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      Structure and Biomechanics of Peripheral Nerves: Nerve Responses to Physical Stresses and Implications for Physical Therapist Practice

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      Physical Therapy
      Oxford University Press (OUP)

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          A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man

          A peripheral mononeuropathy was produced in adult rats by placing loosely constrictive ligatures around the common sciatic nerve. The postoperative behavior of these rats indicated that hyperalgesia, allodynia and, possibly, spontaneous pain (or dysesthesia) were produced. Hyperalgesic responses to noxious radiant heat were evident on the second postoperative day and lasted for over 2 months. Hyperalgesic responses to chemogenic pain were also present. The presence of allodynia was inferred from the nocifensive responses evoked by standing on an innocuous, chilled metal floor or by innocuous mechanical stimulation, and by the rats' persistence in holding the hind paw in a guarded position. The presence of spontaneous pain was suggested by a suppression of appetite and by the frequent occurrence of apparently spontaneous nocifensive responses. The affected hind paw was abnormally warm or cool in about one-third of the rats. About one-half of the rats developed grossly overgrown claws on the affected side. Experiments with this animal model may advance our understanding of the neural mechanisms of neuropathic pain disorders in humans.
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            Vascular ischaemia and reperfusion injury.

            Although restoration of blood flow to an ischaemic organ is essential to prevent irreversible tissue injury, reperfusion per se may result in a local and systemic inflammatory response that may augment tissue injury in excess of that produced by ischaemia alone. Cellular damage after reperfusion of previously viable ischaemic tissues is defined as ischaemia-reperfusion (I-R) injury. I-R injury is characterized by oxidant production, complement activation, leucocyte-endothelial cell adhesion, platelet-leucocyte aggregation, increased microvascular permeability and decreased endothelium-dependent relaxation. In its severest form, I-R injury can lead to multiorgan dysfunction or death. Although our understanding of the pathophysiology of I-R injury has advanced significantly in the last decade, such experimentally derived concepts have yet to be fully integrated into clinical practice. Treatment of I-R injury is also confounded by the fact that inhibition of I-R-associated inflammation might disrupt protective physiological responses or result in immunosuppression. Thus, while timely reperfusion of the ischaemic area at risk remains the cornerstone of clinical practice, therapeutic strategies such as ischaemic preconditioning, controlled reperfusion, and anti-oxidant, complement or neutrophil therapy may significantly prevent or limit I-R-induced injury in humans.
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              The anatomy and physiology of nerve injury.

              Nerves have a structure of considerable complexity with features of special relevance to nerve injury and nerve regeneration. These include variations in the cross-sectional areas devoted to fascicular and epineurial tissue, the fascicular redistribution and mixing of different branch fibers brought about by fascicular plexuses, and the numbers of nerve fibers representing individual branches. The elasticity and tensile strength of nerve trunks and their capacity to resist traction deformation reside in the fascicular tissue, while the epineurium provides a protective cushion against compression. The microstructure of nerve trunks provides the basis for a classification of nerve injuries into five degrees of severity with partial and mixed types--each with a clearly defined pathology and distinguishing clinical features. Following a transection injury, changes occur in the severed axons, endoneurial tubes, fasciculi, and nerve trunk. The type of injury and the nature of these changes determine the outcome of axon regeneration.
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                Author and article information

                Journal
                Physical Therapy
                Oxford University Press (OUP)
                0031-9023
                1538-6724
                January 01 2006
                January 01 2006
                : 86
                : 1
                : 92-109
                Article
                10.1093/ptj/86.1.92
                16386065
                3271f46c-d16b-4bc4-8f92-2fe1eb8de222
                © 2006
                History

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