Autonomic Nerve Research Articles

Background: The mechanistic linkage of complex fractionated atrial electrograms (CFAEs) and the relationship with the autonomic nervous system in the development of persistent atrial fibrillation are complex and not well understood. Objective: To test the hypothesis that CFAEs are accompanied by an increase in parasympathetic nerve firing, enhancing the development of persistent AF. We also hypothesized that the CFAE prevalence and CFAE variability increase over time in the development of persistent AF. Methods: Persistent AF was induced in 5 dogs (> 1 year old, 25 to 35kg) by rapid atrial pacing (RAP) (600 beats/min) for 3 to 17 weeks. We recorded parasympathetic nerve recordings using implanted telemetry (DSI, Harvard Bioscience) in the superior left ganglionic plexi (SLGP) (1 hour) (high and low pass filter 150, 1000Hz) over weeks of RAP. Parasympathetic nerve activity (PNA) was assessed by integrating the signal amplitude over time in 5 minute segments (Matlab). We synchronously analyzed electrograms (EGMs) (high and low pass filter 10, 100Hz) and quantified complex fractionated electrograms (CFAEs) with peak-to-peak sensitivity of 0.05 mV. We also assessed the prevalence of CFAEs (percentage CFAE (%)) as times when CFAEs were observed vs. total time and the CFAE variability as the standard deviation of CFAE length. Results: PNA increased with increasing weeks of RAP (R=0.5, P<0.05) ( Figure 1 ). Over RAP weeks, CFAE length (R=0.5, P<0.05), CFAE prevalence (R=0.5, P<0.05), and CFAE variability (standard deviation of CFAE length) (R=0.5, P<0.05) increased ( Figure 1).: We detected a clear relationship between parasympathetic nerve activity and CFAEs. CFAEs were synchronously overlying PNA, and CFAE length correlated with PNA (R=0.7, P<0.05) ( Figure 2 ). Conclusion: Persistent atrial fibrillation develops over time with increasing parasympathetic nerve activity and increasing CFAE lengths, CFAE prevalence, and CFAE variability. This data provides new insights into the mechanistic linkage between the heart rate, autonomic nerve activity, and overlying CFAEs in the development of persistent AF.

Background: Reactive oxygen species (ROS), complex fractionated atrial electrograms (CFAEs), and the autonomic nervous system play an important role in atrial fibrillation (AF). However, their mechanisms are complex, and their real time feedback responses to ROS scavenging remain unsettled. Objective: We hypothesized that parasympathetic nerve activity (PNA) and overlying CFAEs are uniquely sensitive to acute ROS scavenging with N acetylcysteine (NAC). Methods: We induced persistent AF in 15 dogs (> 1 year old, 25 to 35kg) by rapid atrial pacing (RAP) (600 beats/min) for 3 to 17 weeks and performed high-density epicardial mapping pre/post-NAC, intravenous, 100mg/kg) using an epicardial mapping-plaque in the posterior left atrium (PLA) (130 electrodes, electrode-distance 2.5mm). In 4 dogs, we recorded parasympathetic nerve recordings using implanted telemetry (Data Sciences International, Harvard Bioscience Inc.) in the superior left ganglionic plexi (SLGP) using a high pass (150 Hz) and low pass (1000 Hz) filter pre and post-NAC (intravenous, 100mg/kg) at baseline and in persistent AF. We assessed parasympathetic nerve activity (PNA) by integrating the nerve signal amplitude (1 to 2 hours) over time in 5 minute segments (Matlab, MathWorks) and analyzed synchronous real time electrograms EGMs (high and low pass filter setting 10, 100Hz) and CFAEs. We quantified CFAEs with peak to peak sensitivity of 0.05 mV to avoid sensing noise. Results: In high-resolution mapping, >20% of the fractionated signals were sensitive to ROS scavenging in persistent AF in the PLA. In persistent AF, at the SLGP, we discovered a clear relationship between simultaneous recordings of PNA and overlying CFAEs (Figure 1). PNA correlated with CFEAs (R=0.6, P<0.01) at the SLGP (Figure 1). Post-NAC administration, at the SLGP, CFAEs were significantly reduced by 35% in persistent AF (P<0.05). NAC led to a significant reduction of PNA of 81% (P<0.05) in persistent AF at the SLGP (Figure 2). Conclusion: Acute scavenging of ROS with NAC reduces CFAEs and parasympathetic nerve activity in persistent AF. This data provides evidence for a mechanistic linkage between mitochondrial ROS, autonomic nerve activity, and overlying CFAEs in AF.

