Ipsilateral S1 Research Articles

FMRI Activation in Sensorimotor Regions at 6 Weeks After Anterior Cruciate Ligament Reconstruction.

Brain activity during knee movements is altered throughout the sensorimotor network after anterior cruciate ligament reconstruction (ACLR). Patients at 2 to 5 years after surgery appear to require greater neural activity to perform basic knee movement patterns, but it is unclear if brain activity differences within sensorimotor regions are present early after surgery. It is also unknown whether uninvolved knee movements elicit similar or unique activity compared with involved knee movements. To examine brain activity in sensorimotor regions during involved and uninvolved knee movements in patients at 6 weeks after ACLR compared with control participants. Cohort study; Level of evidence, 2. A total of 15 patients who underwent ACLR (mean age, 21.9 ± 4.3 years [range, 17-29 years]; 8 female) and 15 control participants performed 30-second blocks of repeated knee flexion and extension, followed by 30 seconds of rest, during functional magnetic resonance imaging. Regions of interest included the right and left primary motor cortex (M1), right and left primary somatosensory cortex (S1), supplementary motor area (SMA), precuneus, and lingual gyrus. Activity from task-relevant voxels (move > rest) was extracted, and generalized estimating equations evaluated the main effect of group and group-by-limb interaction. Effect sizes were calculated using the Cohen d. Reduced brain activity during knee flexion and extension was observed in the ACLR group in the ipsilateral M1 and S1, contralateral S1, SMA, and precuneus during movements of the involved and uninvolved knees. There were no group-by-limb interaction effects, indicating no significant differences between the involved knee and uninvolved knee in the ACLR group. Medium to large effect sizes were identified for between-group differences in all regions. At 6 weeks after ACLR, patients exhibited bilateral reductions in brain activity during knee movements in multiple sensorimotor regions. These identified regions are associated with motor planning, motor execution, somatosensory function, and sensorimotor integration. These data indicate that ACLR affected sensorimotor brain activity in both limbs during the early postoperative phase of rehabilitation.

Cortical response characteristics of passive, active, and resistance movements: a multi-channel fNRIS study.

This study aimed to explore the impact of exercise training modes on sensory and motor-related cortex excitability using functional near-infrared spectroscopy technology (fNIRS) and reveal specific cortical effects. Twenty participants with no known health conditions took part in a study involving passive, active, and resistance tasks facilitated by an upper-limb robot, using a block design. The participants wore functional near-infrared spectroscopy (fNIRS) devices throughout the experiment to monitor changes in cortical blood oxygen levels during the tasks. The fNIRS optode coverage primarily targeted key areas of the brain cortex, including the primary motor cortex (M1), primary somatosensory cortex (S1), supplementary motor area (SMA), and premotor cortex (PMC) on both hemispheres. The study evaluated cortical activation areas, intensity, and lateralization values. Passive movement primarily activates M1 and part of S1, while active movement mainly activates contralateral M1 and S1. Resistance training activates brain regions in both hemispheres, including contralateral M1, S1, SMA, and PMC, as well as ipsilateral M1, S1, SMA, and PMC. Resistance movement also activates the ipsilateral sensorimotor cortex (S1, SMA, PMC) more than active or passive movement. Active movement has higher contralateral activation in M1 compared to passive movement. Resistance and active movements increase brain activity more than passive movement. Different movements activate various cortical areas equally on both sides, but lateralization differs. The correlation between lateralization of brain regions is significant in the right cortex but not in the left cortex during three movement patterns. All types of exercise boost motor cortex excitability, but resistance exercise activates both sides of the motor cortex more extensively. The PMC is crucial for intense workouts. The right cortex shows better coordination during motor tasks than the left. fNIRS findings can help determine the length of treatment sessions.

