Neurophysiological Functions Research Articles

A retrospective, observational study of real-world clinical data from the Cognitive Function Development Therapy program

IntroductionCognitive deficits are common in psychiatric and mental health disorders, making the assessment of cognitive function in mental health treatment an important area of research. Cognitive Function Development Therapy (CFDT) is a novel therapeutic modality designed to enhance cognitive function and regulate the autonomic nervous system through targeted exercises and activities focused on attention networks and memory systems. The therapy is tracked and based on Primary Cognitive Function (PCF) scores.MethodsThis retrospective, observational study analyzed real world data from 183 children and adults undergoing CFDT to evaluate changes in cognition over time, incorporating both cognitive performance measures and an exploratory analysis of neurophysiological function. Objective neurophysiological measures in the form of the brain vital signs framework, based in event-related potentials (ERPs), were measured in a small subset of clients to explore the frameworks use in CFDT.ResultsOur findings indicate that CFDT holds promise for improving cognitive performance, as evidenced by increased PCF scores at the group level compared to pre-treatment levels [F (5, 173) = 7.087, p < 0.001, ηp2 = 0.170]. Additionally, a weak effect of age [Spearman’s Rho range: −0.301 to −0.340, p < 0.001] was found to influence the degree of cognitive improvement, suggesting the importance of early intervention for maximizing cognitive gains. The exploratory analysis suggested that CFDT may affect neurophysiological measures of information processing, particularly in basic attention, as reflected in increased amplitude in P300 measures.DiscussionWhile these initial findings are encouraging, caution is warranted due to the retrospective nature of the study, though overall, the results suggest a positive impact of CFDT on cognitive function.

Decreased prefrontal glutamatergic function is associated with a reduced astrocyte-related gene expression in treatment-resistant depression

Glutamatergic dysfunction is involved in the pathophysiology of treatment-resistant depression (TRD). However, few physiological studies have evaluated its pathophysiology in vivo in individuals with TRD. Transcranial magnetic stimulation-electroencephalography (TMS-EEG) techniques can assess intracortical facilitation (ICF), which reflects glutamatergic neurophysiological function in specific cortical regions. The objectives of this study were (1) to compare glutamatergic receptor-mediated function as indexed with ICF TMS-EEG in the dorsolateral prefrontal cortex (DLPFC) between participants with TRD and healthy controls (HCs) and (2) to explore the relationships between cell-specific gene expression levels and the group difference in glutamatergic neural propagation using virtual histology approach. Sixty participants with TRD and thirty HCs were examined with ICF TMS-EEG measure (80 single-pulse TMS and paired-pulse ICF) in the left DLPFC. Both sensor and source-level ICF measures were computed to compare them between the TRD and HC groups. Furthermore, we conducted spatial correlation analyses interregionally between ICF glutamatergic activity and cell-specific gene expression levels employing the Allen Human Brain Atlas dataset. DLPFC-ICF at the sensor level was not significantly different between the two groups, whereas DLPFC-ICF at the source level was reduced in the TRD group compared with the HC group (p = 0.026). Moreover, the reduced ICF signal propagation of TRD correlated with astrocyte-specific gene expression level (p < 0.0001). The glutamatergic neural activities indexed by ICF in the left DLPFC were decreased in participants with TRD. Additionally, a relative reduction in glutamatergic signal propagation originating from the DLPFC in TRD may be associated with astrocytic abnormality.

Scoping review on shamanistic trances practices

BackgroundShamanism is a spiritual tradition in which trance practitioners deliberately modify their state of consciousness to seemingly interact with an invisible world to resolve their community members’ problems. This review aims to provide a multidisciplinary overview of scientific research on shamanic trance.MethodsThe search was performed using PubMed and Google Scholar databases. Twenty-seven articles were found to be eligible, and their data were classified into four dimensions, namely, a) phenomenology, b) psychology, c) neuro-physiological functions, and d) clinical applications.ResultsThese studies suggest that these trances are non-pathological, different from normal states of consciousness in terms of phenomenology and neurophysiology, and influenced by multiple personal and environmental variables. Furthermore, while trances may offer therapeutic potential, their scope should be approached cautiously, underscoring the need for rigorous studies to assess the effectiveness of shamanic approaches for complementary therapies.ConclusionOverall, shamanic trance and its potential benefits remain an intriguing and multifaceted area of scientific study, offering insights into the intersections of consciousness, spirituality, and possibly therapy.

