Degraded tactile coding in the Cntnap2 mouse model of autism.

Atypical sensory processing is common in autism, but how neural coding is disrupted in sensory cortex is unclear. We evaluate whisker touch coding in L2/3 of somatosensory cortex (S1) in Cntnap2-/- mice, which have reduced inhibition. This classically predicts excess pyramidal cell spiking, but this remains controversial, and other deficits may dominate. We find that c-fos expression is elevated in S1 of Cntnap2-/- mice under spontaneous activity conditions but is comparable to that of control mice after whisker stimulation, suggesting normal sensory-evoked spike rates. GCaMP8m imaging from L2/3 pyramidal cells shows no excess whisker responsiveness, but it does show multiple signs of degraded somatotopic coding. This includes broadened whisker-tuning curves, a blurred whisker map, and blunted whisker point representations. These disruptions are greater in noisy than in sparse sensory conditions. Tuning instability across days is also substantially elevated in Cntnap2-/-. Thus, Cntnap2-/- mice show no excess sensory-evoked activity, but a degraded and unstable tactile code in S1.

Cholinergic upregulation by optogenetic stimulation of nucleus basalis after photothrombotic stroke in forelimb somatosensory cortex improves endpoint and motor but not sensory control of skilled reaching in mice.

A network of cholinergic neurons in the basal forebrain innerve the forebrain and are proposed to contribute to a variety of functions including cortical plasticity, attention, and sensorimotor behavior. This study examined the contribution of the nucleus basalis cholinergic projection to the sensorimotor cortex on recovery on a skilled reach-to-eat task following photothrombotic stroke in the forelimb region of the somatosensory cortex. Mice were trained to perform a single pellet skilled reaching task and their pre and poststroke performance, from Day 4 to Day 28 poststroke, was assessed frame-by-frame by video analysis with endpoint, movement and sensorimotor integration measures. Somatosensory forelimb lesions produced impairments in endpoint and movement component measures of reaching and increased the incidence of fictive eating, a sensory impairment in mistaking a missed reach for a successful reach. Upregulated acetylcholine (ACh) release, as measured by local field potential recording, elicited via optogenetic stimulation of the nucleus basalis improved recovery of reaching and improved movement scores but did not affect sensorimotor integration impairment poststroke. The results show that the mouse cortical forelimb somatosensory region contributes to forelimb motor behavior and suggest that ACh upregulation could serve as an adjunct to behavioral therapy for acute treatment of stroke.

Direct Evidence of Plasticity within Human Primary Motor and Somatosensory Cortices of Patients with Glioblastoma.

Glioblastoma multiforme (GBM) is a devastating disease without cure. It is also the most common primary brain tumor in adults. Although aggressive surgical resection is standard of care, these operations are limited by tumor infiltration of critical cortical and subcortical regions. A better understanding of how the brain can recover and reorganize function in response to GBM would provide valuable clinical data. This ability, termed neuroplasticity, is not well understood in the adult human brain. A better understanding of neuroplasticity in GBM could allow for improved extent of resection, even in areas classically thought to have critical, static function. The best evidence to date has demonstrated neuroplasticity only in slower growing tumors or through indirect measures such as functional MRI or transcranial magnetic stimulation. In this novel study, we utilize a unique experimental paradigm to show direct evidence of plasticity via serial direct electrocortical stimulation (DES) within primary motor (M1) and somatosensory (S1) cortices in GBM patients. Six patients with glioblastoma multiforme in or near the primary motor or somatosensory cortex were included in this retrospective observational study. These patients had two awake craniotomies with DES to map cortical motor and sensory sites in M1 and S1. Five of six patients exhibited at least one site of neuroplasticity within M1 or S1. Out of the 51 total sites stimulated, 32 (62.7%) demonstrated plasticity. Of these sites, 14 (43.7%) were in M1 and 18 (56.3%) were in S1. These data suggest that even in patients with GBM in or near primary brain regions, significant functional reorganization is possible. This is a new finding which may lead to a better understanding of the fundamental factors promoting or inhibiting plasticity. Further exploration may aid in treatment of patients with brain tumors and other neurologic disorders.

