Pain
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The nociceptive flexion reflex (NFR) is a physiological, polysynaptic reflex allowing for painful stimuli to activate an appropriate withdrawal response. NFR is easily measurable in clinical setting, and is a reliable and objective tool for measurement of an individual's pain experience. An exhaustive review of the literature, covering multiple search engines, indicates that the NFR method is valuable in studying the impact of diverse pharmacological and non-pharmacological interventions on the flexion reflex, in conditions of acute pain and in healthy volunteers. More recently, the NFR method has gained particular attention as a research tool in studies of central sensitization and persistent or chronic pain.
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Research has demonstrated that women report more pain than men, and clinical observations suggest that attenuated adrenocortical activity is associated with high pain sensitivity. The extent to which cortisol concentrations and hemodynamics contribute to gender differences in pain sensitivity has not been investigated. Thirty-four women and 31 men performed the hand cold pressor test (CPT). ⋯ Systolic blood pressure (BP) and stroke volume correlated negatively with pain reports only in women (Ps<0.05). Controlling for potential confounding variables did not alter these relationships. The negative association between pre-CPT cortisol and pain perception in men and the association between BP and pain in women demonstrate different physiological predictors of pain perception in men and women.
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Various animal models of neuropathic pain have been developed which involve creating a lesion in a spinal root. We describe a human correlate in which patients developed a neuropathic pain syndrome after having one spinal nerve surgically divided. In some patients with brachial plexus lesions, the C7 spinal nerve from the opposite side is divided and used as a nerve transfer to re-innervate the injured brachial plexus. ⋯ The pain and hyperalgesia persisted during a phentolamine infusion, which produced a sympathetic blockade. Only mild parasthesia persisted at a 1 year follow up. Thus, surgical division of a single spinal nerve in humans can lead to the development of neuropathic pain.
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N-type calcium channels modulate the release of key pro-nociceptive neurotransmitters such as glutamate and substance P (SP) in the central nervous system. Considerable research interest has focused on the therapeutic potential of the peptidic omega-conopeptides, GVIA and MVIIA as novel analgesic agents, due to their potent inhibition of N-type calcium channels. Recently, the novel peptidic N-type calcium channel blocker, AM336, was isolated from the venom of the cone snail, Conus catus. ⋯ Following acute i.t. dosing, AM336 evoked dose-dependent antinociception (ED50 approximately 0.110 nmol) but the doses required to produce side-effects were an order of magnitude larger than the doses required to produce antinociception. For i.t. doses of MVIIA
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Comparative Study
Neurogenic hyperalgesia versus painful hypoalgesia: two distinct mechanisms of neuropathic pain.
Patients with sensory disturbances of painful and non-painful character show distinct changes in touch and/or pain sensitivity. The patterns of sensory changes were compared to those of human surrogate models of neuropathic pain to assess the underlying mechanisms. We investigated 30 consecutive in-patients with dysaesthesia of various origins (peripheral, spinal, and brainstem lesions) and 15 healthy subjects. ⋯ Our findings suggest that neuropathic pain is based on two distinct mechanisms: (I) central sensitization (neurogenic hyperalgesia; in patients with minor sensory impairment) and (II) partial nociceptive deafferentation (painful hypoalgesia; in patients with major sensory deficit). This distinction as previously postulated for postherpetic neuralgia, is obviously valid also for other conditions. Our findings emphasize the significance of a mechanism-based classification of neuropathic pain.