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At least 19 recordsLinked to original sources

PubMed2026

Sacral Neuromodulation in the Management of Refractory Pediatric Lower Urinary Tract Dysfunction.

INTRODUCTION: Sacral neuromodulation is currently used in the pediatric patient population for refractory lower urinary tract dysfunction (LUTD). Evidence, however, is currently limited for institutional experiences of long-term outcomes for sacral neuromodulation in the pediatric patient population. OBJECTIVE: The objective of this study is to perform a retrospective review of a large multi-institutional cohort of pediatric patients that underwent sacral neuromodulation (SNM) for refractory LUTD, focused on rates of symptom improvement, quality of life, and bowel-bladder dysfunction measures following device implantation. Secondary objectives included assessing device complication rates and device removals due to failure or successful resolution of symptoms. METHODS: We performed a retrospective cohort study of pediatric patients at three children's hospitals that underwent SNM device implantation for refractory LUTD. Patients 4-18 years of age who were diagnosed with refractory LUTD and managed at a participating institution with follow-up were included. Outcomes were evaluated at baseline and post-operatively after two-stage device implantation at initial follow-up and annually until device removal or final follow-up. RESULTS: From 2010 to 2022, a total of 205 children underwent SNM procedures at three pediatric hospital centers. 204 patients completed the two-stage procedure for permanent device implantation with a median follow-up of 3.4 years (1.3, 4.9). One hundred seventy-eight patients reported partial (25%) or complete (54%) device response/symptom improvement by final follow-up. Comparison of patient-reported validated questionnaires completed at baseline and by final follow-up visit revealed significant improvement in median Pediatric Quality of Life Inventory (PedsQL) (p = 0.004) and Vancouver Nonneurogenic Lower Urinary Tract Dysfunction/Dysfunctional Elimination Syndrome bowel-bladder dysfunction (BBD) scores (p < 0.001). Of those with any device complication (n = 43;21%), 19 patients required device revision, and 20 required complete device removal. Separately, twenty-eight patients (13%) underwent device removal due to resolution of symptoms or treatment success at a median period of 5 years (4,7). CONCLUSION: SNM use demonstrated a majority of patients reporting at least partial subjective symptom improvement following device implantation across multiple institutions by final follow-up. SNM is a viable treatment option for refractory LUTD in the pediatric patient if willing to undergo an invasive procedure and in which thorough counseling of risks and benefits has occurred.

Humans↗

PubMed2026

Neuromodulation for Subjective Tinnitus: A Systematic Review and Meta-Analysis of Randomized Trials.

OBJECTIVE: To evaluate the effectiveness and safety of neuromodulation and bimodal stimulation for chronic subjective tinnitus in randomized controlled trials (RCTs). DATA SOURCES: PubMed/MEDLINE, Web of Science, and EMBASE (January 2015-December 2025) searched per PRISMA 2020. REVIEW METHODS: Adult RCTs (≥ 18 years) with chronic subjective tinnitus (> 3 months) assessing validated outcomes (THI, TFI, TQ) for neuromodulation/bimodal interventions vs. sham/controls. Two-stage screening, Cochrane RoB-2 risk-of-bias assessment. Random-effects meta-analyses (REML) were performed when ≥ 3 comparable trials were available; effects reported as standardized mean differences (SMD) with 95% CIs. Main Outcomes and measures included change in tinnitus severity (THI/TFI/TQ) while secondary outcomes included loudness (VAS/NRS), durability, and adverse events. RESULTS: Twenty-six RCTs (n = 1576) met criteria: tES (11; n = 372), rTMS (8; n = 432), acoustic coordinated reset (1; n = 100), vagus nerve stimulation (2; n = 90), and bimodal stimulation (4; n = 582). Meta-analysis showed a nonsignificant pooled effect for tDCS (SMD -0.36; 95% CI -0.75 to 0.02; I 2 = 51%) and rTMS (SMD -0.15; 95% CI -0.37 to 0.07; I 2 = 0%). Single-trial evidence for coordinated reset showed no advantage over broadband noise. VNS demonstrated modest benefits with safety concerns limited to implanted approaches. Bimodal stimulation yielded consistent, clinically meaningful reductions (often ≥ 10-20 points on THI/TFI), with durability up to 12 months. Adverse events were mild/transient across noninvasive modalities. CONCLUSIONS: Noninvasive neuromodulation appears safe with average benefits; among modalities, bimodal stimulation shows the most consistent and durable clinical improvements. Standardized, adequately powered RCTs with harmonized protocols and long-term follow-up are needed to refine targets and dosing.