Differences in EEG patterns between tonic and high frequency spinal cord stimulation in chronic pain patients.

OBJECTIVE: To investigate the differences in neural patterns between spinal cord stimulation (SCS) waveforms (60-Hz tonic vs 10-KHz high frequency stimulation, HFS) and their correlation to stimulation-induced pain relief. METHODS: We recorded 10-channel electroencephalogram (EEG) in response to stimulation ON and OFF in 9 chronic pain patients (4 women, 5 men) during SCS surgery and examined the intraoperative spatio-spectral EEG features. RESULTS: We discovered stronger relative alpha power in the somatosensory region and higher trend in alpha/theta peak power ratio in frontal cortex with HFS. We also observed a shift in peak frequency from theta to alpha rhythms in HFS as compared to baseline and tonic stimulation, where slower theta activity was maintained. Further, a positive correlation was found between changes in Oswestry disability index (ODI) scores (from preoperative to postoperative) and HFS-induced alpha/theta peak power ratio in frontal and somatosensory regions. CONCLUSIONS: Altogether, our findings suggest that dynamic spectral interactions in theta-alpha band and their spatial distributions might be the first intraoperative neural signatures of pain relief induced by HFS in chronic pain. SIGNIFICANCE: Examining electrophysiological changes intraoperatively has a potential to elucidate response to SCS therapy prior to device selection, reducing the healthcare expenditures associated with failed implants.

EEG patterns associated with present cortical SSEP after cardiac arrest.

BACKGROUND: After cardiac arrest (CA), present cortical somatosensory evoked potentials (N20 response of SSEPs) have low predictive value for good outcome and might be redundant with EEG. AIMS: To determine whether specific features, or rather global, standardized EEG assessments, are reliably associated with cortical SSEP occurrence after cardiac arrest (CA). METHODS: In a prospective CA registry, EEGs recorded within 72 hours were scored according to the ACNS nomenclature, and also categorized into "benign," "malignant," and "highly malignant." Correlations between EEGs and SSEPs (bilaterally absent vs present), and between EEGs/SSEPs and outcome (good: CPC 1-2) were assessed. RESULTS: Among 709 CA episodes, 532 had present N20 and 366 "benign EEGs." While EEG categories as well as background, epileptiform features, and reactivity differed significantly between patients with and without N20 (each P < .001), only "benign EEG" was almost universally associated with present N20: 99.5% (95%CI: 97.9%-99.9%) PPV. The combination of "benign EEG" and present N20 showed similar PPV for good outcome as "benign" EEG alone: 69.0% (95% CI: 65.2-72.4) vs 68.6% (95% CI: 64.9-72.0). CONCLUSION: Global EEG ("benign") assessment, rather than single EEG features, can reliably predict cortical SSEP occurrence. SSEP adjunction does not increase EEG prognostic performance toward good outcome. SSEP could therefore be omitted in patients with "benign EEG."

Activity in grafted human iPS cell-derived cortical neurons integrated in stroke-injured rat brain regulates motor behavior.

Stem cell transplantation can improve behavioral recovery after stroke in animal models but whether stem cell-derived neurons become functionally integrated into stroke-injured brain circuitry is poorly understood. Here we show that intracortically grafted human induced pluripotent stem (iPS) cell-derived cortical neurons send widespread axonal projections to both hemispheres of rats with ischemic lesions in the cerebral cortex. Using rabies virus-based transsynaptic tracing, we find that at 6 mo after transplantation, host neurons in the contralateral somatosensory cortex receive monosynaptic inputs from grafted neurons. Immunoelectron microscopy demonstrates myelination of the graft-derived axons in the corpus callosum and that their terminals form excitatory, glutamatergic synapses on host cortical neurons. We show that the stroke-induced asymmetry in a sensorimotor (cylinder) test is reversed by transplantation. Light-induced inhibition of halorhodopsin-expressing, grafted neurons does not recreate the impairment, indicating that its reversal is not due to neuronal activity in the graft. However, we find bilateral decrease of motor performance in the cylinder test after light-induced inhibition of either grafted or endogenous halorhodopsin-expressing cortical neurons, located in the same area, and after inhibition of endogenous halorhodopsin-expressing cortical neurons by exposure of their axons to light on the contralateral side. Our data indicate that activity in the grafted neurons, probably mediated through transcallosal connections to the contralateral hemisphere, is involved in maintaining normal motor function. This is an example of functional integration of efferent projections from grafted neurons into the stroke-affected brain's neural circuitry, which raises the possibility that such repair might be achievable also in humans affected by stroke.

