Department of Anaesthesia, Perioperative Medicine and Critical Care, Clínica Universidad de Navarra, Pamplona, Spain; Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain.
University of Navarra, CIMA, Program of Neuroscience, Systems Neuroscience Lab, Pamplona, Spain; Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain.
Br J Anaesth. 2021 Aug;127(2):245-253. doi: 10.1016/j.bja.2021.01.036. Epub 2021 Apr 23.
Dexmedetomidine is frequently used for sedation during deep brain stimulator implantation in patients with Parkinson's disease, but its effect on subthalamic nucleus activity is not well known. The aim of this study was to quantify the effect of increasing doses of dexmedetomidine in this population.
Controlled clinical trial assessing changes in subthalamic activity with increasing doses of dexmedetomidine (from 0.2 to 0.6 μg kg h) in a non-operating theatre setting. We recorded local field potentials in 12 patients with Parkinson's disease with bilateral deep brain stimulators (24 nuclei) and compared basal activity in the nuclei of each patient and activity recorded with different doses. Plasma levels of dexmedetomidine were obtained and correlated with the dose administered.
With dexmedetomidine infusion, patients became clinically sedated, and at higher doses (0.5-0.6 μg kg h) a significant decrease in the characteristic Parkinsonian subthalamic activity was observed (P<0.05 in beta activity). All subjects awoke to external stimulus over a median of 1 (range: 0-9) min, showing full restoration of subthalamic activity. Dexmedetomidine dose administered and plasma levels showed a positive correlation (repeated measures correlation coefficient=0.504; P<0.001).
Patients needing some degree of sedation throughout subthalamic deep brain stimulator implantation for Parkinson's disease can probably receive dexmedetomidine up to 0.6 μg kg h without significant alteration of their characteristic subthalamic activity. If patients achieve a 'sedated' state, subthalamic activity decreases, but they can be easily awakened with a non-pharmacological external stimulus and recover baseline subthalamic activity patterns in less than 10 min.
EudraCT 2016-002680-34; NCT-02982512.
在帕金森病患者的深部脑刺激器植入术中，常使用右美托咪定进行镇静，但它对丘脑底核活动的影响尚不清楚。本研究的目的是量化在该人群中增加右美托咪定剂量的效果。
在非手术环境中，评估了在 12 名双侧深部脑刺激器的帕金森病患者中，随着右美托咪定剂量（从 0.2 增加到 0.6μg/kg/h）的增加，丘脑底核活动的变化。我们记录了每位患者的 24 个核的局部场电位，并比较了每个核的基础活动和不同剂量下记录的活动。获得了右美托咪定的血浆水平，并与给予的剂量相关联。
随着右美托咪定输注，患者出现临床镇静，在较高剂量（0.5-0.6μg/kg/h）时观察到典型的帕金森丘脑底核活动明显下降（β活动 P<0.05）。所有患者在中位数为 1（范围：0-9）分钟内对外界刺激苏醒，表现出丘脑底核活动的完全恢复。给予的右美托咪定剂量和血浆水平呈正相关（重复测量相关系数=0.504；P<0.001）。
在帕金森病的丘脑底核深部脑刺激器植入术中需要一定程度镇静的患者，可能可以接受高达 0.6μg/kg/h 的右美托咪定，而不会显著改变其典型的丘脑底核活动。如果患者达到“镇静”状态，丘脑底核活动减少，但可以用非药物性外部刺激很容易唤醒，并在 10 分钟内恢复基线丘脑底核活动模式。
EudraCT 2016-002680-34；NCT-02982512。
