Efferent Pathways Research Articles

Impact of Pesticide Exposure on Auditory Health: Mechanisms, Efferent System Disruption, and Public Health Implications.

Pesticide exposure has been linked to adverse effects on auditory health, impacting both peripheral and central auditory systems. Studies suggest that organophosphate, carbamate, organochlorine, and pyrethroid pesticides disrupt auditory processing through oxidative stress, neuroinflammation, and interference with cholinergic signaling. These disruptions may compromise sensory hair cells, spiral ganglion neurons, and auditory pathways, impairing precise signal transmission. The auditory efferent system, responsible for cochlear protection and auditory signal modulation, appears particularly susceptible to pesticide-induced alterations. This system relies on cholinergic transmission to regulate cochlear amplification and selective attention, functions that may be disrupted by pesticide exposure. Evidence from epidemiological and experimental studies highlights the potential for long-term auditory dysfunction in populations exposed to pesticides, with agricultural workers and their families facing elevated risks due to prolonged contact with agrochemicals. This review integrates findings on pesticide exposure and its implications for auditory health, discussing potential peripheral and central ototoxicity pathways. The cumulative effects of chronic exposure are emphasized, including the gradual degradation of auditory processing capabilities. Additionally, the need for targeted interventions, such as audiological monitoring and enhanced safety protocols, is addressed. Further research is critical to elucidate the mechanisms underlying pesticide-induced auditory damage and identify protective strategies. Such investigations can inform evidence-based policies to mitigate the public health impact of pesticide exposure while maintaining agricultural productivity. A multidisciplinary approach is essential to safeguard auditory health in vulnerable populations exposed to these environmental hazards.

OP15 ECCO Topical Review on Pouch Disorders

Abstract Background Pouch disorders are common and may present with symptoms of increased stool frequency, urgency, incontinence, pelvic cramping, and perianal drainage, leading to poor sleep, fatigue, and disability. This topical review provides expert consensus recommendations for the diagnosis and management of the most common inflammatory, functional, structural and neoplastic pouch disorders. Methods An open-call for participation was made to all ECCO members. Four working groups were formed each focusing on a specific category of pouch disorders. Each group member performed a comprehensive literature review for their assigned disorder using appropriate key words and drafted summary texts. Sections were reviewed and integrated into a single manuscript by MK, GB, and MF. Results Symptoms that arise and persist immediately following pouch construction may indicate surgical issues, while those that gradually develop after a prolonged period of wellness may suggest inflammatory or functional disorders. Symptoms of increased stool frequency, abdominal cramping, and urgency are suggestive of an inflammatory disorder, and a short trial of oral antibiotics may confirm the most likely diagnosis of pouchitis, though a pouchoscopy is preferable to exclude other causes. In case of persistent or recurrent symptoms of pouchitis, additional evaluation via stool studies, pouchoscopy and cross-sectional imaging should be considered to rule out chronic antibiotic-dependent or –refractory pouchitis, or Crohn’s-like disease of the pouch. Symptoms of chronic pelvic pain, intermittent obstruction, and incomplete evacuation suggest a structural disorder. Evaluation with pouchography, MR defaecography, pouchoscopy and examination under anaesthesia should be performed to evaluate for pouch prolapse or volvulus, afferent or efferent limb syndrome, anastomotic leakage, strictures or fistulae. Symptoms of incomplete evacuation, incontinence, and pelvic pain that occur in the absence of an inflammatory or structural abnormality point to a functional disorder. Assessment with anorectal manometry, balloon expulsion tests, and defaecography should be conducted to evaluate pelvic floor dynamics and rule out pelvic floor dyssynergia or irritable pouch syndrome. Conclusion A multidisciplinary approach is essential for the diagnosis and management of most pouch disorders. Centres with a specialized pouch care team are often best equipped to manage these complex cases, providing the expertise necessary for accurate diagnosis and tailored interventions.

