Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
Dysrhythmias IV: Characteristics of Bradyarrhythmias01:18

Dysrhythmias IV: Characteristics of Bradyarrhythmias

Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...
Local Anesthetics: Clinical Application as Intravenous Regional Anesthesia01:16

Local Anesthetics: Clinical Application as Intravenous Regional Anesthesia

Intravenous regional anesthesia or the Bier block technique is used to anesthetize a specific limb or extremity. It uses exsanguinated or blood-drained vessels to transport local anesthetics or LAs to the peripheral nerve trunks. Lidocaine without vasoconstrictors like epinephrine is most commonly used for this technique. Other drugs used are prilocaine, ropivacaine, and chloroprocaine. Bupivacaine is not recommended for this technique due to its high cardiac toxicity.
One of the advantages of...
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clinical and neurophysiological findings in patients with hereditary neuropathy with liability to pressure palsy and chromosome 17p11.2 deletion.

Neurologia·2022
Same author

Clinical and neurophysiological findings in patients with hereditary neuropathy with liability to pressure palsy and chromosome 17p11.2 deletion.

Neurologia·2019
Same author

Corrigendum to "Identification procedure in a model of single fibre action potential - Part I: Estimation of fibre diameter and radial distance" [J. Electromyogr. Kinesiol. 20(2) (2010) 264-273].

Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology·2016
Same author

Corrigendum to "Analysis of the peak-to-peak ratio of extracellular potentials in the proximity of excitable fibres" [J. Electromyogr. Kinesiol. 20(5) (2010) 868-878].

Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology·2016
Same author

Corrigendum to "Effects of changes in the shape of the intracellular action potential on the peak-to-peak ratio of single muscle fibre potentials" [J. Electromyogr. Kinesiol. 22(1) (2012) 88-97].

Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology·2016
Same author

Corrigendum to "Identification procedure in a model of single fibre action potential - Part II: Global approach and experimental results" [J. Electromyogr. Kinesiol. 20(2) (2010) 274-283].

Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology·2016

Related Experiment Video

Updated: Jun 20, 2026

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat
08:05

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat

Published on: November 21, 2025

[Pseudo-conduction block in nonsystemic vasculitic neuropathy].

R M Pabón Meneses1, L Gila, J Urriza

  • 1Servicio de Neurofisiología Clínica, Hospital Virgen del Camino, Pamplona, 31008, Spain.

Anales Del Sistema Sanitario De Navarra
|September 10, 2009
PubMed
Summary

Nonsystemic vasculitic neuropathy (NSVN) can initially mimic conduction block on nerve studies. Early diagnosis requires repeated neurophysiologic assessments to differentiate transient pseudo-conduction block from permanent axonal damage.

More Related Videos

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure
09:34

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Published on: August 27, 2019

Related Experiment Videos

Last Updated: Jun 20, 2026

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat
08:05

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat

Published on: November 21, 2025

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure
09:34

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Published on: August 27, 2019

Area of Science:

  • Neurology
  • Vascular Medicine
  • Neurophysiology

Background:

  • Nonsystemic vasculitic neuropathy (NSVN) is an inflammatory condition affecting the vasa nervorum, typically presenting as mononeuritis multiplex.
  • Early detection and characterization of NSVN are crucial for timely intervention and management.

Observation:

  • A 36-year-old woman presented with sensory and motor deficits in her right hand and left foot.
  • Initial neurophysiologic examination revealed low amplitude of the right median nerve compound muscle action potential (CMAP) with proximal stimulation.
  • Subsequent examination demonstrated evidence of axonal damage in multiple nerves, including the right median nerve.

Findings:

  • Acute ischemic nerve damage in NSVN can manifest as a conduction block pattern on electroneurography.
  • This pattern, termed "pseudo-conduction block," is transient and can evolve into axonal neuropathy.
  • The case highlights the importance of serial neurophysiologic studies for accurate diagnosis.

Implications:

  • Recognizing pseudo-conduction block is vital for differentiating early NSVN from other neuropathies.
  • Repeated neurophysiologic evaluations are essential for comprehensive characterization of vasculitic neuropathy.
  • This case underscores the diagnostic utility of electrophysiologic testing in early-stage NSVN.