Somatosensory Pathways Research Articles

Emergence of a brainstem somatosensory tonotopic map for substrate vibration.

Perceiving substrate-borne vibrations is a fundamental component of tactile perception. How location (somatotopy) and frequency tuning (tonotopy) of vibrations are integratively processed is poorly understood. Here we addressed this question using in vivo electrophysiology and two-photon calcium imaging along the dorsal column-medial lemniscal pathway. We found that both frequency and location are organized into structured maps in the dorsal column nuclei (DCN). Both maps are intimately related at the fine spatial scale, with parallel map gradients that are consistent across the depth of the DCN and preserved along the ascending pathway. The tonotopic map only partially reflects the distribution of end organs in the skin and deep tissue; instead, the emergence of the fine-scale tonotopy is due to the selective dendritic sampling from axonal afferents, already at the first synaptic relay. We conclude that DCN neural circuits are key to the emergence of these two fine-scale topographical organizations in early somatosensory pathways.

MDMA modulates human sensorimotor cortical pathways during gentle touch

Abstract The stimulant ± 3,4-methylenedioxymethamphetamine (MDMA) has been shown to enhance the perceived pleasantness of touch. However, the underlying neural processes contributing to touch-related effects of MDMA are not well understood. Using a double-blind, randomized, within-subject design, this study used fMRI to examine hemodynamic changes following MDMA (1.5 mg/kg) vs. lactose placebo administration during gentle touch stimulation in a healthy sample (N = 18). Participants were stroked on the forearm at a slower, more pleasant (3 cm/s), and a faster (30 cm/s), less pleasant speed. For the MDMA session, participants’ affective ratings of touch stimulation were higher than their placebo ratings. Increase in plasma oxytocin (OT) levels was also greater during the MDMA session. On the neural level, primary sensorimotor areas showed greater hemodynamic changes during the MDMA than during the placebo session for both touch speeds, indicating a relatively early influence within somatosensory pathways. Changes in OT levels showed an interaction with drug in an occipitotemporal region, area MT+, associated with motion perception. However, posterior insula did not show preferential activation for the slower stroking speed. These initial findings provide a basis for extending our knowledge of the neural processes underlying the effect of MDMA on affective touch.

Transformation of neural coding for vibrotactile stimuli along the ascending somatosensory pathway

In mammals, action potentials fired by rapidly adapting mechanosensitive afferents are known to reliably time lock to the cycles of a vibration. How and where along the ascending neuraxis is the peripheral afferent temporal code transformed into a rate code are currently not clear. Here, we probed the encoding of vibrotactile stimuli with electrophysiological recordings along major stages of the ascending somatosensory pathway in mice. We discovered the main transformation step was identified at the level of the thalamus, and parvalbumin-positive interneurons in thalamic reticular nucleus participate in sharpening frequency selectivity and in disrupting the precise spike timing. When frequency-specific microstimulation was applied within the brainstem, it generated frequency selectivity reminiscent of real vibration responses in the somatosensory cortex and could provide informative and robust signals for learning in behaving mice. Taken together, these findings could guide biomimetic stimulus strategies to activate specific nuclei along the ascending somatosensory pathway for neural prostheses.

Brain activity changes after high/low frequency stimulation in a nonhuman primate model of central post-stroke pain

Central post-stroke pain (CPSP) is a chronic pain resulting from a lesion in somatosensory pathways. Neuromodulation techniques, such as repetitive transcranial magnetic stimulation (rTMS) that target the primary motor cortex (M1), have shown promise for the treatment of CPSP. High-frequency (Hf) rTMS exhibits analgesic effects compared to low-frequency (Lf) rTMS; however, its analgesic mechanism is unknown. We aimed to elucidate the mechanism of rTMS-induced analgesia by evaluating alterations of tactile functional magnetic resonance imaging (fMRI) due to Hf- and Lf-rTMS in a CPSP monkey model. Consistent with the patient findings, the monkeys showed an increase in pain threshold after Hf-rTMS, which indicated an analgesic effect. However, no change after Lf-rTMS was observed. Compared to Lf-rTMS, Hf-rTMS produced enhanced tactile-evoked fMRI signals not only in M1 but also in somatosensory processing regions, such as the primary somatosensory and midcingulate cortices. However, the secondary somatosensory cortex (S2) was less active after Hf-rTMS than after Lf-rTMS, suggesting that activation of this region was involved in CPSP. Previous studies showed pharmacological inhibition of S2 reduces CPSP-related behaviors, and the present results emphasize the involvement of an S2 inhibitory system in rTMS-induced analgesia. Verification using the monkey model is important to elucidate the inhibition system.

