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Related Concept Videos

Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

Local Anesthetics: Differential Sensitivity of Nerve Fibers

Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...
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...
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...
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...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...

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Related Experiment Video

Updated: Jun 15, 2026

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

Multifocal conduction blocks in sarcoid peripheral neuropathy.

Setsu Sawai1, Sonoko Misawa, Makoto Kobayashi

  • 1Department of Neurology, Graduate School of Medicine, Chiba University.

Internal Medicine (Tokyo, Japan)
|March 2, 2010
PubMed
Summary

Sarcoidosis can cause peripheral neuropathy, often leading to axonal damage. This study highlights three cases where sarcoidosis initially presented as multiple mononeuropathy with conduction blocks, which improved with corticosteroid treatment.

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Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat
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Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat

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Last Updated: Jun 15, 2026

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

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat
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Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat

Published on: November 21, 2025

Area of Science:

  • Neurology
  • Immunology
  • Pathology

Background:

  • Sarcoidosis is a multisystem inflammatory disease.
  • Peripheral neuropathy is a rare but recognized manifestation of sarcoidosis.
  • Previous research indicated axonal degeneration as the primary pathology in neurosarcoidosis.

Observation:

  • Three patients with sarcoidosis presented with multiple mononeuropathy as their initial symptom.
  • Nerve conduction studies revealed significant multifocal conduction blocks in the intermediate nerve trunks.
  • These conduction blocks were rapidly resolved following corticosteroid administration.

Findings:

  • The electrodiagnostic findings suggest demyelinative or ischemic-functional conduction blocks as the cause of neuropathy.
  • This presentation challenges the notion that axonal degeneration is the sole pathology.
  • The study identified three new cases of acute conduction block neuropathy in sarcoidosis.

Implications:

  • Acute conduction block neuropathy may be an underdiagnosed manifestation of sarcoidosis.
  • Early diagnosis and corticosteroid treatment can lead to significant clinical improvement.
  • Further research is warranted to understand the prevalence and mechanisms of conduction block in neurosarcoidosis.