Conduction Velocity Distribution Research Articles

Protective vs. Therapeutic Effects of Mitochondria-Targeted Antioxidant MitoTEMPO on Rat Sciatic Nerve Crush Injury: A Comprehensive Electrophysiological Analysis.

Protective vs. Therapeutic Effects of Mitochondria-Targeted Antioxidant MitoTEMPO on Rat Sciatic Nerve Crush Injury: A Comprehensive Electrophysiological Analysis. Peripheral nerve injuries often result in long-lasting functional deficits, prompting the need for effective interventions. MitoTEMPO (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride) is a mitochondria-targeted antioxidant that has shown protective and therapeutic effects against pathologies associated with reactive oxygen species. This study explores the utilization of MitoTEMPO as a therapeutic and protective agent for sciatic nerve crush injuries. By employing advanced mathematical approaches, the study seeks to comprehensively analyze nerve conduction parameters, nerve excitability, and the distribution of nerve conduction velocities to gauge the potential. Forty Wistar-Albino rats were randomly divided into following groups: (I) SHAM-animals subjected to sham operation and treated intraperitoneally (i.p.) with vehicle (bidistilled water) for 14 days; (II) CI (crush injury)-animals subjected to CI and treated with vehicle 14 days; (III) MiP-animals subjected to 7 days i.p. MitoTEMPO treatment before CI (0.7 mg/kg/day dissolved in vehicle) and, only vehicle for 7 days after CI, protective MitoTEMPO; and (IV) MiT-animals i.p. treated with only vehicle for 7 days before CI and 7 days with MitoTEMPO (0.7 mg/kg/day dissolved in vehicle) after CI, therapeutic MitoTEMPO. Nerve excitability parameters were measured, including rheobase and chronaxie, along with compound action potential (CAP) recordings. Advanced mathematical analyses were applied to CAP recordings to determine nerve conduction velocities and distribution patterns. The study revealed significant differences in nerve excitability parameters between groups. Nerve conduction velocity was notably reduced in the MiP and CI groups, whereas CAP area values were diminished in the MiP and CI groups compared to the MiT group. Furthermore, CAP velocity was lower in the MiP and CI groups, and maximum depolarization values were markedly lower in the MiP and CI groups compared to the SHAM group. The distribution of nerve conduction velocities indicated alterations in the composition of nerve fiber groups following crush injuries. In conclusion, postoperative MitoTEMPO administration demonstrated promising results in mitigating the detrimental effects of nerve crush injuries.

Motor fiber function in spinal muscular atrophy-analysis of conduction velocity distribution.

The motor neuron survival protein, which is deficient in spinal muscular atrophy (SMA), performs numerous cellular functions. Currently, SMA is believed to be a multi-organ disease, including lesion of various structures of the central and peripheral nervous systems. Motor nerve damage, especially in milder SMA types, is controversial. This prompted the conduct of the electrophysiological studies in adults with SMA types 2 and 3 presented in this paper. The study group consisted of 44 adult patients with SMA types 2 and 3. All patients underwent neurological examination with Hammersmith Functional Motor Scale-Expanded (HFMSE) assessment. Standard electrophysiological studies in the ulnar nerve and conduction velocity distribution (CVD) tests were performed in all patients and controls. A prolongation of the distal latency and lowering of the motor potential amplitude with no changes in CVD were found in the whole patient group. There were no dependencies on the number of gene copies. Patients with low HFSME value had slower standard conduction velocity, CVD in upper and median quartiles, and narrower CVD spread; in milder SMA, CVD spread was greater than in controls. The significant reduction in motor response amplitude in SMA seems to be primarily related to motor neuron loss and directly proportional to its severity. The coexisting rearrangement in the peripheral nerve structure is present in SMA, and this could be partially caused by a coexisting demyelinating process. Nerve remodeling mainly affects large fibers and occurs in more severe SMA types with significant disability.