The location of pain in cluster headache: Data from the International Cluster Headache Questionnaire.

To identify the most common locations of cluster headache pain from an international, non-clinic-based survey of participants with cluster headache, and to compare these locations to other cluster headache features as well as to somatotopic maps of peripheral, brainstem, thalamic, and cortical areas. Official criteria for cluster headache state pain in the orbital, supraorbital, and/or temporal areas, yet studies have noted pain extending beyond these locations, and the occipital nerve appears relevant, given the effectiveness of suboccipital corticosteroid injections and occipital nerve stimulation. Furthermore, cranial autonomic features vary between patients, and it is not clear if the trigeminovascular reflex is dermatome specific (e.g., do patients with maxillary or V2 division pain have more rhinorrhea?). Finally, functional imaging studies show early activation of the posterior hypothalamus in a cluster headache attack. However, the first somatosensory area to be sensitized is unclear; the first area can be hypothesized based on the complete map of pain locations. The International Cluster Headache Questionnaire was an internet-based cross-sectional survey that included a clickable pain map of the face. These data were compared to several other datasets: (1) a meta-analysis of 22 previous publications of pain location in cluster headache (consisting of 6074 patients); (2) four cephalic dermatome maps; (3) participants' survey responses for demographics, autonomic features, and effective medications; and (4) previously published somatotopic maps of the brainstem, thalamus, primary somatosensory cortex, and higher order somatosensory cortex. One thousand five hundred eighty-nine participants completed the pain map portion of the survey, and the primary locations of pain across all respondents was the orbital, periorbital, and temporal areas with a secondary location in the lower occiput; these primary and secondary locations were consistent with our meta-analysis of 22 previous publications. Of the four cephalic dermatomes (V1, V2, V3, and a combination of C2-3), our study found that most respondents had pain in two or more dermatomes (range 85.7% to 88.7%, or 1361-1410 of 1589 respondents, across the four dermatome maps). Dermatomes did not correlate with their respective autonomic features or with medication effectiveness. The first area to be sensitized in the canonical somatosensory pathway is either a subcortical (brainstem or thalamus) or higher order somatosensory area (parietal ventral or secondary somatosensory cortices) because the primary somatosensory cortex (area 3b) and somatosensory area 1 have discontinuous face and occipital regions. The primary pain locations in cluster headache are the orbital, supraorbital, and temporal areas, consistent with the official International Classification of Headache Disorders criteria. However, activation of the occiput in many participants suggests a role for the occipital nerve, and the pain locations suggest that somatosensory sensitization does not start in the primary somatosensory cortex.

Spiking networks that efficiently process dynamic sensory features explain receptor information mixing in somatosensory cortex.

How do biological neural systems efficiently encode, transform and propagate information between the sensory periphery and the sensory cortex about sensory features evolving at different time scales? Are these computations efficient in normative information processing terms? While previous work has suggested that biologically plausible models of of such neural information processing may be implemented efficiently within a single processing layer, how such computations extend across several processing layers is less clear. Here, we model propagation of multiple time-varying sensory features across a sensory pathway, by extending the theory of efficient coding with spikes to efficient encoding, transformation and transmission of sensory signals. These computations are optimally realized by a multilayer spiking network with feedforward networks of spiking neurons (receptor layer) and recurrent excitatory-inhibitory networks of generalized leaky integrate-and-fire neurons (recurrent layers). Our model efficiently realizes a broad class of feature transformations, including positive and negative interaction across features, through specific and biologically plausible structures of feedforward connectivity. We find that mixing of sensory features in the activity of single neurons is beneficial because it lowers the metabolic cost at the network level. We apply the model to the somatosensory pathway by constraining it with parameters measured empirically and include in its last node, analogous to the primary somatosensory cortex (S1), two types of inhibitory neurons: parvalbumin-positive neurons realizing lateral inhibition, and somatostatin-positive neurons realizing winner-take-all inhibition. By implementing a negative interaction across stimulus features, this model captures several intriguing empirical observations from the somatosensory system of the mouse, including a decrease of sustained responses from subcortical networks to S1, a non-linear effect of the knock-out of receptor neuron types on the activity in S1, and amplification of weak signals from sensory neurons across the pathway.