Humans↗

PubMed2026

Efficacy of targeted neuromodulation treatments: a clinical report.

BACKGROUND: Peripheral neuropathy is a debilitating condition characterized by chronic pain, numbness, tingling, burning, and tightness/swelling. Conventional therapies often focus on symptom management, and some patients experience chronic and refractory symptoms. RESEARCH DESIGN AND METHODS: This retrospective clinical analysis evaluated the clinical outcomes of neuromodulation neuropathy treatment using the NeuroGen-Series device in patients with diabetic peripheral neuropathy (DPN) or idiopathic peripheral neuropathy (IPN). 9,805 unique patients who underwent 133,741 treatments between 18 August 2017, and 23 July 2024, were analyzed. Patients were divided into treatment completers (≥24 sessions) and noncompleters (<24 sessions). Paired t-tests confirmed statistically significant reductions in pre- and post-treatment symptom scores (p < 0.001). RESULTS: Among completers, symptom severity decreased by an average of 46.2%. Tingling and pain showed the greatest improvement, while tightness/swelling and numbness showed the least reduction. 64% of patients reported improvement after one session, and 84% reported improvement after 24 sessions. Nonresponders accounted for 5.8% of patients overall. Younger patients and those with higher initial symptom severity were more likely to discontinue treatment. CONCLUSIONS: Overall, neuromodulation treatment resulted in statistically significant reductions in symptom severity, though nonresponders and high attrition rate highlight the need for individualized treatment strategies and further investigation.

Humans↗

PubMed1979

Neurotransmitters and neuromodulators and their mediation by cyclic nucleotides.

An effort has been made here to devise criteria allowing discrimination between neurotransmitters, modulators and mediators. However, after consideration of several technical pitfalls in studies of these criteria, and examination of the properties of two examples of neuroactive agents (norepinephrine and endorphins) often referred to as "modulators", it is still difficult to classify these agents in all cases. Thus, in most central targets where NE-fibers are known to terminate, the synaptic actions of NE appear to have properties of both a neuromodulator and a neurotransmitter. Although much more research needs to be pursued, the opioid peptides may be neuromodulators for some neurons (spinal cord neurons) and neurotransmitters for others (myenteric plexus and spinal cord neurons). It may be that classification of such peptide agonists will need to be done on a cell-by-cell basis, with the endogenous peptides subserving a multi-faceted role in central and peripheral neuronal communication. As more and more endogenous ligands and transmitter-like substances are extracted from brain, it begins to appear that the language of neuronal communication is much richer than originally imagined from responses of spinal neurons to the fast-acting classical neurotransmitters. Indeed, it may evolve that the "deviant" forms of communication or transmission are more the rule than the exception. In the final analysis, each neurotransmitter may possess its own "fingerprint" of holistic actions attesting to the unique individuality of neuron types and their neurotransmitters. Such individualities might be expected to accomplish more sophisticated integrative operations, and hence behaviors, than could simple rapid "yes" or "no" messages.

Acetylcholine↗

PubMed2026

Predictive value of anal sphincter electromyography for sacral neuromodulation test-phase outcomes.