Benefit of right inferior pacing on conduction across Bachmanns Bundle

Abstract Background Bachmann's Bundle (BB) is the main preferential route for interatrial conduction and plays an important role in initiation and perpetuation of atrial tachyarrhythmia such as atrial fibrillation (AF). Especially in patients with inter- and intra-atrial conduction disorders, the conventional site for placement of right atrial (RA) pacing lead in the RA appendage (RAA) has been questioned as it results in a higher incidence of AF. However, it remains unknown how pacing from various sites affects conduction at BB. Purpose To examine the impact of programmed stimulation from the left and right atrium on activation and electrophysiological features of BB. Methods Intra-operative high-resolution epicardial mapping of BB was performed during sinus rhythm (SR) and programmed stimulation in 32 patients (29 male, 65±10 years). Programmed stimulation included a fixed rate sequence of average SR cycle length minus 50 ms provided from the RAA, junction of the RA with inferior caval vein (RAinf) and left atrial appendage (LAA). Electrophysiological features included unipolar voltage, conduction velocity, potential type (single, short/long double and fractionated) and conduction delay/block (CDCB). Results The average cycle length during SR was 962 [869–1085] ms. Pacing from RAA resulted in comparable activation patterns as during SR. As expected, pacing from LAA resulted in left-to-right conduction across BB. However, during pacing from RAinf in most patients activation started in the centre of BB. Compared to SR, the least amount of differences in electrophysiological features was found during pacing from the RAA, followed by pacing from RAinf and LAA. Unipolar voltages, conduction velocity and potential type distribution were similar. However, during pacing from RAinf, total activation time decreased compared to SR (44 [38–62] ms vs 60 [51–67] ms, P=0.012), while total activation time increased by pacing from LAA (66 [60–72] ms, P=0.020). The total activation time during pacing from RAinf was lower compared to LAA (P<0.001) and RAA pacing (P=0.001). During pacing from LAA, the amount of CDCB increased compared to SR (6.6 [4.1–9.9] % vs 8.7 [5.6–12.8] %, P=0.009), while there were no differences in CDCB between SR and pacing from both RAA and RAinf. Reduction of CDCB was most often achieved during pacing from RAinf (12 patients), especially in patients who already had a higher amount of CDCB during SR (8.0 [7.3–11.2] % vs 4.3 [3.0–5.9] %, P<0.001). Reduction of both CDCB and total activation time was achieved in 10 patients by pacing from RAinf, while only 6 patients benefitted from RAA pacing. These patients had similar amount of conduction disorders. Conclusions Pacing from the inferior RA results in a remarkable decrease of total activation time and conduction disorders compared to pacing from the LAA or RAA. As specific patients may benefit more from inferior RA pacing, locations for pacing lead placement should be individualized. Funding Acknowledgement Type of funding sources: None.

Adaptation of the Two-CAP Method for Conduction Velocity Distribution Estimation in Multi-Channel Recordings.

Closed-loop neural interfaces capable of both stimulating and recording from peripheral nerves have the potential to enhance the long-term efficacy of neural implants. One challenge associated with closed loop interfaces is the accurate estimation of the distribution of active fibre conduction velocities (DCV) when recording the immediate effect of stimulation. DCV estimation has been performed in monopolar surface recordings using the Two-CAP method. This work extends the Two-CAP method and demonstrates its application to bipolar in-vivo recordings made with multiple-electrode arrays. A sensitivity analysis was conducted using simulated data with ground truth to ascertain the stability and limits of the algorithm before experimental data was examined. The sensitivity analysis highlighted that recording distance shows a considerable impact on the performance of this extended Two-CAP method, as well as the velocity interval chosen when creating the model. The in-vivo data was also compared against an equivalent simulated model, and a relatively low mean squared error was obtained when comparing the two distributions.

Meshless Electrophysiological Modeling of Cardiac Resynchronization Therapy—Benchmark Analysis with Finite-Element Methods in Experimental Data

Computational models of cardiac electrophysiology are promising tools for reducing the rates of non-response patients suitable for cardiac resynchronization therapy (CRT) by optimizing electrode placement. The majority of computational models in the literature are mesh-based, primarily using the finite element method (FEM). The generation of patient-specific cardiac meshes has traditionally been a tedious task requiring manual intervention and hindering the modeling of a large number of cases. Meshless models can be a valid alternative due to their mesh quality independence. The organization of challenges such as the CRT-EPiggy19, providing unique experimental data as open access, enables benchmarking analysis of different cardiac computational modeling solutions with quantitative metrics. We present a benchmark analysis of a meshless-based method with finite-element methods for the prediction of cardiac electrical patterns in CRT, based on a subset of the CRT-EPiggy19 dataset. A data assimilation strategy was designed to personalize the most relevant parameters of the electrophysiological simulations and identify the optimal CRT lead configuration. The simulation results obtained with the meshless model were equivalent to FEM, with the most relevant aspect for accurate CRT predictions being the parameter personalization strategy (e.g., regional conduction velocity distribution, including the Purkinje system and CRT lead distribution).

