Articles: peripheral-nerve-injuries.
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Anasthesiol Intensivmed Notfallmed Schmerzther · May 2012
Review[Nerve injury due to peripheral nerve blocks: Pathophysiology and aetiology].
Permanent nerve injury as a complication of peripheral regional anaesthesia is fortunately rare with an estimated incidence of 0,03%. However, transient neurological symptoms are more frequent with an occurrence of 3-8%. ⋯ Regarding pathophysiology, trauma-related inflammation should be acknowledged as an important interference during nerve recovery. Needle-nerve contacts, nerve perforation and local cytotoxicity of local anaesthetics should be reduced to a minimum by application of nerve stimulation, ultrasound and an adequate dosage of local anaesthetics with less locotoxicity.
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Anasthesiol Intensivmed Notfallmed Schmerzther · May 2012
Review[Nerve injuries associated with nerve blocks: clinic and incidence].
Persistent nerve injuries in context of peripheral nerve blocks are uncommon. Previous surveys and prospectively designed studies have specified neurological dysfunctions in different ways, which may cause the variability of data about incidence; so it has to be reckoned with about 5% after 1 week, 1% after 1 month and 0,01% after 6 months. ⋯ Dysfunctions manifest as numbness, parasthesia, tingling sensation and/or amyasthenia. Fortunately long-term lesions, caused by nerve blocks are a rarity.
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Several nerve guidance conduits (NGCs) and nerve protectant wraps are approved by the US Food and Drug Administration (FDA) for clinical use in peripheral nerve repair. These devices cover a wide range of natural and synthetic materials, which may or may not be resorbable. ⋯ In this context, this review provides a comprehensive reference for clinicians which may facilitate optimal material/device selection for peripheral nerve repair. For materials scientists, this review highlights predicate devices and evaluation methodologies, offering an insight into current deficiencies associated with state-of-the-art materials and may help direct new technology developments and evaluation methodologies thereof.
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Experimental neurology · Apr 2012
ReviewATP receptors gate microglia signaling in neuropathic pain.
Microglia were described by Pio del Rio-Hortega (1932) as being the 'third element' distinct from neurons and astrocytes. Decades after this observation, the function and even the very existence of microglia as a distinct cell type were topics of intense debate and conjecture. However, considerable advances have been made towards understanding the neurobiology of microglia resulting in a radical shift in our view of them as being passive bystanders that have solely immune and supportive roles, to being active principal players that contribute to central nervous system pathologies caused by disease or following injury. ⋯ Microglia express several P2 receptor subtypes, and of these the P2X4, P2X7, and P2Y12 receptor subtypes have been implicated in neuropathic pain. The P2X4 receptor has emerged as the core microglia-neuron signaling pathway: activation of this receptor causes release of brain-derived neurotrophic factor (BDNF) which causes disinhibition of pain-transmission neurons in spinal lamina I. The present review highlights recent advances in understanding the signaling and regulation of P2 receptors expressed in microglia and the implications for microglia-neuron interactions for the management of neuropathic pain.
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Experimental neurology · Apr 2012
ReviewPurinergic systems, neuropathic pain and the role of microglia.
We have learned various data on the role of purinoceptors (P2X4, P2X7, P2Y6 and P2Y12) expressed in spinal microglia and several factors that presumably activate microglia in neuropathic pain after peripheral nerve injury. Purinergic receptor-mediated spinal microglial functions make a critical contribution to pathologically enhanced pain processing in the dorsal horn. Microglial purinoceptors might be promising targets for treating neuropathic pain. A predicted therapeutic benefit of interfering with microglial purinergic receptors may be that normal pain sensitivity would be unaffected since expression or activity of most of these receptors are upregulated or enhanced predominantly in activated microglia in the spinal cord where damaged sensory fibers project.