Variations in touch representation in the hummingbird and zebra finch forebrain

Somatosensation is essential for animals to perceive the external world through touch, allowing them to detect physical contact, temperature, pain, and body position. Studies on rodent vibrissae have highlighted the organization and processing in mammalian somatosensory pathways.1,2 Comparative research across vertebrates is vital for understanding evolutionary influences and ecological specialization on somatosensory systems. Birds, with their diverse morphologies, sensory abilities, and behaviors, serve as ideal models for investigating the evolution of somatosensation. Prior studies have uncovered tactile-responsive areas within the avian telencephalon, particularly in pigeons,3,4,5,6 parrots,7 and finches,8 but variations in somatosensory maps and responses across avian species are not fully understood. This study aims to explore somatotopic organization and neural coding in the telencephalon of Anna's hummingbirds (Calypte anna) and zebra finches (Taeniopygia guttata) by using invivo extracellular electrophysiology to record activity in response to controlled tactile stimuli on various body regions. These findings reveal unique representations of body regions across distinct forebrain somatosensory nuclei, indicating significant differences in the extent of areas dedicated to certain body surfaces, which may correlate with their behavioral importance.

Thalamocortical Dynamics during Rapid Eye Movement Sleep in the Mouse Somatosensory Pathway.

Rapid eye movement (REM) sleep, also referred to as paradoxical sleep for the striking resemblance of its electroencephalogram (EEG) to the one observed in wakefulness, is characterized by the occurrence of transient events such as limb twitches or facial and rapid eye movements. Here, we investigated the local activity of the primary somatosensory or barrel cortex (S1) in naturally sleeping head-fixed male mice during REM. Through local field potential recordings, we uncovered local appearances of spindle waves in the barrel cortex during REM concomitant with strong delta power, challenging the view of a wakefulness-like activity in REM. We further performed extra- and intracellular recordings of thalamic cells in head-fixed mice. Our data show high-frequency thalamic bursts of spikes and subthreshold spindle oscillations in approximately half of the neurons of the ventral posterior medial nucleus which further confirmed the thalamic origin of local cortical spindles in S1 in REM. Cortical spindle oscillations were suppressed, while thalamus spike firing increased, associated with rapid mouse whisker movements and S1 cortical activity transitioned to an activated state. During REM, the sensory thalamus and barrel cortex therefore alternate between high (wake-like) and low (non-REM sleep-like) activation states, potentially providing a neuronal substrate for mnemonic processes occurring during this paradoxical sleep stage.

Beneficial Effects of Acupuncture for Depression-A Possible Mediation of Peripheral Sensory Stimulation and Central Oxytocin Release

In modern society, depression is one of the most common mental disorders. It is generally thought that depression is due to the disorders of neuronal circuits and chemical balance in the brain. Patients with depression often receive treatment with selective serotonin reuptake inhibitors (SSRIs). However, recent studies suggest that the magnitude of benefit of pharmacological treatment is quite limited for these patients. Although recent studies propose acupuncture as a non-pharmacological approach to managing depression, the mechanism of its beneficial effects is not well understood. Somatosensory pathways stimulated by acupuncture relay to the central nervous system (CNS). In animal studies, acupuncture has demonstrated the potential to ameliorate neural abnormalities associated with depression. As complex daily life stress is highly associated with depression, the procedure that suppresses stress responses would be a good candidate to treat depression. Oxytocin (OXT) is a hormone produced at the hypothalamus and mediates social bonding and stress reduction. OXT inhibits stress-induced corticotropin-releasing factor (CRF) expression at the hypothalamus, resulting in anti-stress and anti-anxiety effects. Research has demonstrated that acupuncture stimulates the release of hypothalamic OXT through somatosensory stimulation. Thus, stress-related mental disorders can be treated, at least in part, by acupuncture. It is proposed that somatosensory stimulations induced by acupuncture are a possible candidate as a non-pharmacological approach for depression.

