Somatosensory Pathways Research Articles

Does Forward Head Posture Influence Somatosensory Evoked Potentials and Somatosensory Processing in Asymptomatic Young Adults?

The current investigation used somatosensory evoked potentials (SEPs) to assess differences in sensorimotor integration and somatosensory processing variables between asymptomatic individuals with and without forward head posture (FHP). We assessed different neural regions of the somatosensory pathway, including the amplitudes of the peripheral N9, spinal N13, brainstem P14, peak-to-peak amplitudes of parietal N20 and P27, and frontal N30 potentials. Central conduction time (N13-N20) was measured as the difference in peak latencies of N13 and N20. We measured these variables in 60 participants with FHP defined as a craniovertebral angle (CVA) < 50° and 60 control participants matched for age, gender, and body mass index (BMI) with normal FHP defined as CVA > 55°. Differences in variable measures were examined using the parametric t-test. Pearson's correlation was used to evaluate the relationship between the CVA and sensorimotor integration and SEP measurements. A generalized linear model (GLM) was used to compare the SEP measures between groups, with adjustment for educational level, marital status, BMI, and working hours per week. There were statistically significant differences between the FHP group and control group for all sensorimotor integration and SEP processing variables, including the amplitudes of spinal N13 (p < 0.005), brainstem P14 (p < 0.005), peak-to-peak amplitudes of parietal N20 and P27 (p < 0.005), frontal N30 potentials (p < 0.005), and the conduction time N13-N20 (p = 0.004). The CVA significantly correlated with all measured neurophysiological variables indicating that as FHP increased, sensorimotor integration and SEP processing became less efficient. FHP group correlations were: N9 (r = -0.44, p < 0.001); N13 (r = -0.67, p < 0.001); P14 (r = -0.58, p < 0.001); N20 (r = -0.49, p = 0.001); P27 (r = -0.58, p < 0.001); N30 potentials (r = -0.64, p < 0.001); and N13-N20 (r = -0.61, p < 0.001). GLM identified that increased working hours adversely affected the SEP measures (p < 0.005), while each 1° increase in the CVA was associated with improved SEP amplitudes and more efficient central conduction time (N13-N20; p < 0.005). Less efficient sensorimotor integration and SEP processing may be related to previous scientific reports of altered sensorimotor control and athletic skill measures in populations with FHP. Future investigations should seek to replicate our findings in different spine disorders and symptomatic populations in an effort to understand how improving forward head posture might benefit functional outcomes of patient care.

Botulinum Toxin-A Treatment of Post-Stroke Spasticity Is Associated with Changes in Interhemispheric Parietal Cortex Connectivity (P12-8.001)

<h3>Objective:</h3> To assess resting-state functional connectivity (rsFC) of the ipsilesional superior parietal lobule (SPL) and intraparietal sulcus (IPS) using functional magnetic resonance imaging (fMRI) in chronic stroke patients with hemiparesis both with and without post-stroke spasticity (PSS) and to explore the relationship between SPL/IPS resting-state functional connectivity (rsFC) and PSS severity. <h3>Background:</h3> Posts-stroke spasticity hampers effective rehabilitation of the paretic arm and lowers the quality of life. Effective PSS treatment with botulinum neurotoxin (BoNT) is associated with transient decrease in task-related fMRI activation of the ipsilesional SPL and IPS. We hypothesized that this would be reflected in changes in rsFC of the SPL/IPS. <h3>Design/Methods:</h3> Fourteen chronic stroke patients with upper limb weakness and PSS (the PSS group) and 8 patients with comparable weakness but no PSS (the control group) underwent clinical and spasticity evaluation and 3 fMRI examinations, at baseline (W0) and 4 and 11 weeks after BoNT (W4 and W11, respectively). Seed-based rsFC of the atlas-based SPL and IPS was evaluated using a group×time interaction analysis and the change in rsFC of SPL/IPS was correlated with change in PSS (modified Ashworth scale), integrity of the ipsilesional somatosensory afferent pathway (evoked potential N20 latency), and age. <h3>Results:</h3> In the PSS group, transient improvement in PSS was associated with increase in rsFC between the ipsilesional IPS and the contralesional SPL at W4. The interhemispheric connectivity was negatively correlated with PSS severity at baseline and with PSS improvement at W4. These changes in the posterior parietal interhemispheric rsFC suggest that previously observed task-related changes in SPL/IPS were independent of actual task performance. <h3>Conclusions:</h3> We propose adaptation of the internal forward model as the possible underlying mechanism and discuss its potential association with increased limb use or improved motor performance, as well as its potential contribution to the clinical effects of BoNT. <b>Disclosure:</b> The institution of Prof. Hlustik has received research support from Czech Health Research Council (AZV CR). Dr. Hok has nothing to disclose. Tomas Veverka has nothing to disclose. Markéta Trnecková has nothing to disclose. Pavel Otruba has nothing to disclose. Jana Zapletalova has nothing to disclose. Zbynek Tudos has nothing to disclose. Prof. Lotze has received publishing royalties from a publication relating to health care. Dr. Kanovsky has nothing to disclose.

