Pathophysiology
Postherpetic neuralgia is thought to be nerve damage caused by herpes zoster. The damage causes nerves in the affected dermatomic area of the skin to send abnormal electrical signals to the brain. These signals may convey excruciating pain, and may persist or recur for months, years or for life.
A key factor in the neural plasticity underlying neuropathic pain is altered gene expression in sensory dorsal root ganglia (DRG) 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, downregulation of the TTX-resistant Nav1.8 (sensory neuron specific, SNS1) channel and upregulation of TTX-sensitive Nav1.3 (brain type III) 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 PHN.
Read more about this topic: Postherpetic Neuralgia