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

Diabetic Neuropathy01:22

Diabetic Neuropathy

59
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...
59
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation01:21

Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

764
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...
764
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

22
Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
22
Endocarditis II: Clinical Features of Infective Endocarditis01:25

Endocarditis II: Clinical Features of Infective Endocarditis

929
Endocarditis can present various clinical features depending on the causative organism and the patient's underlying health conditions. Initially, the clinical features of infective endocarditis develop gradually, presenting with nonspecific symptoms that can be easily mistaken for other illnesses.General SymptomsEarly symptoms of infective endocarditis are fever, chills, weakness, malaise, fatigue, and weight loss. These symptoms reflect the systemic nature of the infection and the body's...
929
Vascular Spasm01:16

Vascular Spasm

4.9K
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
4.9K
Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

Local Anesthetics: Differential Sensitivity of Nerve Fibers

1.8K
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...
1.8K

You might also read

Related Articles

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

Sort by
Same author

Racial Disparities in the Diagnosis and Prognosis of ALS Patients in the United States.

Journal of racial and ethnic health disparities·2024
Same author

Autoimmune polyneuropathies.

Handbook of clinical neurology·2023
Same author

Vasculitic Neuropathies.

Seminars in neurology·2019
Same author

Diagnosis and management of sensory polyneuropathy.

BMJ (Clinical research ed.)·2019
Same author

Sensory Polyneuropathies.

Continuum (Minneapolis, Minn.)·2017
Same author

Sensory neuronopathies.

Muscle & nerve·2015
Same journal

Resolution of expression of concern-Serotonergic pathology and disease burden in the premotor and motor phase of A53T α-synuclein parkinsonism: a cross-sectional study.

The Lancet. Neurology·2026
Same journal

UCL Queen Square Institute of Neurology: 75 years of innovation.

The Lancet. Neurology·2026
Same journal

Correction to Lancet Neurol 2026; 25: 631.

The Lancet. Neurology·2026
Same journal

Epstein-Barr virus and multiple sclerosis: from associations to mechanisms to potential therapies.

The Lancet. Neurology·2026
Same journal

Correction to Lancet Neurol 2025; 24: 740-52.

The Lancet. Neurology·2026
Same journal

Correction to Lancet Neurol 2026; 25: 357-67.

The Lancet. Neurology·2026
See all related articles

Related Experiment Video

Updated: May 4, 2026

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
09:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

9.1K

Vasculitic neuropathies.

Kelly Graham Gwathmey1, Ted Michael Burns1, Michael Paul Collins2

  • 1University of Virginia, Charlottesville, VA, USA.

The Lancet. Neurology
|December 17, 2013
PubMed
Summary
This summary is machine-generated.

Vasculitic neuropathies involve painful nerve damage from inflamed blood vessels. A simple classification based on vessel size aids prompt diagnosis and treatment for better outcomes.

More Related Videos

Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies
08:56

Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies

Published on: October 7, 2021

3.3K
A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments
07:30

A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments

Published on: November 9, 2017

8.9K

Related Experiment Videos

Last Updated: May 4, 2026

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
09:39

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

9.1K
Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies
08:56

Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies

Published on: October 7, 2021

3.3K
A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments
07:30

A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments

Published on: November 9, 2017

8.9K

Area of Science:

  • Neurology
  • Immunology
  • Pathology

Background:

  • Vasculitic neuropathies present with acute-onset painful sensory and motor deficits.
  • These neuropathies stem from inflammatory destruction of nerve blood vessels, leading to ischemic injury.
  • They are associated with primary systemic vasculitis and secondary conditions like rheumatoid arthritis, viral infections, and diabetic neuropathy.

Purpose of the Study:

  • To present a simplified classification scheme for vasculitic neuropathies.
  • To aid neurologists in prompt recognition and treatment initiation.
  • To correlate vessel size with clinical course and prognosis.

Main Methods:

  • A dichotomous classification system for vasculitic neuropathies.
  • Categorization based on the size of the involved blood vessels: large arteriole vasculitis vs. nerve microvasculitis.

Main Results:

  • The classification divides vasculitic neuropathies into two main groups based on vessel size.
  • Vessel size in vasculitic neuropathy correlates with clinical presentation and prognosis.

Conclusions:

  • A simplified classification of vasculitic neuropathies based on vessel size is proposed.
  • Prompt recognition and treatment are crucial for preventing morbidity and mortality.
  • Understanding vessel size aids in predicting the clinical course and prognosis of vasculitic neuropathy.