Articles: peripheral-nerve-injuries-physiopathology.
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In upper brachial plexus palsy patients, loss of shoulder function and elbow flexion is obvious as the result of paralysed muscles innervated by the suprascapular, axillary and musculocutaneus nerve. Shoulder stabilisation, restoration of abduction and external rotation are important as more distal functions will be affected by the shoulder situation. ⋯ Combined nerve transfer by using the spinal accessory nerve for suprascapular nerve neurotisation and one of the triceps nerve branches for axillary nerve and teres minor branch neurotisation is an excellent choice for shoulder abduction and external rotation restoration.
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To determine whether transfer to only the anterior branch of the axillary nerve will restore useful function after axillary nerve injury with persistent posterior deltoid and teres minor paralysis. ⋯ By quantifying the biomechanical role of muscles during submaximal movement, in addition to quantifying muscle contributions to maximal shoulder strength, we can inform preoperative planning and permit more accurate predictions of functional outcomes.
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Annals of neurology · Feb 2013
Matrix metalloproteinase 3 deletion preserves denervated motor endplates after traumatic nerve injury.
Traumatic peripheral nerve injuries often produce permanent functional deficits despite optimal surgical and medical management. One reason for the impaired target organ reinnervation is degradation of motor endplates during prolonged denervation. Here we investigate the effect of preserving agrin on the stability of denervated endplates. Because matrix metalloproteinase 3 (MMP3) is known to degrade agrin, we examined the changes in endplate structure following traumatic nerve injury in MMP3 knockout mice. ⋯ These results demonstrate a critical role for MMP3 in motor endplate remodeling, and reveal a potential target for therapeutic intervention to prevent motor endplate degradation following nerve injury.
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Experimental neurology · Feb 2013
Comparative StudyDifferential effects of activity dependent treatments on axonal regeneration and neuropathic pain after peripheral nerve injury.
Activity treatments are useful strategies to increase axonal regeneration and functional recovery after nerve lesions. They are thought to benefit neuropathy by enhancing neurotrophic factor expression. Nevertheless the effects on sensory function are still unclear. ⋯ ES speeded up expression of BDNF and GDNF in DRG, and of BDNF and NT3 in the ventral horn. TR reduced the levels of pro-nociceptive factors such as BDNF, NGF and GDNF in DRG. Combination of ES and TR induced intermediate levels suggesting an optimal balancing of treatment effects.
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Neuropathic pain is a highly debilitating chronic pain state that is a consequence of nerve injury or of diseases such as diabetes, cancer, infection, autoimmune disease, or trauma. Neuropathic pain is often resistant to currently available analgesics. There is a rapidly growing body of evidence indicating that signalings from spinal microglia play crucial roles in the pathogenesis of neuropathic pain. ⋯ Inhibiting function or expression of these microglial molecules strongly suppresses pain hypersensitivity to innocuous mechanical stimuli (tactile allodynia), a hallmark symptom of neuropathic pain. A recent study also reveals that the transcription factor IRF8 (interferon regulatory factor 8) is a critical regulator of the nerve injury-induced gene expression in microglia. The present review article highlights the recent advances in our understanding of spinal microglia in neuropathic pain.