Cerebellar Mutism/Posterior Fossa Syndrome Following Resection of Posterior Fossa Tumor in Pediatric Patients: Assessing Pathophysiology, Risk Factors, and Neuroradiographic Features

Background Cerebellar mutism syndrome (CMS) is a postoperative syndrome of decreased speech seen in children associated with neurobehavioral abnormalities, the incidence of which is up to 40%. Objective To evaluate pediatric patients with posterior fossa tumors for incidence, clinical characteristics, pathophysiology, risk factors, and neuroradiographic features of this syndrome. Materials and Methods The study included 60 pediatric patients with a posterior fossa tumor who underwent surgery by a telovelar approach. Detailed pre- and postoperative clinical and radiological evaluations were done. Patients with CMS were analyzed and compared with those without mutism to find risk factors for CMS. The presentation and characteristics of cerebellar mutism were studied along with the following risk factors:The preoperative, immediate postoperative, and 1-year postoperative imaging results were reviewed to assess the neuroradiographic features in the two groups. Results The incidence of this syndrome was 20%. The mutism was accompanied by some neurobehavioral abnormalities (p-value = 0.05). The most significant finding was the presence of a period of cerebellar dysarthria after the resolution of the muteness (p-value < 0.001) in all cases. Brainstem and related structures' involvement was the most significant risk factor (p-value = 0.03). The presence of brainstem and peduncular edema in the immediate postoperative period (p-value = 0.04) and gross atrophy of posterior fossa structures at 1 year (p-value = 0.01) showed significance toward the development of CMS. There was delayed neurological recovery in patients with CMS with a poor Glasgow Outcome Score at 1 year of follow-up. Conclusion The clinical presentation of this syndrome in context with neuroradiographic features suggests that it results from transient impairment of the afferent and/or efferent pathways of dentate nuclei that are involved in initiating complex volitional movements and are associated with brainstem involvement of tumor and poor functional outcome.

Noise-induced hearing loss enhances Ca2+-dependent spontaneous bursting activity in lateral cochlear efferents.

Exposure to loud and/or prolonged noise damages cochlear hair cells and triggers downstream changes in synaptic and electrical activity in multiple brain regions, resulting in hearing loss and altered speech comprehension. It remains unclear however whether or not noise exposure also compromises the cochlear efferent system, a feedback pathway in the brain that fine-tunes hearing sensitivity in the cochlea. We examined the effects of noise-induced hearing loss on the spontaneous action potential (AP) firing pattern in mouse lateral olivocochlear (LOC) neurons. This spontaneous firing exhibits a characteristic burst pattern dependent on Ca2+ channels, and we therefore also examined the effects of noise-induced hearing loss on the function of these and other ion channels. The burst pattern was sustained by an interaction between inactivating Ca2+ currents contributed largely by L-type channels, and steady outward currents mediated by Ba2+-sensitive inwardly-rectifying and two-pore domain K+ channels. One week following exposure to loud broadband noise, hearing thresholds were significantly elevated, and the duration of AP bursts was increased, likely as a result of an enhanced Ca2+ current. Additional effects of noise-induced hearing loss included alteration of Ca2+-dependent inactivation of Ca2+ currents and a small elevation of outward K+ currents. We propose that noise-induced hearing loss enhances efferent activity and may thus amplify the release of neurotransmitters and neuromodulators (i.e., neuropeptides), potentially altering sensory coding within the damaged cochlea.

