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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...
Diabetic Foot Ulcer01:31

Diabetic Foot Ulcer

Definition A diabetic foot ulcer (DFU) is a chronic, non-healing wound that develops in individuals with diabetes. It typically occurs on pressure-bearing areas such as the heel, metatarsal heads, or hallux, and carries a high risk of infection and amputation.Pathophysiology • The development of DFUs can be explained by four interconnected mechanisms: neuropathy, ischemia, infection, and impaired wound healing. • Neuropathy is the most common factor. Sensory neuropathy reduces pain perception,...
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...
Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

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Related Experiment Video

Updated: Jun 24, 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

Acute neuropathies.

Mark B Bromberg

    Frontiers of Neurology and Neuroscience
    |April 8, 2009
    PubMed
    Summary
    This summary is machine-generated.

    Acute neuropathies like Guillain-Barré syndrome involve immune attacks on nerves. Early, aggressive pain management is crucial, though treatment data for these conditions remain limited.

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    Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies
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    Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies

    Published on: October 7, 2021

    Related Experiment Videos

    Last Updated: Jun 24, 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

    Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies
    08:56

    Nerve Ultrasound Protocol to Detect Dysimmune Neuropathies

    Published on: October 7, 2021

    Area of Science:

    • Neurology
    • Immunology
    • Clinical Medicine

    Background:

    • Acute neuropathies, including Guillain-Barré syndrome, present with rapid symptom onset and some recovery.
    • An immune-mediated mechanism is suspected, supported by molecular mimicry evidence in Guillain-Barré syndrome.
    • Antecedent infections may trigger immune responses targeting nerve gangliosides.

    Purpose of the Study:

    • To review the clinical features of acute neuropathies.
    • To outline the diagnostic process for these conditions.
    • To discuss pathophysiologic mechanisms and available treatment data.

    Main Methods:

    • Literature review of clinical presentations.
    • Analysis of diagnostic criteria and imaging findings.
    • Examination of immunologic studies and treatment trial data.

    Main Results:

    • Acute neuropathies are characterized by rapid progression (<4 weeks) and partial spontaneous recovery.
    • Immune-mediated mechanisms, particularly molecular mimicry, are implicated in Guillain-Barré syndrome.
    • Pain is a common and significant symptom at onset, requiring aggressive management.

    Conclusions:

    • Further research is needed to guide immune-modulating treatments for acute neuropathies.
    • Aggressive pain management is a critical component of acute neuropathy care.
    • Understanding pathophysiologic mechanisms is key to developing effective therapies.