Articles: neuralgia.
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Herpes zoster neuralgia and post-zoster neuralgia (PZN) are common disabling pain syndromes. While pain from acute herpes zoster is self-limited in most cases, as pain may disappear without treatment, post-zoster neuralgia is difficult to manage. Pathological findings in acute herpes zoster include infiltration of ganglia, demyelinization and loss of axons; yet the pathogenesis of pain remains largely unknown. ⋯ The same is true for specific zoster hyperimmunoglobulins and non-specific immunoglobulins; however, there are no definite results. In the future, controlled, double-blind studies on the effect of therapeutic measures in preventing postzosteric neuralgia need to be conducted. So far, the positive effect of sympathetic blocks in preventing the late pain complications of herpes zoster can only be suggested and recommended based on subjective experience.
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Herpes zoster is an infection caused by reactivation of dormant varicella-zoster virus. The acute course of herpes zoster is generally benign; however, some patients will experience postherpetic neuralgia characterized by severe, relentless, and at times disabling pain that is often refractory to treatment. While herpes zoster responds to acyclovir, cost-benefit considerations limit the drug's usefulness to only a select group. Postherpetic neuralgia requires a holistic approach, including pharmacologic therapy using several different classes of drugs.
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Under normal conditions acute stimulation and sensitization of polymodal nociceptive C-fibres cause pain and, due to afferent axon reflex activation, a local skin vasodilatation, flare reaction and skin temperature increase. Two questions arise: (i) Do sensitized C-nociceptors signal allodynia in chronic postherpetic neuralgia? (ii) If not, does ongoing peripheral nociceptive C-fibre input maintain a central process that accounts for allodynia? Ten patients with postherpetic neuralgia and tactile allodynia and 10 control subjects were studied using a laser Doppler perfusion monitor. Peripheral nociceptive C-fibre function was assessed by quantitative measurement of the axon reflex vasodilatation and flare reaction induced by histamine iontophoresis and compared with non-neural vasodilatation induced by local skin heating. ⋯ Changes in CNS processing may occur after zoster infection that strengthen the synaptic ties between central pain signalling pathways and low-threshold mechanoreceptors with A beta-fibres. This altered central processing is not maintained by ongoing cutaneous nociceptive C-fibre input, at least in some patients with postherpetic neuralgia. On the contrary, an anatomical synaptic reorganization depending on afferent C-fibre degeneration seems to be more likely, particularly in advanced stages of postherpetic neuralgia.
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A case of bilateral fenestration of the vertebral artery at the level of the atlas in a patient who had occipital neuralgia and cervical myelopathy is presented. MRI and vertebral angiogram demonstrated the fenestrated vertebral artery compressing the upper cervical cord. Surgical decompression for the C-1 and C-2 sensory roots and the upper cervical cord was performed. ⋯ However, considering the pathway of the fenestrated vertebral artery, it is quite possible that the fenestrated vertebral artery might compress the neural structures, resulting in some clinical problems. Although occipital neuralgia may result from a variety of causes, this case was caused by the fenestrated vertebral artery compressing the C-1 and C-2 sensory roots. The authors wish to emphasize that microsurgical vascular decompression may be the only effective treatment in such cases as well as in facial spasm and trigeminal neuralgia.