Abstract
The IASP defines postherpetic neuralgia as “chronic pain with skin changes in a dermatomal distribution following acute herpes zoster”. Postherpetic neuralgia is a severe painful neuropathic pain and is one of the most intractable pain.
The patients complained of constant spontaneous burning pain, brief recurrent shooting, tic-like pain and a sharp radiating pain evoked by very light touching of the skin which is called allodynia. Clinical investigations show that sensory deficits area and extremely painful area to light touch may coexist within the affected dermatome.
What kinds of pathophysiological mechanisms are contributing to the pain?
Tissue injury or inflammation leads to release of substance P from nerve endings and release of pain producing substances resulting in sensitization of nociceptors. Characteristic feature of sensitized nociceptors are ongoing discharge, a lowered activation threshold for thermal and mechanical stimuli, and an enhanced discharge to noxious stimulation. This process is called peripheral sensitization. Massive or prolonged C nociceptor input produces dramatic changes in the response of the spinal dorsal hom neurons. The response of neurons are enhanced to all afferent inputs and the size of be neurons receptive field is expanded. This process is called central sensitization. When central sensitization is produced, A beta fibers which normally are sensitive to innocuous tactile stimuli activate the sensitized neuron in the dorsal hom. Thus, gentle moving tactile stimuli become capable of evoking pain. This phenomenon is called dynamic allodynia. Some patients have this condition: the patients have minimal sensory loss and severe allodynia. Other neuralgic patients have pain associated with C fiber degenerations. Under this condition, C fibers synaptic contacts with dorsal hom neurons are reduced, but the central terminals of A beta fiber become directly contact with nociceptive neurons in the dorsal hom. This anatomical reorganization may lead to allodynia. In some patients, temperature sensations are profoundly impaired but light mechanical stimuli can produce severe pain. Other patients have differentiation pain. When the peripheral nerve is injured and primaiy afferent is partially or completely lost, important biological changes are produced on the nervous system.
The sequence of events following nerve injury are
Afferent nerve fiber
post injury nerve discharge nerve sprouting increased sensitivity of sprouts to mechanical and chemical stimuli Dorsal root ganglion cell
spontaneous activity, increased evoked activity increased innervations of large cells by sympathetic terminal Spinal cord
sprouting of A beta terminals into nociceptive laminae central sensitization expansion of receptive fields dorsal hom reorganization (plasticity)
There is some evidence that sink process may underlie the pain of postherpetic neuralgia. Some patients have severe pain, profound sensory loss but no hyperalgesia or allodynia. These patients presumably have deafferentation pain. The pain is likely due to increased spontaneous activity in the deaffereted dorsal hom neurons as well as dorsal root ganglion cells.
At last, after nerve lesion the sympathetic nervous system might interact with afferent neurons. Thus activity in sympathetic fibers can induce further activity in irritable nociceptor and enhance pain and allodynia.
In conclusion, three distinct peripheral and central pathophysiological mechanisms contribute to pain generation. It is likely that more than one mechanism is operative in one individual. It is also possible that pain mechanism changes during the course of the disease and these three types of mechanisms may even coexist in individual patient. The treatment of postherpetic neuralgia is required mechanism-based intervention for each of the different mechanisms.
Pain generated by peripheral and central sensitization are treated with NSAIDS and opioid. Topical application of lidocaine, aspirin or capsaicin is moderately effective in some patients.
Allodynia resulting from C fiber degeneration and deaffemation pain are very difficult to treat. Antidepressant therapy remains standard subcutaneously.
To inhibit the spontaneous discharge of dorsal root ganglion and nerve sprout, Na ion channel blocker is recommended. It is reported that systemic lidocaine silences ectopic neuroma and dorsal root ganglion discharges. Intrathecal N type Ca channel blockers also are effective.
Though there are many drugs and methods to treat the postherpetic neuralgia, their effects are not satisfactory. We are still looking for a better method.
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