Effect of U-92032, T-Type Ca2+ Channel Blocker, on Rats with Genetic Absence Epilepsy.

INTRODUCTION: Absence epilepsy is associated with diffuse spike-and-wave discharges (SWD) on the electroencephalogram (EEG). Recent studies have demonstrated that the primary somatosensory cortex is also implicated in the generation of the SWDs. OBJECTIVE: This study investigated the effects of systemic and local administrations of U-92032 into the brain of Genetic Absence Epilepsy Rats from Strasbourg (GAERS). METHODS: GAERS animals underwent stereotaxic surgery for the placement of EEG recording electrodes and guide cannulas for U-92032 administration into the lateral ventricle (intracerebroventricular [i.c.v.]), upper lips area (S1Ulp) or barrel field area (S1B) of primary somatosensory cortex. Following 7 days of recovery, electrical activity was recorded continuously for 1 h before and 6 h after intraperitoneal (0.25; 1; 5 mg/kg i.p.) or local U-92032 or dimethyl sulfoxide (DMSO) injections. RESULTS: No changes were detected in the cumulative duration, mean duration, and number of SWDs following i.p. U-92032 injections. Local i.c.v. injections of U-92032 caused a significant decrease in the cumulative duration (i.c.v., 50 and 100 nmol/L), mean duration (i.c.v., 50, 100, and 250 nmol/L), and the number (i.c.v., 250 nmol/L) of SWDs compared to DMSO groups. Intra-cortical (S1Ulp and S1B) U-92032 injections caused a significant decrease in all 3 parameters compared to DMSO groups, as well. CONCLUSION: Intra-cortical injection of U-92032 caused almost complete removal of SWDs in GAERS and i.c.v. administration resulted in a significant reduction. However, systemic i.p. administration did not cause a significant change with the applied -doses.

The influence of nociceptive and neuropathic pain states on the processing of acute electrical nociceptive stimulation: A dynamic causal modeling study.

INTRODUCTION: Despite the worldwide increase in prevalence of chronic pain and the subsequent scientific interest, researchers studying the brain and brain mechanisms in pain patients have not yet clearly identified the exact underlying mechanisms. Quantifying the neuronal interactions in electrophysiological data could help us gain insight into the complexity of chronic pain. Therefore, the aim of this study is to examine how different underlying pain states affect the processing of nociceptive information. METHODS: Twenty healthy participants, 20 patients with non-neuropathic low back-related leg pain and 20 patients with neuropathic failed back surgery syndrome received nociceptive electrical stimulation at the right sural nerve with simultaneous electroencephalographic recordings. Dynamic Causal Modeling (DCM) was used to infer hidden neuronal states within a Bayesian framework. RESULTS: Pain intensity ratings and stimulus intensity of the nociceptive stimuli did not differ between groups. Compared to healthy participants, both patient groups had the same winning DCM model, with an additional forward and backward connection between the somatosensory cortex and right dorsolateral prefrontal cortex. DISCUSSION: The additional neuronal connection with the prefrontal cortex as seen in both pain patient groups could be a reflection of the higher attention towards pain in pain patients and might be explained by the higher levels of pain catastrophizing in these patients. CONCLUSION: In contrast to the similar pain intensity ratings of an acute nociceptive electrical stimulus between pain patients and healthy participants, the brain is processing these stimuli in a different way.

Effects of gabapentinoids on responses of primary cultures from rat dorsal root ganglia to inflammatory or somatosensory stimuli.