Delays in latencies of median-nerve evoked magnetic fields in patients with succinic semialdehyde dehydrogenase deficiency

ObjectiveSuccinic semialdehyde dehydrogenase deficiency (SSADHD) is a genetic disorder resulting in abnormal regulation of γ-aminobutyric acid, lipid metabolism, and myelin biogenesis, leading to ataxia, seizures, and cognitive impairment. Since the myelin sheath is thinner in a murine model of SSADHD compared to a wild type, we hypothesized that this also holds for human brain. We tested whether the conduction velocity in the somatosensory pathway is accordingly delayed. MethodsSomatosensory evoked magnetic fields (SEF) produced by transcutaneous electrical stimulation of the median nerve were measured in 13 SSADHD patients, 11 healthy and 14 disease controls with focal epilepsy. The peak latencies of the initial four components (M1, M2, M3 and M4) were measured. ResultsThe SEF waveforms and scalp topographies were comparable across the groups. The latencies were statistically significantly longer in the SSADHD group compared to the two controls. We found these latencies for the SSADHD, healthy and disease controls respectively to be: M1: (21.9 ± 0.8 ms [mean ± standard error of the mean], 20.4 ± 0.6 ms, and 21.0 ± 0.4 ms) (p < 0.05); M2: (36.1 ± 1.0 ms, 33.1 ± 0.6 ms, and 32.1 ± 1.1 ms) (p < 0.005); M3: (62.5 ± 2.4 ms, 54.7 ± 2.0 ms, and 49.9 ± 1.8 ms) (p < 0.005); M4: (86.2 ± 2.3 ms, 78.8 ± 2.8 ms, and 73.5 ± 2.9 ms) (p < 0.005). ConclusionsThe SEF latencies are delayed in patients with SSADHD compared with healthy controls and disease controls. SignificanceThis is the first study that compares conduction velocities in the somatosensory pathway in SSADHD, an inherited disorder of GABA metabolism. The longer peak latency implying slower conduction velocity supports the hypothesis that myelin sheath thickness is decreased in SSADHD.

Soft Tissue Conduction Activates the Auditory Pathway in the Brain.

Soft tissue conduction is a mode of hearing which differs from air and bone conduction since the soft tissues of the body convey the audio-frequency vibrations to the ear. It is elicited by inducing soft tissue vibrations with an external vibrator applied to sites on the body or by intrinsic vibrations resulting from vocalization or the heartbeat. However, the same external vibrator applied to the skin sites also excites cutaneous mechanoreceptors, and attempts have been made to assist patients with hearing loss by audio-tactile substitution. The present study was conducted to assess the contribution of the auditory nerve and brainstem pathways to soft tissue conduction hearing. The study involved 20 normal hearing students, equipped with ear plugs to reduce the possibility of their response to air-conducted sounds produced by the external vibrator. Pure tone audiograms and speech reception (recognition) thresholds were determined in response to the delivery of the stimuli by a clinical bone vibrator applied to the cheek, neck and shoulder. Pure tone and speech recognition thresholds were obtained; the participants were able to repeat the words they heard by soft tissue conduction, confirming that the auditory pathways in the brain had been stimulated, with minimal involvement of the somatosensory pathways.

Whole Body Vibration's Potential to Improve Balance and Function in Cerebral Palsy in Weight and Non-Weight Bearing Positions: A Hypothesis Study

