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BIOMECHANICS AND PAINFUL INJURIES: TISSUE CNS RESPONSES FOR NERVE ROOT MECHANICAL INJURIES

机译:生物力学和疼痛性损伤:组织和中枢神经系统对神经根机械损伤的反应

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摘要

Pain affects as many as 50 million Americans, with annual costs estimated as high as $90 billion. Unfortunately, the mechanism of injuries leading to persistent pain syndromes remain largely uncharacterized. A common painful injury results due from mechanical loading of nerve roots, which can occur for spinal injuries in both the low back and neck. Relationships have been demonstrated between tissue compression and behavioral hypersensitivity responses in animal models, with differential patterns of sensitivity depending on the nature of the mechanical insult (Colburn et al., 1999). Mechanical allodynia (MA) is an increased behavioral sensitivity to a non-noxious stimulus and is observed in the dermatome of the injured tissue. It can be measured by the frequency of paw withdrawals elicited by stimulation with normally non-noxious von Frey filaments. Allodynia is a clinical measure of sensitivity and, therefore, provides a useful gauge of nociceptive responses. Animal studies have shown that compression of neural structures initiates a variety of physiologic responses, including decreased electrical activity, increased edema formation, and increased endoneurial pressure in the region of compression (Lundborg et al., 1983; Olmarker et al., 1989, 1990; Pedowitz et al., 1992). While these studies document physiologic changes immediately following injury, they do not describe the temporal nature of these changes following tissue loading as they relate to pain behaviors. Moreover, despite this evidence of edema formation and increased endoneurial pressure locally in the nerve roots, no study has simultaneously documented local changes in nerve root geometry following compressive injury and how these changes may be linked to the onset and/or maintenance of pain-associated behaviors. Therefore, this study examines injury biomechanics for pain-behaviors in a radiculopathy (nerve root injury) model and temporally characterizes the local geometric changes in the nerve root for a series of postsurgical time points following compressive injury. While these results indicate that compression magnitude clearly modulates pain responses, the local nerve root swelling does not appear to directly drive behavioral changes. This suggests a complicated physiology for injury which likely contributes to the manifestation of pain. Findings are also presented for preliminary investigatations into tissue rebound/recovery responses for varied mechanical insult magnitudes to begin to understand potential injury mechanisms leading to pain.
机译:疼痛影响着多达5000万美国人,每年的损失估计高达900亿美元。不幸的是,导致持续性疼痛综合症的伤害机制在很大程度上仍未阐明。常见的疼痛性损伤是由神经根的机械负荷引起的,这种损伤可能发生在下背部和颈部的脊柱损伤中。在动物模型中,组织压迫与行为超敏反应之间存在关系,其敏感性的差异取决于机械损伤的性质(Colburn等,1999)。机械性异常性疼痛(MA)对非有害刺激的行为敏感性增加,并且在受伤组织的皮肤刀中观察到。可以用正常无毒的冯·弗雷丝刺激引起的爪子缩回频率来测量。异常性疼痛是敏感性的临床量度,因此提供了伤害感受反应的有用量度。动物研究表明,神经结构受压会引发各种生理反应,包括受压区域内电活动减少,水肿形成增加和神经内膜压力升高(Lundborg等,1983; Olmarker等,1989,1990)。 ; Pedowitz等,1992)。尽管这些研究记录了受伤后立即发生的生理变化,但由于它们与疼痛行为有关,因此并未描述组织负荷后这些变化的时间性质。此外,尽管有证据表明神经根局部有水肿形成和神经内膜压力升高,但没有研究同时记录压迫性损伤后神经根几何形状的局部变化以及这些变化如何与疼痛相关的发作和/或维持相关联行为。因此,本研究检查了神经根病(神经根损伤)模型中疼痛行为的损伤生物力学,并在压迫性损伤后的一系列术后时间点上,暂时表征了神经根的局部几何变化。这些结果表明,压迫程度可以明显调节疼痛反应,而局部神经根肿胀似乎并不能直接驱动行为改变。这表明损伤的生理机制很复杂,可能导致疼痛的表现。还提供了用于初步调查各种机械损伤幅度的组织反弹/恢复反应的发现,以开始了解导致疼痛的潜在损伤机制。

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