Dexmedetomidine on Basal Ganglia Neuronal Activity in Parkinson's Disease

Overview

The implantation of a deep brain stimulator (DBS) is an established option to improve the symptoms of Parkinson's disease (PD) in patients that do not respond adequately to medical therapy. Most centers perform this surgery using a technique that involves microelectrode recording (MER) of neuronal activity for localization of the target nucleus, microstimulation of identified targets, and neurological intraoperative testing in a cooperative patient. Dexmedetomidine, a α2-adrenergic receptors agonist, is a potent anxiolytic that acts at subcortical areas of the brain without involving GABA receptors. It provides excellent sedation without respiratory depression; also, it has an analgesic component and a predictable hemodynamic response. Low maintenance doses do not appear to interfere with MER. The possible effect of dexmedetomidine in the PD symptoms is still unclear.

The implantation of a deep brain stimulator (DBS) is an established option to improve the symptoms of Parkinson's disease (PD) in patients that do not respond adequately to medical therapy. Most centers perform this surgery using a technique that involves microelectrode recording (MER) of neuronal activity for localization of the target nucleus, microstimulation of identified targets, and neurological intraoperative testing in a cooperative patient. This surgery is usually performed in two stages. In the first stage, and under conscious sedation (CS), the target nucleus is localized and the DBS is implanted. About 5 days later, and under general anaesthesia, a programmable pulse generator is implanted and connected to the DBS. The anesthetic approach varies depending on the institution, ranging from local anesthesia only with monitored care, conscious sedation, and the "asleep-awake" or "asleep-awake-asleep" technique. But sedative drugs can affect the quality of MER by suppressing the firing rate of basal ganglia structures, and alter PD symptoms. Propofol is the drug most commonly used. Its real influence on the quality of MER and PD symptoms is still today controversial. In recent years, some studies have suggested using dexmedetomidine as the main sedative agent for this intervention. Dexmedetomidine, a α2-adrenergic receptors agonist, is a potent anxiolytic that acts at subcortical areas of the brain without involving GABA receptors. It provides excellent sedation without respiratory depression; also, it has an analgesic component and a predictable hemodynamic response. Low maintenance doses do not appear to interfere with MER. The possible effect of dexmedetomidine in the PD symptoms is still unclear. All these characteristics make it a good choice for sedation of PD patients undergoing DBS surgery. Studying the influence of anesthetic drugs on basal ganglia activity and PD motor symptoms in humans and in a clinical setting is complicated. First, it is difficult to establish a control group to compare effects in different nuclei. There is some data concerning clinical outcomes (clinical symptoms or long term stimulation parameters) but without electrophysiological data. MERs data has been compared between different patients or in the same patient but between contralateral targets. Few studies analyze electrophysiological data with or without one sedative drug in the same target.