Sphingosine 1-phosphate receptor subtype 1 (S1P1) activity in the course of Alzheimer's disease

Some specific lipid molecules in the brain act as signaling molecules, neurotransmitters, or neuromodulators, by binding to specific G protein-coupled receptors (GPCR) for neurolipids. One such receptor, sphingosine 1-phosphate receptor subtype 1 (S1P1), is coupled to Gi/o proteins and is involved in cell proliferation, growth, and neuroprotection. S1P1 constitutes an interesting target for neurodegenerative diseases like multiple sclerosis and Alzheimer's disease (AD), in which changes in the sphingolipid metabolism have been observed. This study analyzes S1P1 receptor-mediated activity in healthy brains and during AD progression using postmortem samples from controls and patients at different Braak's stages. Additionally, the distribution of S1P1 receptor activity in human brains is compared to that in commonly used rodent models, rats and mice, through functional autoradiography, measuring [35S]GTPγS binding stimulated by the S1P1 receptor selective agonist CYM-5442 to obtain the distribution of functional activity of S1P1 receptors.S1P1 receptor-mediated activity, along with that of the cannabinoid CB1 receptor, is one of the highest recorded for any GPCR in many gray matter areas of the brain, reaching maximum values in the cerebellar cortex, specific areas of the hippocampus and the basal forebrain. S1P1 signaling is crucial in areas that regulate learning, memory, motor control, and nociception, such as the basal forebrain and basal ganglia. In AD, S1P1 receptor activity is increased in the inner layers of the frontal cortex and underlying cortical white matter at early stages, but decreases in the hippocampus in advanced stages, indicating ongoing brain impairment. Importantly, we identified significant correlations between S1P1 receptor activity and Braak stages, suggesting that S1P1 receptor dysfunction is associated to disease progression, particularly in memory-related regions. The S1P signaling via S1P1 receptor is a promising neurological target due to its role in key neurophysiological functions and its potential to modify the progression of neurodegenerative diseases. Finally, rats are suggested as a preferred experimental model for studying S1P1 receptor-mediated responses in the human brain.

Hyperexcitability and translational phenotypes in a preclinical mouse model of SYNGAP1-related intellectual disability

Disruption of SYNGAP1 directly causes a genetically identifiable neurodevelopmental disorder (NDD) called SYNGAP1-related intellectual disability (SRID). Without functional SynGAP1 protein, individuals are developmentally delayed and have prominent features of intellectual disability (ID), motor impairments, and epilepsy. Over the past two decades, there have been numerous discoveries indicating the critical role of Syngap1. Several rodent models with a loss of Syngap1 have been engineered, identifying precise roles in neuronal structure and function, as well as key biochemical pathways key for synapse integrity. Homozygous loss of SYNGAP1/Syngap1 is lethal. Heterozygous mutations of Syngap1 result in a broad range of behavioral phenotypes. Our in vivo functional data, using the original mouse model from the Huganir laboratory, corroborated behaviors including robust hyperactivity and deficits in learning and memory in young adults. Furthermore, we described impairments in the domain of sleep, characterized using neurophysiological data that was collected with wireless, telemetric electroencephalography (EEG). Syngap1+/− mice exhibited elevated spiking events and spike trains, in addition to elevated power, most notably in the delta power frequency. For the first time, we illustrated that primary neurons from Syngap1+/− mice displayed: 1) increased network firing activity, 2) greater bursts, 3) and shorter inter-burst intervals between peaks, by utilizing high density microelectrode arrays (HD-MEA). Our work bridges in vitro electrophysiological neuronal activity and function with in vivo neurophysiological brain activity and function. These data elucidate quantitative, translational biomarkers in vivo and in vitro that can be utilized for the development and efficacy assessment of targeted treatments for SRID.

Development of in vitro model of exosome transport in microfluidic gut-brain axis-on-a-chip.

The gut communicates with the brain in a variety of ways known as the gut-brain axis (GBA), which is known to affect neurophysiological functions as well as neuronal disorders. Exosomes capable of passing through the blood-brain-barrier (BBB) have received attention as a mediator of gut-brain signaling and drug delivery vehicles. In conventional well plate-based experiments, it is difficult to observe the exosome movement in real time. Here, we developed a microfluidic-based GBA chip for co-culturing gut epithelial cells and neuronal cells and simultaneously observing exosome transport. The GBA-chip is aimed to mimic the in vivo situation of convective flow in blood vessels and convective and diffusive transport in the tissue interstitium. Here, fluorescence-labeled exosome was produced by transfection of HEK-293T cells with CD63-GFP plasmid. We observed in real time the secretion of CD63-GFP-exosomes by the transfected HEK-293T cells in the chip, and transport of the exosomes to neuronal cells and analyzed the dynamics of GFP-exosome movement. Our model is expected to enhance understanding of the roles of exosome in GBA.

