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Related Concept Videos

Analgesia and Pain Management01:25

Analgesia and Pain Management

Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
Nociception01:44

Nociception

Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain. Thus, pain helps the...
Pain01:20

Pain

Pain serves as a critical warning signal that alerts the body to potential or actual harm. When mechanical pressure on the skin is intense, such as from a sharp pinch, the sensation transitions from touch to pain. Similarly, extreme temperatures, like a hot pot handle, convert the sensation of heat into pain. Pain can also result from overstimulation of other senses, such as blinding light, loud noise, or the intense heat from habañero peppers. This ability to sense pain is essential for...
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...
Blood and Nerve Supply to the Bones01:29

Blood and Nerve Supply to the Bones

Bones are dynamic organs that require a rich supply of oxygen and nutrients. Around 5% to 10% of the cardiac output supplies blood to the bones. A typical long bone has three main sources: the nutrient artery, the metaphyseal and epiphyseal arteries, and the periosteal arteries.
Nutrient Artery
The nutrient artery is the main blood vessel that enters the diaphysis via the nutrient foramen. While most long bones have only one nutrient foramen, large bones, such as the femur, may have two. This...

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Neuropathic pain: a clinical perspective.

Ralf Baron1

  • 1Sektion Neurologische Schmerzforschung und Therapie, Klinik für Neurologie, Christian-Albrechts-Universität Kiel, Schittenhelmstr. 10, 24105 Kiel, Germany. r.baron@neurologie.uni-kiel.de

Handbook of Experimental Pharmacology
|August 6, 2009
PubMed
Summary

Neuropathic pain arises from nervous system damage, causing spontaneous and evoked pain. Current treatments are unsatisfactory, highlighting the need for mechanism-based approaches for personalized pain management.

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Area of Science:

  • Neurology
  • Pain Medicine
  • Neuroscience

Background:

  • Neuropathic pain results from peripheral or central nervous system lesions or diseases.
  • It is characterized by spontaneous pain (e.g., ongoing, paroxysmal) and evoked pain (e.g., hyperalgesia, allodynia).
  • Pathophysiological mechanisms include molecular changes in nociceptors and central sensitization, leading to hyperexcitability.

Purpose of the Study:

  • To review the mechanisms underlying neuropathic pain.
  • To discuss current treatment strategies and their limitations.
  • To propose a mechanism-based approach for optimizing individual patient treatment.

Main Methods:

  • Review of existing literature on neuropathic pain mechanisms and treatments.
  • Analysis of molecular and cellular changes in nociceptive neurons and central processing.
  • Discussion of pharmacological interventions including antidepressants, anticonvulsants, tramadol, opioids, capsaicin, and local anesthetics.

Main Results:

  • Nerve lesions trigger molecular changes in nociceptors (e.g., altered sodium and vanilloid receptors), causing spontaneous and evoked pain.
  • Central sensitization leads to hyperexcitability in the spinal cord and brain, manifesting as allodynia.
  • Current treatments offer general pain relief but often fail to achieve complete pain reduction due to a lack of mechanism-specific targeting.

Conclusions:

  • Neuropathic pain treatment remains largely unsatisfactory, necessitating a shift towards personalized medicine.
  • A proposed concept involves analyzing pain based on underlying mechanisms for targeted therapy.
  • Systematic clinical examination and phenotypic characterization combined with mechanism-specific drugs can optimize treatment for individual patients.