Introduction: Atrial fibrillation (AF) is the most common arrhythmia and is a major risk factor for stroke. Existing therapies including ablation remain suboptimal. An increase in autonomic nerve signaling – both parasympathetic and sympathetic – is thought to contribute to AF genesis and progression. Therapies targeting atrial autonomic signaling may therefore attenuate arrhythmogenic substrate for AF. Hypothesis: Combined gene therapy targeting parasympathetic (Gαi and Gαo), and sympathetic (Gαs) signaling will attenuate autonomic effects on atrial electrophysiology (EP), delaying AF onset and progression. Methods: A polycistronic plasmid encoding inhibitory peptides for Gαi, Gαo, and Gαs (separated by P2A sequences) was injected in the canine (n=3) atria followed by electroporation to facilitate gene delivery. Controls included scrambled-sequence-injected and uninjected animals (n=10). Persistent AF (PersAF) was induced by rapid atrial pacing (RAP) over 12 weeks. Residual AF was evaluated at terminal EP study (Panel A). Results: Controls developed persAF (100% AF burden) after 3.6±1.4 weeks of RAP. Combined (Gαi+Gαo+Gαs) gene therapy attenuated AF development – two animals developed persAF at 8±3 weeks, one animal never reached 100% AF burden and was mainly in atrial flutter until the terminal. The last day of sinus rhythm was extended (54±27 vs 22±13 days, treatment vs control). AF burden was significantly reduced by 35±20% at all timepoints (Panel B, p<0.05). AF at the terminal experiment displayed lower frequency and less fractionation in gene therapy animals (panel C), with one animal spontaneously converting to sinus rhythm. Conclusion: Gene-based inhibition of parasympathetic and sympathetic signaling in the atria by expression of Gαi, Gαo, and Gαs inhibitory peptides successfully delays onset of AF and attenuates AF burden. These data emphasize an important mechanistic role for autonomic nerve activity in genesis and progression of AF. Future optimization of this multi-target gene therapy approach may offer promising novel treatments for AF.

To evaluate the impact of pulsed-field ablation (PFA) and radiofrequency catheter ablation (RFCA) on cardiac autonomic nerve system (ANS) function after pulmonary vein isolation (PVI) by monitoring heart rate (HR) and heart rate variability (HRV) changes. In this prospective cohort clinical study, patients with paroxysmal atrial fibrillation (AF) were enrolled consecutively into PFA or RFCA groups. HRV was assessed using the standard deviation of NN intervals (SDNN) and the standard deviation of the average NN intervals over 5-min periods (SDANN). HR, SDNN, and SDANN were measured before PVI and 3 months after PVI using 24-hour Holtermonitoring. Acute electrical isolation was achieved in 100% of pulmonary veins (PVs) in the 72 patients. Over the 3-month follow-up, 36 of 36 patients in the PFA group and 36 of 36 patients in the RFCA group remained free from atrial arrhythmia episodes >30s. In the PFA group, there were no significant changes in HR, SDNN, and SDANN before and after PVI (all p>0.05). The increase in HR in the PFA group was significantly lower than in the RFCA group (3.19±10.50vs. 10.86±9.30bpm; p=0.0008). The decrease in HRV indices SDNN and SDANN in the PFA group was also significantly less than in the RFCA group (-10.72±33.89vs. -28.33±30.55ms; p=0.012, -4.67±32.55vs. -22.03±27.46ms; p=0.009). PFA results in less damage to cardiac ANS function and preserves more cardiac ANS function compared with RFCA during PVI for paroxysmal AF.

Inherited Peripheral Neuropathies.