The Relevance of Collision Tests and Quantitative Sensory Testing in Diagnostics and Postoperative Outcome Prediction in Carpal Tunnel Syndrome.

BackgroundThe gold standards for the diagnosis and treatment of carpal tunnel syndrome (CTS) and its outcome are undecided. Using clinical and electrophysiological methods, we tried to establish which fibers achieved full postoperative recovery, and the possibility of using non-standard electrophysiological tests as outcome predictors.MethodsThe study group consisted of 35 patients and controls. The Historical–Objective Scale, standard neurography, conduction velocity distribution tests (CVD), and quantitative sensory testing (QST) were performed before and after CTS surgery.ResultsClinical improvement was observed on average in 54.3% of the patients, higher in less advanced CTS. All parameters improved significantly after surgery, except for CVD; most remained worse than in the controls. Only QST parameters fully returned to normal limits. Patient age and CTS severity were important in the estimation of the risk of no improvement.ConclusionsThe efficiency of minimally invasive CTS surgery is higher in younger patients with less advanced CTS. Complete recovery was present only in small fibers; larger fibers could most likely be responsible for residual signs. We did not notice any benefits in CTS diagnosis using methods of small fiber assessment. QST seemed to be useful in the diagnosis of residual signs, and in deciding upon possible reoperation.

Distribution of innervation zone and muscle fiber conduction velocity in the biceps brachii muscle

The spatial distributions of muscle innervation zone (IZ) and muscle fiber conduction velocity (CV) were examined in nine healthy young male participants. High-density surface electromyography (EMG) was collected from the biceps brachii muscle when subjects performed isometric elbow flexions at 20% to 80% of the maximal voluntary contraction (MVC). A total of 9498 samples of IZs were identified and CVs were calculated using the Radon transform. The center and width of IZ sample distribution were compared within four different force levels and six medial to lateral electrode column positions using repeated measures ANOVA and multiple comparison tests. Significant shifts of IZ center were observed in the medial columns (Columns 5, 6, and 7) compared with the lateral columns (Columns 3 and 4) (p < 0.05). Similarly, significant differences in the IZ width were found in Column 7 and 8 compared to Column 3 (p < 0.05). In contrast, muscle CV was unaffected by column position. Instead, muscle CV was faster at 40% and 80% MVC compared to 20% MVC (p < 0.05). The findings of this study add further insights into the physiological properties of the biceps brachii muscle.

Dissecting whole-brain conduction delays through MRI microstructural measures

Network models based on structural connectivity have been increasingly used as the blueprint for large-scale simulations of the human brain. As the nodes of this network are distributed through the cortex and interconnected by white matter pathways with different characteristics, modeling the associated conduction delays becomes important. The goal of this study is to estimate and characterize these delays directly from the brain structure. To achieve this, we leveraged microstructural measures from a combination of advanced magnetic resonance imaging acquisitions and computed the main determinants of conduction velocity, namely axonal diameter and myelin content. Using the model proposed by Rushton, we used these measures to calculate the conduction velocity and estimated the associated delays using tractography. We observed that both the axonal diameter and conduction velocity distributions presented a rather constant trend across different connection lengths, with resulting delays that scale linearly with the connection length. Relying on insights from graph theory and Kuramoto simulations, our results support the approximation of constant conduction velocity but also show path- and region-specific differences.

LSTM Neural Network for Inferring Conduction Velocity Distribution in Demyelinating Neuropathies.

Waveform analysis of compound muscle action potential (CMAP) is important in the detailed analysis of conduction velocities of each axon as seen in temporal dispersion. This understanding is limited because conduction velocity distribution cannot be easily available from a CMAP waveform. Given the recent advent of artificial intelligence, this study aimed to assess whether conduction velocity (CV) distribution can be inferred from CMAP by the use of deep learning algorithms. Simulated CMAP waveforms were constructed from a single motor unit potential and randomly created CV histograms (n = 12,000). After training the data with various recurrent neural networks (RNNs), CV inference was tested by the network. Among simple RNNs, long short-term memory (LSTM) and gated recurrent unit, the best accuracy and loss profiles, were shown by two-layer bidirectional LSTM, with training and validation accuracies of 0.954 and 0.975, respectively. Training with the use of a recurrent neural network can accurately infer conduction velocity distribution in a wide variety of simulated demyelinating neuropathies. Using deep learning techniques, CV distribution can be assessed in a non-invasive manner.