Saying goodbye to an unwelcome guest: Towards robust methods for controlling multi-sensory confounds in TMS-EEG research.

Saying goodbye to an unwelcome guest: Towards robust methods for controlling multi-sensory confounds in TMS-EEG research.

GPR55 contributes to neutrophil recruitment and mechanical pain induction after spinal cord compression in mice

Pain transmission and processing in the nervous system are modulated by various biologically active substances, including lysophospholipids, through direct and indirect actions on the somatosensory pathway. Lysophosphatidylglucoside (LysoPtdGlc) was recently identified as a structurally unique lysophospholipid that exerts biological actions via the G protein-coupled receptor GPR55. Here, we demonstrated that GPR55-knockout (KO) mice show impaired induction of mechanical pain hypersensitivity in a model of spinal cord compression (SCC) without the same change in the models of peripheral tissue inflammation and peripheral nerve injury. Among these models, only SCC recruited peripheral inflammatory cells (neutrophils, monocytes/macrophages, and CD3+ T-cells) in the spinal dorsal horn (SDH), and GPR55-KO blunted these recruitments. Neutrophils were the first cells recruited to the SDH, and their depletion suppressed the induction of SCC-induced mechanical hypersensitivity and inflammatory responses in compressed SDH. Furthermore, we found that PtdGlc was present in the SDH and that intrathecal administration of an inhibitor of secretory phospholipase A2 (an enzyme required for producing LysoPtdGlc from PtdGlc) reduced neutrophil recruitment to compressed SDH and suppressed pain induction. Finally, by screening compounds from a chemical library, we identified auranofin as a clinically used drug with an inhibitory effect on mouse and human GPR55. Systemically administered auranofin to mice with SCC effectively suppressed spinal neutrophil infiltration and pain hypersensitivity. These results suggest that GPR55 signaling contributes to the induction of inflammatory responses and chronic pain after SCC via the recruitment of neutrophils and may provide a new target for reducing pain induction after spinal cord compression, such as spinal canal stenosis.

Interhemispheric parietal cortex connectivity reflects improvement in post-stroke spasticity due to treatment with botulinum toxin-A

In post-stroke spasticity (PSS), effective treatment with botulinum neurotoxin (BoNT) is associated with transient decrease in activation of the ipsilesional superior parietal lobule (SPL) and intraparietal sulcus (IPS). We hypothesized that this would be reflected in changes in resting-state functional connectivity (rsFC) of the SPL/IPS. Our aim was therefore to assess rsFC of the ipsilesional SPL/IPS in chronic stroke patients with hemiparesis both with and without PSS and to explore the relationship between SPL/IPS rsFC and PSS severity. To this end, fourteen chronic stroke patients with upper limb weakness and PSS (the PSS group) and 8 patients with comparable weakness but no PSS (the control group) underwent clinical evaluation and 3 fMRI examinations, at baseline (W0) and 4 and 11 weeks after BoNT (W4 and W11, respectively). Seed-based rsFC of the atlas-based SPL and IPS was evaluated using a group×time interaction analysis and a correlation analysis with PSS severity (modified Ashworth scale), integrity of the ipsilesional somatosensory afferent pathway (evoked potential N20 latency), and age. In the PSS group, transient improvement in PSS was associated with increase in rsFC between the ipsilesional IPS and the contralesional SPL at W4. The interhemispheric connectivity was negatively correlated with PSS severity at baseline and with PSS improvement at W4. We propose adaptation of the internal forward model as the putative underlying mechanism and discuss its possible association with increased limb use, diminished spastic dystonia, or improved motor performance, as well as its potential contribution to the clinical effects of BoNT.