Analyzing Fusion Pore Dynamics and Counting the Number of Acetylcholine Molecules Released by Exocytosis.

Acetylcholine (ACh) is a critical neurotransmitter influencing various neurophysiological functions. Despite its significance, quantitative methods with adequate spatiotemporal resolution for recording a single exocytotic ACh efflux are lacking. In this study, we introduce an ultrafast amperometric ACh biosensor that enables 50 kHz electrochemical recording of spontaneous single exocytosis events at axon terminals of differentiated cholinergic human SH-SY5Y neuroblastoma cells with sub-millisecond temporal resolution. Characterization of the recorded amperometric traces revealed seven distinct current spike types, each displaying variations in shape, time scale, and ACh quantities released. This finding suggests that exocytotic release is governed by complex fusion pore dynamics in these cells. The absolute number of ACh molecules released during exocytosis was quantified by calibrating the sensor through the electroanalysis of liposomes preloaded with varying ACh concentrations. Notably, the largest quantal release involving approximately 8000 ACh molecules likely represents full exocytosis, while a smaller release of 5000 ACh molecules may indicate partial exocytosis. Following a local administration of bafilomycin A1, a V-ATPase inhibitor, the cholinergic cells exhibited both a larger quantity of ACh released and a higher frequency of exocytosis events. Therefore, this ACh sensor provides a means to monitor minute amounts of ACh and investigate regulatory release mechanisms at the single-cell level, which is vital for understanding healthy brain function and pathologies and optimizing drug treatment for disorders.

Effect of different food matrices on the bioaccessibility of vitamin D3 in beverage systems: Comparison between juice and liquid milk

Vitamin D plays a crucial role in bone, immunology, and neurophysiological functions but has inadequate bioavailability in the human body. In this paper, six different liquid beverages were used for vitamin D3 fortification, investigating the effect of different food matrices on the bioaccessibility of vitamin D. Not from concentrate (NFC) apple juice (9.34%) and NFC orange juice (8.12%) presented about 20% higher bioaccessibility of vitamin D3 than soybean and skim milk, and achieved a similar value of whole milk (8.04%). Meanwhile, the bioaccessibility of NFC apple and orange juice was markedly about 120% higher than that of apple clear juice. From the correlation analysis, the bioaccessibility of VD3 indicated significant correlations with small intestine retention (0.82) and viscosity (0.66). But small intestinal particle size showed a negative effect on bioaccessibility (−0.78). Therefore, food components, delivery matrices, and physicochemical properties of digesta were key factors to achieve higher bioaccessibility for guiding formulation design.

Effects of 6-Month Combined Physical Exercise and Cognitive Training on Neuropsychological and Neurophysiological Function in Older Adults with Subjective Cognitive Decline: A Randomized Controlled Trial.

Multidomain intervention may delay or ameliorate cognitive decline in older adults at risk of Alzheimer's disease, particularly in the memory and inhibitory functions. However, no study systematically investigates the changes of brain function in cognitively-normal elderly with subjective cognitive decline (SCD) when they receive multidomain intervention. We aimed to examine whether a multidomain intervention could improve neuropsychological function and neurophysiological activities related to memory and inhibitory function in SCD subjects. Eight clusters with a total of 50 community-dwelling SCD older adults were single-blind, randomized into intervention group, which received physical and cognitive training, or control group, which received treatment as usual. For the neuropsychological function, a composite Z score from six cognitive tests was calculated and compared between two groups. For the neurophysiological activities, event-related potentials (ERPs) of memory function, including mismatch negativity (MMN) and memory-P3, as well as ERPs of inhibitory function, including sensory gating (SG) and inhibition-P3, were measured. Assessments were performed at baseline (T1), end of the intervention (T2), and 6 months after T2 (T3). For the neuropsychological function, the effect was not observed after the intervention. For the neurophysiological activities, improved MMN responses of ΔT2-T1 were observed in the intervention group versus the control group. The multidomain intervention produced a sustained effect on memory-P3 latencies of ΔT3-T1. However, there were no significant differences in changes of SG and inhibition-P3 between intervention and control groups. While not impactful on neuropsychological function, multidomain intervention enhances specific neurophysiological activities associated with memory function.

