Therefore, while nerve injury may have laid the foundation for World War I, treatments for PNIs were vastly improved by innovative surgeons during the war.Īlthough PNS axons have the capacity to regrow, functional recovery in humans is often incomplete. Nerve grafting, which is the current gold standard for PNIs with gaps, was refined during this time. It is bittersweet irony that many of the most effective treatments for peripheral nerve injury (PNI) were developed during the war: 18% of extremity injuries included trauma to peripheral nerves, allowing physicians to experiment with new therapies. Therefore, obstetric brachial plexus injury - and events precipitated by the injury - were instrumental in moulding the Kaiser's perspective and character which ultimately may have started a devastating world war. His mother, Victoria, favoured her healthier children over her flawed eldest son, which created deep-seated insecurities and bitterness in the future Kaiser. According to historical records ( but see ), the Kaiser's petulant and outspoken demeanour had foundations laid during childbirth: complications during his breech delivery likely caused injury to his brachial plexus nerves, which led to a permanently limp left arm. Rather than acting with diplomacy, Kaiser Wilhelm II - leader of Germany and Prussia - engaged in warfare with Serbia, ultimately starting World War I. In 1914, Austria's Archduke Ferdinand was assassinated in Sarajevo. Future research will help determine how to manipulate PNS and CNS inflammatory responses in order to improve tissue repair and functional recovery. Rather than efficiently removing debris before resolving the inflammatory response as in other tissues, macrophages infiltrating the CNS exacerbate cell death and damage by releasing toxic pro-inflammatory mediators over an extended period of time. The efficacy of the PNS inflammatory response (although transient) stands in stark contrast with that of the CNS, where the response of nearby cells is associated with inhibitory scar formation, quiescence, and degeneration/apoptosis. Macrophages take over the bulk of phagocytosis within days of PNI, before exiting the nerve by the circulation once remyelination has occurred. Denervated Schwann cells respond to injury by shedding myelin, proliferating, phagocytosing debris, and releasing cytokines that recruit blood-borne monocytes/macrophages. The inflammatory response is initiated by axonal disintegration in the distal nerve stump: this causes blood-nerve barrier permeabilization and activates nearby Schwann cells and resident macrophages via receptors sensitive to tissue damage. In addition to requiring a robust regenerative response from the injured neuron itself, successful axon regeneration is dependent on the coordinated efforts of non-neuronal cells which release extracellular matrix molecules, cytokines, and growth factors that support axon regrowth. Therefore, studying PNI could be instructive for both improving PNS regeneration and recovery after CNS injury. In addition, the growth-supportive milieu of PNS axons is not sustained over time, precluding long-distance regeneration. Nevertheless, peripheral nervous system (PNS) axon regrowth is hampered by nerve gaps created by injury. In contrast with central nervous system (CNS) axons, those in the periphery have the remarkable ability to regenerate after injury. We then consider the initiation, progression, and resolution of the cellular inflammatory response after PNI, before comparing the PNI inflammatory response with that induced by spinal cord injury (SCI). In this review, we first provide a brief historical perspective, discussing how peripheral nerve injury (PNI) may have caused World War I.
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