Subthreshold electrical stimulation with pink noise enhances feedback control as evaluated by scaling exponent of postural sway

Subthreshold somatosensory stimulation with pink noise has been shown to attenuate postural sway better than stimulation with white noise. This might be due to the different frequency structures of the noise signals. However, their effects on the underlying somatosensory feedback pathway are still unknown. Thus, we aimed to determine whether pink noise enhances the somatosensory feedback pathway more effectively than other noises with different frequency structures, such as white and red noises. Sixteen young adults stood quietly for 65 s under four stimulation conditions: no stimulation and stimulations with white-, pink-, and red-noise-like signals. Based on a stabilogram-diffusion analysis, we calculated the long-term diffusion coefficient and scaling exponent in the radial direction to evaluate the effects of these noise signals on their somatosensory feedback control. The root mean square (CoPRMS) and mean velocity of the foot center of pressure were also computed to assess the amount of postural sway. The results showed that the stimulation condition had a significant effect on the scaling exponent, with the value under the pink-noise-like signal significantly lower than that under the no-stimulation condition. We also found that among the participants, the percentage of reduction in CoPRMS by the pink-noise-like signal was positively correlated with the CoPRMS value under the no-stimulation condition. Altogether, the somatosensory feedback control for balancing for quiet standing posture was improved by pink noise, and its effect on the variability of postural sway correlated with inherent postural sway variability.

Bayesian surprise shapes neural responses in somatosensory cortical circuits.

Numerous psychophysical studies show that Bayesian inference governs sensory decision-making; however, the specific neural circuitry underlying this probabilistic mechanism remains unclear. We record extracellular neural activity along the somatosensory pathway of mice while delivering sensory stimulation paradigms designed to isolate the response to the surprise generated by Bayesian inference. Our results demonstrate that laminar cortical circuits in early sensory areas encode Bayesian surprise. Systematic sensitivity to surprise is not identified in the somatosensory thalamus, rather emerging in the primary (S1) and secondary (S2) somatosensory cortices. Multiunit spiking activity and evoked potentials in layer 6 of these regions exhibit the highest sensitivity to surprise. Gamma power in S1 layer 2/3 exhibits an NMDAR-dependent scaling with surprise, as does alpha power in layers 2/3 and 6 of S2. These results show a precise spatiotemporal neural representation of Bayesian surprise and suggest that Bayesian inference is a fundamental component of cortical processing.

Hemodynamic transient and functional connectivity follow structural connectivity and cell type over the brain hierarchy

The neural circuit of the brain is organized as a hierarchy of functional units with wide-ranging connections that support information flow and functional connectivity. Studies using MRI indicate a moderate coupling between structural and functional connectivity at the system level. However, how do connections of different directions (feedforward and feedback) and regions with different excitatory and inhibitory (E/I) neurons shape the hemodynamic activity and functional connectivity over the hierarchy are unknown. Here, we used functional MRI to detect optogenetic-evoked and resting-state activities over a somatosensory pathway in the mouse brain in relation to axonal projection and E/I distribution. Using a highly sensitive ultrafast imaging, we identified extensive activation in regions up to the third order of axonal projections following optogenetic excitation of the ventral posteriomedial nucleus of the thalamus. The evoked response and functional connectivity correlated with feedforward projections more than feedback projections and weakened with the hierarchy. The hemodynamic response exhibited regional and hierarchical differences, with slower and more variable responses in high-order areas and bipolar response predominantly in the contralateral cortex. Electrophysiological recordings suggest that these reflect differences in neural activity rather than neurovascular coupling. Importantly, the positive and negative parts of the hemodynamic response correlated with E/I neuronal densities, respectively. Furthermore, resting-state functional connectivity was more associated with E/I distribution, whereas stimulus-evoked effective connectivity followed structural wiring. These findings indicate that the structure-function relationship is projection-, cell-type- and hierarchy-dependent. Hemodynamic transients could reflect E/I activity and the increased complexity of hierarchical processing.

Static Balance in Hereditary Spastic Paraplegias: a Cross-sectional Study.

