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

机译:生物力学和疼痛伤:组织和CNS对神经根机械损伤的反应

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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:疼痛影响多达5000万美国人,年费估计高达900亿美元。不幸的是,导致持续疼痛综合征的伤害机制仍然很大程度上是无表情的。由于神经根的机械荷载,这是一种常见的痛苦损伤结果,这可能在低背部和颈部脊柱损伤发生。在动物模型中的组织压缩和行为超敏反应之间的关系已经证明了与机械损伤性质的差异敏感程度(Colburn等,1999)。机械异常性疼痛(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病中观察到。它可以通过用通常非有害的von Frey长丝刺激引发的爪子提取的频率来衡量。 Allodynia是一种敏感性的临床测量,因此提供了有用的伤害反应仪表。动物研究表明,神经结构的压缩引发了各种生理反应,包括降低的电活性,增加水肿形成,并在压缩区域增加了内牙髓压力(Lundborg等,1983; Olmarker等,1989,1990 ; Pedowitz等,1992)。虽然这些研究在受伤后立即进行生理变化,但由于它们与疼痛行为相关,但它们不会描述这些变化的时间性。此外,尽管在神经根部局部地形成的水肿形成和内牙髓压力增加的证据,但在压缩损伤之后没有同时记录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疼痛和/或维持联系行为。因此,本研究检查了放射性病变(神经根损伤)模型中疼痛行为的损伤生物力学,并且在压缩损伤后一系列后尿针的局部几何变化暂时表征了局部几何变化。虽然这些结果表明压缩幅度清楚地调节疼痛反应,但局部神经根肿胀似乎没有直接驱动行为变化。这表明对伤害的复杂生理学可能有助于疼痛的表现。还介绍了对组织回弹/恢复响应的初步调查,以便开始了解潜在的伤害机制导致疼痛的潜在伤害机制。

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