Time synchronization between parietal–frontocentral connectivity with MRCP and gait in post-stroke bipedal tasks

BackgroundIn post-stroke rehabilitation, functional connectivity (FC), motor-related cortical potential (MRCP), and gait activities are common measures related to recovery outcomes. However, the interrelationship between FC, MRCP, gait activities, and bipedal distinguishability have yet to be investigated.MethodsTen participants were equipped with EEG devices and inertial measurement units (IMUs) while performing lower limb motor preparation (MP) and motor execution (ME) tasks. MRCP, FCs, and bipedal distinguishability were extracted from the EEG signals, while the change in knee degree during the ME phase was calculated from the gait data. FCs were analyzed with pairwise Pearson’s correlation, and the brain-wide FC was fed into support vector machine (SVM) for bipedal classification.ResultsParietal–frontocentral connectivity (PFCC) dysconnection and MRCP desynchronization were related to the MP and ME phases, respectively. Hemiplegic limb movement exhibited higher PFCC strength than nonhemiplegic limb movement. Bipedal classification had a short-lived peak of 75.1% in the pre-movement phase. These results contribute to a better understanding of the neurophysiological functions during motor tasks, with respect to localized MRCP and nonlocalized FC activities. The difference in PFCCs between both limbs could be a marker to understand the motor function of the brain of post-stroke patients.ConclusionsIn this study, we discovered that PFCCs are temporally dependent on lower limb gait movement and MRCP. The PFCCs are also related to the lower limb motor performance of post-stroke patients. The detection of motor intentions allows the development of bipedal brain-controlled exoskeletons for lower limb active rehabilitation.

Does Transcranial Direct Current Stimulation Affect Potential P300-Related Events in Vascular Dementia? Considerations from a Pilot Study.

Vascular dementia, the second most common type of dementia, currently lacks a definitive cure. In the pursuit of therapies aimed at slowing its progression and alleviating symptoms, transcranial direct current stimulation (tDCS) emerges as a promising approach, characterized by its non-invasive nature and the ability to promote brain plasticity. In this study, the primary objective was to investigate the effects of a two-week cycle of tDCS on the dorsolateral prefrontal cortex (DLPFC) and neurophysiological functioning in thirty patients diagnosed with vascular dementia. Each participant was assigned to one of two groups: the experimental group, which received anodal tDCS to stimulate DPCFL, and the control group, which received sham tDCS. Neurophysiological functions were assessed before and after tDCS using P300 event-related potentials (ERPs), while neuropsychological function was evaluated through a Mini-Mental State Examination (MMSE). The results showed a reduction in P300 latency, indicating a faster cognitive process; an increase in P300 amplitude, suggesting a stronger neural response to cognitive stimuli; and a significant improvement in MMSE scores compared to the control group, indicating an overall enhancement in cognitive functions. These findings suggest that tDCS could represent a promising therapeutic option for improving both neurophysiological and cognitive aspects in patients with vascular dementia.

Imbalance in Unc80 RNA Editing Disrupts Dynamic Neuronal Activity and Olfactory Perception.

A-to-I RNA editing, catalyzed by the ADAR protein family, significantly contributes to the diversity and adaptability of mammalian RNA signatures, aligning with developmental and physiological needs. Yet, the functions of many editing sites are still to be defined. The Unc80 gene stands out in this context due to its brain-specific expression and the evolutionary conservation of its codon-altering editing event. The precise biological functions of Unc80 and its editing, however, are still largely undefined. In this study, we first demonstrated that Unc80 editing occurs in an ADAR2-dependent manner and is exclusive to the brain. By employing the CRISPR/Cas9 system to generate Unc80 knock-in mouse models that replicate the natural editing variations, our findings revealed that mice with the "gain-of-editing" variant (Unc80G/G) exhibit heightened basal neuronal activity in critical olfactory regions, compared to the "loss-of-editing" (Unc80S/S) counterparts. Moreover, an increase in glutamate levels was observed in the olfactory bulbs of Unc80G/G mice, indicating altered neurotransmitter dynamics. Behavioral analysis of odor detection revealed distinctive responses to novel odors-both Unc80 deficient (Unc80+/-) and Unc80S/S mice demonstrated prolonged exploration times and heightened dishabituation responses. Further elucidating the olfactory connection of Unc80 editing, transcriptomic analysis of the olfactory bulb identified significant alterations in gene expression that corroborate the behavioral and physiological findings. Collectively, our research advances the understanding of Unc80's neurophysiological functions and the impact of its editing on the olfactory sensory system, shedding light on the intricate molecular underpinnings of olfactory perception and neuronal activity.