Reduction in calcium responses to whisker stimulation in the primary somatosensory and motor cortices of the model mouse with trigeminal neuropathic pain

ObjectiveChronic constriction injury (CCI) of the infraorbital nerve induces neuropathic pain, such as allodynia and hyperalgesia, in the orofacial area. However, the changes in the local circuits of the central nervous system following CCI remain unclear. This study aimed to identify the changes following CCI in Thy1-GCaMP6s transgenic mice. MethodsNeural activity in the primary somatosensory cortex (S1) and motor cortex (M1) following whisker stimulation was assessed using in vivo Ca2+ imaging. CCI-induced changes in responses were analyzed. ResultsBefore CCI, whisker stimulation induced a greater Ca2+ response in the contralateral S1 than in the ipsilateral S1 and contralateral M1. The peak Ca2+ response amplitude in the bilateral S1 and contralateral M1 decreased two days after CCI compared to before CCI. Decreased Ca2+ response amplitude in these regions was observed until four days after CCI. Seven days after CCI, the Ca2+ response amplitude in the contralateral S1 decreased, whereas that in the ipsilateral S1 and contralateral M1 recovered to control levels. ConclusionThese results suggest that neural activity in regions receiving excitatory inputs via corticocortical pathways recovers earlier than in regions receiving thalamocortical inputs. (185/250 words)

Human orbitofrontal cortex signals decision outcomes to sensory cortex during behavioral adaptations

The ability to respond flexibly to an ever-changing environment relies on the orbitofrontal cortex (OFC). However, how the OFC associates sensory information with predicted outcomes to enable flexible sensory learning in humans remains elusive. Here, we combine a probabilistic tactile reversal learning task with functional magnetic resonance imaging (fMRI) to investigate how lateral OFC (lOFC) interacts with the primary somatosensory cortex (S1) to guide flexible tactile learning in humans. fMRI results reveal that lOFC and S1 exhibit distinct task-dependent engagement: while the lOFC responds transiently to unexpected outcomes immediately following reversals, S1 is persistently engaged during re-learning. Unlike the contralateral stimulus-selective S1, activity in ipsilateral S1 mirrors the outcomes of behavior during re-learning, closely related to top-down signals from lOFC. These findings suggest that lOFC contributes to teaching signals to dynamically update representations in sensory areas, which implement computations critical for adaptive behavior.

Electroacupuncture Induces Bilateral S1 and ACC Epigenetic Regulation of Genes in a Mouse Model of Neuropathic Pain

Clinical and animal studies have shown that acupuncture may benefit controlling neuropathic pain. However, the underlying molecular mechanisms are poorly understood. In a well-established mouse unilateral tibial nerve injury (TNI) model, we confirmed the efficacy of electroacupuncture (EA) in reducing mechanical allodynia and measured methylation and hydroxy-methylation levels in the primary somatosensory cortex (S1) and anterior cingulate cortex (ACC), two cortical regions critically involved in pain processing. TNI resulted in increased DNA methylation of both the contra- and ipsilateral S1, while EA only reduced contralateral S1 methylation. RNA sequencing of the S1 and ACC identified differentially expressed genes related to energy metabolism, inflammation, synapse function, and neural plasticity and repair. One week of daily EA decreased or increased the majority of up- or downregulated genes, respectively, in both cortical regions. Validations of two greatly regulated genes with immunofluorescent staining revealed an increased expression of gephyrin in the ipsilateral S1 after TNI was decreased by EA; while TNI-induced increases in Tomm20, a biomarker of mitochondria, in the contralateral ACC were further enhanced after EA. We concluded that neuropathic pain is associated with differential epigenetic regulations of gene expression in the ACC and S1 and that the analgesic effect of EA may involve regulating cortical gene expression.

P 65 Functional adaptations of the sensorimotor cortex in degenerative cervical myelopathy