Role of Gut-Microbiome-Brain-Axis in Neurodegenerative Diseases: A Review on Mechanisms and Potential Therapeutics

Neurodegenerative diseases encompass a group of disorders with diverse etiologies characterized by the accumulation of neurotoxic substances that contribute to neuronal damage and brain degeneration. The integration of the microbiota-intestine-brain axis mechanism occurs via afferent and efferent pathways with the assistance of the vagus nerve and peripheral circulation. The gut microbiota produces pathogenic proteins and other harmful substances that can cross the blood-brain barrier and develop into even more pathogenic proteins when in contact with the bloodstream. The microbial metabolites most commonly associated with neurodegenerative diseases are butyrate and amyloid, although the precise role and mechanism of their relationship with the microbiota have yet to be fully elucidated. Additionally, in Parkinson's disease, the microbiome is directly linked to an increase in opportunistic pathogens, a decrease in beneficial anti-inflammatory species, and higher levels of carbohydrate metabolizers.

Continuous vital sign monitoring of patients recovering from surgery on general wards: a narrative review.

Most postoperative deaths occur on general wards, often linked to complications associated with untreated changes in vital signs. Monitoring in these units is typically intermittent checks each shift or maximally every 4-6 h, which misses prolonged periods of subtle changes in physiology that can herald a critical downstream event. Continuous monitoring of vital signs is therefore intuitively necessary for patient safety. The past five decades have seen monitoring systems evolve rapidly, and today entirely wireless, wearable, and portable continuous surveillance of vital signs is possible on general wards. Introduction of this technology has the potential to modify both the sensing (afferent) and response (efferent) limbs of monitoring, and will allow earlier detection of vital signs perturbations. But this comes with challenges, including but not limited to issues with connectivity, data handling, alarm fatigue, information overload, and lack of meaningful clinical interventions. Evidence from before and after studies and retrospective propensity-matched data suggests that continuous ward monitoring decreases the risk of intensive care unit (ICU) admissions, rapid response calls, and in some instances, mortality. This review summarises the history of general ward monitoring and describes future directions, including opportunities to implement these devices using artificial intelligence, pattern detection, and user-friendly interfaces. Pragmatic, well designed and appropriately powered trials, and real-world implementation data are necessary to make continuous monitoring standard practice at every hospital bed.

Effects of stimuli and contralateral noise levels on auditory cortical potentials recorded in school-age children.

One of the functions attributed to the auditory efferent system is related to the processing of acoustic stimuli in noise backgrounds. However, clinical implications and the neurophysiological mechanisms of this system are not yet understood, especially on higher regions of the central nervous system. Only a few researchers studied the effects of noise on cortical auditory evoked potentials (CAEP), but the lack of studies in this area and the contradictory results, especially in children, point to the need to investigate different protocols and parameters that could allow the study of top-down activity in humans. For this reason, the aim of this study was to analyze the effect of varying levels of contralateral noise on efferent activity in children by recording CAEPs with tone burst stimuli. Additionally, we aimed at verifying the effects of contralateral noise on cortical processing of speech stimuli. Monaural CAEPs were recorded using tone burst stimuli in quiet and with contralateral white noise at 60 dB and at 70 dB in 65 typically developing school-aged children (experiment 1), and using speech stimuli with contralateral white noise at 60 dB in 41 children (experiment 2). In experiment 1, noise induced changes were observed only for P1 and P300 components. P1 latency was prolonged at both noise level conditions, P300 latency was prolonged only in the condition with noise at 70 dB, and P300 amplitude was reduced only in the condition with noise at 60 dB. In experiment 2, noise induced latency delays were observed on P1, P2, N2, and P300 components and amplitude reduction was observed only for N1. The effects of noise stimulation were observed on all CAEP components elicited by speech, but the same was not observed in the experiment with tone bursts. The study of noise effects on CAEPs can provide electrophysiological evidence on how difficult listening situations affect sound discrimination and stimulus evaluation at thalamocortical regions.

Computational modelling of cardiac control following myocardial infarction using an in silico patient cohort.

