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Related Concept Videos

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...
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...
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation01:21

Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
Local Anesthetics: Adverse Effects01:12

Local Anesthetics: Adverse Effects

While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
Olfactory Receptors: Location and Structure01:03

Olfactory Receptors: Location and Structure

The process of olfaction, also known as the sense of smell, is a sophisticated chemical response system. The specialized sensory neurons that facilitate this process, known as olfactory receptor neurons, are situated in an upper segment of the nasal cavity, known as the olfactory epithelium. Olfactory sensory neurons are bipolar, with their dendrites extending from the epithelium's apex into the mucus that lines the nasal cavity. Airborne molecules, when inhaled, traverse the olfactory...

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Updated: Jun 16, 2026

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Peripheral neuropathy following nitrous oxide abuse.

Philip G Richardson1

  • 1Department of Emergency Medicine, Royal Brisbane & Women's Hospital, Butterfield St., Herston, Brisbane, QLD 4029, Australia. philip_richardson@health.qld.gov.au

Emergency Medicine Australasia : EMA
|February 16, 2010
PubMed
Summary

Prolonged nitrous oxide abuse can cause neurological damage, leading to peripheral neuropathy. This case highlights the importance of considering substance abuse in undifferentiated neurological presentations in the emergency department.

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Area of Science:

  • Neurology
  • Toxicology
  • Emergency Medicine

Background:

  • Undifferentiated neurological presentations are common in emergency departments.
  • Vitamin B12 deficiency can cause demyelination and peripheral neuropathy.
  • Nitrous oxide is an anesthetic adjuvant but also a drug of abuse.

Purpose of the Study:

  • To report a case of peripheral neuropathy resulting from nitrous oxide abuse.
  • To highlight the neurological risks associated with nitrous oxide misuse.

Main Methods:

  • Case report of a patient presenting with neurological symptoms.
  • Review of patient's history and substance use.
  • Clinical and diagnostic evaluation for peripheral neuropathy.

Main Results:

  • The patient developed a peripheral neuropathy.
  • Prolonged and intensive nitrous oxide abuse was identified as the cause.
  • Neurological deficits were progressive due to demyelination and axonal lesions.

Conclusions:

  • Nitrous oxide abuse can lead to severe peripheral neuropathy.
  • Emergency departments should consider substance abuse in patients with unexplained neurological symptoms.
  • Awareness of nitrous oxide's abuse potential is crucial for clinicians.