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Received Jul 21, 2017; Revised Sep 18, 2017; Accepted Oct 1, 2017
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1. Introduction
Peripheral nerve injury requires a long recovery period, and recovery, once attained, usually is incomplete [1]. Peripheral nerve damage can, by manifesting as serious disability, negatively impact upon patients’ daily life as well as quality of life (QoL). Indeed, patients might lose as much as 21% of their accustomed daily activities, and such activity loss is strongly associated with depression. And certainly, the higher the pain, disability, and depression levels, the worse the QoL [2, 3]. Crush injuries are more likely to be accompanied by peripheral nerve injuries, which are sustained most commonly by young people aged between 21 and 30 [4]. Management for recovery of peripheral nerve injury is important in terms of not only QoL but also medical (and therefore social) costs.
Dexmedetomidine (DXM), a selective α2-adrenergic receptor agonist that has an eightfold affinity to the receptor relative to clonidine, has anxiolytic, sedative, and analgesic effects. Widely used in anesthesia and intensive care medicine, DXM’s characteristic sedative effect appears without respiratory suppression. Its most common side effects are bradycardia and hypotension. Animal models and human studies show evidence of potential neuroprotective effects on the brain [5]. In the developing rat brain, for example, DXM contributes to neuroprotection via effectively reducing ketamine-induced or propofol-induced neuroapoptosis [6, 7].
However, whereas its neuroprotective effects have been well documented, there is as yet no data on any peripheral nerve neuroprotective effects. If it can...