Cerebral palsy is one of the most prevalent neurological conditions in children. It has classical features of spasticity, poor balance and coordination, muscle weakness, proprioception, and inter-limb coordination. The primary cause is brain damage which affects certain circuits of the central nervous system. It has been reported that D1 inhibition is affected by cerebral palsy. The corticospinal and somatosensory pathways are also affected in the central nervous system along with abnormal activation of the motor neuron pool. There is abnormal presynaptic inhibition and post-activation depression of Ia afferents, while Group II facilitation is strongly enhanced. There are various therapies available to treat the symptoms of cerebral palsy, among which whole-body vibration therapy is considered to change the spinal transmission and somatosensory input. WBVT is typically administered in a weight bearing stance, targeting the lower extremities only. To the best of our knowledge, there is no research available exploring the cross-training effect of WBVT applied to upper and lower extremities, both weight and non-weight bearing positions, either alone on altogether. Hence, we propose that administering the WBVT across various configurations, incorporating weight and non-weight bearing positions for both upper and lower extremities could induce neural plasticity through cross training effect. We expect that by engaging all extremities in weight bearing positions may yield more significant outcomes compared to focusing solely on either upper or lower extremities.

Mechanisms of ocular surface pain

Ocular pain is evoked upon activation of a small number of nociceptive neurons located at the trigeminal ganglion whose peripheral projections profusely innervate the cornea and conjunctiva. In healthy conditions, nerve impulse activity originated at peripheral nerve endings of these primary sensory neurons in response to noxious or potentially noxious stimuli acting on the ocular surface travels centrally and reaches second‐order neurons located at the trigeminal brain stem complex. In turn, these brainstem neurons send their axons to the contralateral posterior thalamic nuclei, where the third neurons along the ocular nociceptive pathway are found. Thalamic neurons send their axons to the primary somatosensory area of the brain cortex and, after brain cortex processing if this sensory inflow, nociceptive pain sensation is experienced.The activity of ocular nociceptor neurons is modified under inflammation. Inflammatory mediators released at the ocular surface increase the excitability of the nerve terminals. As a result, the impulse response of primary nociceptor neurons to noxious stimuli is increased, which constitutes the basis of hyperalgesia and leads to pain and other sensations such as gritty eyes, foreign body sensation, etc. experienced under ocular inflammation.After a lesion (including surgery) or disease that affects any nerve or neuron of the ocular somatosensory pathway, the activity and connectivity of the neurons involved in ocular pain is altered, sometimes permanently. The excitability of damaged neurons is long‐lasting increased, leading to ocular dysesthesia and development of neuropathic pain referred to the eye.(Supported by PID2020‐115934RB‐I00 from DOI: MCIN/AEI/10.13039/50110001103, and CIPROM/2021/48 from the Generalitat Valenciana, Spain)

Evoked potential response in patients with idiopathic Parkinson’s disease and atypical parkinsonian syndromes: A comparative study

Patients with idiopathic Parkinson&amp;rsquo;s disease (IPD) and atypical parkinsonian syndromes (APSs) suffer from a range of disorders, especially in balance and locomotion, which necessitate visual, auditory, and somatosensory inputs. In this study, IPD patients, APS patients, and healthy controls (HCs) (n = 50 per group) underwent a series of assessments for visual evoked potentials (VEP), brainstem auditory evoked response (BAER), and short-latency somatosensory evoked potentials (SSEP). Results showed that VEP P100 latency was prolonged in multiple system atrophy-cerebellar type (MSA-C), multiple system atrophy-parkinsonian type (MSA-P), and corticobasal ganglionic degeneration (CBD) patients. The latency of peaks III and V was prolonged in IPD, MSA-C, dementia with Lewy bodies (DLB), and Parkinson&amp;rsquo;s disease dementia (PDD). BAER I-III and I-V interpeak latency were prolonged in IPD, DLB, and PDD, whereas BAER I-III, III-V, and I-V interpeak latencies were increased and the V/I amplitude ratio was decreased in MSA-C. The central sensory conduction time (N20-N13) was increased in MSA-P and MSA-C in SSEP. IPD patients had prolonged VEP P100 latency (P &lt; 0.001), lower VEP N75-P100 amplitude (P &lt; 0.001), prolonged BAER I, II, II, IV, V peak latencies (P &lt; 0.001), I-III, I-V interpeak latencies (P &lt; 0.001), lower BAER V/I amplitude ratio (P &lt; 0.001), and prolonged SSEP N13, N20, central sensory conduction time (N20-N13) (P &lt; 0.001) than HCs. IPD patients also had prolonged BAER I, II, II, IV, V peak latencies (P &lt; 0.001), prolonged I-III, I-V interpeak latencies (P &lt; 0.001), and shorter SSEP N13, N20, central sensory conduction time (N20-N13) (P &lt; 0.001) than APS patients. Moreover, APS patients had prolonged VEP P100 and N145 latencies (P &lt; 0.001) and decreased N75-N145 amplitude (P &lt; 0.001) compared to HCs. APS patients also had prolonged BAER II, II, IV, V peak latencies (P &lt; 0.001), prolonged I-III, III-V, I-V interpeak latencies (P &lt; 0.001), decreased V/I amplitude ratio, and prolonged SSEP N13, N20, central sensory conduction time (N20-N13) (P &lt; 0.001) than HCs. Postural instability and gait disorder (PIGD) IPD had significantly prolonged BAER III, V peak latencies (P &lt; 0.05), and prolonged III-V interpeak latencies (P &lt; 0.05) compared to tremor-dominant IPD. Overall, the IPD and APS patients had significant VEP, BAER, and SSEP abnormalities of demyelination and axonal variety in the visual, auditory, and somatosensory pathways. The changes were also correlated with the disease duration and severity. Although the diseases are predominantly motor disorders with significant non-motor components, these electrophysiological abnormalities might open a new avenue to assess the non-motor symptoms.