BACKGROUND: Sacral neuromodulation (SNM) is an established therapy for refractory pelvic organ dysfunction. Anal sphincter electromyography (EMG) is commonly used preoperatively to assess sacral and peripheral nerve integrity. However, the prognostic significance of chronic neurogenic EMG changes for SNM outcomes remains unclear. OBJECTIVE: To evaluate whether chronic neurogenic changes on preoperative anal sphincter EMG predict the outcome of the SNM test phase. METHODS: We retrospectively analysed 62 consecutive patients with bladder and/or bowel dysfunction or pelvic pain who were candidates for SNM treatment and who underwent preoperative anal sphincter EMG. EMG findings were classified as normal or showing chronic neurogenic changes. SNM test-phase success was defined as a ≥50% improvement of symptoms at 24 days. Outcomes were compared between EMG groups. RESULTS: Of the 62 patients (49 women, 13 men), 30 (48%) had normal EMG findings and 32 (52%) showed chronic neurogenic changes. Overall, the SNM test phase was successful in 47 patients (76%). Success rates were similar in patients with normal EMG (72%) and neurogenic EMG changes (79%), with no statistically significant difference (p = 0.878). Sex-stratified analyses revealed no significant association between EMG findings and test-phase success in women or men. CONCLUSIONS: Chronic neurogenic changes on anal sphincter EMG do not predict SNM test-phase outcomes. These findings suggest that abnormal sphincter EMG results should not be used as a standalone criterion to exclude patients from SNM therapy. SIGNIFICANCE: Signs of neurogenic damage on anal sphincter EMG are not an indicator of reduced neuromodulatory capacity or diminished clinical response to SNM.

Humans↗

PubMed2026

Assessment of blinding in pharmacotherapy and noninvasive neuromodulation randomized controlled trials for neuropathic pain in adults.

In randomized controlled trials (RCTs), study participants and research personnel are often blinded to minimize biases related to knowing treatment allocation. To determine if blinding was effective, participants may be asked which treatment they believe they received ("treatment guess"). This descriptive review characterized blinding assessment (BA) reporting in pharmacotherapy and neuromodulation neuropathic pain RCTs. Of 288 papers, 36 (12.5%) reported a BA. One paper reported the results of 2 studies, so in total 37 studies with a BA were assessed. Of these, 19 were crossover, 17 parallel, and 1 partial crossover in design. All 37 studies assessed participant blinding, and 10 also assessed investigator blinding. Approximately 27% included an "unsure" answer option for treatment guess, and 38% asked the reason for the guess. There were no clear patterns in BA reporting across time nor based on treatment type. Seventeen trials provided sufficient data to calculate Bang Blinding Index (BI) to determine blinding success. Participants remained blinded (BI = 0 ± 0.2) in 10/17 placebo and 10/17 treatment arms, 6 placebo and 5 treatment arms had a BI > 0.2 suggesting possible unblinding, whereas 1 placebo and 2 treatment arms had a BI < -0.2 suggesting misinformed guessing. Overall, we found that BAs are done in a minority of published neuropathic pain trials and with variable methodology. Given the importance of minimizing risk of bias because of treatment unblinding, future studies should consider including BAs, and further consensus building is necessary to determine if and how BAs should be conducted and interpreted in analgesic clinical trials.

Bias↗

PubMed1992

Lateral hypothalamic area neurotransmission and neuromodulation of the specific cardiac effects of insular cortex stimulation.

Microstimulation of the rat posterior insular cortex in phase with the ECG R wave elicits pure cardiac effects unaccompanied by changes in blood pressure or respiration. This technique has successfully demonstrated cardiac chronotropic organisation and arrhythmogenesis within the insula. Pathways exist linking the insular cortex with the lateral hypothalamic area (LHA). Similarly, the LHA has previously been shown to mediate the sympathetic and blood pressure effects of insular cortex stimulation. Therefore it was anticipated that the tachycardia elicited by insular phasic microstimulation would be responsive to LHA manipulations. Insular tachycardia sites in 28 chloralose-anesthetised male Wistar rats were phasically stimulated once with each cardiac cycle using 500 microA for 1 min before and after microinfusions (390 nl) into the LHA. The insular tachycardia response was abolished by LHA microinfusions of the synaptic blocker cobaltous chloride (4 mM). LHA microinjection of kynurenic acid (250 mM) attenuated insular tachycardia by 95%. Microinjection of naloxone (30 mM) similarly attenuated the tachycardia by 95%. Met-enkephalin (3.5 mM) was without effect on this response whereas Leu-enkephalin (3.5 mM) and neuropeptide Y (0.01 mM) (NPY) doubled the magnitude of the tachycardia. Dynorphin (0.12 mM), a specific kappa opioid receptor agonist, augmented the response to stimulation of insular tachycardia sites 8-fold. Consequently, it is suggested that the LHA contains an obligatory synapse mediating insular tachycardia and that glutamate is the likely neurotransmitter at this site. Neuromodulation of insular tachycardia may be effected by opiate kappa and NPY receptors, a finding of considerable clinical relevance.