Pelvic surgeries frequently injure the pelvic autonomic plexus, represented in rats by the major pelvic ganglia (MPG), resulting in refractory erectile dysfunction (ED) with limited therapeutic options. Sacral neural crest (NC) cells, the embryonic progenitors of MPG neurons and glial cells, offer a developmentally matched cell source for targeted neural repair. We developed a stable and expandable sacral NC cell population derived from human pluripotent stem cells (hPSCs) and transplanted these cells into a rat model of MPG crush injury to assess engraftment efficacy and functional outcomes. Transplantation of sacral NC cells resulted in robust engraftment and significant erectile functional recovery, as evidenced by elevated intracavernosal pressure/mean arterial pressure (ICP/MAP) ratios. Mechanistically, MPG repair involves dual pathways: differentiation into nitrergic and cholinergic neurons and glial cells, which is coupled with the sustained secretion of neurotrophic factors (BDNF/GDNF/NGF). MPG restoration thereby re-established autonomic innervation of the penis, driving structural recovery characterized by reduced apoptosis and fibrosis, as well as the restoration of smooth muscle and endothelial integrity-essential for erectile functional rehabilitation. Our results demonstrate that hPSC-derived sacral NC cells represent a novel therapeutic strategy for neurogenic ED, restoring pelvic autonomic nerve structure and function through both neurogenic differentiation and sustained neurotrophic support.

Expressive writing is the disclosure of negative events in a safe and non-threatening environment while focusing on the feelings and emotions associated with an experience. Studies have proposed that alternative expressive writing instructions can influence expressive writing outcomes and shed light on the benefits of the intervention. Thus, we created two novel expressive writing instructions susceptible to inducing emotion regulation: a reappraisal and a self-compassion instruction. Sixty-six college students at a university were randomly assigned to either reappraisal or a self-compassion expressive group. Positive and negative affect, emotion regulation, anxiety, and alexithymia were measured before and after writing. ECG was recorded during the experiment to examine the effects of the writing exercise on the Autonomous Nervous System. We found that expressive writing decreased HR (d = 0.63) and alexithymia (d = 0.55) in both groups. In addition, LF/HF ratio was higher in the reappraisal expressive group (d = 0.70). These findings support the use of expressive writing as a tool to promote emotion regulation.

Leprosy, caused by Mycobacterium leprae, leads to peripheral neuropathy and significant functional disability if its diagnosis is delayed. Infrared thermography may offer a non-invasive method for the detection of neurological complications. A cross-sectional study was conducted with 100 leprosy patients and 20 healthy controls. Participants were assessed for cutaneous temperature using infrared thermography at defined areas corresponding to peripheral nerve innervation points (hands, feet, and face). Sensory neuropathy was analyzed using the Semmes-Weinstein (SW) monofilament test, while autonomic nerve dysfunction was evaluated through the sympathetic skin response (SSR). Data were analyzed with the aim of verifying whether changes in skin temperature clinically correlated with sensory loss, autonomic nerve dysfunction, and distinct forms of the leprosy spectrum. Leprosy patients had significantly lower skin temperature compared to controls, with a mean temperature of 32.5°C ± 2.3°C vs. 35.2°C ± 0.4°C for hands (p < 0.001) and 24.1°C ± 2.8°C vs. 34.8°C ± 0.5°C for feet (p < 0.001). Temperature differences were most pronounced in body areas showing sensory neuropathy (e.g., 30.1°C ± 2.2°C for hands with absent sensation vs. 34.1°C ± 1.6°C with normal sensation, p < 0.001). Strong linear correlations were found between cutaneous temperature and sensory loss assessed using SW filaments (p < 0.001) and between cutaneous temperature and SSR (p < 0.001). Disability grade also correlated with lower temperatures, with hands at 34.3°C for no disability, 31.3°C for Grade 1, and 31.5°C for Grade 2 disability. Infrared thermography is a promising, non-invasive tool for the detection of peripheral sensory impairment in leprosy. The results obtained by infrared thermography show a strong correlation with those obtained using standard tests for sensory loss and autonomic nerve dysfunction.