Objective: Degenerative Cervical Myelopathy (DCM) shows growing prevalence in industrial nations. However, the surgical decision-making is still challenging due to the lack of sufficiently reliable predictors of disease progression and surgical outcome. Neither the interplay of involved pathomechanisms, nor the effect on neural networks within the central nervous system has been investigated sufficiently, yet. Recently, the compensatory potential of reorganization processes within the cerebrospinal motor network has been discussed (Zdunczyk et al., 2018). Somatosensory impairment as an early but often overlooked symptom of DCM, however, was not in the main focus of research so far. Therefore, we investigated how not only the motor, but also the primary and secondary somatosensory cortex (S1 & S2) adapt in DCM. Methods: A cohort of 18 right-handed participants, consisting of 9 DCM patients (age 56 ± 12 years, 7 male, mean JOA score 13.3 ± 2.3) and 9 age- and gender-matched healthy control subjects (age 57 ± 12 years, 7 male) underwent a fMRI (3T) session using a block design. DCM patients were assessed before and 3 months after surgical decompression. The fMRI procedure consisted i.a. of alternating, passive somatosensory stimulation of the subjects' hands and feet by means of a felt stick. Using MATLAB® 2019a and the SPM12 software package, a ROI-wise analysis of BOLD-response was performed at the group level using a three-way ANOVA, including the factors “group” (patients/controls), “limb” (hand/foot) and “side” (left/right). Results : In both, patients and controls, we found a strongly left-lateralized cortical response in S1 and S2 (p≤0.05, FWE-corrected) regarding the somatosensory stimulation of the right (dominant) hand. However, activation in patients was lower than in healthy control subjects (p≤0.001, uncorrected). Regarding the other task conditions, controls showed significant responses within the somatosensory cortex (p≤0.05, FWE-corrected), including a consistent activation within the ipsilateral S2. In contrast, patients showed only weak activation in S1 (p≤0.001, uncorrected) and a much scarcer involvement of ipsilateral areas. Discussion: Our results imply that DCM patients show reduced cortical responsiveness to peripheral stimuli. The cortical somatosensory representation of the right (preferred) hand seems to be more robust to deviations due to DCM than the representations of the other tested limbs. It remains to be investigated whether clinical impairment is correlated with cortical somatosensory responsiveness and if the alterations outlined above are reversible after surgical decompression. References Zdunczyk A, Schwarzer V, Mikhailov M, Bagley B, Rosenstock T, Picht T, Vajkoczy P. The Corticospinal Reserve Capacity: Reorganization of Motor Area and Excitability As a Novel Pathophysiological Concept in Cervical Myelopathy. Neurosurgery. 2018 Oct 1;83(4):810-818. doi: 10.1093/neuros/nyx437. PMID: 29165642.

FV 9. How Degenerative Cervical Myelopathy Affects the Functional Imaging Correlates of the Somatosensory Cortex

Question. Degenerative Cervical Myelopathy (DCM) shows growing prevalence in industrial nations due to the demographic development. Nevertheless, the surgical decision-making is still challenging due to the lack of sufficiently reliable predictors of disease progression and surgical outcome. Neither the interplay of involved pathomechanisms, nor the definite effect on neural networks within the central nervous system has been investigated sufficiently, yet. Recently, the compensatory potential of reorganization processes within the cerebrospinal motor network has been discussed. Somatosensory impairment as an early but often overlooked symptom of DCM, however, was not in the main focus of research so far. We, therefore, investigated how the primary and secondary somatosensory cortex (S1 & S2) adapt in DCM. Methods. A cohort of 18 right-handed participants, consisting of 9 DCM patients (age 56 ± 12 years, 7 male, mean JOA score 13.3 ± 2.3) and 9 age- and gender-matched healthy control subjects (age 57 ± 12 years, 7 male) underwent an fMRI (3T) session using a block design. The fMRI procedure consisted of alternating, passive somatosensory stimulation of the subjects' hands and feet by means of a felt stick. Using MATLAB® 2019a and the SPM12 software package, a ROI-wise analysis of BOLD-response was performed at the group level using a three-way ANOVA, including the factors “group” (patients/controls), “limb” (hand/foot) and “side” (left/right). Results. In both, patients and controls, we found a strongly left-lateralized cortical response in S1 and S2 (p ≤ 0.05, FWE-corrected) regarding the somatosensory stimulation of the right (dominant) hand. However, activation in patients was lower than in healthy control subjects (p≤0.001, uncorrected). Regarding the other task conditions, controls showed significant responses within the somatosensory cortex (p ≤ 0.05, FWE-corrected), including a consistent activation within the ipsilateral S2. In contrast, patients showed only weak activation in S1 (p ≤ 0.001, uncorrected) and a much scarcer involvement of ipsilateral areas. Conclusions. Our results imply that DCM patients show reduced cortical responsiveness to peripheral stimuli. The cortical somatosensory representation of the right (preferred) hand seems to be more robust to deviations due to DCM than the representations of the other tested limbs. It remains to be investigated whether clinical impairment is correlated with cortical somatosensory responsiveness and if the alterations outlined above are reversible after surgical decompression.