Loss of cardiac physiological function following myocardial infarction (MI) is accompanied by neural adaptations in the baroreflex that are compensatory in the short term, but then become associated with long-term disease progression. One marker of these adaptations is decreased baroreflex sensitivity, a strong predictor of post-MI mortality. The relative contributions of cardiac remodelling and neural adaptation in the sensory, central brainstem and peripheral ganglionic loci to baroreflex sensitivity changes remain underexplored. We used a computational model-based approach that accounts for the short-term dynamics of closed-loop human cardiac control to integrate disparate experimental studies on neural adaptation following MI into a unified quantitative framework. We developed an ensemble of 59 distinct model parameterizations that account for the clinically observed heterogeneity of cardiac control in healthy individuals. We simulated an in silico cohort of 35,400 patients with MI, corresponding to six scenarios of one or more loci of neural adaptation coupled with cardiac remodelling. We evaluated the range of MI-induced shifts in arterial pressure, heart rate and baroreflex curve responses. Our results show that adaptation in any single neural locus coupled with cardiac remodelling is sufficient to account for the MI-induced haemodynamic and autonomic changes observed experimentally. Of the adaptation pathways, we found that individuals with central or peripheral vagal efferent adaptation and preserved baroreceptor gain could maintain high baroreflex sensitivity after ischaemic injury. These results suggest that there are a multitude of adaptive pathways for tuning the baroreflex circuit to shift cardiac control physiology, potentially explaining patient heterogeneity post-MI. KEY POINTS: Baroreflex sensitivity is a strong indicator of post-myocardial ischaemia survival and is variable among individuals. We fine-tuned a computational model ensemble based on physiological observations to develop an in silico patient cohort consistent with the range of baroreflex responses observed experimentally. Simulation and analysis of the in silico cohort show that individuals with a functional afferent pathway and the ability to adapt along the vagal efferent pathway can maintain baroreflex sensitivity post-cardiac ischaemia.

Neuroimaging of postoperative pediatric cerebellar mutism syndrome: a systematic review.

Postoperative pediatric cerebellar mutism syndrome (ppCMS) poses serious morbidity after posterior fossa tumor surgery. Neuroimaging studies aim to understand its pathophysiology, yet these vary in methodology and outcome measures. Therefore, we systematically reviewed the current literature to evaluate the evidence for differences in neuroimaging features between children with and without ppCMS. Following PRISMA guidelines, a systematic review was conducted by searching for original articles on neuroimaging in children undergoing posterior fossa tumor surgery, comparing patients with and without ppCMS. Articles were selected based on predefined eligibility criteria. Data were systematically extracted, and risk of bias was evaluated. From the 866 articles identified, 50 studies fulfilled the inclusion criteria. Studies were categorized into 3 imaging domains: structural, diffusion, and functional imaging. Risk of bias assessment revealed a medium risk in most articles, predominantly due to unclear ppCMS definition and qualitative image analysis without blinding for ppCMS diagnosis. Preoperative structural imaging showed the association of ppCMS with midline tumor localization and involvement of the brainstem, superior cerebellar peduncle (SCP), or middle cerebellar peduncle. Postoperative structural and diffusion imaging highlighted SCP injury with reduced white matter integrity, while functional imaging demonstrated hypoperfusion in frontal lobes. Late follow-up showed T2-weighted hyperintensities in the inferior olivary nuclei of ppCMS patients. Neuroimaging features suggest that ppCMS is associated with efferent cerebellar pathway injury and hypoperfusion in frontal lobes, with level 2 a/b evidence. Large-scale prospective longitudinal neuroimaging studies comparing pre- and postoperative imaging are needed to further elucidate the pathophysiological mechanism of ppCMS.