Background Gabapentinoids are known to reduce neuropathic pain. The aim of this experimental study was to investigate whether gabapentinoids exert anti-inflammatory and/or anti-nociceptive effects at the cellular level using primary cultures of rat dorsal root ganglia (DRG). Methods Cells from rat DRG were cultured in the presence of gabapentin or pregabalin, and we tested the effects of subsequent stimulation with lipopolysaccharide (LPS) on the expression of genes (real-time polymerase chain reaction) and production of tumor necrosis factor-α (TNFα) and interleukin-6 (IL-6) by specific bioassays. Using Ca2+ imaging, we further investigated in neurons the effects of gabapentinoids upon stimulation with the TRPV-1 agonist capsaicin. Results There is a small influence of gabapentinoids on the inflammatory response to LPS stimulation, namely, a significantly reduced expression of IL-6. Pregabalin and gabapentin further seem to exert a moderate inhibitory influence on capsaicin-induced Ca2+ signals in DRG neurons. Conclusions Although the single inhibitory effects of gabapentinoids on inflammatory and nociceptive responses are moderate, a combination of both effects might provide an explanation for the proposed function of these substances as an adjuvant for the reduction of neuropathic pain.

Small damage of brain parenchyma reliably triggers spreading depolarization.

Objectives: Spreading depolarization (SD) is a well-recognized component of the stress response of the cortex to its acute injury. Cortical SD has been shown to occur in severe brain insults and standard neurosurgical procedures in patients and is supposed to promote delayed secondary brain injuries. Stereotactic surgery and site-specific intracerebral microinjections produce a small tissue injury when a thin needle is inserted directly into the brain parenchyma (via the cannula guide). The present study was designed to examine whether such a parenchymal damage can trigger SD.Methods: Experiments were performed in awake freely moving rats with simultaneous video-monitoring of behavior and recording of SD-related DC potentials in the cortex and striatum. A parenchymal damage was produced by 1-mm protruding of thin (0.3-mm diameter) cannula beyond the tip of cannula guide preliminary implanted into the amygdala or deep cortical layers.Results: We found that the micro-injury of the brain parenchyma the volume of which did not exceed 0.3 mm3 was sufficient to initiate SD in a very high proportion of rats (75-100%). The amygdala showed increased resistance against the injury-induced SD compared to the cortex. We further showed that SD triggered by the local micro-injury invaded remote intact regions of the cortico-striatal system and evoked specific changes in spontaneous animal behavior.Discussion: The findings indicate that SD may represent a previously unidentified side effect of local parenchymal injury during site-specific microinjections and stereotactic surgery.

A magnetoencephalographic study of longitudinal brain function alterations following carpal tunnel release.

We investigate changes in brain function before and after carpal tunnel release. Magnetoencephalography (MEG), during which we recorded somatosensory evoked cortical magnetic fields (SEFs), and a clinical evaluation were performed before surgery and 6 months after. The distance on the vertical axis between the equivalent current dipoles (ECDs) for the first and third digits before surgery was significantly less than after surgery. There were no significant differences in values between the control participant and patients after surgery. In terms of distal motor latency, there was a negative correlation with the distance. The recovery function of the root mean square (RMS) before surgery for the N20m was less suppressed at 10 ms of ISI in patients, compared to controls. There were no significant differences in the RMS values for patients before and after surgery. Our results indicate that treating peripheral nerve lesions, such as in carpal tunnel release, positively modifies brain function.

Early recovery of neuronal functioning in the sensory cortex after nerve reconstruction surgery.

BACKGROUND: Nerve reconstructive surgery induces a transient loss and a prolonged and a gradual return of sensory inputs to the brain. It is unknown whether, following this massive peripheral denervation, the brain will experience a prolonged period of severe, intrinsic dysfunction. OBJECTIVE: We aim to investigate the mechanisms of return of processing function in cortical neurons. METHODS: We used the whisker model in rats to evaluate the functional recovery in the somatosensory cortex after a nerve reconstruction surgery. Multi-unit recording in the barrel cortex was performed in lightly anesthetized rats while their whiskers were stimulated by a whisker stimulator. RESULTS: We observed a loss of neuronal responses to whisker stimulation 1 week after surgery, which started to recover 2 weeks after surgery. Following the surgery, only 11.8% of units had principle whiskers (PWs) returned to their original status while 17.7% had PWs different from their original status, indicating the effect of aberrant reinnervation on the whisker response map. CONCLUSIONS: Robust neuronal responses to sensory stimulation even when only sparse sensory inputs are available in the early recovery phase. During this phase, aberrant reinnervation induces disorganized whisker tuning, a finding that might be account for the hypoesthesia and paresthesia during early recovery after nerve reconstruction.