Parkinson's disease (PD) is characterized by pathological α-synuclein (α-syn) aggregation, yet the origin of α-syn pathology (central or peripheral) remains debated. The synuclein origin and connectome (SOC) model proposes two subtypes, including brain-first (pathology initiating in brain structures) and body-first (originating in peripheral autonomic nerves) subtypes. This study aimed to delineate cutaneous α-syn signatures between these subtypes to validate the SOC model. In this cross-sectional study, 126 brain-first PD patients, 79 body-first PD patients, and 60 healthy controls were enrolled. Subtype classification was based on the presence of REM sleep behavior disorder preceding motor symptoms. All participants underwent skin biopsies at two anatomical sites: the distal leg (DL) and the posterior cervical region (C7). Intraepidermal, sudomotor, and pilomotor nerve fiber densities were quantified. Phosphorylated α-syn (p-α-syn) deposition was assessed by immunostaining, and α-syn seeding activity was evaluated using real-time quaking-induced conversion (RT-QuIC). Clinical correlations and diagnostic performance were systematically analyzed. Body-first PD patients exhibited more prominent non-motor symptoms (e.g., REM sleep behavior disorder, autonomic dysfunction) and severe autonomic denervation (reduced sweat gland and pilomotor nerve densities; P < 0.01). Immunostaining revealed significantly higher p-α-syn positivity (92.4% vs. 61.9%) and a greater p-α-syn diffusion coefficient (0.2 vs. 0.0) in body-first versus brain-first PD patients. Body-first PD patients displayed a distal-to-proximal α-syn gradient (DL:86.1% vs. C7:55.7%), contrasting the proximal-dominant pattern in brain-first PD patients (DL:40.5% vs. C7:50.8%). Body-first PD patients also demonstrated accelerated α-syn seeding activity (higher maximum fluorescence intensity, shorter time to reach threshold; P < 0.001). Cutaneous α-syn parameters strongly correlated with non-motor symptom severity in body-first PD patients (P < 0.05). Receiver operating characteristic analysis showed that DL α-syn signatures have discriminative power for subtype differentiation (AUC = 0.774). Our findings provide direct pathological evidence for the body-first versus brain-first PD framework and highlight the value of skin biopsy as a minimally invasive biomarker for PD subtyping. This study contributes to precision medicine approaches targeting α-syn pathology-specific propagation pathways in PD.

Numerous reports have been published on the putative mechanisms of development of insulin resistance in diabetes mellitus. However, no unified view has been established yet, especially in regard to involvement of the nervous system in the regulation of insulin sensitivity. In this study, we investigated the involvement of the autonomic nervous system in cellular glucose uptake by blocking Group C nerve fibers (C fibers) in the rat pancreas with capsaicin. When the junction of the proximal pancreatic duct and common bile duct was treated with capsaicin, glucose uptake was enhanced, probably due to increased insulin sensitivity. This suggests that capsaicin may partially block the vagal nerve fibers innervating the pancreas, resulting in enhanced insulin sensitivity. In other words, our finding suggests that pancreatic autonomic nerves may be involved in the regulation of insulin sensitivity and that partial blockade of these nerves may improve insulin sensitivity.

Individualized paced deep breathing training with autonomic nervous function as rehab targets in patients with chronic heart failure: a randomized clinical trial

BackgroundDegeneration of organ-specific nervous systems precede major clinical conditions such as heart failure, dementia, diabetic retinopathy, and diabetic neuropathy. Glucagon-like peptide-1 receptor (GLP1R) agonists may have neuroprotective effects, independent of their glucose-lowering effects, and as such may be tools for early prevention of neurodegeneration. We investigated whether genetic variation in the GLP1R protein encoding region, assessed using a genetic score, was associated with neurodegeneration measured in the heart, brain, retina, and peripheral nerves.MethodsData from up to 7446 individuals from The Maastricht Study were used (mean [standard deviation (SD)] age 59.5 ([8.7] years, 49.4% men, and 20.0% with type 2 diabetes [by design]). A GLP1R score (0–8 points) was calculated using four genetic variants located in the GLP1R protein encoding region, with putative functional consequences on GLP1R activity (rs1042044, rs1004280, rs10305423, rs880067). Multivariable regression analysis was used to examine the associations between GLP1R genetic score and neural measures of the heart (time- and frequency-domain heart rate variability [HRV]), brain (magnetic resonance imaging-assessed local and global structural connectivity indices, brain volume, and global cognitive performance), retina (retinal nerve fiber layer thickness and retinal sensitivity) and peripheral nerves (conduction velocity). Associations were adjusted for age, sex, and HbA1c. Interaction with sex, age, and glucose metabolism status was examined.ResultsIn fully adjusted analyses, higher GLP1R genetic score (corresponding to higher predicted GLP1R protein expression) was significantly associated with higher time-domain HRV (per SD higher GLP1R score, 0.031 (0.006, 0.056) SD) and similarly, but not statistically significantly, with higher frequency-domain HRV (0.024 (− 0.001, 0.048) SD). The GLP1R genetic score was not significantly associated with brain, retinal, or peripheral nerves measures. Associations did not consistently differ as a function of age, sex, or glucose metabolism status.ConclusionsHigher putative GLP1R protein expression, assessed from genetic variation in the GLP1R protein encoding region, was significantly associated with lower levels of neurodegeneration in the heart, but not in the brain, retina, and peripheral nerves. Future clinical trials should test whether use of GLP1R agonists can contribute to prevention of cardiac autonomic nerve degeneration and associated clinical disease.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12933-025-02888-1.