Cognitive Network Changes After Exposure to Haptic Vibrotactile Trigger Technology: Results From The ENHANCE Study

The conceptual framework of cognitive networks, or cognits, represents a system of working memory, especially long-term memory arrays that are intrinsically designed to attain certain behavioral ends and that are activated by a neural structure. Despite the fact that cognitions can be used in a plethora of systems, current technologies allow manipulations of the central nervous system (CNS) to execute certain sensory and motor functions. Sensation and tactual perception by the skin are an innate mechanism for human survival and represent our adaptive somatosensorial ability to apprehend information via haptics—the active touch for object recognition and perception by higher centers of the brain. The somatosensation, which is identified by a set of channels and receptors sensitive to a variety of stimuli (thermal, tactile, and mechanical), is critical to survival, balance control, cognition, and pain modulation. Cognits are cutting-edge tools and modalities that provide a landscape of theoretical assets, evidencebased experimental protocols, computational intelligence schemes, and direct empirical modalities that facilitate the understanding of the complex functionalities of the human brain. By evaluating neuroimaging data after somatosensory stimulation and collected via electroencephalogram (EEG), cognition response and change can be obtained that allows researchers to gain a better understanding of emerging scientific approaches aimed at understanding human behavioral outcomes. An emerging technology, haptic vibrotactile trigger technology (VTT), incorporates somatosensory patterns in compression sleeves. eSmartr Smart Compression Sleeves (Srysty Holdings Inc., Mississauga, ON, Canada) with VTT and its Cognitive Boost Technology (CBT) pattern is designed to optimize neural communications for improved mindful wellness. This technology has also been incorporated into patches, braces, apparel (socks), wrist bands, and other routes of delivery. Mindful wellness is considered an outcome of somatosensory intervention that modulates the behavioral responses associated with cognitive networks. Currently, there is limited research exploring these modalities, exposing the need to study new technologies and their influence on somatosensory pathways and cognitive networks. The purpose of this IRB-approved study was to explore the effects of forearm VTT stimulation patterns on cognitive networks by comparing a baseline EEG to an EEG after placing a sleeve incorporating VTT on the right or left forearm of adult healthy individuals. Materials and methods: A baseline EEG was recorded over 5 minutes from 19 scalp locations on 20 subjects ranging in age from 17.6 years to 41.9 years (n=7 females, 13 males). The subject’s dominant arm was then fitted with the eSmartr Smart Compression Sleeve for 20 minutes and another 5-minute EEG was recorded. Both the LORETA (Low Resolution Electromagnetic Tomography Analysis) inverse solution and a power spectral analysis of the surface EEG were calculated. Additionally, for 10 distinct networks, the current sources from 88 Brodmann areas were computed. The variables were absolute power and absolute current density in 1 Hz increments in 10 frequency bands (delta, theta, alpha-1, alpha-2, beta-1, beta-2, beta-3, and hi-beta). Paired t-tests were computed for each individual for all EEG parameters, as well as group paired t-tests, between the baseline EEG and followup EEG. Results: The results showed statistically significant t-test differences (P &lt; 0.01) in both the surface EEG and the LORETA current sources between the baseline measurement and the follow-up ‘sleeve-on’ measurement. The largest differences were detected with a prominent downregulation of alpha and beta frequency powers at both the surface EEG and the LORETA current sources with the “sleeve-on,” as compared to baseline. In addition, the maximal effects of the “sleeve-on” condition were in the left frontal and left temporal surface EEGs and on the medial bank of the somatosensory cortex in the range of the alpha frequency. Changes in the default network and attention network were also prominent. Conclusions: Study results indicate that these non-pharmacologic, non-invasive, haptic vibrotactile trigger technology (VTT) patterned compression sleeves elicited a response in multiple cognitive networks. These networks play a key role in executive function, memory, attention, mood, and information flow. There was a prominent effect of the haptic vibrotactile trigger technology with the CBT- patterned sleeves on the EEG that was primarily located in alpha and beta frequency bands. The substantial impacts on the homuncular projection of the arm to the medial somatosensory cortex as well as the default network demonstrated activity influenced by the patterned sleeve. The mechanisms of action of the VTT sleeve on the brain, neuropathways, and the EEG spectrum are still being investigated. If results are confirmed with further research, this novel VTT technology could be a promising addition as a non-invasive and non-drug treatment approach for a variety of conditions and therapeutic applications.

