ec50 of dexmedetomidine in deep brain stimulation implantation of patients with parkinson's disease

Conditions: PD - Parkinson's Disease

Summary: dexmedetomidine (dex) sedation is widely used in deep brain stimulation implantation (dbsi) of patients with parkinson's disease. however, intraoperative application of dex may affect the discharge activity of deep brain nuclei and reduce the discharge frequency of subthalamic nucleus (stn) neurons. at present, there is still a lack of prospective intervention research to explore the optimal dose that does not affect mer mapping in patients with parkinson's disease. the present study uses the dixon and massey up-and-down method to analyze the ec50 of dex in patients with pd undergoing stn-dbs sedation, to clarify the balance meets the sufficient comfort of patients without affecting the accurate target of mer and the optimal dosage of dex for boundary recognition.

deep brain stimulation (dbs) is an effective treatment to improve the motor symptoms of parkinson's disease (pd). subthalamic nucleus (stn) is one of the most commonly used targets in the treatment of pd-dbs. the accuracy of the final implantation position of deep brain electrodes is the key to the success of surgery. sedation-awake-sedation anesthesia is widely used in dbs. dexmedetomidine (dex) mainly acts on the central locus coeruleus nucleus and spinal cord α receptor, which has sedative and analgesic effect and little respiratory inhibition. dex can produce natural non eye movement sleep that is conducive to the recovery of the body. within a certain dose range, patients are easy to wake up and have the characteristics of conscious sedation. patients can make corresponding actions according to the instructions of neurosurgeons and cooperate with doctors to complete the operation. its sedative safety has been confirmed. however, intraoperative application of dex may delay the recovery of cognitive function, affect the discharge activity of deep brain nuclei and reduce the discharge frequency of stn neurons, even after stopping the use of sedatives. the result may be related to the residual effect of sedatives. dex can reduce the activity of stn neurons in a dose-dependent manner. a smaller dose of dex may not meet the effects of surgical sedation and analgesia, and the effect of high concentration is better than that of low concentration. some existing studies have recommended a reasonable dose range of dex for dbs, but these studies have a small number of research populations, and of great heterogeneity in target selection, anesthetic dose and strategy. at present, there is still a lack of prospective intervention research to explore the optimal dose that the application of dex sedation does not affect mer mapping in patients with parkinson's disease. the present study uses the up and down method to analyze the ec50 and ec95 of dex in patients with pd undergoing stn-dbs sedation, to clarify the balance meets the sufficient comfort of patients without affecting the accurate target of mer and the optimal dosage of dex for boundary recognition.

Eligibility criteria:
inclusion criteria: 1. 50-80 years old, asa grade ii-iii; 2. bilateral stn-dbs of patients with parkinson's disease; 3. signed informed consent. exclusion criteria: 1. obstructive sleep apnea; 2. bmi \> 30kg/m2; 3. estimated difficult airway; 4. severe preoperative anxiety; 5. serious dysfunction of important organs such as heart, liver and kidney; 6. previous allergy to dexmedetomidine; 7. pregnant or lactating women.