Comparative fMRI and MEG localization of cortical sensorimotor function: Bimodal mapping supports motor area reorganization in glioma patients.

INTRODUCTION: Preoperative functional mapping in the vicinity of brain lesion is of high importance for avoiding complications in surgical management. However, space-occupying lesions may lead to functional reorganization or decreased BOLD activity. METHODS: Therefore in 13 patients with cerebral gliomas or brain arterio-venous malformations/ hemangioma fMRI- and MEG-based cortical localizations of motor and somatosensory cortical activation pattern were compared in order to investigate their congruency. RESULTS: Localization of cortical sensorimotor areas with fMRI and MEG showed good congruency with a mean spatial distance of around 10 mm, with differences depending on the localization method. The smallest mean differences for the centroids were found for MEF with MNE 8 mm and SEF with sLORETA 8 mm. Primary motor area (M1) reorganization was found in 5 of 12 patients in fMRI and confirmed with MEG data. In these 5 patients with M1-reorganization the distance between the border of the fMRI-based cortical M1-localization and the tumor border on T1w MR images varied between 0-4 mm, which was significant (P = 0.025) different to the distance in glioma patients without M1-reorganization (5-26 mm). CONCLUSION: Our multimodal preoperative mapping approach combining fMRI and MEG reveals a high degree of spatial congruence and provided high evidence for the presence of motor cortex reorganization.

Aberrant Somatosensory Processing and Connectivity in Mice Lacking Engrailed-2.

Overreactivity and defensive behaviors in response to tactile stimuli are common symptoms in autism spectrum disorder (ASD) patients. Similarly, somatosensory hypersensitivity has also been described in mice lacking ASD-associated genes such as Fmr1 (fragile X mental retardation protein 1). Fmr1 knock-out mice also show reduced functional connectivity between sensory cortical areas, which may represent an endogenous biomarker for their hypersensitivity. Here, we measured whole-brain functional connectivity in Engrailed-2 knock-out (En2-/-) adult mice, which show a lower expression of Fmr1 and anatomical defects common to Fmr1 knock-outs. MRI-based resting-state functional connectivity in adult En2-/- mice revealed significantly reduced synchronization in somatosensory-auditory/associative cortices and dorsal thalamus, suggesting the presence of aberrant somatosensory processing in these mutants. Accordingly, when tested in the whisker nuisance test, En2-/- but not WT mice of both sexes showed fear behavior in response to repeated whisker stimulation. En2-/- mice undergoing this test exhibited decreased c-Fos-positive neurons (a marker of neuronal activity) in layer IV of the primary somatosensory cortex and increased immunoreactive cells in the basolateral amygdala compared with WT littermates. Conversely, when tested in a sensory maze, En2-/- and WT mice spent a comparable time in whisker-guided exploration, indicating that whisker-mediated behaviors are otherwise preserved in En2 mutants. Therefore, fearful responses to somatosensory stimuli in En2-/- mice are accompanied by reduced basal connectivity of sensory regions, reduced activation of somatosensory cortex, and increased activation of the basolateral amygdala, suggesting that impaired somatosensory processing is a common feature in mice lacking ASD-related genes.SIGNIFICANCE STATEMENT Overreactivity to tactile stimuli is a common symptom in autism spectrum disorder (ASD) patients. Recent studies performed in mice bearing ASD-related mutations confirmed these findings. Here, we evaluated the behavioral response to whisker stimulation in mice lacking the ASD-related gene Engrailed-2 (En2-/- mice). Compared with WT controls, En2-/- mice showed reduced functional connectivity in the somatosensory cortex, which was paralleled by fear behavior, reduced activation of somatosensory cortex, and increased activation of the basolateral amygdala in response to repeated whisker stimulation. These results suggest that impaired somatosensory signal processing is a common feature in mice harboring ASD-related mutations.

