Action Potential Conduction Velocity Research Articles

Motor unit action potential conduction velocity estimated from surface electromyographic signals using image processing techniques.

In surface electromyography (surface EMG, or S-EMG), conduction velocity (CV) refers to the velocity at which the motor unit action potentials (MUAPs) propagate along the muscle fibers, during contractions. The CV is related to the type and diameter of the muscle fibers, ion concentration, pH, and firing rate of the motor units (MUs). The CV can be used in the evaluation of contractile properties of MUs, and of muscle fatigue. The most popular methods for CV estimation are those based on maximum likelihood estimation (MLE). This work proposes an algorithm for estimating CV from S-EMG signals, using digital image processing techniques. The proposed approach is demonstrated and evaluated, using both simulated and experimentally-acquired multichannel S-EMG signals. We show that the proposed algorithm is as precise and accurate as the MLE method in typical conditions of noise and CV. The proposed method is not susceptible to errors associated with MUAP propagation direction or inadequate initialization parameters, which are common with the MLE algorithm. Image processing -based approaches may be useful in S-EMG analysis to extract different physiological parameters from multichannel S-EMG signals. Other new methods based on image processing could also be developed to help solving other tasks in EMG analysis, such as estimation of the CV for individual MUs, localization and tracking of innervation zones, and study of MU recruitment strategies.

Local Gradients in Electrotonic Loading Modulate the Local Effective Refractory Period: Implications for Arrhythmogenesis in the Infarct Border Zone.

Ectopic electrical activity that originates in the peri-infarct region can give rise to potentially lethal re-entrant arrhythmias. The spatial variation in electrotonic loading that results from structural remodelling in the infarct border zone may increase the probability that focal activity will trigger electrical capture, but this has not previously been investigated systematically. This study uses in-silico experiments to examine the structural modulation of effective refractory period on ectopic beat capture. Informed by 3-D reconstructions of myocyte organization in the infarct border zone, a region of rapid tissue expansion is abstracted to an idealized representation. A novel metric is introduced that defines the local electrotonic loading as a function of passive tissue properties and boundary conditions. The effective refractory period correlates closely with local electrotonic loading, while the action potential duration, conduction, and upstroke velocity reduce in regions of increasing electrotonic load. In the presence of focal ectopic stimuli, spatial variation in effective refractory period can cause unidirectional conduction block providing a substrate for reentrant arrhythmias. Consequently, based on the observed results, a possible novel mechanism for arrhythmogenesis in the infarct border zone is proposed.

Tuning of Ranvier node and internode properties in myelinated axons to adjust action potential timing.

Action potential timing is fundamental to information processing; however, its determinants are not fully understood. Here we report unexpected structural specializations in the Ranvier nodes and internodes of auditory brainstem axons involved in sound localization. Myelination properties deviated significantly from the traditionally assumed structure. Axons responding best to low-frequency sounds had a larger diameter than high-frequency axons but, surprisingly, shorter internodes. Simulations predicted that this geometry helps to adjust the conduction velocity and timing of action potentials within the circuit. Electrophysiological recordings in vitro and in vivo confirmed higher conduction velocities in low-frequency axons. Moreover, internode length decreased and Ranvier node diameter increased progressively along the distal axon segments, which simulations show was essential to ensure precisely timed depolarization of the giant calyx of Held presynaptic terminal. Thus, individual anatomical parameters of myelinated axons can be tuned to optimize pathways involved in temporal processing.

Purification and Characterization of Nk-3FTx: A Three Finger Toxin from the Venom of North East Indian Monocled Cobra.

Snake venom three finger toxins (3FTxs) are a non-enzymatic family of venom proteins abundantly found in elapids. We have purified a 7579.5 ± 0.591 Da 3FTx named as Nk-3FTx from the venom of Naja kaouthia of North East India origin. The primary structure was determined by a combination of N-terminal sequencing and electrospray ionization liquid chromatography-mass spectrometry/mass spectrometry. Biochemical and biological characterization reveal that it is nontoxic to human cell lines and exhibit mild anticoagulant activity when tested on citrated human plasma. Nk-3FTx was found to affect the compound action potential (CAP) and nerve conduction velocity of isolated toad sciatic nerve. This is the first report of a non-conventional 3FTx from Naja kaouthia venom that reduces CAP for its neurotoxic effect. Further studies can be carried out to understand the mechanism of action and to explore its potential therapeutic application.

