Articles: peripheral-nerve-injuries.
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Abnormal pain-related behaviour that accompanies peripheral nerve injury may be the result of altered spinal neuronal function. The long-term loss of inhibitory function by GABA neurons in particular may be a mechanism by which abnormal neural hyperactivity occurs, leading to exaggerated sensory processing following nerve injury. In order to assess this, changes in spinal GABA immunoreactivity at several time points following constriction nerve injury were quantified in parallel with behavioural assessments of abnormal sensory responses to noxious and innocuous stimuli. ⋯ Parallel improvements in sensory responses to innocuous and noxious stimuli were also observed in these animals. The results of this study indicate that peripheral nerve injury can result in severe losses in spinal inhibitory mechanisms, possibly leading to exaggerated sensory processes in persistent pain states. In addition, adrenal medullary transplants may provide a neuroprotective function in promoting recovery and improving long-term survival of GABAergic neurons in the spinal dorsal horn which have been damaged by excitotoxic injury.
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Brain-derived neurotrophic factor (BDNF) is produced in Schwann cells and fibroblasts in the peripheral nerve, and is considered to play an important role in survival, maintenance, development and repair of the peripheral neuron. In this study, the effect of human recombinant BDNF on the regeneration of nerve fibers following a crush injury to the sciatic nerves of Sprague-Dawley rats was evaluated. In the experimental group, 20 mg/kg of BDNF was injected subcutaneously three times a week for 4 weeks in seven rats. ⋯ Therefore, BDNF may promote the myelination. However, such an effect on myelination seems not to be clinically significant, because such an effect was not demonstrated in other morphometric evaluations reflecting the myelination condition. Therefore, taking all the data obtained in this study into consideration, we concluded that there was no definite evidence that BDNF promoted the regeneration of nerve fibers at least under these experimental conditions.
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Autotomy in experimental animals following peripheral nerve section has been interpreted as a sign of pain corresponding to the chronic pain observed in patients with extensive nerve lesions. Such pain may be alleviated by spinal cord stimulation. In the present study, the effect of such stimulation, via chronically implanted electrodes, on autotomy behavior following sciatic nerve section was assessed in the rat. ⋯ It seems that spinal cord stimulation, albeit applied only once daily and during a limited time period, can protect the spinal cord from developing the state of hyperexcitability believed to be the major cause of autotomy behavior. Peripheral mechanisms may also play a role by the antidromic activity evoked by the stimulation in the sectioned peripheral nerve. This study shows that spinal cord stimulation, which is a commonly employed method for treating chronic neurogenic pain, may have long-lasting effects on plasticity changes in the spinal cord following peripheral nerve injury, even when the stimulation is applied for short periods of time.
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We describe the clinical application and utility of high-resolution magnetic resonance neurography (MRN) techniques to image the normal fascicular structure of peripheral nerves and its distortion by mass lesions or trauma in the lower extremity. ⋯ MRN proved useful in the preoperative evaluation and planning of surgery in patients with peripheral nerve lesions.