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INTRODUCTION

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Preexisting disorders of the peripheral nervous system, central nervous system, and spinal canal present a unique challenge to both patients and anesthesiologists who desire to use regional anesthetic techniques. Because each of these clinical conditions involves compromise to neural structures, the concern is that further insult from surgical (eg, intraoperative stretch or compression, tourniquet ischemia, hemorrhage) or anesthetic (eg, mechanical trauma, vasoconstrictor-induced ischemia, local anesthetic toxicity) causes may result in new or worsening postoperative neurologic deficits.

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Regardless of the underlying etiology, the presence of chronic neural compromise secondary to mechanical (eg, spinal stenosis or compressive radiculopathy), ischemic (eg, peripheral vascular disease), toxic (eg, vincristine or cisplatin chemotherapy), metabolic (eg, diabetes mellitus), or autoimmune (eg, multiple sclerosis) derangements may place patients at increased risk of further neurologic injury.1,2,3 Upton and McComas1 were the first to describe the “double-crush phenomenon,” which suggests that patients with preexisting neural compromise may be more susceptible to injury at another site when exposed to a secondary insult (Figure 49–1). Secondary insults may include a variety of acute surgical or anesthetic risk factors, including those of regional anesthetic techniques. Osterman2 emphasized that not only are two low-grade insults along a peripheral nerve trunk worse than just one at a single site, but that the damage of the dual injury far exceeds the expected additive damage caused by each isolated insult. It may be further postulated that the second insult need not be along the peripheral nerve trunk itself, but rather at any point along the neural transmission pathway. Therefore, the performance of peripheral or neuraxial regional techniques in patients with preexisting neurologic disorders may place them at increased risk of the double-crush phenomenon.

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Figure 49–1.

Neural lesions resulting in denervation. Axoplasmic flow is indicated by the degree of shading. Complete loss of axoplasmic flow results in denervation (C, D, E). A: Normal neuron. B: Mild neuronal injury at a single site (x) is insufficient to cause denervation distal to the insult. C: Mild neuronal injury at two separate sites (x1 and x2) may cause distal denervation (ie, “double crush”). D: Severe neuronal injury at a single site (X) may also cause distal denervation. E: Axon with a diffuse, preexisting underlying disease process (toxic, metabolic, ischemic) may have impaired axonal flow throughout the neuron, which may or may not be symptomatic but predisposes the axon to distal denervation following a single minor neural insult at x (ie, “double crush”). (Reproduced with permission from Mayo Foundation for Medical Education and Research.)

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Unfortunately, the data available regarding any association of pre-existing neurologic disease and post-regional anesthesia dysfunction often conflicting in terms of outcomes and conclusions. As a result, definitive recommendations can rarely be made from the existing scientific literature. However, the following discussion provides a comprehensive review of the ...

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