Motor and somatosensory pathway dysfunction due to degeneration of long tracts in hereditary spastic paraplegias (HSP) indicates that postural abnormalities may be a relevant disease feature. However, balance assessments have been underutilized to study these conditions. How does the static balance of individuals with HSP with eyes open and closed differ from healthy controls, and how does it relate to disease severity? This cross-sectional case-control study assessed the static balance of 17 subjects with genetically confirmed HSP and 17 healthy individuals, evaluating the center of pressure (COP) variables captured by a force platform. The root-mean-square of velocities and mean of displacements amplitudes in mediolateral and anteroposterior axes were correlated with disease severity. All COP parameters' performances were significantly impaired in HSP subjects compared to controls (p < 0.001 for all comparisons). COP with eyes open and closed differed for all variables within the HSP group, whereas in the control group, differences were observed only for anteroposterior velocity and amplitude. Spastic Paraplegia Rating Scale presented moderate direct correlations with the most COP variables (Rho = - 0.520 to - 0.736). HSP individuals presented significant postural instability with eyes open and to a greater extent with eyes closed, corroborating the clinical findings of somatosensorial and proprioceptive pathways dysfunction. The degrees of proprioceptive and motor impairments are mutually correlated, suggesting that similar pathophysiological mechanisms operate for the degeneration of these long tracts. COP parameters can be seen as disease severity biomarkers of HSP, and they should be assessed in future clinical trials.

Electron Microscopic Study in the Rat Model of Electrically Injured Myelopathy: Preliminary Report.

The patient with electrically injured myelopathy showed mild motor weakness without somatosensory pathway abnormalities. Few reports have been reported on the pathophysiological mechanisms of electrically injured myelopathy, and there is controversy about the exact pathological causes. This study aimed to investigate the ultrastructural changes in the electron microscopic findings of electrical spinal cord injury. Nine rats were used in this study. We performed 7 electrical shocks (frequency, 120 Hz; pulse width, 0.9 ms; duration, 3 seconds; current, 99 mA) using an electroconvulsive therapy (ECT) apparatus (57800 ECT unit; UGO BASILE). We used one ear and one contralateral hind limb as entry and exit sites, respectively. We only enrolled rats with hind limb weakness and performed electron microscopy evaluations of the spinal cord on the first day and 4 weeks after injury. On the first day after injury, an electron microscopic examination showed a directly damaged area that appeared to be torn as physical damage, damaged myelin sheath, vacuolated axons in the myelin sheath, swollen Golgi apparatus, and injured mitochondria. Looking at changes in motor and sensory nerves, the sensory neurons showed recovered mitochondria and Golgi apparatus 4 weeks after injury; however, motor neurons still showed injured mitochondria, swollen Golgi apparatus, and endoplasmic reticulum. This study showed that recovery from ultrastructural injury was more rapid in sensory neurons than in motor neurons.

Lumbar trans-spinal direct current stimulation: A modeling-experimental approach to dorsal root ganglia stimulation.

The excitability of spinal motor neurons (MN) can be altered through subthreshold currents, such as transcutaneous spinal direct-current stimulation (tsDCS). Current evidence shows that tsDCS can interfere with ascending somatosensory pathways and lower motor neurons' (LMN) excitability, which points to its therapeutic potential for repairing altered spinal responses. We aim to define the best tsDCS montage for maximizing the electric field (E-field) in the lumbar spinal cord (L-SC) by computer modeling; and to apply this montage to measure the effect on LMN excitability and somatosensory evoked potentials (SSEP). A human volume conductor model was obtained from an available database. The E-field distribution was calculated considering three different electrode settings aiming at maximizing the field at L-SC and right dorsal root ganglia (DRG). The best electrode setting was then selected and applied in a blind crossover pseudo-randomized study including 14 subjects. tsDCS was delivered for 15 min (cathodal vs. sham) over L2 vertebra level (4 mA, 144 mC/cm2), and its effect on F-waves, H-reflex (including homosynaptic depression, HD) and SSEPs was investigated in the lower limbs. All simulated montages showed higher current density and E-field magnitudes between the electrodes (>0.15 V/m), with a major longitudinal component and with rostral-caudal direction. The induced E-field involved the sensory ganglia and was maximum in the right T8-left L2 montage, which was the one selected for the experimental protocol. We disclosed a statistically significant increase of the H-reflex amplitude at 0.1 Hz, after cathodal tsDCS (c-tsDCS) on both sides. No other significant change was observed. Our results can suggest the c-tsDCS applied to the L-SC and DRG can modulate synaptic efficiency increasing lower motor neurons response to Ia fibers excitation. The possible implications of our findings for treating clinical conditions will be addressed in future studies.