Aberrant central plasticity underlying synchronous sensory phenomena in brachial plexus injuries after contralateral cervical seventh nerve transfer.

BackgroundsContralateral cervical seventh (C7) nerve transfer aids motor and sensory recovery in total brachial plexus avulsion injuries (TBPI), but synchronous sensation often persists postoperatively. The mechanism underlying synchronous sensory phenomena remain largely unknown.ObjectiveTo investigate the role of central plasticity in sensory recovery after contralateral C7 nerve transfer.MethodsSixteen right TBPI patients who received contralateral C7 nerve transfer for more than 2 years were included. Sensory evaluations included Semmes–Weinstein monofilament assessment (SWM), synchronous sensation test, and sensory evoked action potential (SNAP) test. Smaller value in the SWM assessment and larger amplitude of SNAP indicates better tactile sensory. Functional magnetic resonance imaging was performed while stimulations delivered to each hand separately in block‐design trials for central plasticity analysis.ResultsThe SWM value of the injured right hand was increased compared with the healthy left side (difference: 1.76, 95% confidence interval: 1.37–2.15, p < .001), and all 16 patients developed synchronous sensation. In functional magnetic resonance imaging analysis, sensory representative areas of the injured right hand were located in its ipsilateral S1, and 23.4% of this area overlapped with the representative area of the left hand. The ratio of overlap for each patient was significantly correlated with SWM value and SNAP amplitude of the right hand.ConclusionThe tactile sensory functioning of the injured hand was dominated by its ipsilateral SI in long‐term observation, and its representative area largely overlapped with the representative area of the intact hand, which possibly reflected a key mechanism of synchronous sensation in patients with TBPI after contralateral C7 transfer.

Secondary somatosensory area is involved in vibrotactile temporal-structure processing: MEG analysis of slow cortical potential shifts in humans

Purpose: Temporal-structure discrimination is an essential dimension of tactile processing. Exploring object surface by touch generates vibrotactile input with various temporal dynamics, which gives diversity to tactile percepts. Here, we examined whether slow cortical potential shifts (SCPs) (<1 Hz) evoked by long vibrotactile stimuli can reflect active temporal-structure processing.Materials and methods: Vibrotactile-evoked magnetic brain responses were recorded in 10 right-handed healthy volunteers using a piezoelectric-based stimulator and whole-head magnetoencephalography. A series of vibrotactile train stimuli with various temporal structures were delivered to the right index finger. While all trains consisted of identical number (15) of stimuli delivered within a fixed duration (1500 ms), temporal structures were varied by modulating inter-stimulus intervals (ISIs). Participants judged regularity/irregularity of ISI for each train in the active condition, whereas they ignored the stimuli while performing a visual distraction task in the passive condition. We analysed the spatiotemporal features of SCPs and their behaviour using the minimum norm estimates with the dynamic statistical parametric mapping.Results: SCPs were localized to contralateral primary somatosensory area (S1), contralateral superior temporal gyrus, and contralateral as well as ipsilateral secondary somatosensory areas (S2). A significant enhancement of SCPs was observed in the ipsilateral S2 (S2i) in the active condition, whereas such effects were absent in the other regions. We also found a significant larger amplitude difference between the regular- and irregular-stimulus evoked S2i responses during the active condition than during the passive condition.Conclusions: This study suggests that S2 subserves the temporal dimension of vibrotactile processing.

Ipsilateral S2 nerve root transfer to pudendal nerve for restoration of external anal and urethral sphincter function: an anatomical study

Patients suffer bilateral sacral plexus injuries experience severe problems with incontinence. We performed a cadaveric study to explore the anatomical feasibility of transferring ipsilateral S2 nerve root combined with a sural nerve graft to pudendal nerve for restoration of external anal and urethral sphincter function. The sacral nerve roots and pudendal nerve roots on the right side were exposed in 10 cadavers. The length from S2 nerve root origin to pudendal nerve at inferior border of piriformis was measured. The sural nerve was used as nerve graft. The diameters and nerve cross-sectional areas of S2 nerve root, pudendal nerve and sural nerve were measured and calculated, so as the number of myelinated axons of three nerves on each cadaver specimen. The length from S2 nerve root to pudendal nerve was 10.69 ± 1.67 cm. The cross-sectional areas of the three nerves were 8.57 ± 3.03 mm2 for S2, 7.02 ± 2.04 mm2 for pudendal nerve and 6.33 ± 1.61 mm2 for sural nerve. The pudendal nerve contained approximately the same number of axons (5708 ± 1143) as the sural nerve (5607 ± 1305), which was a bit less than that of the S2 nerve root (6005 ± 1479). The S2 nerve root in combination with a sural nerve graft is surgically feasible to transfer to the pudendal nerve for return of external urethral and anal sphincter function, and may be suitable for clinical application in patients suffering from incontinence following sacral plexus injuries.

