Anesthesia for Deep Brain Stimulation

Parkinsons Disease Clinical Trial

Official title:

Anesthesia for Deep Brain Stimulation for the Treatment of Parkinsons Disease

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01789385
• Other study ID #: DILEKPARKINSON
• Status: Completed
• Phase: Phase 4
• First received: February 2, 2013
• Last updated: May 19, 2014
• Start date: February 2013
• Est. completion date: April 2013

Study information

• Verified date: February 2013
• Source: Diskapi Teaching and Research Hospital
• Contact: n/a
• Is FDA regulated: No
• Health authority: Turkey: Ministry of Health
• Study type: Interventional

Clinical Trial Summary

Deep brain stimulation for the treatment of Parkinson's disease has unique surgical stages and anesthesia needs. In the first stage the electrodes are inserted in the targeted brain areas and in the second stage the pulse generator is implanted. The technique for establishing sedation and analgesia for functional neurosurgery may differ among institutions. In this study it was aimed to investigate our anesthesia methods, intra-operative adverse events in the first stage of deep brain stimulation and the post operative pain therapy of the patients.

Description:

This study included patients underwent deep brain stimulation (DBS) in the treatment of patients with Parkinson disease (PD). After obtaining ethical approval and patient consent, consecutive patients underwent deep brain stimulation with a predetermined anesthesia protocol were studied.

The anesthetic procedure was explained to the patients in detail by the responsible anesthetist. Patients requiring general anesthesia, suffering from dementia, obstructive sleep apnea, gastroesophageal reflux and with a mallampati score>2, musculoskeletal problems causing difficulty with long term surgical positioning were excluded. The following parameters were recorded:Gender, age, body mass index (BMI), ASA classification, co existing diseases, anti Parkinson medications, sedative drugs and doses, level of conscious sedation, local anesthetic agents and doses, total duration of procedure, adverse events and complications, post operative pain therapy.

Preoperative sedation was not administered. At arrival in the operating room patients were monitored for heart rate (HR) non invasive blood pressures (systolic arterial pressure; SAP, diastolic arterial pressure; DAP, mean arterial pressure; MAP) peripheral oxygen saturation (SPO2), respiratory rate (RR), BIS, baseline values were recorded and recordings were continued with 5 min intervals. Urinary catheterization was not applied. Adequate attention was payed to assure all patients to be in a comfortable position. A peripheral intravenous catheter was inserted and Ringers lactate solution was infused 50-100 ml h-1. All patients received oxygen 2 L min-1 via a nasal cannula. Nasal airway, LMA and ET was prepared as rescue airway devices. Periods of SPO2 < 92 and a RR ≤ 8 min were documented. Maneuvers needed to manipulate airway patency was recorded. A 20% difference in the initial hemodynamic parameters and the use of hypotensive or inotrope, vasopressor medications were recorded.

Initial sedation was employed with a 1 mg kg-1min-1 loading dose of dexmedetomidine (Precedex®,Hospira Inc, Rocky Mountain, USA) for 10 minutes. Sedation was maintained with dexmedetomidine at a 0.2-0.8 mg kg-1h-1 infusion rate. Invasive blood pressure monitoring will be applied after sedation is commenced. After achieving an adequate sedation level which is defined as a BIS value of 65-85 and the Ramsay sedation score 3, the scalp block was performed as previously described by Girvin. A superficial cervical plexus block was also performed. Bupivacaine was used for the nerve blocks. Lidocaine was used for local anesthetic scalp infiltration in case of insufficient analgesia was observed during the insertion of the head pins or at any time the patient complained having pain. Ephedrine 1/200000 was added to the local anesthetics. Local anesthetic agents were diluted with equivalent volumes of saline (1/1 volume). The total doses of local anesthetics was recorded at the end of the procedure. Propofol was used with incremental intravenous boluses for rescue sedation when needed and the total dose will be documented. Sedation was discontinued before the micro electrode recordings (MER's) and macro stimulation. Time to emergence was defined as the time between the discontinuation of the sedatives and the time between the patients are able to cooperate with the neurologic examination. All intra-operative events and complications and complaints regarding pain and restlessness were documented. The total duration of the procedure includes initial sedation, performance of regional anesthesia, stereotactic frame insertion, magnetic resonance (MRI) or computerized tomography (CT) imaging, MER's, macro stimulation and closure.

After completion of procedure patients were transferred to the post anesthesia care unit (PACU). Postoperative pain was evaluated in the PACU at arrival and then at 1, 6, 12, 24 h using a 0-10 cm verbal analog scale (VAS)(zero: no pain, 10: maximal pain). Patients received 50 mg tramadol 8 hourly and PCA with morphine(5 mg loading dose, 2 mg bolus, 15 min lockout time) was initiated when the VAS ≥ 3. Morphine consumption was measured at 24 h.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 26
• Est. completion date: April 2013
• Est. primary completion date: April 2013
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 19 Years to 85 Years

Eligibility

Inclusion Criteria:

• Patients undergoing DBS for the treatment of PD

Exclusion Criteria:

• Patients required general anesthesia,

• suffered from dementia,

• obstructive sleep apnea,

• gastro esophageal reflux and with a mallampati score > 2,

• musculoskeletal problems causing difficulty with long term surgical positioning were excluded.

Study Design

Endpoint Classification: Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Related Conditions & MeSH terms

• Parkinson Disease
• Parkinsons Disease

Intervention

Drug:
• Dexmedetomidine
Starting with a 1 mg kg-1min-1 loading dose and than continued with a0.2-0.8 mg kg-1h-1 infusion rate.

Locations

Country	Name	City	State
Turkey	Ankara Diskapi Yildirim Beyazit Teaching and Research Hospital	Ankara

Sponsors (1)

Lead Sponsor	Collaborator
Diskapi Teaching and Research Hospital

Country where clinical trial is conducted

Turkey, 

References & Publications (3)

Genty S, Derrey S, Pouplin S, Lefaucheur R, Chastan N, Gérardin E, Maltête D. Pain due to osteoarthritis may impair the early outcome of deep brain stimulation in Parkinson's disease. Clin Neurol Neurosurg. 2011 Dec;113(10):864-7. doi: 10.1016/j.clineuro.2011.06.006. Epub 2011 Jul 19. — View Citation

Stoneham MD, Cooper R, Quiney NF, Walters FJ. Pain following craniotomy: a preliminary study comparing PCA morphine with intramuscular codeine phosphate. Anaesthesia. 1996 Dec;51(12):1176-8. — View Citation

Yagar S, Yavas S, Karahalil B. The role of the ADRA2A C1291G genetic polymorphism in response to dexmedetomidine on patients undergoing coronary artery surgery. Mol Biol Rep. 2011 Jun;38(5):3383-9. doi: 10.1007/s11033-010-0446-y. Epub 2010 Nov 23. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Other	postoperative pain scores	visual analog pain scores of the patients at postoperative 1, 6, 12 and 24th hours	postopertive 1 day	No
Primary	Doses of the sedative agents	Dexmedetomidine, propofol and midazolam will be used for sedation. We will determine the doses needed to tolerate surgery and to allow MER's and macrostimulation	1 day	No
Secondary	Time to emergence	time from discontinuation of sedative drugs to time that the patients are able to cooperate with macrostimulation	1 day	No