Omega-3 fatty acids supplementation prevents learning and memory impairment induced by chronic ethanol consumption in adolescent male rats through restoration of inflammatory and oxidative responses.

Ethanol (Eth) intake is known to cause numerous detrimental effects on the structure and function of the brain, and it is commonly used as a psychostimulant drug by adolescents. Conversely, omega-3 (O3) can reduce the risk of cognitive decline and promote the maintenance of neurophysiological functions. In this study, we investigated the protective effects of O3 on behavioral alterations, oxidative stress, and interleukin-6 (IL-6) levels induced by chronic Eth intake during adolescence in rats. Adolescent male rats (21 days old) were divided as follows: (1) Vehicle, (2) Eth (Eth in drinking water [20%]), (3-5) Eth + O3 (50/100/150 mg/kg), and (6) O3 (150 mg/kg). After 5weeks, Morris water maze (MWM) and passive avoidance (PA) tests were performed, and the hippocampal and cortical levels of oxidative stress markers and inflammatory indices were measured. Adolescent Eth intake impairs learning and memory function in MWM and PA tests (groups × day, p< 0.05 and p< 0.001, respectively). It was shown that Eth induced oxidative stress and neuroinflammation. O3 improved learning and impairment induced by Eth by reducing the adverse effects of Eth on the oxidant/antioxidant balance in the hippocampi (for malondialdehyde [MDA]/thiol: p< 0.01, p< 0.001, respectively) and for superoxide dismutase (SOD)/catalase (CAT): p< 0.01 and p< 0.05, respectively). Furthermore, we found that O3 prevented the Eth-induced increase of hippocampal IL-6 (p< 0.001). O3 supplementation acts as an effective approach to prevent learning and memory impairments induced by chronic Eth consumption during adolescence. In this respect, the antioxidant and anti-inflammatory properties of O3 seem to be the main underlying mechanisms of neuroprotection.

Should the Struggle Against Authoritarian Regimes Be Based on Aristotle’s or Freud’s Psychology, or Rather on Neuroscience?

The prevailing global social and geopolitical situation is perceived as unfavorable by most people. According to the authors, many worrying threats are linked to the mental state of the planet's inhabitants. Thus, they believe that the emergence of authoritarian regimes, the constant instigation of wars, and the poor living conditions in many communities require explanations grounded in accurate psychological concepts. The authors refer to their previous work that connects authoritarian regimes with conservative personality traits, particularly those found in far-right, populist groups. These regimes often promote a patriarchal social structure and rely on religious taboos to maintain control. The authors expand on this theory by exploring Sigmund Freud's concepts of "totem" and "taboo," examining how these ideas might explain the behavior of authoritarian regimes. They also refer to Carl Jung's theory of the Shadow and the collective sense of inferiority. The article concludes with suggestions on how to counter the spread of authoritarian regimes. The authors advocate for a balanced approach that focuses on finding ways to coexist with authoritarian individuals. They draw parallels between the different neurophysiological functions of the brain's two hemispheres and the potential coexistence of multiple geopolitical blocs. The authors reflect on a country that recently shifted from far-right, populist, national governance back to a liberal democratic pattern. They also propose a tool to record personal civic feelings, which can help assess whether a particular region is moving toward or away from autocratic governance.

HAT and HDAC: Enzyme with Contradictory Action in Neurodegenerative Diseases.