Effects of thalamic infarction on the structural and functional connectivity of the ipsilesional primary somatosensory cortex.

To identify regions causally influenced by thalamic stroke by measuring white matter integrity, cortical volume, and functional connectivity (FC) among patients with thalamic infarction (TI) and to determine the association between structural/functional alteration and somatosensory dysfunction. Thirty-one cases with TI-induced somatosensory dysfunction and 32 healthy controls underwent magnetic resonance imaging scanning. We reconstructed the ipsilesional central thalamic radiation (CTR) and assessed its integrity using fractional anisotropy (FA), assessed S1 ipsilesional changes with cortical volume, and identified brain regions functionally connected to TI locations and regions without TI to examine the potential effects on somatosensory symptoms. Compared with controls, TI patients showed decreased FA (F = 17.626, p < 0.001) in the ipsilesional CTR. TI patients exhibited significantly decreased cortical volume in the ipsilesional top S1. Both affected CTR (r = 0.460, p = 0.012) and S1 volume (r = 0.375, p = 0.049) were positively correlated with somatosensory impairment in TI patients. In controls, the TI region was highly functionally connected to atrophic top S1 and less connected to the adjacent middle S1 region in FC mapping. However, T1 patients demonstrated significantly increased FC between the ipsilesional thalamus and middle S1 area, which was adjacent to the atrophic S1 region. TI induces remote changes in the S1, and this network of abnormality underlies the cause of the sensory deficits. However, our other finding that there is stronger connectivity in pathways adjacent to the damaged ones is likely responsible for at least some of the recovery of function. • TI led to secondary impairment in the CTR and cortical atrophy in the ipsilesional top of S1. • TI patients exhibited significantly higher functional connectivity with the ipsilateral middle S1 which was mainly located within the non-atrophic area of S1. • Our results provide neuroimaging markers for non-invasive treatment and predict somatosensory recovery.

Cortical lateralization of cheirosensory processing in callosal dysgenesis.

The paradoxical absence of a split-brain syndrome in most cases of callosal dysgenesis has originated three main hypotheses, namely, (i) bilateral cortical representation of language, (ii) bilateral thalamocortical projections of somatosensory pathways conveyed by the spinothalamic-medial lemniscus system, and (iii) a variable combination of (i) and (ii). We used functional neuroimaging to investigate the cortical representation and lateralization of somatosensory information from the palm of each hand in six cases of callosal dysgenesis (hypothesis [ii]). Cortical regions of interest were contralateral and ipsilateral S1 (areas 3a and 3b, 1 and 2 in the central sulcus and postcentral gyrus) and S2 (parts of areas 40 and 43 in the parietal operculum). The degree of cortical asymmetry was expressed by a laterality index (LI), which may assume values from −1 (fully left-lateralized) to +1 (fully right-lateralized). In callosal dysgenesis, LI values for the right and the left hands were, respectively, −1 and + 1 for both S1 and S2, indicating absence of engagement of ipsilateral S1 and S2. In controls, LI values were − 0.70 (S1) and − 0.51 (S2) for right hand stimulation, and 0.82 (S1) and 0.36 (S2) for left hand stimulation, reflecting bilateral asymmetric activations, which were significantly higher in the hemisphere contralateral to the stimulated hand. Therefore, none of the main hypotheses so far entertained to account for the callosal dysgenesis-split-brain paradox have succeeded. We conclude that the preserved interhemispheric transfer of somatosensory tactile information in callosal dysgenesis must be mediated by a fourth alternative, such as aberrant interhemispheric bundles, reorganization of subcortical commissures, or both.

