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Shingles is caused by varicella zoster virus (VZV), an alpha-herpesvirus. Initial VZV infection usually occurs in childhood causing chickenpox. After this resolves, the virus is not eliminated from the body, but remains latent in the nerve cell bodies of the dorsal root or trigeminal ganglia, without causing symptoms.
Shingles, also known as herpes zoster or zona, [6] is a viral disease characterized by a painful skin rash with blisters in a localized area. [2] [7] Typically the rash occurs in a single, wide mark either on the left or right side of the body or face. [1]
Similar to the herpes simplex viruses, after primary infection with VZV (chickenpox), the virus lies dormant in neurons, including the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Many years after the person has recovered from initial chickenpox infection, VZV can reactivate to cause shingles. [4]
Postherpetic neuralgia (PHN) is neuropathic pain that occurs due to damage to a peripheral nerve caused by the reactivation of the varicella zoster virus (herpes zoster, also known as shingles). PHN is defined as pain in a dermatomal distribution that lasts for at least 90 days after an outbreak of herpes zoster. [ 1 ]
The dorsal root ganglion contains cell bodies for sensory nerves including large, myelinated Aβ fibers which carry proprioception and tactile touch sensation to the brain via the dorsal column–medial lemniscus pathway and small, unmyelinated C fibers which carry thermal and pain sensation to the brain via the spinothalamic tract. [2]
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Tabes dorsalis is a late consequence of neurosyphilis, characterized by the slow degeneration (specifically, demyelination) of the neural tracts primarily in the dorsal root ganglia of the spinal cord (nerve root). These patients have lancinating nerve root pain which is aggravated by coughing, and features of sensory ataxia with ocular ...
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