Animals↗

PubMed2026

Neurophysiological signatures of Stanford Neuromodulation Therapy in treatment resistant depression.

Treatment-resistant depression (TRD) affects approximately 30% of patients with major depressive disorder. Stanford Neuromodulation Therapy (SNT), a high-dose intermittent theta-burst transcranial magnetic stimulation protocol, produces rapid antidepressant effects, but its neurophysiological mechanisms remain unclear. Here, we used longitudinal TMS-EEG to characterize the progressive neurophysiological changes induced by SNT, assess their site-specificity, and explore whether baseline neural markers are associated with clinical response. We conducted a double-blind, randomized, sham-controlled trial at Stanford University (2017-2018; analysis August 2024-October 2025) in 24 TMS-naïve participants with TRD (Montgomery-Åsberg Depression Rating Scale ≥20; ≥1 failed antidepressant trial). Participants were randomized to active (n = 12) or sham (n = 12) SNT, consisting of 10 sessions per day over 5 consecutive days targeting the left dorsolateral prefrontal cortex (90,000 pulses). TMS-EEG was acquired at two baseline sessions, before and after each treatment session, and at 1-month follow-up (14 TMS-EEG sessions in total). Active SNT progressively reduced cortical excitability at the treatment site, with significant decreases by day 3 in the early window component (-27.9%; P < 0.01), while no changes were observed at the vertex control site. Site-specific comparisons confirmed early window reductions only at the left dorsolateral prefrontal cortex (t₂₂ = -3.82; P < 0.001). SNT also selectively decreased estimated medial prefrontal source activity consistent with the subgenual anterior cingulate cortex (sgACC) across sessions (F₁₃,₂₂₂ = 4.93; P < 0.001), with effects persisting at 1-month follow-up. In an exploratory analysis in the active group (n = 12), higher baseline estimated sgACC source activity was associated with greater clinical improvement (r = -0.67; P = 0.023); although promising, the latter preliminary finding requires replication in larger, adequately powered samples before predictive utility can be established. These findings indicate that SNT induces progressive, site-specific cortical modulation and selective downstream effects on estimated sgACC source activity. Early cortical excitability changes represent candidate neurophysiological markers of SNT response, while the observed association between baseline sgACC activity and clinical outcome, while preliminary, motivates prospective investigation of subcortical source activity as a potential predictor of treatment response in larger trials. ClinicalTrials.gov Identifier: NCT03068715.

Journal Article↗

PubMed1979

Prostaglandin D2, a neuromodulator.

The distribution of prostaglandin D synthetase activity was determined in various tissues of rat by using the supernatant fraction (10,000 x g, 20 min) of the homogenates. The highest activity was found in brain, spinal cord, and alimentary tract. The activity was uniquitously distributed in all parts of brain, and the highest specific activity was found in hypothalamus and thalamus. Homogenates of two neuroblastoma cell lines were found to produce prostaglandin D2, whereas a glioma cell line was almost inactive. Prostaglandin D2 is a potent and specific activator of the adenylate cyclase system of cultured neuroblastoma cells, suggesting the possibility that it may act as a neuromodulator in the central nervous system.

Animals↗

PubMed2026

Assessment of Surgical Salvage Outcomes for Exposed Cranial Neuromodulating Devices.

OBJECTIVES: Implanted neuromodulating devices (NMDs) such as cochlear implants (CIs) and deep brain stimulators (DBSs) are commonly used in modern medicine. Rarely, complications arise post-operatively, including hardware exposure. Traditional teaching suggests that these devices require removal if exposed; however, surgical salvage is a high risk, high reward alternative. We review our single institution experience managing NMD exposure with surgical salvage. METHODS: Retrospective chart review was performed on individuals who had a NMD implanted and underwent an attempt at surgical salvage for exposure during the study period (January 01, 2021 through December 31, 2023). Study outcome success was defined as maintaining a functional NMD 1 year after salvage was attempted. Surgical techniques associated with successful salvage were compared. RESULTS: Nine of 729 patients (1.2%) implanted with NMDs experienced hardware exposure during this 2-year study period. Nine subjects were referred for NMD salvage; however, only 6 of 9 subjects (66.7%, CI = 3; DBS = 3) underwent NMD salvage attempts. Four of the subjects had successful salvage demonstrated successful salvage with a functioning NMD and without wound healing concerns 1 year after their salvage procedure. CONCLUSIONS: Classic teaching states that exposed NMDs require explantation. However, this approach necessarily imposes time without benefit from the NMD between explantation and reimplantation. Our experience demonstrates that surgical salvage can be a successful alternative for the majority (66.7%) of individuals.

