Articles: neuralgia.
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In 12 zoster patients who had developed postherpetic neuralgia with dynamic mechanical allodynia and in six zoster patients who had recovered without pain, the functional role of nociceptive C-fibers in allodynia was assessed by quantifying axon reflex reactions induced by histamine iontophoresis within allodynic regions and in their contralateral sites. In patients with postherpetic neuralgia, histamine responses were reduced or abolished within allodynic areas, indicating degeneration of nociceptive C-fibers. ⋯ These results demonstrate that sensitized nociceptive C-fibers are not involved in signaling and maintenance of allodynia. Alteration in CNS processing may reorganize synaptic ties between central pain-signaling pathways and mechanoreceptive A beta-fibers depending on afferent C-fiber degeneration rather than ongoing C-fiber input.
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This article concerns traction lesions of the brachial plexus in adults, focusing on management and recovery. Open wounds of the plexus are now treated surgically as soon as possible. The subsequent rehabilitation is the same as that for closed traction lesions of the brachial plexus in which significant recovery is expected.
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The aim of the present study was to investigate the role of primary afferent fibres with polymodal nociceptors in the various pain symptoms and signs associated with post-herpetic neuralgia (PHN). Forty-four patients with PHN affecting thoracic dermatomes were examined clinically for evidence of sensory disturbance to touch and pinprick and compared to 14 normal subjects and 9 subjects with evidence of past herpes zoster infection but no pain. ⋯ The 2 groups with allodynia had significantly decreased neurogenic flare responses compared to PHN subjects without allodynia and the 2 control groups. These results suggest that allodynia in patients with post-herpetic neuralgia may be a consequence of disrupted function of primary afferent fibres.
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The oxygen-15 water bolus positron emission tomography (PET) method was used to image regional brain activity in 4 patients with chronic post-traumatic neuropathic pain confined to one lower limb and in 1 patient with post-herpetic neuralgia. In comparison to 13 normal subjects, scans of the patients disclosed a statistically significant decrease in thalamic activity contralateral to the symptomatic side. Examination of the right/left ratio for all the subjects showed that the values for the patients fell at the extremes of the normal range, according to the side of the affected body part. These initial observations suggest that functional alterations in thalamic pain processing circuits may be an important component of chronic neuropathic pain.
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We have tested the effects of cutaneous application of noradrenaline in 35 patients presenting with neuropathic pain. Depending on the outcome of sympatholytic interventions the patients were considered to have sympathetically maintained pain (SMP; n = 25) or sympathetically independent pain (SIP; n = 10). Iontophoretic application or cutaneous injection of noradrenaline into symptomatic skin aggravated pain and mechanical or thermal hyperalgesia in 7/25 SMP patients. ⋯ None of these 4 and none of the 7 initially noradrenaline-unresponsive patients experienced pain to the noradrenaline challenge at follow-up. Thus, cutaneous noradrenaline application can aggravate the pain in some, but not all SMP patients. THe abnormal noradrenaline reaction can change over time as can the pain relieving effects of sympatholytic therapy.