The Physiological Significance of A-Waves in Early Diabetic Neuropathy: Assessment of Motor Nerve Fibers by Neurophysiological Techniques.

Objective: This study aimed to investigate how early A-waves could occur in type II diabetes, and what it implied functionally.Methods: We performed conduction velocity distribution (CVD) test in peroneal nerves of 37 type II diabetic patients with normal nerve conduction study (NCS) and 22 age-matched controls. The electrophysiological data and clinical information were analyzed.Results: A-waves were observed in 45.9% of diabetic patients and only in 1 person in healthy controls, all detected in the tibial nerves. The diabetic patients with A-waves showed faster conduction velocity in all quartiles in the motor peroneal nerves compared to the patients without A-waves, and their CVD histograms were shifted to the right side, consisting of a significantly larger percentage of fast conducting fibers. There was no significant difference in the CVD values of the upper extremity nerves among the patients with and without A-waves and the healthy controls.Conclusion: A-waves could occur in type II diabetes as early as when NCS showed normal, and represented as a sign of neuropathy as well as a sign of rescued motor nerve function.

Can MitoTEMPO protect rat sciatic nerve against ischemia-reperfusion injury?

Abdominal ischemia-reperfusion (I/R) is known to cause both structural and functional damage to sciatic nerve which is related to the oxidative stress. We investigated the protective effects of mitochondria-targeted antioxidant (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride (MitoTEMPO) on ischemia-reperfusion-induced nerve damage by using the conduction velocity distribution (CVD) calculations from in vitro compound nerve action potential (CNAP) recordings from rat sciatic nerve. Adult male Wistar albino rats were divided into three groups. The IR and IR + MT groups had aortic cross-clamping for 1h followed by 2h reperfusion, while SHAM group had the same procedure without cross-clamping. IR + MT group received 0.7mg/kg/day MitoTEMPO injection for 28days before I/R, while other groups received vehicle alone. Ischemia-reperfusion resulted in a significant decrease (p < .05) in maximum depolarizations (mV), areas (mV.ms), and maximum and minimum upstroke velocities (mV/ms) of CNAPs, while injection of MitoTEMPO showed a complete protective effect on these impairments. The histograms for CVD showed that I/R blocked the contribution of fast-conducting fibers (> 60m/s). MitoTEMPO prevented that blockage and caused a shift in the CVD. Functional nerve damage caused by I/R can be prevented by MitoTEMPO, which can enter mitochondria, the main source of reactive oxygen species (ROS).

Comparison of nerve conduction velocity distribution methods by cold exposure and ischemia

Purpose Non-invasive estimation of the conduction velocity distribution (CVD) of a peripheral nerve has the potential to both improve clinical diagnoses of pathology and to observe the progress of the disease or the efficacy of treatments. Comparisons were made of the performance of three non-invasive CVD estimation methods proposed by independent research groups on peripheral nerve bundles under different conditions. Methods The first method (Cummins) uses a nerve compound action potential (CAP) with temporal dispersion and a mathematical single fiber action potential (SFAP). The second method (Barker) uses two CAPs and a non-mathematical SFAP waveform. The third method (Hirose) uses two CAPs recorded from distal and proximal sites. The Cummins and Barker methods have iterative solutions in the time domain while the Hirose method is a deconvolution estimator in the frequency domain. In order to compare these methods, we used cold exposure to affect primarily motor fibers and ischemia to affect primarily sensory fibers on rat caudal nerve bundles. Results The Cummins method is sensitive to changes in motor and sensory fiber percentages in CVD if it is used with the volume conductor model. The Barker and Hirose methods are sensitive to motor fiber percentages in CVD but they cannot detect changes in sensory fiber percentages accurately. Conclusions Estimation of the CVD using a priori SFAP created with a volume conductor model can non-invasively supply accurate and precise information about fiber groups in a peripheral nerve bundle.

Measuring conduction velocity distributions in peripheral nerves using neurophysiological techniques

ObjectiveTo determine how long it takes for neural impulses to travel along peripheral nerve fibers in living humans. MethodsA collision test was performed to measure the conduction velocity distribution of the ulnar nerve. Two stimuli at the distal and proximal sites were used to produce the collision. Compound muscle or nerve action potentials were recorded to perform the measurements on the motor or mixed nerve, respectively. Interstimulus interval was set at 1–5 ms. A quadri-pulse technique was used to measure the refractory period and calibrate the conduction time. ResultsCompound muscle action potential produced by the proximal stimulation started to emerge at the interstimulus interval of about 1.5 ms and increased with the increment in interstimulus interval. Two groups of motor nerve fibers with different conduction velocities were identified. The mixed nerve showed a wider conduction velocity distribution with identification of more subgroups of nerve fibers than the motor nerve. ConclusionsThe conduction velocity distributions in high resolution on a peripheral motor and mixed nerve are different and this can be measured with the collision test. SignificanceWe provided ground truth data to verify the neuroimaging pipelines for the measurements of latency connectome in the peripheral nervous system.