Immunohistochemical Identification of Sensory Neuropeptides Calcitonin Gene-Related Peptide, Substance P, and Pituitary Adenylate Cyclase-Activating Polypeptide in Efferent Vestibular Nucleus Neurons

Introduction: The efferent vestibular system (EVS) originates in brainstem efferent vestibular nuclei (EVN) and modifies afferent vestibular signals at their source, in peripheral vestibular organs. Recent evidence suggests that EVS is also involved in the development of motion sickness symptoms, including vertigo and nausea, but the underlying mechanism is unknown. One possible link between EVN and motion sickness symptoms is through the neuropeptide calcitonin gene-related peptide (CGRP). CGRP often co-exists with substance P and pituitary adenylate cyclase-activating polypeptide (PACAP), two neuropeptides with similar vasodilatory effects. Collectively, these sensory neuropeptides have been associated with vestibular migraine pathophysiology and motion sickness. While CGRP and the fast EVS neurotransmitter, acetylcholine (ACh), have previously been identified in EVN neurons and their peripheral terminals, the presence of substance P and PACAP in the EVN has not yet been described. Methods: We used fluorescent immunohistochemistry combined with confocal microscopy to examine the distribution of these three neuropeptides in the mouse EVN. In transgenic choline acetyltransferase (ChAT)-gCaMP6f mice, EVN neurons were positively identified using the fluorescent expression of gCaMP6f. In wild-type C57/BL6 mice, EVN neurons were confirmed using ChAT immunolabelling. Results: Consistent with previous studies, CGRP was labelled in a subset of cholinergic EVN neurons. Additionally, we also show evidence for substance P and PACAP expression in EVN of transgenic and wild-type mice. Conclusion: The presence of CGRP, substance P, and PACAP in EVN neurons suggests a complex peptidergic modulation of cholinergic signalling, whose release into local blood vessels may contribute to motion sickness symptoms.

In vivo AAV9-Myo7a gene rescue restores hearing and cholinergic efferent innervation in inner hair cells.

In the mammalian cochlea, sensory hair cells are crucial for the transduction of acoustic stimuli into electrical signals, which are then relayed to the central auditory pathway via spiral ganglion neuron (SGN) afferent dendrites. The SGN output is directly modulated by inhibitory cholinergic axodendritic synapses from the efferent fibers originating in the superior olivary complex. When the adult cochlea is subjected to noxious stimuli or aging, the efferent system undergoes major rewiring, such that it reestablishes direct axosomatic contacts with the inner hair cells (IHCs), which occur only transiently during prehearing stages of development. The trigger, origin, and degree of efferent plasticity in the cochlea remains largely unknown. Using functional and morphological approaches, we demonstrate that efferent plasticity in the adult cochlea occurs as a direct consequence of mechanoelectrical transducer current dysfunction. We also show that, different from prehearing stages of development, the lateral olivocochlear - but not the medial olivocochlear - efferent fibers are those that form the axosomatic synapses with the IHCs. The study also demonstrates that in vivo restoration of IHC function using AAV-Myo7a rescue reestablishes the synaptic profile of adult IHCs and improves hearing, highlighting the potential of using gene-replacement therapy for progressive hearing loss.

Failure to rescue—rapid response systems: A making healthcare safer rapid review

Background Rapid response systems (RRSs) were developed to respond to early warnings of unexpected deterioration, but their effectiveness may be limited by factors impacting RRS activation (afferent limb) or response (efferent limb). Despite decades of RRS implementation, patients still experience unrecognized deterioration with associated worse outcomes. Methods This rapid review used modified search strategies to focus on the most valuable studies performed in the United States. Citations were screened by one reviewer with artificial intelligence as a second reviewer at the title/abstract review stage. The full text of eligible articles was then reviewed by a single team member to confirm eligibility. One reviewer completed the data abstraction, and a second reviewer checked the first reviewer's abstraction. Results Three categories of interventions were identified: implementation of a new RRS, and modifications to the afferent limb and/or efferent limb of an existing RRS. RRSs may have a large impact in reducing in-hospital mortality and an even greater impact in reducing cardiorespiratory arrest on hospital general wards in adults but the effect is unclear in children. Their impact on unanticipated intensive care unit admission is unclear. Modifications to the afferent and/or efferent limb were associated with a reduction in mortality and the incidence of cardiorespiratory arrest for adults. Conclusions RRS may have a large beneficial effect on hospital mortality and in-hospital cardiorespiratory arrest, but the strength of the evidence is low due to methodological weaknesses of the studies. Innovations in afferent and efferent limb structures show promise for increased benefit.