Focal vibrations enhance somatosensory facilitation in healthy subjects: A pilot study on Equistasi® and high-frequency oscillations.

Equistasi® is a vibrotactile device composed of nanotechnology fibers that converts temperature change into mechanical energy by self-producing a focal vibration. It is used in non-pharmacological rehabilitation in patients with movement disorders and multiple sclerosis sequelae. Nonetheless, the mechanism underlying such an improvement in motor functions is still poorly understood. We designed a small uncontrolled pilot trial to explore the effect of Equistasi® on the somatosensory pathway through the analysis of high-frequency oscillations (HFOs). For all the included subjects, we recorded somatosensory-evoked potentials (SEPs) at the baseline (T0) and at 60 min after the application of Equistasi® (T1) on the seventh cervical vertebra level and at the forearm over each flexor carpi radialis, bilaterally. Then, we extracted the HFOs from the N20 signal and compared the HFO duration and area under the curve pre- and post-Equistasi® application. In a head-to-head comparison of T0 to T1 data, there was a statistically significant reduction in the total HFO area (p < 0.01), which was prominent for the late component (p = 0.025). No statistical differences have been found between T0 and T1 HFO duration (p > 0.05). We further evaluated the N20 amplitude from the onset to the N20 peak to avoid possible interpretational bias. No statistical differences have been found between T0 and T1 (p = 0.437). Our clinical hypothesis, supported by preliminary data, is that vibrotactile afference delivered by the device could work by interfering with the somatosensory processing, rather than by peripheral effects.

Differential changes in somatosensory evoked potentials and motor performance: pursuit movement task versus force matching tracking task.

Force modulation relies on accurate proprioception, and force-matching tasks alter corticocerebellar connectivity. Corticocerebellar (N24) and corticomotor pathways are impacted following the acquisition of a motor tracing task (MTT), measured using both somatosensory evoked potentials (SEPs) and transcranial magnetic stimulation. This study compared changes in early SEP peak amplitudes and motor performance following a force-matching tracking task (FMTT) to an MTT. Thirty (18 females) right-handed participants, aged 21.4 ± 2.76, were electrically stimulated over the right-median nerve at 2.47 Hz and 4.98 Hz (averaged 1,000 sweeps/rate) to elicit SEPs, recorded via a 64-channel electroencephalography cap, before, and after task acquisition using the right abductor pollicis brevis muscle. Retention was measured 24 h later. Significant time-by-group interactions occurred for the N20 SEP: 6.3% decrease post-FMTT versus 5.5% increase post-MTT (P = 0.013); P25 SEP: 4.0% decrease post-FMTT versus 10.3% increase post-MTT (P = 0.006); and N18 SEP: 113.4% increase post-FMTT versus 4.4% decrease post-MTT (P = 0.006). N18 and N30 showed significant effect of time (both P < 0.001). Motor performance: significant time-by-group interactions-postacquisition: FMTT improved 15.3% versus 24.3% for MTT (P = 0.025), retention: FMTT improved 17.4% and MTT by 30.1% (P = 0.004). Task-dependent differences occurred in SEP peaks associated with cortical somatosensory processing (N20 and P25), and cerebellar input (N18), with similar changes in sensorimotor integration (N30), with differential improvements in motor performance, indicating important differences in cerebellar and sensory processing for tasks reliant on proprioception.NEW & NOTEWORTHY This study demonstrates neurophysiological differences in cerebellar and somatosensory cortex pathways when learning a motor task requiring visuomotor tracking versus a task that requires force-matching modulation, in healthy individuals. The clear neurophysiological differences in early somatosensory evoked potentials associated with cortical somatosensory processing, cerebellar input, and sensorimotor integration between these two tasks demonstrate some of the neural correlates of force modulation and validate the force-matching task for use in future work.

Ras GTPase-activating proteins control neuronal circuit development in barrel cortex layer 4.

The cerebral cortex comprises a complex and exquisite network of neuronal circuits that is formed during development. To explore the molecular mechanisms involved in cortical circuit formation, the tactile somatosensory pathway that connects the whiskers and cortex of rodents is a useful model. Here, we analyzed the roles of Ras GTPase-activating proteins (RasGAPs) in the circuit formation in the somatosensory cortex layer 4 (L4). We suppressed the function of RasGAPs in L4 neurons using Supernova RNAi, a plasmid vector-based sparse cell gene knockdown (KD) system. The results showed disrupted dendritic pattern formation of L4 spiny stellate neurons on the barrel edge by RasGAP KD. Furthermore, the number of presynaptic boutons on L4 neurons was reduced by RasGAP KD. These results demonstrate the essential roles of RasGAPs in circuit formation in the cerebral cortex and imply that developmental changes in dendrites and synapses in RasGAP KD neurons may be related to cognitive disabilities in RasGAP-deficient individuals, such as patients with neurofibromatosis type 1.