Autonomic nerves regulate the innervation and function of the bladder, uterus, and rectum via their terminal branches. This section emphasizes the superior hypogastric plexus, hypogastric nerve, pelvic splanchnic nerves, inferior hypogastric plexus, and its terminal branches, namely the vesical, rectal, and uterine nerves. Somatic nerves traverse the pelvis, providing motor and/or sensory innervation to the pelvic floor and lower limbs. It is important to recognize the obturator nerve, genitofemoral nerve, lateral femoral cutaneous nerve, lumbosacral trunk, and femoral nerve.

Autonomic imbalance is a key driver of cardiovascular disease progression, arising from disrupted interactions between sympathetic and parasympathetic signaling. This review explores the molecular mechanisms underpinning autonomic dysfunction, emphasizing the roles of β-adrenergic receptor (βAR) signaling, cyclic AMP (cAMP) compartmentation, and cholinergic regulation. Dysregulated cAMP nanodomain signaling, βAR desensitization, impaired vagal tone, and maladaptive autonomic nerve remodeling collectively promote structural, electrophysiological, and functional deterioration. Advances in high-resolution imaging and molecular mapping have revealed previously unrecognized pathways governing second-messenger compartmentation and neuromodulatory feedback loops. These insights are driving the development of next-generation therapeutics designed to selectively restore autonomic balance. Promising strategies include isoform-specific phosphodiesterase (PDE) inhibitors, vagus nerve stimulation (VNS), and axonal modulation therapy (AMT), which target norepinephrine (NE) and acetylcholine (ACh) pathways while preserving physiological responsiveness. Integrating pharmacological, neuromodulatory, and molecular approaches represents an evolving frontier for cardiovascular therapeutics. Future strategies will benefit from precision mapping of autonomic circuits, patient-specific profiling, and optimization of therapeutic timing. By linking fundamental molecular signaling with translational advances, this review highlights opportunities to improve treatment precision and efficacy for autonomic dysfunction in cardiovascular disease.

Background: Autonomic nerve dysfunction has been noted in type 2 diabetes mellitus (T2DM). It needs not only medical management but also lifestyle modification. Regular practice of yoga based deep relaxation technique (DRT) cause improvement of autonomic nerve function by increasing heart rate variability (HRV) in healthy subjects. Objective: To observe the effect of yoga based DRT on non linear measures HRV by Poincare plot analysis in T2DM patients. Methods: This prospective interventional study was done in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSSMU), Dhaka in 2016 on 30 female diagnosed T2DM patients aged 50-55 years with duration of diabetes of 5-10 years. They performed DRT (20 minutes twice daily) for 3 months. 30 apparently healthy female with similar age who did not perform DRT or any other form of exercise, were included as control. To assess the cardiac autonomic nerve function, non linear HRV parameters were recorded by a data acquisition device Power Lab 8/35 (Australia) and Poincare analysis of data was auto generated by Lab chart software. HRV data of all subjects were collected at baseline (Pre) and also after 3 months of DRT(Post) in patients as well as in control without DRT. For statistical analysis, paired and independent sample t-test were used. Results: The pre-intervention non linear values of standard deviation of long axis(SD1) of scatterplots and standard deviation of short axis (SD2) of scatterplots (p&lt;0.001) and SD1/SD2 ratio (p&lt;0.01) were significantly lower in all diabetic patients compared to control. After 3 months of DRT, there was significant increment in SD1, SD2 (p&lt;0.001) and SD1/SD2 ratio (p&lt;0.05) compared to their pre-intervention values. Conclusion: Cardiac autonomic nerve dysfunction may occur in T2DM and 3 month’s regular exercise of DRT may improve cardiac autonomic nerve function and sympathovagal balance in Type 2 Diabetes Mellitus. J Bangladesh Soc Physiol 2025;20(1): 32-38