Cortical tracking of postural sways during standing balance

Maintaining an upright stance requires the integration of sensory inputs from the visual, vestibular and somatosensory-proprioceptive systems by the central nervous system to develop a corrective postural strategy. However, it is unclear whether and how the cerebral cortex monitors and controls postural sways. Here, we asked whether postural sways are encoded in ongoing cortical oscillations, giving rise to a form of corticokinematic coherence (CKC) in the context of standing balance. Center-of-pressure (CoP) fluctuations and electroencephalographic cortical activity were recorded as young healthy participants performed balance tasks during which sensory information was manipulated, by either removal or alteration. We found that postural sways are represented in ongoing cortical activity during challenging balance conditions, in the form of CKC at 1–6 Hz. Time delays between cortical activity and CoP features indicated that both afferent and efferent pathways contribute to CKC, wherein the brain would monitor the CoP velocity and control its position. Importantly, CKC was behaviorally relevant, as it predicted the increase in instability brought by alteration of sensory information. Our results suggest that human sensorimotor cortical areas take part in the closed-loop control of standing balance in challenging conditions. Importantly, CKC could serve as a neurophysiological marker of cortical involvement in maintaining balance.

Novel Concepts on the Functional Neuroanatomy of the Anorectum: Implications for Anorectal Neuropathy and Neuromodulation Therapy

Anorectal neuropathy causes anorectal dysfunction, yet it is poorly recognized. This stems from both a lack of understanding of the extrinsic and intrinsic innervation of the anorectum and tools for evaluation of neuronal function. Our objective was to provide an improved understanding of the neuronal networks of the anorectum and discuss its functional significance. We performed a comprehensive and up-to-date review of the published literature on anorectal neuroanatomy to generate our findings. Anorectal nerve innervation appears to be much more complex than hitherto known with an extensive overlap, intercommunications, and variations. The innervations arise from 5 sources as evidenced by immunohistochemical markers: Sympathetic innervation arises from the superior hypogastric plexus, hypogastric plexus, and splanchnic nerves (T1-L2); the parasympathetic from pelvic splanchnic nerves (S1-S4); the mixed autonomic from inferior hypogastric plexus; the somatic from pudendal nerves; and the intercommunicating nerves. Furthermore, they are fine, closely packed nerves susceptible to damage from obstetric or spinal cord injury, or pelvic surgery that may not manifest with bowel problems immediately but later in life. This illustrated review provides a new understanding of the afferent and efferent pathways between the rectum, spinal cord, and brain, and a framework for clinical implications of anorectal neuropathy, such as anal sphincter or rectal sensory or rectal accommodation dysfunction, causing bowel problems. Insights into the functional neuroanatomy provide an improved mechanistic understanding of anorectal symptoms and could facilitate the development of neurophysiological tests such as translumbosacral anorectal magnetic stimulation and neuromodulation treatments such as sacral neuromodulation and translumbosacral neuromodulation treatment.

Auditory evoked brainstem responses and medial olivocochlear efferent system in migraine patients with phonophobia

ABSTRACT Objective This study aims to investigate Auditory Evoked Brainstem Responses (ABR) and Distortion Product Otoacoustic Emission (DPOAE) suppression in migraine patients with and without phonophobia. Methods Thirty-two migraine patients with normal hearing and 30 healthy individuals were included in the study. Migraine characteristics and phonophobia status of migraine patients were noted. The patients were divided into two groups according to their phonophobia status. All participants underwent ABR, DPOAE and DPOAE suppression. Results Migraine patients had less DPOAE suppression (1481 and 2222 hz) and shorter ABR wave latencies compared to the control group (p < 0.05). Twelve (37.5%) of the migraine patients did not have phonophobia, and 20 (62.5%) had phonophobia. Phonophobia was not found to affect DPOAE suppression (p > 0.05). However, ABR wave I and V latencies in migraine patients with phonophobia were shorter than in healthy individuals (p < 0.05). Conclusion There are changes in the auditory evoked brainstem responses and medial olivocochlear efferent system of migraine patients. While phonophobia in migraine patients does not affect the medial olivocochlear efferent system, it may affect auditory evoked brainstem responses.

