Intraoperative Neuromonitoring in Thyroid and Parathyroid Surgery.

Background: It has been reported that the incidence of recurrent laryngeal nerve (RLN) injury is higher in an operational procedure in the thyroid and parathyroid region. Elevating voice pitch is achieved by the cricothyroid contraction, which in turn is innervated by the external branch of the superior laryngeal nerve (EBSLN). Due to the subtle nature and clinical variability of EBSLN damage, diagnosis may be difficult. The use of intraoperative neuromonitoring (IONM) as a supplement to enhance surgical identification in thyroid and parathyroid operation appeared to have collected momentum with operators. Methods: IONM clinical usage rationale, efficiency, and safety profile are discussed in this overview in thyroid and parathyroid surgery. Results: IONM usage incurred numerous skepticisms in decreasing the frequency of EBSLN or RLN injury. However, a recent article has shown the efficacy and benefits of using IONM in thyroid and parathyroid procedures. IONM facilitates the recognition of RLN and EBSLN, verifies its functional integrity, localizes the site of a nerve injury, and gives postsurgical function feedback. This technique has been successful in reducing rates of bilateral laryngeal paralysis, with the elevated safety profile for surgical patients. Conclusions: It is recommended using IONM in all thyroidectomies and in high-risk parathyroidectomies.

Both PI3K/Akt and ERK1/2 pathways participate in the protection by dexmedetomidine against transient focal cerebral ischemia/reperfusion injury in rats.

Dexmedetomidine (Dex) has been demonstrated to provide neuroprotection against ischemia/reperfusion (I/R) injury. However, the exact mechanism of this protection remains unknown. Here, we explored the neuroprotective effect of Dex in rats exposed to cerebral I/R-induced by middle cerebral artery occlusion (MCAO) and the role of phosphatidylinositol 3-kinase (PI3K)/Akt, extracellular signal-regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase-3ß (GSK-3ß) in this protective action. Adult male Sprague-Dawley rats were subjected to MCAO for 90 min followed by reperfusion for 24h and Dex (15 µg/kg, i.v.) was administered immediately after the onset of MCAO. The neurological deficit score, cerebral infarct volume, brain edema, and neuron survival were evaluated at 24h of reperfusion. The effect of Dex on p-Akt, p-ERK1/2 and p-GSK-3ß expression in the ischemic hemisphere was assayed by Western blot. Treatment of rats exposed to I/R with Dex caused not only marked reduction in the neurological deficit score, cerebral infarct volume, and brain edema (P <0.01 vs. I/R alone), but also a decrease in neuron death in hippocampal CA1 and cortex (P<0.01 vs. I/R alone). The Dex-induced increment of neuron survival in the ischemic CA1 and cortex was diminished by the PI3K inhibitor LY294002 and the MEK inhibitor U0126. The increasing expressions of p-Akt and p-ERK1/2 induced by Dex in the ischemic hemisphere were markedly inhibited by LY294002 (or wortmannin) and U0126 (or PD98059), respectively. The up-regulation of p-GSK-3ß by Dex in the ischemic hemisphere was significantly decreased by both LY294002 (or wortmannin) and U0126 (or PD98059). Our data demonstrated that treatment with Dex reduced cerebral injury in rats exposed to transient focal I/R, and this was mediated by the activation of the PI3K/Akt and ERK1/2 pathways as well the phosphorylation of downstream GSK-3ß.