Humans↗

PubMedDate not supplied

[Neuromediators and neuromodulators. Evolution of compounds and the evolution of hypotheses].

Probable peculiarities of evolution of neurotransmitters (NM) and neuromodulators (NR) of various types are discussed. The hypothesis of higher evolutionary rate of peptide NM and NR, and of more diverse possibilities of the formation of this type of NM and NR is suggested. Monomolecular MN and NR are presumably more conservative, although they exhibit some advantage with respect to strict differentiation of the systems of synthesis and degradation. Probably, the most ancient NM and NR are presented by such compounds as peptides, some amino acids, and ATP.

Adenosine Triphosphate↗

PubMed1979

The behaviorally active neuropeptide ACTH as neurohormone and neuromodulator: the role of cyclic nucleotides and membrane phosphoproteins.

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Adenylyl Cyclases↗

PubMed1992

NE/DA interactions in prefrontal cortex and their possible roles as neuromodulators in schizophrenia.

The monoaminergic innervation of the rat prefrontal cortex arises from well-defined mesencephalic nuclei, with noradrenergic (NE) neurons located in the locus coeruleus, dopaminergic (DA) neurons located in the ventral tegmental area, and serotonergic (5-HT) neurons originating in the raphe nuclei. Specific destruction of the NE bundle was found to induce morphological (i.e., sprouting) as well as metabolic (i.e., changes in rate of DA utilization) modifications of mesocortical DA neurons, suggesting that these two catecholaminergic systems have functional interactions within the prefrontal cortex. This was substantiated by experiments showing that DA afferents modulate the sensitivity of cortical post-synaptic beta-adrenergic receptors and that, reciprocally, NE neurons control the sensitivity of cortical D1 receptors. Behavioural and pharmacological data have further indicated that the stimulation of cortical alpha-1 adrenergic receptors inhibits cortical DA transmission at D1 receptors. Secondly, we have attempted to analyze how such interactions between neuromodulatory systems may be related to the development of mental diseases such as schizophrenia. On the basis of studies in the literature describing the effects produced by the ingestion of hallucinogenic drugs or data collected regarding REM sleep, it is postulated that two modes of brain functioning exist: analogical and cognitive. Each mode is characterized by differences in the relative activities of NE, DA and 5-HT neurons. At birth, during REM sleep, and following the ingestion of hallucinogens, the mode of brain functioning is essentially analogical; in contrast, both analogic and cognitive modes are postulated to coexist in the awake state. Oscillations between these two modes are under the control of monoaminergic systems on which an increase in cortical DA release favours the cognitive processing mode, whereas intermittent activations of NE neurons would switch the brain into the analogical mode of processing. It is proposed that schizophrenic patients with "positive" symptoms suffer from an abnormal preponderance of the analogical mode while awake, whereas "negative" symptoms are due to the excessive presence of the cognitive mode. Although pure biological deficits cannot be excluded, these dysfunctions could be related to the absence of particular environmental variables early in the development of these patients. This condition is probably required to establish normal regulatory control of monoaminergic neuronal activity.

Dopamine↗

PubMed1992

Excitable membranes, lipid messengers, and immediate-early genes. Alteration of signal transduction in neuromodulation and neurotrauma.

