Studies of neuropathic pain patients have shown pathological conditions characterized by zones of skin in which heat hyperalgesia is present in some patients, and larger zones in which mechanical hyperalgesia and/or allodynia is present in all or most patients (17,21,37). Two distinct types of mechanical allodynia have been characterized in neuropathic pain patients. The first is termed low threshold A-beta allodynia (17,37). Its presence is based on several lines of evidence. First, it occurs in response to electrical stimulation of the lowest threshold axons in nerves supplying the pathological zone. Second, it occurs in response to very gentle mechanical stimuli. Third, it is abolished by blockade of the largest fastest conducting axons within nerves (21). Finally, it has a reaction time consistent with conduction in myelinated afferents (21). It is also commonly characterized by the fact that moving stimuli or stimulus onset or offset is more painful than static mechanical stimuli (17,37). The other type of mechanical allodynia is characterized by evidence that A-beta afferents do not seem to be involved (see above) and that more intense but normally painless stimuli are required to evoke pain. For example, 15 to 600 g von Frey filament stimuli, which are well above threshold for A-beta primary mechanoreceptive afferents but are rarely painful under normal circumstances, evoke pain when applied to the pathological zones of these patients. This type of mechanical allody-nia is termed high threshold and it may well be mediated by activation of nociceptive afferents under conditions that normally do not produce pain.
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