Synaptic Origin of Early Sensory-evoked Oscillations in the Immature Thalamus.

During the critical period of postnatal development, brain maturation is extremely sensitive to external stimuli. Newborn rodents already have functional somatosensory pathways and the thalamus, but the cortex is still forming. Immature thalamic synapses may produce large postsynaptic potentials in immature neurons, while non-synaptic membrane currents remain relatively weak and slow. The thalamocortical system generates spontaneous and evoked early gamma and spindle-burst oscillations in newborn rodents. How relatively strong synapses and weak intrinsic currents interact with each other and how they contribute to early thalamic activities remains largely unknown. Here, we performed local field potential (LFP), juxtacellular, and patch-clamp recordings in the somatosensory thalamus of urethane-anesthetized rat pups at postnatal days 6-7 with one whisker stimulation. We removed the overlying cortex and hippocampus to reach the thalamus with electrodes. Deflection of only one (the principal) whisker induced spikes in a particular thalamic cell. Whisker deflection evoked a group of large-amplitude excitatory events, likely originating from lemniscal synapses and multiple inhibitory postsynaptic events in thalamocortical cells. Large-amplitude excitatory events produced a group of spike bursts and could evoke a depolarization block. Juxtacellular recordings confirmed the partial inactivation of spikes. Inhibitory events prevented inactivation of action potentials and gamma-modulated neuronal firing. We conclude that the interplay of strong excitatory and inhibitory synapses and relatively weak intrinsic currents produces sensory-evoked early gamma oscillations in thalamocortical cells. We also propose that sensory-evoked large-amplitude excitatory events contribute to evoked spindle-bursts.

Somatosensory pathway dysfunction in patients with amyotrophic lateral sclerosis in a completely locked-in state

ObjectiveTo investigate somatosensory pathway function in patients with amyotrophic lateral sclerosis (ALS) dependent on invasive ventilation and in a completely locked-in state (CLIS). MethodsWe examined median nerve somatosensory evoked potentials (SEPs) in 17 ALS patients in a CLIS, including 11 patients with sporadic ALS, one with familial ALS with genes not examined, four with a Cu/Zn superoxide-dismutase-1 (SOD1) gene variant (Val118Leu, Gly93Ser, Cys146Arg), and one with a fused-in-sarcoma gene variant (P525L). We evaluated N9, N13, N20 and P25, and central conduction time (CCT); the data were compared with those of 73 healthy controls. ResultsN20 and N13 were abolished in 12 and 10 patients, and their latencies was prolonged in four and three patients, respectively. The CCT was prolonged in five patients with measurable N13 and N20. Two patients with SOD1 gene mutations had absent or slightly visible N9. Compared to the CCT and latencies and amplitudes of N13 and N20 in the controls, those in the patient cohort were significantly abnormal. ConclusionsThe central somatosensory pathway is severely involved in patients with ALS in a CLIS. SignificanceOur findings suggest that median nerve SEP cannot be utilized for communication in patients with ALS in a CLIS.