Continuum of sensory profiles in diabetes mellitus patients with and without neuropathy and pain.

Quantitative sensory testing (QST) assesses the functional integrity of small and large nerve fibre afferents and central somatosensory pathways; QST was assumed to provide insight into the mechanisms of neuropathy. We analysed QST profiles and phenotypes in patients with diabetes mellitus to study whether these could differentiate patients with and without pain and neuropathy. A standardized QST protocol was performed and 'loss and gain of function' abnormalities were analysed in four groups of subjects: diabetic patients with painful (pDSPN; n=220) and non-painful distal symmetric polyneuropathy (nDSPN; n=219), diabetic patients without neuropathy (DM; n=23) and healthy non-diabetic subjects (n=37). Based on the QST findings, diabetic subjects were further stratified into four predefined prototypic phenotypes: sensory loss (SL), thermal hyperalgesia (TH), mechanical hyperalgesia (MH) and healthy individuals. Patients in the pDSPN group showed the greatest hyposensitivity ('loss of function'), and DM patients showed the lowest, with statistically significant increases in thermal, thermal pain, mechanical and mechanical pain sensory thresholds. Accordingly, the frequency of the SL phenotype was significantly higher in the pDSPN subgroup (41.8%), than expected (p &lt; 0.0042). The proportion of 'gain of function' abnormalities was low in both pDSPN and nDSPN patients without significant differences. There is a continuum in the sensory profiles of diabetic patients, with a more pronounced sensory loss in pDSPN group probably reflecting somatosensory nerve fibre degeneration. An analysis of 'gain of function' abnormalities (allodynia, hyperalgesia) did not offer a key to understanding the pathophysiology of spontaneous diabetic peripheral neuropathic pain. This article, using quantitative sensory testing profiles in large cohorts of diabetic patients with and without polyneuropathy and pain, presents a continuum in the sensory profiles of diabetic patients, with more pronounced 'loss of function' abnormalities in painful polyneuropathy patients. Painful diabetic polyneuropathy probably represents a 'more progressed' type of neuropathy with more pronounced somatosensory nerve fibre degeneration. The proportion of 'gain of function' sensory abnormalities was low, and these offer limited understanding of pathophysiological mechanisms of spontaneous neuropathic pain.

Somatosensory and trigeminal pathway abnormalities in Chinese patients with trigeminal neuralgia.

This study aimed to evaluate somatosensory function in Chinese patients with trigeminal neuralgia (TN) using a standard quantitative sensory testing (QST) battery and electrophysiological tests consisting of contact heat-evoked potentials (CHEPs) and blink reflex (BR). Twenty patients with TN and 20 sex- and age-matched healthy controls were recruited for this study. A standard QST protocol recommended by the German Research Network on Neuropathic Pain was carried out on the patients' painful and contralateral faces, the controls' right faces, and all participants' right hands. The CHEPs and BR were recorded at the Cz electrode and bilateral lower bellies of the orbicularis oculi, respectively, with thermal stimuli applied to both sides of the patient's face and the control's right face. The cold detection threshold, heat pain threshold, and mechanical pain threshold on the painful face were lower than those of healthy controls (P < 0.05), whereas the cold pain threshold and mechanical detection threshold were higher (P < 0.05) on the painful faces than those of the contralateral faces from patients or healthy controls. Mechanical pain sensitivity was higher in both test sites than in healthy controls (P < 0.05). Significantly longer N latencies (P < 0.05) and lower N-P amplitudes (P < 0.01) were detected in the patients' painful sites than in the contralateral sites and those of healthy controls. Comprehensive somatosensory abnormalities were found in painful facial sites in patients with TN, suggesting disturbances in the processing of somatosensory stimuli. Deficiencies in electrophysiological tests further revealed unilaterally impaired function of the trigeminal pathway in TN patients.