Sensory and autonomic nerves supply the sinonasal mucosa and contribute to chronic rhinitis, rhinosinusitis, and craniofacial pain. While posterior and posterolateral nasal nerves have been studied anatomically and histologically, nerves supplying the anterolateral nasal wall (ALNW) have been incompletely studied. The purpose of this cadaveric study was to investigate the ALNW's nerve supply. Sixteen fresh cadaver heads were dissected. First, six heads underwent unilateral ALNW dissection to harvest nerves coursing through the bony ALNW, and these were termed anterior nasal nerves (ANNs). Specimens were formalin-fixed, sectioned, and stained with hematoxylin and eosin, as well as for sensory or autonomic neuropeptides and enzymes. Nerve biomarker presence/absence was recorded. Next, 10 heads (20 sides) were utilized for ALNW mucosal area measurement and dissections. Bilateral subperiosteal dissections were performed to count nerves coursing from the ALNW and anterior portion of the inferior turbinate (IT). Of the six ANNs analyzed immunohistochemically, sensory and autonomic nerve markers were identified in each ANN. The other 10 cadavers all had ANNs coursing from the bony ALNW, with significantly more ANNs coursing through the bony ALNW superior to the IT-ALNW mucosal junction (p = 0.001). ANNs were identified in all cadavers, with more supplying the ALNW than the anterior portion of the IT. Sensory and autonomic nerve markers were identified in the ANNs. Future studies should explore the relative contributions of sensory versus autonomic dysfunction in different rhinologic conditions, and whether these aberrations differentially affect the anterior versus posterior nasal cavities.

Small fiber neuropathy (SFN) affects small-diameter sensory and autonomic nerve fibers, leading to chronic pain and autonomic dysfunction. While SFN can be associated with diabetes and autoimmune diseases, a significant proportion of cases are idiopathic. Although immune-mediated mechanisms are being recognized increasingly in SFN, their precise role remains unclear. This study investigates the presence of autoantibodies against interferon-induced GTP-binding protein MX (MX1) in SFN patients and explores their potential pathogenic role. A total of 59 patients with skin biopsy-confirmed SFN and 20 healthy controls were recruited. Serum samples were analyzed for the presence of anti-MX1 autoantibodies using enzyme-linked immunosorbent assay (ELISA). Immunohistochemistry was performed on rat sciatic nerves to assess the localization of patient IgG to unmyelinated nerve fibers, and immunocytochemistry and flow cytometry confirmed specific binding to MX1. Functional characterization of MX1 was conducted using whole-cell patch-clamp recordings in dorsal root ganglion (DRG) neurons overexpressing MX1. Additionally, protein interactions between MX1 and transient receptor potential cation channel subfamily C member 6 (TRPC6) were assessed using co-immunoprecipitation and surface biotinylation assays. Anti-MX1 autoantibody levels were significantly elevated in SFN patients compared to controls (p = 0.0278), particularly in the autoimmune SFN subgroup. Patient sera exhibited IgG binding to unmyelinated nerve fibers, with idiopathic and autoimmune SFN cases showing similar staining patterns, suggesting a similar immune-mediated mechanism. Immunocytochemistry showed binding to HEK293-MX1 cells and flow cytometry revealed higher MX1/WT fluorescence intensity ratios in patient sera, further confirming specific immune recognition of MX1. Patch-clamp recordings demonstrated that MX1 overexpression in DRG neurons led to significant membrane depolarization and increased action potential firing frequency (p < 0.0001), indicating heightened neuronal excitability. However, MX1 did not directly interact with TRPC6 or alter its function, suggesting an alternative pathway for its effects. The addition of anti-MX1 IgG did not further modify DRG electrophysiology, implying that the autoimmune component may contribute to SFN pathogenesis through indirect mechanisms. Our findings support the hypothesis that MX1 influences neuronal excitability and plays a role in SFN pathophysiology. Future studies should validate these findings in larger cohorts and explore potential therapeutic strategies targeting MX1-associated pathways in SFN.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12974-025-03557-6.