Cortical astrocytes prime the induction of spine plasticity and mirror image pain.

Peripheral nerve injury causes maladaptive plasticity in the central nervous system and induces chronic pain. In addition to the injured limb, abnormal pain sensation can appear in the limb contralateral to the injury, called mirror image pain. Because synaptic remodeling in the primary somatosensory cortex (S1) has critical roles in the induction of chronic pain, cortical reorganization in the S1 ipsilateral to the injured limb may also accompany mirror image pain. To elucidate this, we conducted in vivo 2-photon calcium imaging of neuron and astrocyte activity in the ipsilateral S1 after a peripheral nerve injury. We found that cross-callosal inputs enhanced the activity of both S1 astrocytes and inhibitory neurons, whereas activity of excitatory neurons decreased. When local inhibitory circuits were blocked, astrocyte-dependent spine plasticity and allodynia were revealed. Thus, we propose that cortical astrocytes prime the induction of spine plasticity and mirror image pain after peripheral nerve injury. Moreover, this result suggests that cortical synaptic rewiring could be sufficient to cause allodynia on the uninjured periphery.

Brain Functional Changes before, during, and after Clinical Pain

This study used an emerging brain imaging technique, functional near-infrared spectroscopy (fNIRS), to investigate functional brain activation and connectivity that modulates sometimes traumatic pain experience in a clinical setting. Hemodynamic responses were recorded at bilateral somatosensory (S1) and prefrontal cortices (PFCs) from 12 patients with dentin hypersensitivity in a dental chair before, during, and after clinical pain. Clinical dental pain was triggered with 20 consecutive descending cold stimulations (32° to 0°C) to the affected teeth. We used a partial least squares path modeling framework to link patients’ clinical pain experience with recorded hemodynamic responses at sequential stages and baseline resting-state functional connectivity (RSFC). Hemodynamic responses at PFC/S1 were sequentially elicited by expectation, cold detection, and pain perception at a high-level coefficient (coefficients: 0.92, 0.98, and 0.99, P < 0.05). We found that the pain ratings were positively affected only at a moderate level of coefficients by such sequence of functional activation (coefficient: 0.52, P < 0.05) and the baseline PFC-S1 RSFC (coefficient: 0.59, P < 0.05). Furthermore, when the dental pain had finally subsided, the PFC increased its functional connection with the affected S1 orofacial region contralateral to the pain stimulus and, in contrast, decreased with the ipsilateral homuncular S1 regions (P < 0.05). Our study indicated for the first time that patients’ clinical pain experience in the dental chair can be predicted concomitantly by their baseline functional connectivity between S1 and PFC, as well as their sequence of ongoing hemodynamic responses. In addition, this linked cascade of events had immediate after-effects on the patients’ brain connectivity, even when clinical pain had already ceased. Our findings offer a better understating of the ongoing impact of affective and sensory experience in the brain before, during, and after clinical dental pain.

Loss of inhibition in ipsilateral somatosensory areas following altered afferent nerve signaling from the hand

Cutaneous stimulation of the hand results in increased neural activity in the contralateral primary somatosensory cortex (S1) in humans, whereas an inhibition of neurons is seen in the ipsilateral S1.The aim of this study was to assess changes in neural activity in the S1 bilaterally, with a focus on the ipsilateral hemisphere, following altered afferent nerve signaling from the hand. Three cohorts, all with altered afferent nerve signaling from the hand, participated in the study. There were: 18 patients with traumatic median nerve injury, 10 patients with vibration induced neuropathy and 11 healthy subjects who had their dominant hand and wrist immobilized for 72 h. In addition, 36 healthy subjects were included as controls. Each subject was examined using functional magnetic resonance imaging at 3 T. All three study cohorts showed enlarged activation in the contralateral S1 during tactile stimulation compared to healthy controls. Moreover, inhibition of the ipsilateral S1 was significantly decreased or completely lost. Thus, somatosensory areas of both hemispheres respond to changed afferent nerve signaling from the hand. The loss of inhibition of neurons in the ipsilateral S1 suggests an important role of the ipsilateral hemisphere in the cerebral adaptation following a change in afferent nerve signaling.

