Anesthesia for Deep Brain Stimulation
Condition: Parkinsons Disease
MeSH terms: Parkinson Disease
Study type: Interventional
Phase: Phase 4

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.
    

Detailed 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.
    

Intervention name(s): Dexmedetomidine
Intervention type(s): Drug
Intervention description(s): Starting with a 1 mg kg-1min-1 loading dose and than continued with a0.2-0.8 mg kg-1h-1 infusion rate.
Other intervention name(s): Precedex 200 mcg 2 ml
Intervention MeSH terms: Dexmedetomidine
Intervention model: Single Group Assignment
Masking: None (Open Label)
Primary purpose: Treatment
Keywords: Deep brain stimulation; Parkinson