Two-Dimensional Electrically Conductive Metal-Organic Framework Boosts Synaptic Plasticity for Dynamic Image Refresh, Classification, and Efferent Neuromuscular Systems.

We present a two-dimensional (2D) electrically conductive metal-organic framework (EC-MOF)-based artificial synapse. The intrinsic electronic conductivity and subnanometer channels of the EC-MOF facilitate efficient ion diffusion, enable a high density of active redox centers, and significantly enhance capacitance within the artificial synapse. As a result, the synapse operates at an ultralow voltage of 10 mV and exhibits a remarkably low power consumption of approximately 1 fW, along with the longest retention time recorded for two-terminal electrolyte-type artificial synapses to date. The alignment of the quantum size of the subnanometer pores in the EC-MOF with various cations allows for versatile synaptic plasticity. This capability is applied to image refresh, classification, and efferent signal transmission for controlling artificial muscles, thereby offering a methodology for achieving tunable neuromorphic properties. These findings suggest the potential application of metal-organic frameworks in artificial nervous systems for future brain-inspired computation, peripheral interfaces, and neurorobotics.

Impact of the laparoscopic approach, early closure and preoperative stimulation on outcomes of ileostomy closure after rectal resection

AimTo evaluate the clinical outcome of early closure of a protective ileostomy and preoperative stimulation of the efferent limb in a cohort of patients with rectal cancer treated surgically, primarily using the laparoscopic approach. MethodsWe performed an observational retrospective cohort study in a prospectively recorded series of patients with rectal cancer who underwent laparoscopic surgery with a protective loop ileostomy between 2017 and 2022. Ileostomy closure was programmed for within 3 months after surgery. All patients underwent stimulation of the efferent limb. Primary outcomes were morbidity and mortality, length of stay (LOS), and re-admission. ResultsBetween 2017 and 2022, 108 patients underwent resection for rectal cancer and protective ileostomy. The laparoscopic approach was performed in 84.3% of patients (n = 91). Permanent ileostomy was performed in 5 patients (4.6%). Ileostomy closure was thus performed in 95.4% of patients (n = 103). Median time to closure was 74.5 days (range 57–113). In 63.1% (n = 65) of patients, reconstructive surgery was performed within 90 days. Prior to closure, efferent limb stimulation was performed in 77.8% (n = 84) of patients. Global morbidity was 26.2% (n = 27) (85.19%, n = 23 Clavien-Dindo I and 7.41%, n = 2 Clavien-Dindo II). The main causes of morbidity were postoperative ileus (10.7%, n = 11) and rectal bleeding (8.7%, n = 9). Anastomosis leakage occurred in 2 patients. Median hospital stay was 6 days (5–7). Readmission was needed in 6.8% (n = 7) of patients. ConclusionA previous laparoscopic approach, early closure and stimulation of the efferent limb could be a useful strategy to reduce the morbidity and mortality of temporary ileostomy closure.

ATP-gated P2x7 receptor is a major channel type at type II auditory nerves and required for hearing sensitivity efferent controlling and noise protection.

