufficient neural processing responsible for neuromechanical links between the ACL and central nervous system. It remains unclear how the brain of the ACLR patients perceives mechanical loading compared with healthy controls. PURPOSE: To examine brain activity differences between ACLR patients and healthy controls during knee loading. METHODS: Seventeen healthy control (CON: 26.9±5.6yrs, 69.6±1.2kg, 166.3±7.7cm) and seventeen ACLR patients (ACLR: 22.29±3.8yrs, 67.8±18.7kg, 164.5±10.4cm) volunteered. Somatosensory cortical activity was measured using event-related desynchronization (ERD: % decreased power; ERD1, ERD2, ERD3) from electroencephalography (EEG) during each second of an anterior knee loading (3sec) at constant force (45N/sec). Comparisons were made using 2-way ANOVAs with one within factor (limb, 2 levels) and one between factor (group, 2 levels). RESULTS: A significant limb by group interaction was observed for ERD1 (F[1,32] = 8.280, p = .007). The reconstructed knee in the ACLR showed greater increased cortical activity than the matched limb in the CON (36.4±11.5 vs. 25.3±13.2%, p = .013), while the uninjured knee in the ACLR was similar to the CON’s matched limb (25.1±14.2 vs. 28.0±11.5%, p = .506). Additionally, the ACLR showed greater increased ERD1 in the reconstructed limb when compared to the uninjured limb (36.4±11.5 vs. 25.1±14.2%, p = .006). No significant interactions or main effects were observed for ERD2 and ERD3. CONCLUSION: Following an ACL rupture, the injured leg exhibits increased brain responses during early loading compared to the uninjured knee, as well as the matched limb of healthy controls. This may indicate protective neural adaptation in the brain to compensate the altered proprioceptive input from the injured knee, such that reorganized somatosensory cortex activity can optimize neuromuscular control needed for maintaining functional joint stability. Future studies should explore whether this neural adaptation improves joint health and junction after an ACL injury.

Pulse-train Stimulation of Primary Somatosensory Cortex Blocks Pain Perception in Tail Clip Test.

Human studies of brain stimulation have demonstrated modulatory effects on the perception of pain. However, whether the primary somatosensory cortical activity is associated with antinociceptive responses remains unknown. Therefore, we examined the antinociceptive effects of neuronal activity evoked by optogenetic stimulation of primary somatosensory cortex. Optogenetic transgenic mice were subjected to continuous or pulse-train optogenetic stimulation of the primary somatosensory cortex at frequencies of 15, 30, and 40 Hz, during a tail clip test. Reaction time was measured using a digital high-speed video camera. Pulse-train optogenetic stimulation of primary somatosensory cortex showed a delayed pain response with respect to a tail clip, whereas no significant change in reaction time was observed with continuous stimulation. In response to the pulse-train stimulation, video monitoring and local field potential recording revealed associated paw movement and sensorimotor rhythms, respectively. Our results show that optogenetic stimulation of primary somatosensory cortex at beta and gamma frequencies blocks transmission of pain signals in tail clip test.