A Review of the Biological Mechanisms of Dexmedetomidine for Postoperative Neurocognitive Disorders

Abstract

Postoperative neurocognitive disorders are common neurological complications following surgery that are generally characterized by varying degrees of cognitive impairment. Postoperative neurocognitive disorders can exhibit as short-term postoperative delirium and/or long-term postoperative cognitive dysfunction. In addition, postoperative neurocognitive disorders may result in poor outcomes in patients, and are a leading cause of postoperative morbidity and mortality, particularly in elderly patients. Recently, there has been a heightened interest in mechanisms and clinical treatments for postoperative neurocognitive disorders. Though some influencing factors and mechanisms of postoperative neurocognitive disorders have been revealed, they remain troublesome problems in clinical departments. Dexmedetomidine is a commonly used anesthetic adjuvant that may help improve postoperative cognitive impairment, especially the conditions of a postoperative acute event (postoperative delirium, within 1 week after operation) and delayed neurocognitive recovery (postoperative cognitive dysfunction, up to 30 days). In the recent literature, dexmedetomidine has been shown to exert positive effects on cognitive impairment in clinical and animal studies, especially for postoperative neurocognitive disorders. However, not all clinical findings support this efficacy. Though some mechanisms of dexmedetomidine on postoperative neurocognitive disorders have been proposed, such as signaling pathways associated with inflammation and apoptosis, this evidence is fragmentary and disputed in the literature. Therefore, this article aims to review the potential biological mechanisms underlying dexmedetomidine’s effects on postoperative neurocognitive disorders, providing a reference for future studies.

Effects of dexmedetomidine combined with dezocine on T lymphocytes, NK cells and cognitive function in elderly patients with gastrointestinal cancer after radical surgery

“…Dezocine and dexmedetomidine have been used in combination with lung cancer surgery patients. After surgery, the inflammatory factors of patients decreased and their cognitive function improved (16,17). Dezocine can up-regulate PD-L1 and activate the NF-κB pathway, promoting immune escape and glucose metabolism of LC.…”

Study on the application of dexmedetomidine in general anesthesia in elderly patients

“…The subsequent decrease in blood pressure and heart rate is due to the inhibition of central sympathetic outflow and stimulation of presynaptic α-2 receptors, resulting in reduced release of norepinephrine, resulting in a further decrease in blood pressure. [27,28] However, these hemodynamic effects may be harmful in patients with fixed stroke volume, patients using deceleration drugs such as β-blockers, digitalis, etc., and patients with hypovolemia. Dexmedetomidine causes a decrease in cerebral blood flow and cerebral oxygen metabolism requirements, as well as a slight decrease in intracranial pressure.…”

The effect on vital signs of concomitant administration of nicardipine and dexmedetomidine sedation after spinal anesthesia: A double-blind, randomized controlled trial

“…[3][4][5] Previous studies have been conducted on its use in treating insomnia, delirium, and postoperative cognitive dysfunction. [6][7][8][9] In addition, DEX does not suppress the patient's respiratory function and is a desirable option for sedation compared to other traditional agents. [10,11] DEX is administered as a loading dose followed by a maintenance dose.…”