Changes in somatosensory evoked potentials elicited by lateral cerebellar nucleus deep brain stimulation in the naïve rodent

Deep brain stimulation (DBS) of the deep cerebellar nuclei has been shown to enhance perilesional cortical excitability and promote motor rehabilitation in preclinical models of cortical ischemia and is currently being evaluated in patients with chronic, post-stroke deficits. Understanding the effects of cerebellar DBS on contralateral sensorimotor cortex may be key to developing approaches to optimize stimulation delivery and treatment outcomes. Using the naïve rat model, we characterized the effects of DBS of the lateral cerebellar nucleus (LCN) on somatosensory evoked potentials (SSEPs) and evaluated their potential use as a surrogate index of cortical excitability. SSEPs were recorded concurrently with continuous 30 Hz or 100 Hz LCN DBS and compared to the DBS OFF condition. Ratios of SSEP peak to peak amplitude during 100 Hz LCN DBS to DBS OFF at longer latency peaks were significantly>1, suggesting that cortical excitability was enhanced as a result of LCN DBS. Although changes in SSEP peak to peak amplitudes were observed, they were modest in relation to previously reported effects on motor cortical excitability. Overall, our findings suggest that LCN output influences thalamocortical somatosensory pathways, however further work is need to better understand the potential role of SSEPs in optimizing therapy.

Neuromonitoring in Neurosurgery : An imperative redemption

With the refinement in biomedical gadgetry, it has been a modern day requisite to safeguard the indigenous neuro-architecture and henceforth foretell the postoperative neurological outcome. The intraoperative neuro-physiological monitoring (IONM) comes as no surprise to be the only credible paradigm which can cluethe standing of neural pathway directly during general anesthesia. By engaging with the IONM appliance, the operating surgeon can acknowledge the risk of injury to critical neural structure while dealing with the pathology within its vicinity. Based on the province of the encephalon, a disparate methods of IONM such as MEP, SSEP, ABR, VEP, BCR, AMR etc have unfolded over time. Intraoperative monitoring of motor evoked potentials (MEPs) has been believed to be advantageousin preventing postoperative motor dysfunction while coping up with aneurysmal surgery involving the internal carotid artery (ICA) and middle cerebral artery (MCA) and resection of tumor near sensorimotor areas or corticospinal tract.3–6The fundamental essence of MEP monitoring is based on the detection of a pyramidal tract insult expressed as a decrease of the amplitude of the waveform elicited by electrical stimulation. Conversely, Somatosensory evoked potentials (SSEPs) embraces a series of wave forms that emulate sequential activation of neural structures along the somatosensory pathways.7 The representative stimulation sites classically used for clinical diagnostic in the course of SSEPs studies are the median nerve at the wrist, the common peroneal nerve at the knee, and the posterior tibial nerve at the ankle. Over and above that, SSEPs have been used as an indicator of cerebral ischemia during CEA, although far less commonly and as a surrogate alternative to EEG. SSEPs primarily gauge the integrity of the dorsal (sensory) column of the spinal cord. It furnishes with the real-time examination of spinal tracts at risk during surgical manipulation of the spinal cord such as spinal tumor and pedicle screw instrumentation. Likewise, Auditory brainstem response (ABR) is a test which can assess the brain wave activity and diagnose dysfunctions of the auditory pathways within the auditory nerve and brainstem that occurs in response to an stimuli with clicks or certain tones.8This is notably useful in the surgery of CP angle tumor such as vestibular schwannoma, Microvascular decompression for hemifacial spasm and trigeminal neuralgia. In any neurosurgical endeavour, where a visual field impairment is contemplated during the intraoperative period, the monitoring of flash visual evoked potential (VEP) comes as a rescue to evaluate the state of visual function.9This manoeuvre is explicitly virtuous while performing tumorectomy at the optic chiasm of pituitary adenomas, craniopharyngiomas, tuberculum sellae meningiomas, and other tumors; the removal of brain tumors from the optic pathway and structures in its vicinity such as the optic nerve, optic radiation, and occipital lobe; and clip ligation of aneurysm involving the internal carotid artery, which strike a pose of risking injury and impeding blood flow to the ophthalmic artery.9 Monitoring intraoperative flash visual evoked potentials (VEPs) estimate the functionality of the optic pathway from the retina to the visual cortical area, and hence allows visual impairment to be avoided or minimized. The bulbocavernosus reflex (BCR) is anillustrious somatic reflex that is convenient in gaining information about the state of the sacral spinal cord segments.10 When present, it is indicative of an intact spinal reflex arcs (S2–S4 spinal segments) with afferent and efferent nerves through the pudendal nerve. BCR is of the greatest utility for the monitoring of sacral function in detethering of the tethered cord syndrome.11 A surface electrode is used to electrically stimulate the pudendal afferent fibers at the clitoris or penis and recording of the analogous triggered EMG in external anal sphincter using a subdermal needle electrode. The abnormal muscle response (AMR), which is also known as lateral pread response, is adopted in the microvascular decompression (MVD) for hemifacial spasm.12A complete disappearance of AMR after a convincing MVD from root exit zone implicate a postoperative disappearance of the hemifacial spasm. Nonetheless, the persistence of the AMR does not mean incomplete MVD.