In Vivo Femtosecond Laser Subsurface Cortical Microtransections Attenuate Acute Rat Focal Seizures.

Recent evidence shows that seizures propagate primarily through supragranular cortical layers. To selectively modify these circuits, we developed a new technique using tightly focused, femtosecond infrared laser pulses to make as small as ~100 µm-wide subsurface cortical incisions surrounding an epileptic focus. We use this "laser scalpel" to produce subsurface cortical incisions selectively to supragranular layers surrounding an epileptic focus in an acute rodent seizure model. Compared with sham animals, these microtransections completely blocked seizure initiation and propagation in 1/3 of all animals. In the remaining animals, seizure frequency was reduced by 2/3 and seizure propagation reduced by 1/3. In those seizures that still propagated, it was delayed and reduced in amplitude. When the recording electrode was inside the partially isolated cube and the seizure focus was on the outside, the results were even more striking. In spite of these microtransections, somatosensory responses to tail stimulation were maintained but with reduced amplitude. Our data show that just a single enclosing wall of laser cuts limited to supragranular layers led to a significant reduction in seizure initiation and propagation with preserved cortical function. Modification of this concept may be a useful treatment for human epilepsy.

Intraoperative mapping of the sensory cortex by time-resolved thermal imaging.

The resection of brain tumor requires a precise distinction between eloquent areas of the brain and pathological tumor tissue in order to improve the extent of resection as well as the patient's progression free survival time. In this study, we discuss mathematical tools necessary to recognize neural activity using thermal imaging cameras. The main contribution to thermal radiation of the exposed human cortex is regional cerebral blood flow (CBF). In fact, neurovascular coupling links neural activity to changes in regional CBF which in turn affects the cortical temperature. We propose a statistically sound framework to visualize neural activity of the primary somatosensory cortex. The framework incorporates a priori known experimental conditions such as the thermal response to neural activity as well as unrelated effects induced by random neural activity and autoregulation. These experimental conditions can be adopted to certain electrical stimulation protocols so that the framework allows to unveil arbitrary evoked neural activity. The method was applied to semisynthetic as well as two intraoperative cases with promising results as we were able to map the eloquent sensory cortex with high sensitivity. Furthermore, the results were validated by anatomical localization and electrophysiological measurements.

Investigation on the Neural Mechanism of Hypnosis-Based Respiratory Control Using Functional MRI.

Respiratory control is essential for treatment effect of radiotherapy due to the high dose, especially for thoracic-abdomen tumor, such as lung and liver tumors. As a noninvasive and comfortable way of respiratory control, hypnosis has been proven effective as a psychological technology in clinical therapy. In this study, the neural control mechanism of hypnosis for respiration was investigated by using functional magnetic resonance imaging (fMRI). Altered spontaneous brain activity as well as neural correlation of respiratory motion was detected for eight healthy subjects in normal state (NS) and hypnosis state (HS) guided by a hypnotist. Reduced respiratory amplitude was observed in HS (mean ± SD: 14.23 ± 3.40 mm in NS, 12.79 ± 2.49 mm in HS, p=0.0350), with mean amplitude deduction of 9.2%. Interstate difference of neural activity showed activations in the visual cortex and cerebellum, while deactivations in the prefrontal cortex and precuneus/posterior cingulate cortex (PCu/PCC) in HS. Within these regions, negative correlations of neural activity and respiratory motion were observed in visual cortex in HS. Moreover, in HS, voxel-wise neural correlations of respiratory amplitude demonstrated positive correlations in cerebellum anterior lobe and insula, while negative correlations were shown in the prefrontal cortex and sensorimotor area. These findings reveal the involvement of cognitive, executive control, and sensorimotor processing in the control mechanisms of hypnosis for respiration, and shed new light on hypnosis performance in interaction of psychology, physiology, and cognitive neuroscience.