In view of the increasing risk of neurodegenerative diseases, epigenetics plays a fundamental role in the field of neuroscience. Several modifications have been studied including DNA methylation, histone acetylation, histone phosphorylation, etc. Histone acetylation and deacetylation regulate gene expression, and the regular activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs) provides regulatory stages for gene expression and cell cycle. Imbalanced homeostasis in these enzymes causes a detrimental effect on neurophysiological function. Intriguingly, epigenetic remodelling via histone acetylation in certain brain areas has been found to play a key role in the neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. It has been demonstrated that a number of HATs have a role in crucial brain processes such regulating neuronal plasticity and memory formation. The most recent therapeutic methods involve the use of small molecules known as histone deacetylase (HDAC) inhibitors that antagonize HDAC activity thereby increase acetylation levels in order to prevent the loss of HAT function in neurodegenerative disorders. The target specificity of the HDAC inhibitors now in use raises concerns about their applicability, despite the fact that this strategy has demonstrated promising therapeutic outcomes. The aim of this review is to summarize the cross-linking between histone modification and its regulation in the pathogenesis of neurological disorders. Furthermore, these findings also support the notion of new pharmacotherapies that target particular areas of the brain using histone deacetylase inhibitors.

Effects of Transcranial Direct Current Stimulation on Potential P300-Related Events and Alpha and Beta EEG Band Rhythms in Parkinson's Disease.

Parkinson's disease is one of the most common neurodegenerative disorders. While a definitive cure for Parkinson's disease remains elusive, a range of treatments are available to slow its progression and counteract its symptoms. Transcranial direct current stimulation (tDCS) represents a non-invasive method to induce brain plasticity. The aim of this study was to examine the effects of two weeks of tDCS on the left dorsolateral prefrontal cortex (DLPFC) on the neurophysiological functioning of Parkinson's patients. Thirty patients aged between 67 and 82 years with Parkinson's disease participated to the experiment. Fifteen underwent tDCS on the left DLPFC, while fifteen underwent sham tDCS. Neurophysiological functions were assessed before and after tDCS using electroencephalogram methods for alpha and beta band rhythms and P300 event-related potential latency. tDCS led to a reduction in the onset latency of the P300 response and an increase in the power spectrum of the alpha and beta band rhythms. This research enhances our understanding of the potential effects of tDCS in the context of Parkinson's disease treatment, as the reduction in P300 latency and the increase in alpha and beta bands are associated with improvements in cognitive aspects.

Neurophysiological brain function predicts response to cognitive rehabilitation and mindfulness in multiple sclerosis: a randomized trial

BackgroundCognitive treatment response varies highly in people with multiple sclerosis (PwMS). Identification of mechanisms is essential for predicting response.ObjectivesThis study aimed to investigate whether brain network function predicts response to cognitive rehabilitation therapy (CRT) and mindfulness-based cognitive therapy (MBCT).MethodsPwMS with cognitive complaints completed CRT, MBCT, or enhanced treatment as usual (ETAU) and performed three measurements (baseline, post-treatment, 6-month follow-up). Baseline magnetoencephalography (MEG) measures were used to predict treatment effects on cognitive complaints, personalized cognitive goals, and information processing speed (IPS) using mixed models (secondary analysis REMIND-MS study).ResultsWe included 105 PwMS (96 included in prediction analyses; 32 CRT, 31 MBCT, 33 ETAU), and 56 healthy controls with baseline MEG. MEG did not predict reductions in complaints. Higher connectivity predicted better goal achievement after MBCT (p = 0.010) and CRT (p = 0.018). Lower gamma power (p = 0.006) and higher connectivity (p = 0.020) predicted larger IPS benefits after MBCT. These MEG predictors indicated worse brain function compared to healthy controls (p < 0.05).ConclusionsBrain network function predicted better cognitive goal achievement after MBCT and CRT, and IPS improvements after MBCT. PwMS with neuronal slowing and hyperconnectivity were most prone to show treatment response, making network function a promising tool for personalized treatment recommendations.Trial registrationThe REMIND-MS study was prospectively registered in the Dutch Trial registry (NL6285; https://trialsearch.who.int/Trial2.aspx?TrialID=NTR6459).

Paravertebral Muscular Neurophysiological Function as an Independent Outcome Predictor of Recurring Herniation/Low Back Pain after Radiofrequency Ablation: A Prospective Follow-Up and Case-Control Study Based on Surface Electromyography.