Pain-Related Vertex Evoked Potentials. Comparison of Surface Electrical to Heat Stimulation.

Demonstration of nociceptive fiber abnormality is important for diagnosing neuropathic pain and small fiber neuropathies. This is usually assessed by brief heat pulses using lasers, contact heat, or special electrodes. We hypothesized that pain-related evoked potentials to conventional surface electrical stimulation (PREPse) can index Aδ afferences despite tactile Aß fibers coactivation. PREPse may be more readily used clinically than contact heat evoked potentials (CHEPS). Twenty-eight healthy subjects. Vertex (Cz-A1/A2) recordings. Electrical stimulation of middle finger and second toe with conventional ring, and forearm/leg skin with cup, electrodes. Contact heat stimulation to forearm and leg. Compression ischemic nerve blockade. PREPse peripheral velocities were within the midrange of Aδ fibers. N1-P1 amplitude increased with pain numerical rating scale graded (0-10) electrical stimulation (n = 25) and decreased with increasing stimulation frequency. Amplitudes were unchanged by different presentation orders of four stimulation intensities. PREPse N1 (∼130 milliseconds) and N2 (∼345 milliseconds) peaks were approximately 40 milliseconds earlier than that with CHEPS. PREPse and CHEPS N1-N2 interpeak latency (∼207 milliseconds) were similar. PREPse became unrecordable with nerve blockade of Aδ fibers. PREPse earlier N1 and N2 peaks, and similar interpeak N1-N2 latencies and central conduction velocities, or synaptic delays, to CHEPS are consistent with direct stimulation of Aδ fibers. The relation of vertex PREPse amplitude and pain, or the differential effects of frequency stimulation, is similar to pain-related evoked potential to laser, special electrodes, or contact heat stimulation. The relationship to Aδ was validated by conduction velocity and nerve block. Clinical utility of PREPse compared with CHEPS needs validation in somatosensory pathways lesions.

Direct brainstem somatosensory evoked potentials for cavernous malformations.

Brainstem cavernous malformations (CMs) often require resection due to their aggressive natural history causing hemorrhage and progressive neurological deficits. The authors report a novel intraoperative neuromonitoring technique of direct brainstem somatosensory evoked potentials (SSEPs) for functional mapping intended to help guide surgery and subsequently prevent and minimize postoperative sensory deficits. Between 2013 and 2019 at the Stanford University Hospital, intraoperative direct brainstem stimulation of primary somatosensory pathways was attempted in 11 patients with CMs. Stimulation identified nucleus fasciculus, nucleus cuneatus, medial lemniscus, or safe corridors for incisions. SSEPs were recorded from standard scalp subdermal electrodes. Stimulation intensities required to evoke potentials ranged from 0.3 to 3.0 mA or V. There were a total of 1 midbrain, 6 pontine, and 4 medullary CMs-all with surrounding hemorrhage. In 7/11 cases, brainstem SSEPs were recorded and reproducible. In cases 1 and 11, peripheral median nerve and posterior tibial nerve stimulations did not produce reliable SSEPs but direct brainstem stimulation did. In 4/11 cases, stimulation around the areas of hemosiderin did not evoke reliable SSEPs. The direct brainstem SSEP technique allowed the surgeon to find safe corridors to incise the brainstem and resect the lesions. Direct stimulation of brainstem sensory structures with successful recording of scalp SSEPs is feasible at low stimulation intensities. This innovative technique can help the neurosurgeon clarify distorted anatomy, identify safer incision sites from which to evacuate clots and CMs, and may help reduce postoperative neurological deficits. The technique needs further refinement, but could potentially be useful to map other brainstem lesions.