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Related Concept Videos

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

Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

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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...
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Local Anesthetics: Differential Sensitivity of Nerve Fibers01:24

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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...
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Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs but also impacts other areas, such as the arms, thereby impairing overall circulation and organ function.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty deposits inside the arterial...
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Related Experiment Video

Updated: Jun 12, 2025

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

Teresa Sevilla1, Lucía Galán Dávila2

  • 1Unidad de Enfermedades Musculares, Departamento de Neurología, Hospital Universitario y Politécnico La Fe; Grupo de Investigación de Ataxia y Enfermedades Neuromusculares IISLAFE, Valencia, España; Departamento de Medicina, Universidad de Valencia University; Centro de Investigación Neurológica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III, Madrid, España.

Medicina Clinica
|June 10, 2025
PubMed
Summary
This summary is machine-generated.

Small fiber neuropathy (SFN) is a common neurological condition causing pain and autonomic dysfunction. Recent discoveries in SFN causes and genetics may enable more personalized treatments beyond current symptomatic approaches.

Keywords:
Biopsia de pielDisautonomíaDysautonomiaNeuropatía de fibra pequeñaNeuropatía dolorosaPainful neuropathySkin biopsySmall fiber neuropathy

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Area of Science:

  • Neurology
  • Neuroscience
  • Genetics

Background:

  • Small fiber neuropathy (SFN) is a frequent neurological consultation, affecting at least 53 per 100,000 individuals.
  • Key symptoms include neuropathic pain and dysautonomic dysfunction.
  • Diagnosis relies on clinical symptoms, examination, neurophysiologic testing, and skin biopsy.

Purpose of the Study:

  • To summarize current understanding of small fiber neuropathy.
  • To highlight recent advancements in identifying SFN causes.
  • To discuss the implications for future treatment strategies.

Main Methods:

  • Review of clinical presentation and diagnostic methods for SFN.
  • Analysis of recent literature on genetic and immune-related causes of SFN.
  • Evaluation of current symptomatic treatment approaches.

Main Results:

  • SFN is characterized by neuropathic pain and autonomic dysfunction.
  • Emerging causes include sodium channel mutations and immune factors like TS-HDS, FGFR-3, and plexin D1.
  • Current treatments are primarily symptomatic, often using antidepressants and antiepileptics via trial-and-error.

Conclusions:

  • Advances in understanding SFN etiology, including genetic and immune factors, are crucial.
  • This knowledge facilitates improved phenotype and genotype definition.
  • Personalized treatment approaches for SFN are becoming increasingly feasible.