Distinct Corticostriatal and Intracortical Pathways Mediate Bilateral Sensory Responses in the Striatum.

Individual striatal neurons integrate somatosensory information from both sides of the body, however, the afferent pathways mediating these bilateral responses are unclear. Whereas ipsilateral corticostriatal projections are prevalent throughout the neocortex, contralateral projections provide sparse input from primary sensory cortices, in contrast to the dense innervation from motor and frontal regions. There is, therefore, an apparent discrepancy between the observed anatomical pathways and the recorded striatal responses. We used simultaneous in vivo whole-cell and extracellular recordings combined with focal cortical silencing, to dissect the afferent pathways underlying bilateral sensory integration in the mouse striatum. We show that unlike direct corticostriatal projections mediating responses to contralateral whisker deflection, responses to ipsilateral stimuli are mediated mainly by intracortical projections from the contralateral somatosensory cortex (S1). The dominant pathway is the callosal projection from contralateral to ipsilateral S1. Our results suggest a functional difference between the cortico-basal ganglia pathways underlying bilateral sensory and motor processes.

Polarity-Specific Cortical Effects of Transcranial Direct Current Stimulation in Primary Somatosensory Cortex of Healthy Humans.

Transcranial direct current stimulation (tDCS) is a non-invasive stimulation method that has been shown to modulate the excitability of the motor and visual cortices in human subjects in a polarity dependent manner in previous studies. The aim of our study was to investigate whether anodal and cathodal tDCS can also be used to modulate the excitability of the human primary somatosensory cortex (S1). We measured paired-pulse suppression (PPS) of somatosensory evoked potentials in 36 right-handed volunteers before and after anodal, cathodal, or sham stimulation over the right non-dominant S1. Paired-pulse stimulation of the median nerve was performed at the dominant and non-dominant hand. After anodal tDCS, PPS was reduced in the ipsilateral S1 compared to sham stimulation, indicating an excitatory effect of anodal tDCS. In contrast, PPS in the stimulated left hemisphere was increased after cathodal tDCS, indicating an inhibitory effect of cathodal tDCS. Sham stimulation induced no pre–post differences. Thus, tDCS can be used to modulate the excitability of S1 in polarity-dependent manner, which can be assessed by PPS. An interesting topic for further studies could be the investigation of direct correlations between sensory changes and excitability changes induced by tDCS.

The AOSpine Sacral Fracture Classification

Introduction Sacral fractures are complex and heterogeneous injuries that often include involvement of the lumbar spine and/or pelvis. Due to their complex nature, no comprehensive classification system has been accepted. Material and Methods The AOSpine Trauma Knowledge Forum partnered with orthopaedic traumatologists from AOTrauma to develop a straightforward, hierarchical classification system for sacral fractures. The classification was developed via a consensus process of clinical experts, and, prior to finalizing the classification system, a survey was sent to all members of AOSpine and AOTrauma asking for their input on key parts of the classification. Results The new AOSpine Sacral Classification is a hierarchical classification that follows the same structure as the subaxial and thoracolumbar classifications. First injuries are broadly divided into three types: Type A—Lower Sacro-coccygeal Injuries; Type B—Posterior Pelvic Injuries and Type C—Spino-Pelvic Injuries. Type A injuries have no impact on posterior pelvic or spinopelvic instability, however higher grade injuries may be associated with neurologic injuries. Type A injuries are divided into three subtypes; A1—Coccygeal or compression injuries as well as ligamentous avulsion fractures; A2—Non-displaced transverse fractures below the Sacroiliac (SI) joint, and A3—Displaced transverse fractures below the SI joint. Type B injuries are unilateral longitudinal sacral fractures in which the ipsilateral superior S1 facet is not discontinuous with medial portion of the sacrum. These injuries primarily impact posterior pelvic stability and have minimal impact on spino-pelvic stability. Type B injuries are divided into three subtypes based on the likelihood of neurologic injury, and while this is similar to the Denis classification, because B-type injuries exclude fractures with a transverse component, there is little risk of a neurologic injury with an injury medial to the foramen. The three sub-types of B injuries are: B1—Longitudinal fracture medial to the foramen; B2—Longitudinal fracture lateral to the foramen and B3—Longitudinal injury thought the foramen. Type C injuries are Injuries that result in spino-pelvic instability. They are divided into four subtypes: C0—Non displaced sacral U fracture (commonly seen in low energy insufficiency fractures); C1—Any unilateral B-subtype where the ipsilateral superior S1 facet is discontinuous with the medial portion of the sacrum; C2—Bilateral complete B type fracture without a transverse component, and C3—Displaced sacral U type fracture. In addition to the fracture morphology, the new classification also formally considers the neurologic status of the patient: Nx—The patient cannot be examined; N0—No neurological deficits; N1—Transient neurological injury; N2—Nerve root injury and N3—Cauda Equina Syndrome. Lastly there are four patient specific modifiers that may alter the treatment of these fractures: M1—Significant soft tissue injury; M2—Metabolic bone disease; M3—High-energy injury that may be associated with an anterior pelvic ring injury, acetabular fracture or vascular injury, and M4—Altered anatomy of the lumbosacral junction (may be due to a prior fusion or transitional anatomy). Conclusion The AOSpine sacral fracture classification is the first comprehensive sacral classification to consider posterior pelvic and spino-pelvic instability patterns, and validation studies are ongoing.