Hypokalemic Quadriparesis with Electrophysiological Changes in a Child with Distal Renal Tubular Acidosis and Nephrocalcinosis

We report an unusual case of a 4-year-old girl presenting with recurrent episodes of weakness with documented hypokalemia, failure to thrive, and rachitic changes. Nerve conduction study during the episode of weakness revealed reduced compound muscle action potential amplitudes and motor conduction velocity and electromyography revealed reduced interference pattern, which normalized on correction of hypokalemia and subsequent recovery of weakness. The child was diagnosed with distal renal tubular acidosis. Ultrasound revealed medullary nephrocalcinosis, which regressed on long-term treatment with alkali and potassium supplement.

Investigating the Effect of Thermal Stress on Nerve Action Potential Using the Soliton Model

The thermal mechanism of acoustic modulation of the reversible electrical activities of peripheral nerves is investigated using the soliton model, and a numerical solution is presented for its non-homogenous version. Our results indicate that heating a small segment of the nerve will increase the action potential conduction velocity and decrease its amplitude. Moreover, cooling the nerve will have the reverse effects, and cooling to temperatures below the nerve melting point can reflect back a significant portion of the action potentials. These results are consistent with the theory of the soliton model, as well as with the experimental findings. Although there exists a discrepancy between the results of the soliton model and experimental pulse amplitude data, from the free energy point of view, the experiments are compatible with Heimburg and Jackson theory. We conclude that the presented model accompanied by the free energy view is capable of simulating the effects of thermal energy on nerve function. One potential application of the developed theoretical model will be investigation of the reversible and irreversible effects of thermal energy induced by various energy modalities, including therapeutic ultrasound, on nerve function.

Flecainide exerts paradoxical effects on sodium currents and atrial arrhythmia in murine RyR2-P2328S hearts.

AimsCardiac ryanodine receptor mutations are associated with catecholaminergic polymorphic ventricular tachycardia (CPVT), and some, including RyR2-P2328S, also predispose to atrial fibrillation. Recent work associates reduced atrial Nav1.5 currents in homozygous RyR2-P2328S (RyR2S/S) mice with slowed conduction and increased arrhythmogenicity. Yet clinically, and in murine models, the Nav1.5 blocker flecainide reduces ventricular arrhythmogenicity in CPVT. We aimed to determine whether, and how, flecainide influences atrial arrhythmogenicity in RyR2S/S mice and their wild-type (WT) littermates.MethodsWe explored effects of 1 μm flecainide on WT and RyR2S/S atria. Arrhythmic incidence, action potential (AP) conduction velocity (CV), atrial effective refractory period (AERP) and AP wavelength (λ = CV × AERP) were measured using multi-electrode array recordings in Langendorff-perfused hearts; Na+ currents (INa) were recorded using loose patch clamping of superfused atria.ResultsRyR2S/S showed more frequent atrial arrhythmias, slower CV, reduced INa and unchanged AERP compared to WT. Flecainide was anti-arrhythmic in RyR2S/S but pro-arrhythmic in WT. It increased INa in RyR2S/S atria, whereas it reduced INa as expected in WT. It increased AERP while sparing CV in RyR2S/S, but reduced CV while sparing AERP in WT. Thus, RyR2S/S hearts have low λ relative to WT; flecainide then increases λ in RyR2S/S but decreases λ in WT.ConclusionsFlecainide (1 μm) rescues the RyR2-P2328S atrial arrhythmogenic phenotype by restoring compromised INa and λ, changes recently attributed to increased sarcoplasmic reticular Ca2+ release. This contrasts with the increased arrhythmic incidence and reduced INa and λ with flecainide in WT.

Cardiovagal and somatic sensory nerve functions in healthy subjects.

Heart rate response to deep breathing (HRDB), which depends on the integrity of cardiac vagal preganglionic neurons and efferent fibers, and the function of sural nerve fibers are both associated with an age-related decline process. The aim of this study was to determine whether the effects attributed to aging on cardiovagal and sural nerve function decline are associated. HRDB and sural sensory nerve action potential (SNAP) amplitude, latency, and conduction velocity (SCV) were measured in one hundred healthy asymptomatic subjects (aged 14-92 years, 41 women). Multiple and simple linear regressions were used to analyze the relationships between the variables. There were significant linear relationships between sural SNAP amplitude and HRDB with age. There was also a significant linear relationship between sural SNAP amplitude and HRDB (correlation coefficient 0.46, p<0.0001), but the model explained only 21.5% of the variability in HRDB. Cardiovagal function assessed by HRDB is associated with sural SNAP amplitude in healthy subjects. Age-related decline only partially explained the variability seen in the association. Other genetic and environmental factors may also play a role.