Hearing sensitivity and noise protection are mediated and determined by negative feedback of the cochlear efferent system. Type II auditory nerves (ANs) innervate outer hair cells (OHCs) in the cochlea and provide an input to this efferent control. However, little is known about underlying channel information. Here, we report that ATP-gated P2x7 receptor had a predominant expression at type II ANs and the synaptic areas under inner hair cells and OHCs with lateral and medial olivocochlear efferent nerves. Knockout (KO) of P2x7 increased hearing sensitivity with enhanced acoustic startle response (ASR), auditory brainstem response (ABR), and cochlear microphonics (CM) by increasing OHC electromotility, an active cochlear amplifier in mammals. P2x7 KO also increased susceptibility to noise. Middle level noise exposure could impair active cochlear mechanics resulting in permanent hearing loss in P2x7 KO mice. These data demonstrate that P2x7 receptors have a critical role in type II AN function and the cochlear efferent system to control hearing sensitivity; deficiency of P2x7 receptors can impair the cochlear efferent suppression leading to hearing oversensitivity and susceptibility to noise.

Auditory Efferent Pathway Functioning in Individuals with Misophonia

Background and Aim: Misophonia, characterized by a decreased tolerance for specific auditory stimuli, has been insufficiently explored within audiology. Limited research has been conducted, and the auditory mechanisms involved in this disorder remain to be explored. Hence, our study aimed to investigate the auditory efferent systems in individuals with misophonia. By focusing on this specific aspect, we aim to contribute to a better understanding of misophonia and shed light on the underlying auditory mechanisms involved in the condition. Methods: A cross-sectional research was performed with students from Mysore University to investigate misophonia. The severity of misophonia was evaluated using the revised Amsterdam misophonia scale. The participants were divided into two groups based on their misophonia severity: mild (n=15) and moderate-severe (n=15). All participants underwent transient evoked otoacoustic emissions with contralateral suppression to assess the auditory function. The overall amplitude and frequency-specific amplitudes were analyzed and compared across the various groups. Results: The analysis of variance results revealed no significant differences between the groups in global amplitude suppression and suppression of all frequencies. These findings imply that the medial-olivocochlear bundle efferent pathway is intact among individuals with misophonia. Conclusion: Our findings have concluded that the medial olivocochlear bundle appears intact among individuals with misophonia (p&gt;0.05). However, it is essential to note that the generalizability of these findings may be limited due to the relatively small sample size used in our study. Therefore, further research involving a more extensive and diverse population is needed to validate and generalize these conclusions. Keywords: Misophonia; efferent pathway; contralateral suppression; neurophysiology; audiology

Knee joint pathology and efferent pathway dysfunction: Mapping muscle inhibition from motor cortex to muscle force

BackgroundDysfunction in efferent pathways after knee pathology is tied to long-term impairments in quadriceps and hamstrings muscle performance, daily function, and health-related quality of life. Understanding the underlying etiology is crucial for effective treatment and prevention of poor outcomes, such as post-traumatic osteoarthritis or joint replacement. ObjectivesTo synthesize recent evidence of efferent pathway dysfunction (i.e., motor cortex, motor units) among individuals with knee pathology. DesignCommentary. MethodWe summarize the current literature investigating the motor cortex, corticospinal tract, and motoneuron pool in individuals with three common knee pathologies: anterior cruciate ligament (ACL) injury, anterior knee pain (AKP), and knee osteoarthritis (OA). To offer a complete perspective, we draw from studies applying a range of neuroimaging and neurophysiologic techniques. ResultsAdaptations within the motor cortices, corticospinal tract, and motoneuron pool are present in those with knee pathology and underline impairments in quadriceps and hamstrings muscle function. Each pathology has evidence of altered motor system excitability and reduced volitional muscle activation and force-generating capacity, but few impairments were common across ACL injury, AKP, and OA studies. These findings underscore the central role of the motor cortex and motor unit behavior in the long-term outcomes of individuals with knee pathology. ConclusionsAdaptations in the efferent pathways underlie persistent muscle dysfunction across three common knee pathologies. This review provides an overview of these changes and summarizes key findings from neurophysiology and neuroimaging studies, offering direction for future research and clinical application in the rehabilitation of joint injuries.