• J Clin Neurosci · Jul 2010

    Comparative Study

    Delayed awakening in dystonia patients undergoing deep brain stimulation surgery.

    • Carlos Trombetta, Anupa Deogaonkar, Milind Deogaonkar, Zeyd Ebrahim, Ali Rezai, Andre Machado, and Ehab Farag.
    • Anesthesiology Institute, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland Clinic, Cleveland, Ohio 44195, USA.
    • J Clin Neurosci. 2010 Jul 1;17(7):865-8.

    AbstractWe aimed to identify the incidence, duration and causes of delayed emergence from anesthesia in patients with dystonia undergoing surgery for deep brain stimulation (DBS) placement. A retrospective review of patients with dystonia who underwent DBS placement was conducted and the following characteristics were noted: age, gender, comorbid conditions, American Society of Anesthesiologists classification, anesthetic agents used, amount of initial dose, amount of infusion dose, duration of the infusion and the time needed for emergence. Twenty-four patients underwent 33 DBS procedures for dystonia. Propofol was administered to 21 patients, in 29 of the 33 procedures. Dexmedetomidine was administered to three patients, in four procedures. The average propofol loading dose was 0.7mg/kg, and the infusion rate was 80microg/kg per minute (min), for an average duration of 89min. The average time of emergence was 36min. Only 31% of patients emerged from propofol anesthesia during the expected time frame, 69% of patients had some degree of delayed emergence, and 24% had a significant delay in emergence. Delayed emergence was more common in younger patients due to the higher loading doses these patients received. This study shows a 69% incidence of delayed emergence in dystonia patients undergoing DBS surgery. It also suggests an association between delayed emergence and younger patients who receive higher loading doses. A possible cause of delayed emergence is excessive anesthetic potentiation of the low output pallidal state in dystonia which may depress the pallido-thalamo-cortical circuitry. Delayed emergence could also result from depression of the previously affected ventral pallidal inputs to the septo-hippocampal system that mediates general anesthesia and awareness. Complex neurotransmitter disturbances may also be involved.

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