Polyneuropathy improvement following autologous stem cell transplantation for POEMS syndrome.

To study the evolution of the neuropathy and long-term disability in a large cohort of patients with POEMS (polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes) syndrome following autologous stem cell transplantation (ASCT). Retrospective chart review documenting the clinical, electrophysiologic, and laboratory characteristics of patients with POEMS syndrome undergoing ASCT at Mayo Clinic, Rochester. Sixty patients with a median follow-up time of 61 months were studied. All patients had peripheral polyneuropathy and demonstrated neurologic improvement after ASCT (apart from one patient who died early). Before ASCT, 27 patients (45%) required a wheelchair and 17 (29%) required a walker or foot brace. At the end of the follow-up period, no patient was using a wheelchair and 23 patients (38%) were using a foot brace. The median Neuropathy Impairment Score improved from 66 to 48 points at 12 months and to 30 points at most recent follow-up (p < 0.0001). Median Rankin Scale score improved from 3 to 1.5 (p < 0.0001). Vascular endothelial growth factor levels decreased from a median of 452 to 63.5 pg/mL (p < 0.0001). The ulnar compound motor action potential amplitude (median) improved from 4.3 to 7.6 mV (p < 0.0001) and ulnar compound motor action potential conduction velocity (median) improved from 34 to 51 m/s (p < 0.0001). Predicted forced vital capacity improved from 81% to 88% (p < 0.0001). Periengraftment syndrome occurred in 24 patients. Fourteen patients required additional chemotherapy and/or radiation following ASCT, but there was no clinical deterioration in the neuropathy in any of these patients. Six patients died: 1 due to POEMS, 1 due to failed engraftment, and 4 due to other malignancies (2 myelodysplastic syndrome, 1 lymphoma, 1 metastatic lung cancer). Patients with POEMS syndrome who undergo ASCT have a significant and meaningful improvement of their neuropathy by multiple measurements during both short and long-term follow-up, which corresponds to reduction in morbidity and disability (none are in wheelchair long-term). Periengraftment syndrome was common but manageable. Fatal complications, although rare, did occur, usually in association with other malignancies. This study provides Class IV evidence that for patients with POEMS syndrome, ASCT improves neuropathy-related function.

Progressive age-associated activation of JNK associates with conduction disruption in the aged atrium

Connexin43 (Cx43) is critical for maintaining electrical conduction across atrial muscle. During progressive ageing atrial conduction slows associating with increasing susceptibility to arrhythmias. Changes in Cx43 protein expression, or its phosphorylation status, can instigate changes in the conduction of the cardiac action potential. This study investigated whether increased levels of activated c-jun N-terminal kinase (JNK) is responsible for the decline of Cx43 during ageing. Right atria from guinea pigs aged between 1 day and 38 months of age were examined. The area of the intercalated disc increased with age concurrent with a 75% decline in C43 protein expression. An age-dependent increase in activated-JNK correlated with a rise in phosphorylated Cx43, but also slowing of action potential conduction velocity across the atria from 0.38±0.01m/s at 1 month of age to 0.30±0.01m/s at 38 months. The JNK activator anisomycin increased activated JNK in myocytes and reduced Cx43 protein expression simulating ageing. The JNK inhibitor SP600125, was found to eradicate almost all trace of Cx43 protein. We conclude that in vivo activation of JNK increases with age leading to the loss of Cx43 protein resulting in impaired conduction and contributing to the increasing risk of atrial arrhythmias with advancing age.

Local muscle endurance is associated with fatigue-based changes in electromyographic spectral properties, but not with conduction velocity

The purpose of this study was to examine the associations amongst muscle fiber action potential conduction velocity (CV), spectral characteristics of the surface electromyographic (EMG) signal, and endurance time during a sustained submaximal isometric muscle action. Eleven men (mean±SD age=23±4yrs) performed a sustained, submaximal isometric muscle action of the dominant forearm flexors at 60% of the maximum voluntary contraction (MVC) until the designated force level could no longer be maintained. Sixteen separate bipolar surface EMG signals were detected from the biceps brachii with a linear electrode array during this contraction. Two channels from this array were used to measure CV, and one of these two channels was used for further EMG signal processing. The channels that provided the highest signal quality were used for the CV measurements and further data analysis. A wavelet analysis was then used to analyze the bipolar EMG signal, and the resulting wavelet spectrum was decomposed with a nonparametric spectral decomposition procedure. The results showed that the time to exhaustion during the sustained contraction was not correlated with the rate of decrease in CV, but it was highly correlated with both the decrease in high-frequency spectral power (r=0.947) and the increase in low-frequency spectral power (r=0.960). These findings are particularly interesting, considering that the decrease in traditional EMG spectral variables (e.g., mean frequency or median frequency) with fatigue is generally attributed to reductions in CV. While this may indeed be true, the present results suggested that other factors (i.e., other than CV) that can affect the shape of the EMG frequency spectrum during fatigue are more important in determining the endurance capabilities of the muscle than is CV.