Magnetoencephalographic study of hand and foot sensorimotor organization in 325 consecutive patients evaluated for tumor or epilepsy surgery.

ObjectivesThe presence of intracranial lesions or epilepsy may lead to functional reorganization and hemispheric lateralization. We applied a clinical magnetoencephalography (MEG) protocol for the localization of the contralateral and ipsilateral S1 and M1 of the foot and hand in patients with non-lesional epilepsy, stroke, developmental brain injury, traumatic brain injury and brain tumors. We investigated whether differences in activation patterns could be related to underlying pathology.MethodsUsing dipole fitting, we localized the sources underlying sensory and motor evoked magnetic fields (SEFs and MEFs) of both hands and feet following unilateral stimulation of the median nerve (MN) and posterior tibial nerve (PTN) in 325 consecutive patients. The primary motor cortex was localized using beamforming following a self-paced repetitive motor task for each hand and foot.ResultsThe success rate for motor and sensory localization for the feet was significantly lower than for the hands (motor_hand 94.6% versus motor_feet 81.8%, p < 0.001; sensory_hand 95.3% versus sensory_feet 76.0%, p < 0.001). MN and PTN stimulation activated 86.6% in the contralateral S1, with ipsilateral activation < 0.5%. Motor cortex activation localized contralaterally in 76.1% (5.2% ipsilateral, 7.6% bilateral and 11.1% failures) of all motor MEG recordings. The ipsilateral motor responses were found in 43 (14%) out of 308 patients with motor recordings (range: 8.3–50%, depending on the underlying pathology), and had a higher occurrence in the foot than in the hand (motor_foot 44.8% versus motor_hand 29.6%, p = 0.031). Ipsilateral motor responses tended to be more frequent in patients with a history of stroke, traumatic brain injury (TBI) or developmental brain lesions (p = 0.063).ConclusionsMEG localization of sensorimotor cortex activation was more successful for the hand compared to the foot. In patients with neural lesions, there were signs of brain reorganization as measured by more frequent ipsilateral motor cortical activation of the foot in addition to the traditional sensory and motor activation patterns in the contralateral hemisphere. The presence of ipsilateral neural reorganization, especially around the foot motor area, suggests that careful mapping of the hand and foot in both contralateral and ipsilateral hemispheres prior to surgery might minimize postoperative deficits.

Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice.

Transient ischemia produces postischemic tingling sensation. Ischemia also produces nerve conduction block that may modulate spinal neural circuits. In the present study, reduced mechanical thresholds for hindpaw-withdrawal reflex were found in mice after transient hindpaw ischemia, which was produced by a high pressure applied around the hindpaw for 30 min. The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors. Neural activities in the spinal cord and the primary somatosensory cortex (S1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S1 responses, abolished by lesioning the ipsilateral dorsal column, reappeared after ischemic treatment, indicating that postischemic tingling sensation reflects a sensory modality shift from tactile sensation to nociception in the spinal cord. Changes in neural responses were investigated during ischemic treatment in the contralateral spinal cord and the ipsilateral S1. Potentiation already appeared during ischemic treatment for 30 min. The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.