Spinal endoscopy radiofrequency is a minimally invasive technique for lumbar disc herniation (LDH) and low back pain (LBP). However, recurring LDH/LBP following spinal endoscopy radiofrequency is a significant problem. Paravertebral musculature plays a crucial role in spine stability and motor function, and the purpose of the present study was to identify whether patients' baseline lumbar muscular electrophysiological function could be a predictor of recurring LDH/LBP. This was a prospective follow-up and case-control study focusing on elderly patients with LDH who were treated in our department between January 1, 2018, and October 31, 2021. The end of follow-up was recurring LBP, recurring LDH, death, missing to follow-up or 2 years postoperation. The surface electromyography test was performed before the endoscopy C-arm radiofrequency (ECRF) operation to detect the flexion-relaxation ratio (FRR) of the lumbar multifidus (FRRLM ) and the longissimus erector spinae (FRRES ), and the other baseline parameters included the general characteristics, the visual analogue scale, the Japanese Orthopaedic Association score, and the Oswestry Disability Index. Intergroup comparisons were performed by independent t-test and χ2 -test, and further binary logistic regression analysis was performed. Fifty-four patients completed the 2-year follow-up and were retrospectively divided into a recurring LDH/LBP group (Group R) (n = 21) and a no recurring group (Group N) (n = 33) according to their clinical outcomes. FRRLM and FRRES in Group N were much higher than those in Group R (p < 0.001, p = 0.009). Logistic regression analysis showed that only the FRRLM (odds ratio [OR] = 0.123, p = 0.011) and FRRES (OR = 0.115, p = 0.036) were independent factors associated with the ECRF outcome. Lumbar disc herniation patients' baseline FRRLM and FRRES are independent outcome predictors of recurring LDH/LBP after ECRF. For every unit increase in baseline FRRLM , the risk of recurring LDH/LBP is decreased by 87.7%, and for every unit increase in baseline FRRES , the risk of recurring LDH/LBP is decreased by 88.5%.

Multiformity of extracellular microelectrode recordings from Aδ neurons in the dorsal root ganglia: a computational modeling study.

Microelectrodes serve as a fundamental tool in electrophysiology research throughout the nervous system, providing a means of exploring neural function with a high resolution of neural firing information. We constructed a hybrid computational model using the finite element method and multicompartment cable models to explore factors that contribute to extracellular voltage waveforms that are produced by sensory pseudounipolar neurons, specifically smaller A-type neurons, and that are recorded by microelectrodes in dorsal root ganglia. The finite element method model included a dorsal root ganglion, surrounding tissues, and a planar microelectrode array. We built a multicompartment neuron model with multiple trajectories of the glomerular initial segment found in many A-type sensory neurons. Our model replicated both the somatic intracellular voltage profile of Aδ low-threshold mechanoreceptor neurons and the unique extracellular voltage waveform shapes that are observed in experimental settings. Results from this model indicated that tortuous glomerular initial segment geometries can introduce distinct multiphasic properties into a neuron's recorded waveform. Our model also demonstrated how recording location relative to specific microanatomical components of these neurons, and recording distance from these components, can contribute to additional changes in the multiphasic characteristics and peak-to-peak voltage amplitude of the waveform. This knowledge may provide context for research employing microelectrode recordings of pseudounipolar neurons in sensory ganglia, including functional mapping and closed-loop neuromodulation. Furthermore, our simulations gave insight into the neurophysiology of pseudounipolar neurons by demonstrating how the glomerular initial segment aids in increasing the resistance of the stem axon and mitigating rebounding somatic action potentials.NEW & NOTEWORTHY We built a computational model of sensory neurons in the dorsal root ganglia to investigate factors that influence the extracellular waveforms recorded by microelectrodes. Our model demonstrates how the unique structure of these neurons can lead to diverse and often multiphasic waveform profiles depending on the location of the recording contact relative to microanatomical neural components. Our model also provides insight into the neurophysiological function of axon glomeruli that are often present in these neurons.

CONTROL OF ANGIOGENESIS AS PATHOGENETIC SUBSTANTIATED APPROACH TO CHRONIC EPILEPTIC ACTIVITY TREATMENT

The purpose of the work – to carry out an analysis of literary sources regarding theassessment of the effectiveness of the combined use of drugs that affect various links ofthe regulation of neurophysiological functions on the manifestations of chronic epilepticactivity.Conclusions. 1. Based on the analysis of literature data, the perspective of using theconcept of a functional unit of nervous tissue, which includes vessels and microglia inaddition to the neuron, in the pharmacological control of epileptogenic excitation hasbeen determined. 2. The combined use of neuromodulators that affect the excitability ofthe neuron indirectly, through the components of the functional unit of the nervous tissue,provides a synergistic anticonvulsant effect, which is explained by the involvement ofvarious links of intracellular signaling pathways.