Tang-Tong-Fang Confers Protection against Experimental Diabetic Peripheral Neuropathy by Reducing Inflammation.

Tang-tong-fang (TTF) is a Chinese herbal formula that has been shown to be beneficial in diabetic peripheral neuropathy (DPN), a common complication secondary to diabetic microvascular injury. However, the underlying mechanism of protection in nerve ischemia provided by TTF is still unclear. We hypothesized that TTF alleviates DPN via inhibition of ICAM-1 expression. Therefore, we tested the effect of TTF in a previously established DPN model, in which nerve injury was induced by ischemia/reperfusion in streptozotocin-induced diabetic rats. We found that the conduction velocity and amplitude of action potentials of sciatic nerve conduction were reduced in the DPN model group but were rescued by TTF treatment. In addition, TTF treatment also attenuated the effect of DPN on other parameters including histology and ultrastructural changes, expression of ICAM-1, MPO, and TNF-α in rat sciatic nerves, and plasma sICAM-1 and MPO levels. Together, our data suggest that TTF treatment may alleviate DPN via ICAM-1 inhibition.

Computational Approaches to Understanding the Role of Fibroblast-Myocyte Interactions in Cardiac Arrhythmogenesis.

The adult heart is composed of a dense network of cardiomyocytes surrounded by nonmyocytes, the most abundant of which are cardiac fibroblasts. Several cardiac diseases, such as myocardial infarction or dilated cardiomyopathy, are associated with an increased density of fibroblasts, that is, fibrosis. Fibroblasts play a significant role in the development of electrical and mechanical dysfunction of the heart; however the underlying mechanisms are only partially understood. One widely studied mechanism suggests that fibroblasts produce excess extracellular matrix, resulting in collagenous septa. These collagenous septa slow propagation, cause zig-zag conduction paths, and decouple cardiomyocytes resulting in a substrate for arrhythmia. Another emerging mechanism suggests that fibroblasts promote arrhythmogenesis through direct electrical interactions with cardiomyocytes via gap junctions. Due to the challenges of investigating fibroblast-myocyte coupling in native cardiac tissue, computational modeling and in vitro experiments have facilitated the investigation into the mechanisms underlying fibroblast-mediated changes in cardiomyocyte action potential morphology, conduction velocity, spontaneous excitability, and vulnerability to reentry. In this paper, we summarize the major findings of the existing computational studies investigating the implications of fibroblast-myocyte interactions in the normal and diseased heart. We then present investigations from our group into the potential role of voltage-dependent gap junctions in fibroblast-myocyte interactions.

Motor conduction parameters in recently diagnosed and untreated hypothyroidism.

The severity of neuromuscular symptoms and signs in hypothyroidism is known to be related to the duration and degree of hormone deficiency. The present study was aimed to assess whether recently diagnosed and untreated hypothyroidism affects peripheral nervous system. The study included a total of 120 female subjects with age ranging from 20 to 45 years. The motor nerve conduction parameters viz. Distal latency (DL), amplitude of compound muscle action potential (CMAP) and motor nerve conduction velocity (MNCV) were recorded bilaterally in median, ulnar and posterior tibial nerves using standard protocols and settings. The observations revealed significantly prolonged distal motor latencies, reduced CMAP amplitudes and slowed MNCV in the peripheral nerves in hypothyroid. The results indicated that the alteration in motor conduction parameters in recently diagnosed and untreated hypothyroidism might be due to various functional and structural changes in peripheral nerves associated with deficiency of thyroid hormones.

Automated Patch-Clamp Pharmacology Assays using Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes

Recent progress in the field of embryonic and induced pluripotent stem cell (iPSC)-derived cardiomyocytes led to flourishing of a variety of pharmacology and drug safety screening assays, relying on diverse principles, such as optical measurements using wide dynamic range Ca2+-sensitive or transmembrane voltage-sensitive dyes, or multi-electrode arrays allowing field potential measurements, action potential (AP) conduction velocity and 2D local activation mapping, and impedance changes in cultured monolayers.

