Articles: peripheral-nerve-injuries.
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Anesthesia-associated nerve injury is a common cause of patient morbidity and litigation. To identify factors associated with perioperative nerve injuries and rationalize preventive strategies, 44 cases from the American Association of Nurse Anesthetists (AANA) Foundation Closed Malpractice Claims Database pertaining to nerve injuries in which nurse anesthetists provided care were analyzed. Emerging patterns and themes related to the development of injury were identified. ⋯ Documentation on the anesthesia record of the use of intraoperative protective padding and patient position was lacking or inadequate in a majority of the claims. Effective strategies for the prevention of nerve injury during anesthesia are reviewed. Abnormal body habitus, several disease states, anesthesia technique, improper positioning, lack of adequate padding, and tourniquet use have been implicated as risk factors.
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Mouse genetics has contributed significantly to our understanding of molecular mechanisms underlying tissue and nerve injury-induced persistent pain. To create a highly reproducible, relatively noninvasive model of neuropathic pain in the mouse, we examined the behavioral consequences of sparing each of the 3 distal branches of the sciatic nerve in wild-type mice after a model originally described in the rat. ⋯ We found that each of the sciatic branches targets a distinct mediolateral location in inner lamina II and that each of the spared nerve injury models produced a more reproducible pattern of thiamine monophosphatase staining loss than did partial tight ligation. These results improve on previous nerve injury models in mouse, demonstrate similar behavioral changes as in rat, and provide novel information on the topographic organization of small diameter peripheral afferents in the mouse spinal cord.
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Intrathecal clonidine reduces tactile allodynia in animal models of neuropathic pain, and this effect is blocked by atropine. However, the role of tonic spinal cholinergic activity and its interaction with alpha2-adrenergic systems in normal and neuropathic conditions and to different sensory methods has not been systematically examined. The authors examined cholinergic receptor involvement in thermal and mechanical sensitivity in normal and neuropathic animals and its interaction with intrathecal clonidine. ⋯ These data suggest that after nerve injury, mechanical but not thermal antinociception from intrathecal clonidine relies on a muscarinic interaction, because only mechanical antinociception was antagonized by atropine. These results do not favor a regulation of nociceptive transmission by a tonic release of acetylcholine in nerve-injured rats.
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Comparative Study Clinical Trial
Comparison of the pain suppressive effects of clinical and experimental painful conditioning stimuli.
Studies in healthy volunteers suggested that the classical counterirritation phenomenon (i.e. pain inhibits pain effect) might depend on diffuse noxious inhibitory controls (DNIC), which modulate the spinal transmission of nociceptive signals. In the present study, we sought to determine whether similar mechanisms were at play in patients with different subtypes of neuropathic pain. Ten patients presenting with a traumatic peripheral nerve injury associated with dynamic mechano-allodynia (i.e. pain triggered by brushing) or static mechano-allodynia (i.e. pain triggered by light pressure stimuli) were included in this study. ⋯ These effects were similar to those induced by HNCS and were probably due to an increased activation of DNIC. In contrast, in patients with dynamic allodynia, brushing within the allodynic area reduced the pain sensation at the foot, but did not inhibit the electrophysiological responses, suggesting that in this case the counterirritation effect may take place at the supraspinal level. Thus, the mechanisms of counterirritation are not univocal, but depend on the pathophysiological mechanisms of clinical pain.
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J Shoulder Elbow Surg · May 2003
The course of the suprascapular nerve in the supraspinatus fossa and its vulnerability in muscle advancement.
Twenty-four cadaveric shoulders were evaluated to assess damage to the suprascapular nerve in relation to Debeyre's advancement of the supraspinatus muscle for rotator cuff repair. In all cases the neurovascular pedicle was tethered at the suprascapular notch and at the periosteum of the supraspinatus fossa. The medial motor branches were directed to the trigonum spinae or the superior angle of the scapula (group 1). ⋯ Branches of group 1 and the main nerve are at risk of injury when detaching muscle from bone. This risk is minimized by subperiosteal detachment. Branches of group 1 are tensioned when advancing the muscle 1 cm laterally.