Signal Modeling and Simulation of Temporal Dispersion and Conduction Block in Motor Nerves.

Electroneurography is a well-established diagnostic test for supporting the diagnosis of disorders of myelinated peripheral nerves. Neurophysiological quantities are automatically calculated and are used to determine the pathology of the nerve (axonal damage) or its sheath (myelin damage). Specific differential diagnostic criteria are derived from time-domain normative data, which result primarily from a computer simulation in the early 1990s based on animal data, namely rats. However, the rat signals studied differ significantly from those of humans because of anatomical differences. We present a model-based simulation of nerve conduction in healthy and pathological motor nerves. In contrast to earlier simulations, the present model is based on motor unit action potentials extracted from real human measurements facilitating the generation of realistic signals, starting from a conduction velocity distribution. In addition to the modeling of healthy nerves, we model a hereditary peripheral nerve disease as well as an acute and a chronic inflammatory demyelinating condition. Quantitative signal differences based on standard variables in the time-domain are presented. The findings for the demyelinating conditions demonstrate amplitude reductions of 71% and 65% between the distal and proximal responses, which result from an increase in the variance of the nerve fiber conduction velocities. The simulation results closely match those of empirical measurements, indicating that the signal model captures relevant pathological mechanisms. An amplitude reduction of more than 50% in demyelinating conditions is in accordance with routine measurements and shows that temporal dispersion is quite well-modeled compared to previous simulation models. The simulation outcomes can serve as the basis for an improved pathophysiological understanding of peripheral nerve disorders and should aid neurophysiologists to refine their diagnostic armamentarium resulting in a more precise differential diagnosis.

P58-T Electrophysiological assessment of small fibres in carpal tunnel syndrome

Background Conventional nerve conduction techniques have limitations on carpal tunnel syndrome (CTS) diagnosing, because dysfunction of small fibres is beyond the resolution of these studies. The lack of the gold standard of CTS evaluation and common misdiagnosis underlie the treatment failure. Evaluation of small fibres susceptibility to damage and the sequence of decline of different types of fibres in CTS were analyzed. Materials and methods 75 hands, in 43 patients, 35 females, 8 males, with elecrophysiologically confirmed CTS were studied. The control group consisted of 35 volunteers (63 hands), sex and age-matched. Standard motor and antidromic sensory nerve conduction velocity studies in the median and ulnar nerves, with distal onset latency, conduction velocity, and amplitude assessment were done. Conduction velocity distribution test (CVD) was performed in the same nerves with estimation of conduction velocities in 10, 50, 90 decyl, and the conduction spread between 90 and 10 decyl. Quantitative sensory testing (QST) for detection temperature, pain and vibratory theresholds were done from thenar and hypothenar skin. Results CVD values of the median nerve in all decyls differed significantly between the carpal tunnel syndrome group and the control group, without any significant differences in the spread of conduction values. The thresholds of temperature and pain were similar, but the vibratory thresholds were significantly higher in the CTS group. Conclusions Mainly large fibers of the median nerve are damaged in the initial stage of CTS. Evaluation of small fibers is not useful in the early diagnosis of CTS.

How extracellular sodium replacement affects the conduction velocity distribution of rats’ peripheral nerves

How extracellular sodium replacement affects the conduction velocity distribution of rats’ peripheral nerves

Use of collision tests to identify physiological differences between the median and ulnar nerves.

Median and ulnar nerves are used in comparative electrophysiological studies. We analyzed the conduction values in these hand nerves in healthy volunteers to find any physiological differences between them. We performed standard conduction studies and conduction velocity distribution (CVD) tests with estimation of 3 quartiles in 31 healthy right-handed volunteers (17 women, 14 men) with a mean age of 44.8 ± 15.5 years. The conduction velocities in all quartiles of CVD tests were statistically faster in the ulnar nerve (P < 0.00001), with no differences in the spread of conduction values and no differences between sides. In the ulnar nerve, CVD velocities in all quartiles were faster in the female group (P < 0.05). The ulnar nerve has more fibers conducting with high velocities than does the median nerve. Electrophysiological comparisons between hand nerves must be performed carefully. Muscle Nerve 59:470-474, 2019.