Morphological and functional changes in regenerated primary afferent fibres following mental and inferior alveolar nerve transection.

It is important to know the mechanisms underlying pain abnormalities associated with inferior alveolar nerve (IAN) regeneration in order to develop the appropriate treatment for orofacial neuropathic pain patients. However, peripheral mechanisms underlying orofacial pain abnormalities following IAN regeneration are not fully understood. Head withdrawal threshold (HWT), jaw opening reflex (JOR) thresholds, single-fibre recordings of the regenerated mental nerve (MN) fibres, calcitonin gene-related peptide (CGRP), isolectin B4 (IB4), peripherin, neurofilament-200 (NF-200) and transient receptor potential vanilloid 1 (TRPV1) expression in trigeminal ganglion (TG) cells, and electron microscopic (EM) observations of the regenerated MN fibres were studied in MN- and IAN-transected (M-IANX) rats. HWT to mechanical or heat stimulation of the mental skin was significantly lower in M-IANX rats compared with sham rats. Mean conduction velocity of action potentials recorded from MN fibres (n = 124) was significantly slower in M-IANX rats compared with sham rats. The percentage of Fluoro-Gold (FG)-labelled CGRP-, peripherin- or TRPV1-immunoreactive (IR) cells was significantly larger in M-IANX rats compared with that of sham rats, whereas that of FG-labelled IB4- and NF-200-IR cells was significantly smaller in M-IANX rats compared with sham rats. Large-sized myelinated nerve fibres were rarely observed in M-IANX rats, whereas large-sized unmyelinated nerve fibres were frequently observed and were aggregated in the bundles at the distal portion of regenerated axons. These findings suggest that the demyelination of MN fibres following regeneration may be involved in peripheral sensitization, resulting in the orofacial neuropathic pain associated with trigeminal nerve injury.

Optogenetic release of norepinephrine from cardiac sympathetic neurons alters mechanical and electrical function.

Release of norepinephrine (NE) from sympathetic neurons enhances heart rate (HR) and developed force through activation of β-adrenergic receptors, and this sympathoexcitation is a key risk for the generation of cardiac arrhythmias. Studies of β-adrenergic modulation of cardiac function typically involve the administration of exogenous β-adrenergic receptor agonists to directly elicit global β-adrenergic receptor activation by bypassing the involvement of sympathetic nerve terminals. In this work, we use a novel method to activate sympathetic fibres within the myocardium of Langendorff-perfused hearts while measuring changes in electrical and mechanical function. The light-activated optogenetic protein channelrhodopsin-2 (ChR2) was expressed in murine catecholaminergic sympathetic neurons. Sympathetic fibres were then photoactivated to examine changes in contractile force, HR, and cardiac electrical activity. Incidence of arrhythmia was measured with and without exposure to photoactivation of sympathetic fibres, and hearts were optically mapped to detect changes in action potential durations and conduction velocities. Results demonstrate facilitation of both developed force and HR after photostimulated release of NE, with increases in contractile force and HR of 34.5 ± 5.5 and 25.0 ± 9.3%, respectively. Photostimulation of sympathetic fibres also made hearts more susceptible to arrhythmia, with greater incidence and severity. In addition, optically mapped action potentials displayed a small but significant shortening of the plateau phase (-5.5 ± 1.0 ms) after photostimulation. This study characterizes a powerful and clinically relevant new model for studies of cardiac arrhythmias generated by increasing the activity of sympathetic nerve terminals and the resulting activation of myocyte β-adrenergic receptors.

Architectural correlates of myocardial conduction: changes to the topography of cellular coupling, intracellular conductance, and action potential propagation with hypertrophy in Guinea-pig ventricular myocardium.