Increased excitability and reduced GABAergic levels in somatosensory cortex under chronic spinal cord injury

The complete or partial damage of ascending somatosensory pathways produced by a spinal cord injury triggers changes in the somatosensory cortex consisting in a functional expansion of activity from intact cortical regions towards deafferented ones, a process known as cortical reorganization. However, it is still unclear whether cortical reorganization depends on the severity of the spinal cord damage or if a spinal cord injury always leads to a similar cortical reorganization process in the somatosensory cortex. To answer these open questions in the field, we obtained longitudinal somatosensory evoked responses from bilateral hindlimb and forelimb cortex from animals with chronic full-transection or contusive spinal cord injury at thoracic level (T9-T10) to induce sensory deprivation of hindlimb cortex while preserving intact the forelimb cortex. Electrophysiological recordings from the four locations were obtained before lesion and weekly for up to 4 weeks. Our results show that cortical reorganization depends on the type of spinal cord injury, which tends to be more bilateral in full transection while is more unilateral in the model of contusive spinal cord injury. Moreover, in full transection of spinal cord, the deafferented and intact cortex exhibited similar increments of somatosensory evoked responses in both models of spinal cord injury - a feature observed in about 80% of subjects. The other 20% were unaffected by the injury indicating that cortical reorganization does not undergo in all subjects. In addition, we demonstrated an increased probability of triggered up-states in animals with spinal cord injury. This data indicates increased cortical excitability that could be proposed as a new feature of cortical reorganization. Finally, decreased levels of GABA marker GAD67 across cortical layers were only found in those animals with increased somatosensory evoked responses, but not in the unaffected population. In conclusion, cortical reorganization depends on the types of spinal cord injuries, and suggest that the phenomenon is strongly determined by cortical circuits. Moreover, changes in GABAergic transmission at the deprived cortex may be considered one of the mechanisms underlying the process of cortical reorganization and increased excitability.

Evaluation of Sexual Function in Patients with Lower Lumbar Disc Herniation: A Comparison of Pre- and Postoperative Status.

Neuroregulation of sexual functions requires coordination of parasympathetic, sympathetic, and somatosensory neuronal pathways. The nerves formed by the lower lumbar plexus provide the innervation of the urogenital organs. Lower lumbar disc hernias (LDHs) might impair the neuroregulation of sexual functions by compressing the neural structures. This prospective study aims to evaluate the effect of lower LDHs on libido and sexual dysfunctions. A total of 61 sexually active patients diagnosed with single-level LDH who underwent unilateral microdiscectomy were included in the study. The patients' healthy sex partners were included in study as controls. The International Sexual Function Index-5 (IIEF-5) and Female Sexual Function Index (FSFI) were used for sexual assessment of male and female participants, respectively. Visual Analog Scale (VAS) was used for pain assessment. According to the FSFI scores, all 20 female patients had preoperative sexual dysfunction, which improved in 15 (75%) patients after surgery (p < 0.001). According to the IIEF-5 score for men, 38 of 41 male patients had preoperative sexual dysfunction, which improved in 26 (68.4%) patients postoperatively (p < 0.001). The preoperative sexual dysfunctions of LDH patients improved significantly after the microdiscectomy.

ID: 211374 Spinal Cord Stimulation for Diffuse Neuropathic Pain After Spinal Cord Injury

Post spinal cord injury (SCI) patients often develop chronic neuropathic pain [1]. Management of pain in these complex patients is frequently inadequate leading to a significant negative impact on quality of life and rehabilitation. Neuropathic pain is usually diffuse, severely debilitating, and can affect 30-80% of SCI injury patients [2]. Current understanding of the mechanism for this pain is limited and broadly attributed to dysfunctional somatosensory pathways. Neuromodulation as a therapeutic option for SCI neuropathic pain has been poorly studied [3].