Patient-Specific Identification of Atrial Flutter Vulnerability-A Computational Approach to Reveal Latent Reentry Pathways.

Atypical atrial flutter (AFlut) is a reentrant arrhythmia which patients frequently develop after ablation for atrial fibrillation (AF). Indeed, substrate modifications during AF ablation can increase the likelihood to develop AFlut and it is clinically not feasible to reliably and sensitively test if a patient is vulnerable to AFlut. Here, we present a novel method based on personalized computational models to identify pathways along which AFlut can be sustained in an individual patient. We build a personalized model of atrial excitation propagation considering the anatomy as well as the spatial distribution of anisotropic conduction velocity and repolarization characteristics based on a combination of a priori knowledge on the population level and information derived from measurements performed in the individual patient. The fast marching scheme is employed to compute activation times for stimuli from all parts of the atria. Potential flutter pathways are then identified by tracing loops from wave front collision sites and constricting them using a geometric snake approach under consideration of the heterogeneous wavelength condition. In this way, all pathways along which AFlut can be sustained are identified. Flutter pathways can be instantiated by using an eikonal-diffusion phase extrapolation approach and a dynamic multifront fast marching simulation. In these dynamic simulations, the initial pattern eventually turns into the one driven by the dominant pathway, which is the only pathway that can be observed clinically. We assessed the sensitivity of the flutter pathway maps with respect to conduction velocity and its anisotropy. Moreover, we demonstrate the application of tailored models considering disease-specific repolarization properties (healthy, AF-remodeled, potassium channel mutations) as well as applicabiltiy on a clinical dataset. Finally, we tested how AFlut vulnerability of these substrates is modulated by exemplary antiarrhythmic drugs (amiodarone, dronedarone). Our novel method allows to assess the vulnerability of an individual patient to develop AFlut based on the personal anatomical, electrophysiological, and pharmacological characteristics. In contrast to clinical electrophysiological studies, our computational approach provides the means to identify all possible AFlut pathways and not just the currently dominant one. This allows to consider all relevant AFlut pathways when tailoring clinical ablation therapy in order to reduce the development and recurrence of AFlut.

The Corticospinal Discrepancy: Where are all the Slow Pyramidal Tract Neurons?

This feature article focuses on the discrepancy between the distribution of axon diameters within the primate corticospinal tract, determined neuroanatomically, and the distribution of axonal conduction velocities within the same tract, determined electrophysiologically. We point out the importance of resolving this discrepancy for a complete understanding of corticospinal functions, and discuss the various explanations for the mismatch between anatomy and physiology.

Analysis of peripheral nerve and autonomic nervous system function and the stage of microangiopathy in patients with secondary Raynaud's phenomenon in the course of connective tissue diseases.

The pathogenesis of secondary Raynaud's phenomenon (SRP) associated with connective tissue diseases (CTD) is not entirely understood. Nervous system dysfunction and microangiopathy are considered to be causes of this pathology. Peripheral and autonomic nervous system function, the stage of microangiopathy, and the relationships between these in patients with SRP were analyzed. In the study, 20 patients with CTD-related SRP and 30 healthy controls were subject to capillaroscopy, standard conduction velocity tests and conduction velocity distribution (CVD) tests in ulnar and peroneal nerves, heart rate variability (HRV), and sympathetic skin response (SSR) tests. There were no significant differences in the standard motor and sensory conduction velocity tests, or in CVD tests in the ulnar and peroneal nerves in SRP patients compared with the controls. The patients with SRP had a significantly lower SSR amplitude and longer latency in hands and feet. The patients with CTD-related SRP had a significantly lower mean HRV with higher low frequency (LF) values in the spectral analysis and expiration/inspiration ratio (E/I) during deep breathing. There was no correlation between the stage of microangiopathy and neurophysiological test results. Correct standard conduction velocity and CVD testing in patients with SPR suggest that vasomotor disturbances may occur in CTD regardless of peripheral neuropathy. The lack of relationship between SSR and microangiopathy could confirm that these 2 processes occur independently in patients with CTD-related SRP. Autonomic nervous system impairment together with normal peripheral nerve function suggest the central origin of CTD-related SRP.