We tested the hypothesis that alterations to action potential conduction velocity (CV) and conduction anisotropy in left ventricular hypertrophy are associated with topographical changes to gap-junction coupling and intracellular conductance by measuring these variables in the same preparations. Left ventricular papillary muscles were excised from aortic-banded or sham-operated guinea-pig hearts. With intracellular stimulating and recording microelectrodes, CV was measured in 3 dimensions with simultaneous conductance mapping with subthreshold stimuli and correlated with quantitative histomorphometry of myocardial architecture and connexin 43 distribution. In hypertrophied myocardium, CV in the longitudinal axis was smaller and transverse velocity was greater compared with control; associated with similar differences of intracellular conductance, consistent with more cell contacts per cell (5.7 ± 0.2 versus 8.1 ± 0.5; control versus hypertrophy), and more intercalated disks mediating side-to-side coupling (8.2 ± 0.2 versus 10.2 ± 0.4 per cell). Intercalated disk morphology and connexin 43 immunolabelling were not different in hypertrophy. Hypertrophied preparations showed local submillimeter (≈250 μm) regions with slow conduction and low intracellular conductance, which, although not affecting CV on the millimeter scale, were consistent with discontinuities from increased microscopical connective tissue content. With myocardial hypertrophy, altered longitudinal and transverse CV, and greater nonuniformity of CV anisotropy correspond to changes of intracellular conductance. These are associated with alteration of myocardial architecture, specifically the topography of cell-cell coupling and gap-junction connectivity.

CONTROL OF ATRIAL GAP JUNCTION CONDUCTANCE BY INTRACELLULAR PHOSPHATASES

Myocardial action potential conduction velocity is a function of gap junction (GJ) electrical conductance (Gj). The phosphorylation state of GJ proteins, in particular Cx43 determines Gj and the role of protein phosphatases (PPs) remains unclear. This study aims to investigate the role of serine-threonine PPs in regulating Gj, in particular the Ca2+-dependent PP, calcineurin, and the Ca2+-independent PPs, PP1 and PP2A. Left atrial strips were dissected from male, Dunkin-Hartley guinea pigs to estimate Gj by measuring the frequency-dependent intracellular conductance1 in control solution (Na=149.4 mM), or low-Na solution (Na=29.4 mM) to raise [Ca2+]i. Inhibitors to calcinuerin, (cyclosporine-A; 5 µM; calcineurin auto-inhibitory peptide; CAIP, 50 µM); PPI (tautomycin, 5 nM) or PP2A (okadaic acid, 2 nM; fostreicin 100 nM) were used. Western blots were conducted on inhibitor perfused tissue. Values are mean±SEM, normalised to control. Differences were tested by ANOVA; null hypotheses rejected at p Low-Na significantly and reversibly decreased Gj, and in control conditions individual inhibitors had no effect. Cyclosporine-A and CAIP diminished the effects of low-Na (Gj: low-Na, 55±5.8% low-Na+ cyclosporine-A (n=6): 85±9.7%; low-Na+CAIP (n=3): 104±10.2% control). Fostreicin also reduced the low-Na effect (low-Na: 54±2.5%; low-Na+fostreicin (n=6): 77±6.1% control) but not tautomycin (low-Na: 65±4.9%; low-Na+TTM (n=7): 66±3.9%). Phosphorylation of Cx43 during low-Na was diminished by CysA, CAIP and FST. The phosphatases calcineurin and PP2A mediate the decrease of Gj in the left atrium during elevated [Ca2+]i. Connexin43 is one of the targets for calcineurin and PP2A.

Prevalence of accessory deep peroneal nerve in referred patients to an electrodiagnostic medicine clinic

BackgroundAccessory Deep Peroneal Nerve (ADPN) is an anatomic variation that can potentially cause disturbance in electrodiagnostic studies. This anomaly could be detected by nerve conduction studies. There are no recent updates about prevalence of this anatomic variation. Electrodiagnostic medicine clinic is the best environment for detecting presence and prevalence of this nerve, so present study enrolled.Materials & MethodsIn this cross sectional descriptive study that take place from March 2009 to July 2010, 230 cases comprising 460 legs referred for electrodiagnostic studies of upper limbs problems participated in the study. Compound muscle action potential (CMAP) and Nerve conduction Velocity (NCV) of Deep Peroneal Nerve (DPN) were measured by using EMG machine by stimulating DPN at knee, ankle and lateral malleolous areas accordingly, with recording from extensor digitorum brevis muscle. Results were analyzed and conclusion made.ResultsThe study population included 120 females (52%) and 110 (47%) males with mean age of 42.1 ± 13.5 years. ADPN was detected in 28 patients (12%). Among them,10(17.9%) had bilateral ADPN and in remained 18 cases (82.1%) APN was unilateral. In 8 patients there was no recorded CMAP from EDB by proximal and distal stimulation implying EDB agenesis. Gender distribution was similar which means half of the cases (14 patients) belonged to each gender.ConclusionThe prevalence of ADPN in this study was 12.2%, (17.9% bilateral and 82.1% unilateral).