Funct Neurol
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A comparison of the heat- and pilocarpine-induced forehead sweating patterns was carried out in 8 patients with "Hemicrania continua" (HC) and in healthy subjects (n = 17 and 14 for the two tests, respectively). The results were compared with those obtained in 8 patients with chronic paroxysmal hemicrania (CPH). ⋯ The only exception seems to be a significant relative increase in medial forehead sweating on both sides in HC patients when compared to controls during the heating test. With these variables, no evidence for any difference of major importance seems to exist between the two headache forms.
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Age differences in the thresholds for heat pain, warmth and cold were studied in 64 healthy persons from 17 to 63 years of age (32 women, 32 men). The stimuli were applied to the thenar and the dorsum pedis with a contact thermode. ⋯ Furthermore, the quotients of the individual foot and hand thresholds revealed a significant relative increase in all thresholds on the foot. The length of the afferent pathways seems to influence the degree of age-related changes both in heat pain perception and in thermal sensitivity, resulting in a distal-proximal pattern of age-dependent decline.
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Sympathetic skin response and plethysomography were used to assess the sympatholytic effect of the stellate ganglion block with morphine and bupivacaine in patients affected by a sympathetic algodystrophy of the upper limb. Morphine did not show any analgesic or sympatholytic effect. The distribution of the sympatholytic effect and the clinical findings of pain relief without somatic sensory-motor impairments obtained with the local anaesthetic, support the presence of a blockade of the sympathetic efferent pathway as well as of an afferent contingent of fibres probably and mainly involved in sympathetic reflexes.
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Painful neurogenic syndromes commonly diagnosed as reflex sympathetic dystrophy (RSD) may not be the consequence of sympathetic dysfunction. Recent experimental data on the mechanism of hyperalgesia indicate that the primary pathophysiological mechanism of RSD may be sensitization of either peripheral nociceptors, or central neurons, or both. The sympathetic system might be involved in maintaining this condition, but this is not always the case. This presentation is an attempt to interpret clinical neuropathic syndromes on the basis of new scientific knowledge.
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There is a spectrum of conditions which have in common burning pain, often with hyperpathia, hyperalgesia, vasomotor and sudomotor changes. When due to major nerve damage, the condition is known as causalgia; when due to minor nerve damage or other factors, various terms such as algodystrophy or reflex sympathetic dystrophy are employed. ⋯ The classical view that the peripheral sympathetic nervous system is involved in generation of pain is questioned, and the possible roles of the central nervous system and of non-adrenergic mechanisms are summarised. That pain could be due to dysfunction of the polymodal nociceptor neurone is considered.