Articles: peripheral-nerve-injuries.
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The purpose of this review is to summarize the basic science literature related to chronic nerve injuries, and to then use this as the background to provide emerging insights into the promising role of cellular therapy for nerve injury repair. ⋯ There are several avenues of stem cell-based approaches to peripheral nerve repair. One of these, skin-derived precursor cells, are easily accessible, autologous adult stem cells that can survive and myelinate in the peripheral nerve environment and become SC-like in their apparent differentiation.
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Oral Maxillofac Surg Clin North Am · Feb 2009
ReviewNerve injuries and treatment in facial cosmetic surgery.
Surgical intervention remains a popular choice in patients seeking facial rejuvenation. Although uncommon, temporary or permanent peripheral nerve injury may complicate almost any type of invasive aesthetic procedure of the face, resulting in functional and psychological consequences for patients. ⋯ Depending on the type of injury, various interventions may range from observation and close follow-up to interposition nerve grafting. This article reviews the pertinent anatomy of nerves at risk in facial cosmetic surgery and discusses various management strategies for inadvertent injury to peripheral nerves of the face.
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Review
Transplantation of autologous Schwann cells for the repair of segmental peripheral nerve defects.
Peripheral nerve injuries are a source of chronic disability. Incomplete recovery from such injuries results in motor and sensory dysfunction and the potential for the development of chronic pain. The repair of human peripheral nerve injuries with traditional surgical techniques has limited success, particularly when a damaged nerve segment needs to be replaced. ⋯ The authors sought to determine whether the use of SC-filled channels is superior or equivalent to strategies that are currently used clinically (for example, autologous nerve grafts). Finally, although many nerve repair paradigms demonstrate evidence of regeneration within the AGC, the authors further sought to determine if the regeneration observed was physiologically relevant by including electrophysiological, behavioral, and pain assessments. If successful, the development of this reparative approach will bring together techniques that are readily available for clinical use and should rapidly accelerate the process of bringing an effective nerve repair strategy to patients with peripheral nerve injury prior to the development of pain and chronic disability.
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The concept of the nerve tube has been a major topic of research in the field of peripheral nerve regeneration for more than 25 years. The first nerve tubes are currently available for clinical use. This article gives an overview of the experimental and clinical data on nerve tubes for peripheral nerve repair and critically analyzes the data on which the step from laboratory to clinical use is based. In addition, it briefly discusses the different modifications to the common single lumen nerve tubes that may improve the results of generation.
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Review
Pain relief by gabapentin and pregabalin via supraspinal mechanisms after peripheral nerve injury.
The antihypersensitivity actions of gabapentin and pregabalin have been well characterized in a large number of studies, although the underlying mechanisms have yet to be defined. We have been focusing on the supraspinal structure as a possible site for their action and have demonstrated that intracerebroventricular (i.c.v.) administration of gabapentin and pregabalin indeed decreases thermal and mechanical hypersensitivity in a murine chronic pain model involving partial ligation of the sciatic nerve. This novel supraspinally mediated analgesic effect was markedly suppressed by either depletion of central noradrenaline (NA) or blockade of spinal alpha(2)-adrenergic receptors. ⋯ Moreover, gabapentin did not reduce IPSCs in slices taken from mice given a sham operation. Although gabapentin altered neither the amplitude nor the frequency of miniature IPSCs, it reduced IPSCs together with an increase in the paired-pulse ratio, suggesting that gabapentin acts on the presynaptic GABAergic nerve terminals in the LC. Together, the data suggest that gabapentin presynaptically reduces GABAergic synaptic transmission, thereby removing the inhibitory influence on LC neurons only in neuropathic pain states, leading to activation of the descending noradrenergic system.