ABSTRACTPelvic autonomic nerve injury during radical treatment of cervical cancer and postoperative radiotherapy leads to bladder dysfunction and urinary retention. At present, there is no specific treatment. We report a 51‐year‐old patient with cervical adenocarcinoma who developed acute radiation cystitis and urinary retention 2 months after radiotherapy. We used three courses of intravesical injection of platelet‐rich plasma, which improved the patient's bladder emptying function and restored the bladder mucosa. We believe that intravesical injection of platelet‐rich plasma can not only be used to treat acute radiation cystitis, but also be a potential treatment for urinary retention after pelvic tumor surgery. However, further controlled clinical trials are needed to confirm.

ABSTRACTPatients with deep endometriosis of the posterior pelvic compartment might present various lower urinary tract symptoms, including urinary retention, without any prior pelvic surgery in their medical history. These symptoms, including urinary retention, pollakiuria or urge incontinence, urinary urgency, and decreased bladder sensitivity, imply an infiltration of the pelvic autonomic nerves by endometriosis lesions, in combination with inflammatory phenomena. Although there are numerous publications dealing with de novo urinary dysfunction after endometriosis surgery, significantly less scientific information is available on the effect of endometriosis surgery specifically tailored to improve preoperative voiding dysfunction in endometriosis. Therefore, in this case report, we analyze the effect of laparoscopic endometriosis surgery in a 28‐year‐old nulliparous woman with serious preoperative urinary retention mandating clean intermittent self‐catheterization three to four times daily. Patient history revealed neither prior pelvic nor abdominal operation, nor any neurological or other known disease. Uroflowmetry demonstrated significant voiding dysfunction. Filling cystometry showed signs of reduced bladder sensation (normal desire to void at 400 mL) along with preserved bladder compliance. During the pressure‐flow study, the patient was unable to initiate micturition, although abdominal straining and detrusor contraction were registered. The cause of voiding dysfunction was deemed to be pelvic floor dysfunction (dysfunctional voiding) rather than detrusor underactivity. Alpha blocker, muscle relaxant therapy, and pelvic floor relaxation training were introduced, achieving poor short‐term response. Transvaginal ultrasound examination showed hypoechogenic alterations on both uterosacral ligaments in the vicinity of their cervical attachment sites. These areas appeared to be painful while scanning with the probe. MRI examination confirmed the previous finding of transvaginal ultrasound with regard to bilateral alteration of the uterosacral ligaments characteristic of endometriosis. During laparoscopy, we confirmed the presence of endometriotic lesions of both uterosacral ligaments that were completely removed. The patient showed significantly improved emptying function following surgery. Uroflowmetry also demonstrated improved voiding parameters. We conclude that laparoscopic removal of endometriotic lesions of the uterosacral ligaments can significantly improve bladder function in patients suffering from preoperative voiding dysfunction.

Skin wound repair is critically regulated by peripheral nerves. Injury or dysfunction of these nerves represents a key factor impairing the healing of pathological wounds, such as diabetic ulcers and deep burns. The mechanisms by which peripheral nerves participate in cutaneous wound healing primarily involve modulation of immune responses, construction of stem cell niches, and promotion of angiogenesis. Sensory neurons initiate and mediate essential local immune responses, contribute to the epidermal stem cell microenvironment, and support regenerative potential. Sympathetic nerves bidirectionally regulate immune homeostasis via the release of various neuromodulators and precisely control the activation of hair follicle stem cells as well as the homeostasis of melanocyte stem cells. Schwann cells also play pivotal roles in immune modulation, balancing repair processes and mitigating scar formation. During revascularization, sensory and autonomic nerve terminals release neurotransmitters that precisely regulate vasomotor activity and angiogenesis, while Schwann cells facilitate the reconstruction of functional vascular networks via potent paracrine signaling. This review systematically summarizes the crucial roles of peripheral nerves in skin wound repair, with emphasis on their regulatory mechanisms in immune responses, stem cell activation and homeostasis, and vascular dynamics, thereby providing insights into the development of novel therapeutic strategies targeting peripheral nerve regulation.