alexa Postherpetic neuralgia | Belgium | PDF | PPT| Case Reports | Symptoms | Treatment

OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Recommended Conferences

Read more

Recommended Journals

Relevant Topics

Postherpetic Neuralgia

  • Share this page
  • Facebook
  • Twitter
  • LinkedIn
  • Google+
  • Pinterest
  • Blogger
  • Postherpetic neuralgia

    Definition: Postherpetic neuralgia is a nerve pain due to damage caused by the varicella zoster virus. Typically, the neuralgia is confined to a dermatomic area of the skin, and follows an outbreak of herpes zoster (commonly known as shingles) in that same dermatomic area. Disease Symptoms Common signs and symptoms of postherpetic neuralgia include: a) severe pain that continues for more than one to three months in the same place that the shingles occurred, even after the rash goes away; b) burning sensation on the skin, even from the slightest pressure; c) sensitivity to touch or temperature changes.

  • Postherpetic neuralgia

    Topical treatments: a) Some creams that help with shingles pain contain capsaicin, the ingredient in cayenne pepper that gives it a kick. Examples are Capsin and Zostrix. b) Lidoderm is a patch that contains the anesthetic lidocaine. You apply it directly to the painful area of skin.

  • Postherpetic neuralgia

    statistics:A key factor in the neural plasticity underlying neuropathic pain is altered gene expression in sensory dorsal root ganglia neurons. Injury to sensory nerves induces neurochemical, physiological and anatomical modifications to afferent and central neurons, such as afferent terminal sprouting and inhibitory interneuron loss. Following nerve damage, NaCl channel accumulation causes hyperexcitability, and downregulation of the TTX-resistant Nav1.8 (sensory neuron specific, SNS1) channel and upregulation of TTX-sensitive Nav1.3 (brain type III) and TRPV1 channels. These changes contribute to increased NMDA glutamate receptor-dependent excitability of spinal dorsal horn neurons and are restricted to the ipsilateral (injured) side. A combination of these factors could contribute to the neuropathic pain state of postherpetic neuralgia.

 

High Impact List of Articles

Conference Proceedings

adwords