Somatosensory function and pain in extremely preterm young adults from the UK EPICure cohort: sex-dependent differences and impact of neonatal surgery.

BACKGROUND: Surgery or multiple procedural interventions in extremely preterm neonates influence neurodevelopmental outcome and may be associated with long-term changes in somatosensory function or pain response. METHODS: This observational study recruited extremely preterm (EP, <26 weeks' gestation; n=102, 60% female) and term-born controls (TC; n=48) aged 18-20 yr from the UK EPICure cohort. Thirty EP but no TC participants had neonatal surgery. Evaluation included: quantitative sensory testing (thenar eminence, chest wall); clinical pain history; questionnaires (intelligence quotient; pain catastrophising; anxiety); and structural brain imaging. RESULTS: Reduced thermal threshold sensitivity in EP vs TC participants persisted at age 18-20 yr. Sex-dependent effects varied with stimulus intensity and were enhanced by neonatal surgery, with reduced threshold sensitivity in EP surgery males but increased sensitivity to prolonged noxious cold in EP surgery females (P<0.01). Sex-dependent differences in thermal sensitivity correlated with smaller amygdala volume (P<0.05) but not current intelligence quotient. While generalised decreased sensitivity encompassed mechanical and thermal modalities in EP surgery males, a mixed pattern of sensory loss and sensory gain persisted adjacent to neonatal scars in males and females. More EP participants reported moderate-severe recurrent pain (22/101 vs 4/48; χ2=0.04) and increased pain intensity correlated with higher anxiety and pain catastrophising. CONCLUSIONS: After preterm birth and neonatal surgery, different patterns of generalised and local scar-related alterations in somatosensory function persist into early adulthood. Sex-dependent changes in generalised sensitivity may reflect central modulation by affective circuits. Early life experience and sex/gender should be considered when evaluating somatosensory function, pain experience, or future chronic pain risk.

Variability and bias between magnetoencephalography systems in non-invasive localization of the primary somatosensory cortex.

OBJECTIVES: Magnetoencephalography (MEG) provides functional neuroimaging data for pre-surgical planning in patients with epilepsy or brain tumour. For mapping the primary somatosensory cortex (S1), MEG data are acquired while a patient undergoes median nerve stimulation (MNS) to localize components of the somatosensory evoked field (SEF). In clinical settings, only one MEG imaging session is usually possible due to limited resources. As such, it is important to have an a priori estimate of the expected variability in localization. Variability in S1 localization between mapping sessions using the same MEG system has been previously measured as 8 mm. There are different types of MEG systems available with varied hardware and software, and it is not known how using a different MEG system will impact on S1 localization. PATIENTS AND METHODS: In our study, healthy participants underwent the MNS procedure with two different MEG systems (Vector View and CTF). We compared the location, amplitude and latency of SEF components between data from each system to quantify variability and bias between MEG systems. RESULTS: We found 8-11 mm variability in S1 localization between the two MEG systems, and no evidence for a systematic bias in location, amplitude or latency between the two systems. CONCLUSION: These findings suggest that S1 localization is not biased by the type of MEG system used, and that differences between the two systems are not a major contributor to variability in localization.

Negative myoclonus secondary to paroxetine intake.

Outside the context of overdose and serotonin syndrome, seizures and myoclonic movements attributed to selective serotonin reuptake inhibitors (SSRIs) are rare and poorly documented. We present a 77-year-old man, with no history of epilepsy, presenting in the emergency department with whole body jerks since that morning. Two days earlier, due to a prescription mistake, he was started on paroxetine 20 mg instead of his usual fluoxetine 20 mg. The patient's electroencephalogram (EEG), performed in the emergency department, revealed a bilateral synchronous parieto-occipital fast spike activity pattern, which correlated consistently with negative myoclonus. Two days after stopping paroxetine, the patient presented no seizures and no abnormalities in the EEG. We present an EEG documented case of drug-induced seizures, with a bilateral parieto-occipital pattern, secondary to paroxetine intake. A hyperexcitability of the primary somatosensory cortex inhibiting primary motor cortex output could explain the electroclinical correlation.