Articles: neuralgia.
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Clin Neurol Neurosurg · Feb 1997
Case ReportsCoiling of the vertebral artery presenting with neuralgic pain.
A rare case of radicular pain in the arm due to compression of the C6 nerve root by coiling of the vertebral artery is reported; the diagnosis was confirmed by computed tomography (CT), magnetic resonance (MR) angiography and echocolordoppler. Although the enlargement of an intervertebral foramen by a tortuous vertebral artery has been described previously, the occurrence of radicular pain is exceptional. Magnetic resonance imaging (MRI), MR angiography and echocolordoppler allow to differentiate foraminal enlargement due to vascular anomalies of the vertebral artery from that more commonly due to tumor compression, mainly from neurinoma. Surgical decompression may be considered in symptomatic cases.
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Neuropathic pain syndromes are commonly seen in clinical practice and are frequently used as pain models in testing new therapies. However, no pain scale exists with the primary purpose to measure pain in neuropathic syndromes. ⋯ Moreover, the NPS items appear to be sensitive to treatments known to impact neuropathic pain. These findings provide support for the further development of the NPS.
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Neuropathic pains arising from peripheral nerve injury can result in increased sensitivity to both noxious and non-noxious stimuli and are accompanied by a number of neuroplastic alterations at the level of the spinal cord including upregulation of neurotransmitters including dynorphin, cholecystokinin and neuropeptide Y. Additionally, such pain states appear to be associated with activation of excitatory amino acid receptors including the N-methyl-D-aspartate (NMDA) receptor. Neuropathic pains have often been classified as 'opioid resistant' in both clinical and laboratory settings. ⋯ Co-administration, however, of i.t. morphine with MK-801, or i.t. antisera to dynorphin A (1-13) given prior to morphine elicited both a full antiallodynic response and a complete block of the tail-flick reflex in nerve-injured animals. These results suggest that tonic activation of NMDA receptors, following peripheral nerve injury, is involved with the attenuation of the effectiveness of spinal morphine in a model of neuropathic pain. Additionally, this tonic NMDA activity may be mediated, in part, by increased levels of endogenous dynorphin associated with peripheral nerve injury.
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Herpes zoster is a common disease primarily affecting the elderly. Although some individuals experience no symptoms beyond the duration of the acute infection, many develop chronic pain [postherpetic neuralgia (PHN)], which is the commonest complication of herpes zoster infection and remains notoriously difficult to treat once established. It may persist until death and has major implications for quality of life and use of healthcare resources. ⋯ In the future, vaccines may have an important place in reducing the incidence of chickenpox in the population or, through the vaccination of middle-aged individuals, in boosting immunity to varicella zoster virus, thus preventing or modifying the replication of the virus from its latent phase that results in herpes zoster. Developments in the understanding of the pathophysiology of PHN indicate possible directions for improved drug management of established PHN, although no evidence yet exists for efficacy of the drugs concerned. Such agents include new generation anticonvulsants and N-methyl-D-aspartate antagonists.
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Randomized Controlled Trial Clinical Trial
Effect of adrenergic receptor activation on post-herpetic neuralgia pain and sensory disturbances.
Patients with acute herpes zoster, and to a lesser extent post-herpetic neuralgia (PHN), have been reported to respond to local anesthetic blockade of the sympathetic nervous system. In animal models of nerve injury, local injection of adrenergic agonists after nerve injury, but not before, excites nociceptors. In some patients with chronic neuropathic pain, local application of norepinephrine evokes pain. ⋯ After injection of the adrenergic agonist into PHN skin, both overall PHN pain and allodynia severity were significantly greater than after saline injection, peaking at 10-15 min post-injection. Even when PHN has been present for years, adrenergic receptor stimulation in PHN skin increases pain, most likely through direct activation of C-nociceptors in the painful skin. Increased allodynia is most likely mediated centrally and driven by the increase in C-nociceptor input.