Articles: peripheral-nerve-injuries-physiopathology.
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Background Acute pain is a warning mechanism that exists to prevent tissue damage, however pain can outlast its protective purpose and persist beyond injury, becoming chronic. Chronic Pain is maladaptive and needs addressing as available medicines are only partially effective and cause severe side effects. There are profound differences between acute and chronic pain. ⋯ On one hand the delivery of neuron-derived miR-21 to macrophages for example, polarises these cells towards a pro-inflammatory/pro-nociceptive phenotype; on the other hand, silencing miR-21 expression in sensory neurons prevents both development of neuropathic allodynia and recruitment of macrophages in the DRG. Immune system mechanisms in the central nervous system In the dorsal horn of the spinal cord, growing evidence over the last two decades has delineated signalling pathways that mediate neuron-microglia communication such as P2X4/BDNF/GABAA, P2X7/Cathepsin S/Fractalkine/CX3CR1, and CSF-1/CSF-1R/DAP12 pathway-dependent mechanisms. Conclusions and implications Definition of the modalities by which neuron and immune cells communicate at different locations of the pain pathway under neuropathic pain states constitutes innovative biology that takes the pain field in a different direction and provides opportunities for novel approaches for the treatment of chronic pain.
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Outcome after nerve repair of the hand needs standardized psychometrically robust measures. We aimed to systematically review the psychometric properties of available functional, motor, and sensory assessment instruments after nerve repair. ⋯ Few studies included nerve repair in their sample for the psychometric analysis of outcome measures, so moderate evidence could be confirmed. Manual muscle test and Rotterdam Intrinsic Hand Myometer dynamometer had excellent reliability but insufficient data on validity or responsiveness. Touch threshold testing was more responsive than 2PD test. The locognosia test and STI had limited but positive supporting data related to validity. Rosén-Lundborg score had emerging evidence of reliability and validity as a comprehensive outcome following nerve repair. Few questionnaires were considered reliable and valid to assess cold intolerance. There is no patient-reported outcome measurement following nerve repair that provides comprehensive assessment of symptoms and function by patient perspective.
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Neuropathic pain (NP) is caused by lesions of the peripheral fibers and central neurons in the somatosensory nervous system and affects 7-10% of the general population. Although the distinct cause of neuropathic pain has been investigated in primary afferent neurons over the years, pain modulation by central sensitization remains controversial. NP is believed to be driven by cell type-specific spinal synaptic plasticity in the dorsal horn. ⋯ These impairments in GABAergic interneurons may be associated with dysfunctional autophagy, resulting in neuropathic pain. Here, we review an emerging number of investigations that suggest a pivotal role of impaired autophagy of GABAergic interneurons in NP. We discuss relevant research spurring the development of new targets and therapeutic agents of NP and emphasize the need for a multidisciplinary approach to manage NP in the future.
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Regarding nerves as simple cables and electrical conduits is a gross error that does not allow us to understand the anomalies and disorders observed postoperatively. Instead, nerves should be seen as a living tissue of which physiological regulation is as complex as that of the blood-brain barrier. This review describes the basic structure and functions of this blood-nerve barrier and highlights the mechanisms of its breakdown and the resultant disorders. ⋯ This blood supply can adapt in a variety of ways but when these possibilities of adaptation are exceeded, tissue ischaemia may be more extensive. Also, even after the initial injury has subsided, inflammation can cause a secondary insult. This could be particularly important in some patients with subclinical neuropathy.
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Reg Anesth Pain Med · Sep 2015
ReviewPathophysiology and Etiology of Nerve Injury Following Peripheral Nerve Blockade.
This review synthesizes anatomical, anesthetic, surgical, and patient factors that may contribute to neurologic complications associated with peripheral nerve blockade. Peripheral nerves have anatomical features unique to a given location that may influence risk of injury. Peripheral nerve blockade-related peripheral nerve injury (PNI) is most severe with intrafascicular injection. Surgery and its associated requirements such as positioning and tourniquet have specific risks. Patients with preexisting neuropathy may be at an increased risk of postoperative neurologic dysfunction. Distinguishing potential causes of PNI require clinical assessment and investigation; a definitive diagnosis, however, is not always possible. Fortunately, most postoperative neurologic dysfunction appears to resolve with time, and the incidence of serious long-term nerve injury directly attributable to peripheral nerve blockade is relatively uncommon. Nonetheless, despite the use of ultrasound guidance, the risk of block-related PNI remains unchanged. ⋯ Since the 2008 Practice Advisory, new information has been published, furthering our understanding of the microanatomy of peripheral nerves, mechanisms of peripheral nerve injection injury, toxicity of local anesthetics, the etiology of and monitoring methods, and technologies that may decrease the risk of nerve block-related peripheral nerve injury.