Dexmedetomidine improves cognition after carotid endarterectomy by inhibiting cerebral inflammation and enhancing brain-derived neurotrophic factor expression

Carotid endarterectomy (CEA) is a classical method for prevention of life-threatening strokes in patients with severe internal carotid artery stenosis (ICA), regardless of symptoms.1,2 However, there is increasing evidence that subtle cognitive dysfunction may occur in 27%–31% of patients after CEA; this may be caused by cerebral perfusion deficiency related to hemodynamic changes and cerebral emboli, as well as a variety of individual factors.3–5 Brain-derived neurotrophic factor (BDNF) is a well-known member of the neurotrophic family of growth-promoting proteins, which is essential to neuronal survival, axon growth, and synaptic plasticity.6 Elevation of BDNF in the central nervous system is known to prevent hypoxic neuronal death in animal models of stroke,7 and has been implicated in learning and memory processes,8 as well as other advanced neuronal functions. Moreover, BDNF can be detected in blood, and a direct correlation has been observed between cortical and serum levels of BDNF.9–11 Thus, the serum BDNF level may serve as an indicator of changes in BDNF levels in the central nervous system. Dexmedetomidine (DEX) is a highly selective agonist of α2-adrenergic receptors with multiple effects on the human brain, including clinical sedation, anesthesia, and analgesia.12 Moreover, DEX has drawn widespread attention for its neuroprotective effects against stroke in animal models through its actions on α2-adrenergic receptors13–16; this neuroprotection is partly related to the DEX-induced elevation of BDNF levels in the cortex and hippocampus,17,18 as well as concurrent anti-inflammatory effects.19 However, for patients who have undergone CEA, the impacts of DEX on cognition and plasma BDNF level have not yet been determined. Based on the above considerations, we hypothesized that DEX may improve cognition in aged patients after CEA. Here, we aimed to determine the effects of DEX administered intravenously during CEA on postoperative cognitive function, and to assess cerebral inflammation and plasma levels of BDNF, in order to elucidate whether DEX can prevent cognitive dysfunction in patients undergoing CEA.