The physical nature of neuronal cells, particularly in the functional and morphological segregation of synapse, soma, and dendrites, imparts special importance on the integrity of their cell membranes for the localization of function, generation of intrinsic second messengers, and plasticity required for adaptation and repair. The component phospholipids of neural membranes are important sources of bioactive mediators that participate in such diverse phenomena as memory formation and cellular damage following trauma. A common role for PAF in these processes is established through the suppressive effects of its antagonists. Furthermore, being both an extracellular and intracellular agonist of phospholipase activation, in addition to being a product of phospholipase activity, PAF assumes a centralized role in the cellular metabolism following neural stimulation. The linkage of PAF to neural immediate-early gene expression, both in vitro and in vivo, suggests that its effects are initiating to long-term formative and reparative processes. Such a common link between destructive and plastic responses provides an important view of cellular and tissue maintenance in the nervous system.

Animals↗

PubMed1992

The effect of atherosclerosis on neuromodulation of sympathetic neurotransmission by neuropeptide Y and calcitonin gene-related peptide in the rabbit mesenteric artery.

The neuromodulatory actions of neuropeptide Y (NPY) (0.1 microM) and calcitonin gene-related peptide (CGRP) (0.01 microM) on nerve-evoked contractions have been studied in the Watanabe heritable hyperlipidemic (WHHL) rabbit mesenteric artery from 4-, 6- and 12-month-old animals with New Zealand white (NZW) rabbits being used as age- and sex-matched controls. Nerve-evoked contractions in 12-month-old rabbits were smaller in WHHL in comparison to NZW rabbits, with no difference between the two strains of rabbit at 4 and 6 months of age. Both the potentiating effect of NPY and the inhibitory effect of CGRP on nerve-evoked contractions increased significantly at 12 months of age compared with responses measured in younger WHHL rabbits, and were greater than in 12-month-old control NZW rabbits. In contrast, the direct smooth muscle relaxant response of CGRP on raised-tone preparations was not different between the two strains of rabbit at any age. Both NPY-immunoreactive and CGRP-immunoreactive nerve fibres were less varicose in 6- and 12-month-old WHHL rabbits when compared with younger WHHL rabbits and NZW controls. In conclusion, this study shows that while nerve-evoked contractions are reduced, in the 12-month-old WHHL rabbit mesenteric artery, the neuromodulatory actions of NPY and CGRP are augmented.

Age Factors↗

PubMed1992

Neurotransmitter actions in the thalamus and cerebral cortex and their role in neuromodulation of thalamocortical activity.

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Animals↗

PubMed1992

Neuromodulation of vertebrate motor neuron membrane properties.

The short-term function of motor neurons is to integrate synaptic inputs converging onto the somato-dendritic membrane and to transform the net synaptic drive into spike trains. A set of voltage-gated ion channels determines the electro-responsiveness and thereby the motor neuron's input-output function. In addition, several of the decisive ion channels are transmitter controlled, which results in a flexible control of the input-output relationship.

Animals↗

PubMed1992

Introduction to slow synaptic potentials and their neuromodulation by dopamine.

The existence of two muscarinically mediated slow postsynaptic potentials (PSPs) and a noncholinergic (peptidergic) late-slow PSP was established in the 1960s. These have synaptic delays and PSP durations 100-10,000 times those for the nicotinic (fast) excitatory post-synaptic potential (EPSP). Evidence is reviewed for an against the proposal that, in rabbit superior cervical ganglia, the slow (s-) inhibitory postsynaptic potential requires a second transmitter, dopamine, released by muscarinic action on interneurones (the small, intensely fluorescent cells). The s-EPSP in frog ganglia appears only in already depolarized cells by a muscarinic closure of the M (voltage-sensitive K+) channels. But the large s-EPSP in mammalian neurones, not depolarized, is generated largely via other mechanisms, especially one involving cyclic GMP. Dopamine also produces a long-term enhancement (LTE) of the muscarinic slow PSPs in rabbit superior cervical ganglia, whether dopamine is applied exogenously or released intraganglionically by preganglionic nerve impulses at 10 s-1. LTE is producible heterosynaptically, and it persists well over 3 h; a noncholinergic (peptide?) transmitter may contribute to the initial 30 min of LTE. LTE is mediated by a D1 receptor coupled to cyclic AMP; it is blocked by cyclic GMP or low Ca2+ or calmidazolium (a calmodulin inhibitor). The modulatory process of LTE has certain similarities to, but also fundamental differences from, the long-term potentiation known in the hippocampus.

Animals↗