Himmelfarb Health Sciences Library, The George Washington University Health Sciences Research Commons Neurological Surgery Faculty Publications Neurological Surgery 2015 Anesthesia for deep brain stimulation in traumatic brain injury-induced hemidystonia Jill M. Jani Chima O. Oluigbo George Washington University Srijaya K. Reddy George Washington University Follow this and additional works at: http://hsrc.himmelfarb.gwu.edu/smhs_neurosurg_facpubs Part of the Anesthesia and Analgesia Commons, and the Neurology Commons Recommended Citation [epub ahead of print] This Journal Article is brought to you for free and open access by the Neurological Surgery at Health Sciences Research Commons. It has been accepted for inclusion in Neurological Surgery Faculty Publications by an authorized administrator of Health Sciences Research Commons. For more information, please contact [email protected]. CASE REPORT Anesthesia for deep brain stimulation in traumatic brain injury-induced hemidystonia Jill M. Jani1, Chima O. Oluigbo2 & Srijaya K. Reddy1 1Division of Anesthesiology, Children’s National Medical Center, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia 2Division of Neurosurgery, Children’s National Medical Center, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia Correspondence Key Clinical Message Srijaya K. Reddy, Division of Anesthesiology, Children’s National Medical Center, 111 Deep brain stimulation in an awake patient presents several unique challenges Michigan Avenue NW, Washington, DC to the anesthesiologist. It is important to understand the various stages of the 20010. Tel: (202) 476-2025; procedure and the complexities of anesthetic management in order to have a Fax: (202) 476-5999; successful surgical outcome and provide a safe environment for the patient. E-mail: [email protected] Funding Information Keywords No sources of funding were declared for this Awake craniotomy, Deep brain stimulation (DBS), deep sedation, dexmede- study. tomidine, dystonia, traumatic brain injury (TBI). Received: 10 July 2014; Revised: 4 December 2014; Accepted: 20 February 2015 doi: 10.1002/ccr3.289 Introduction dystonic flexor position at the elbow. The surgical plan included implantation of intracranial DBS leads in the Deep brain stimulation (DBS) is a neurosurgical tech- globus pallidus internus in an attempt to relieve the nique aimed at improving “functional” neurologic disor- hemidystonia. A peripheral IV was placed and midazolam ders. To facilitate intraoperative neurophysiologic 2 mg was administered en route to the OR. Standard microelectrode recording (MER) and neurocognitive test- ASA monitors were applied along with 2 L/min of oxygen ing of the eloquent parts of the brain, DBS is commonly via nasal cannula, while the neurosurgical team prepared performed via an “awake” approach under a local anes- for head frame placement. A dexmedetomidine intrave- thetic and conscious sedation. While a deeper plane of nous infusion at 0.5 lg/kg/h was started, and a total of anesthesia can be used during the portion of the proce- 1.2 lg/kg of fentanyl was administered incrementally for dure not involved in testing, an awake and cooperative local anesthetic infiltration at the head frame pin sites. patient with fully preserved brain function is essen- During this period, the patient maintained spontaneous tial during MER to ensure accurate lead placement ventilation and did not react to local infiltration, pin [1, 2]. insertion, or head frame manipulation. A radial arterial line and second peripheral IV were l Case Description placed under local and propofol infusion at 100 g/kg/ min. Before MER and neurocognitive testing, propofol Our case involved a developmentally delayed 24-year old, was turned off in order to transition to the “awake” seg- 80-kg male with traumatic brain injury (TBI) as an infant ment of the procedure. The patient was able to follow with resultant post-traumatic stroke, hydrocephalus, and commands under the dexmedetomidine infusion alone. right upper extremity hemidystonia, causing a prominent Exceptional quality MER recordings were obtained. Once ª 2015 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd. 1 This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. Anesthesia for DBS in TBI-induced Hemidystonia J. M. Jani et al. MER was complete, the propofol infusion was restarted hole drilling, and maintaining this level of supportive care to supplement the dexmedetomidine infusion during sur- over a potentially long surgery; ensuring proper position- gical site closure. The patient’s postoperative course was ing to allow for safe and optimal surgical conditions; and uneventful, and he was discharged home 2 days after the maintaining access to the patient’s airway while anticipat- procedure. At patient’s 6-month follow up clinic visit, he ing emergency airway interventions in the event ventila- had a dramatic reduction in his right upper extremity tre- tory compromise occurs under sedation. This is especially mor and had a significant improvement in his ability to important as the head frame system (Fig. 1) can impair perform daily activities. access to the airway, making mask ventilation problem- atic. Patient cooperation, providing an anesthetic tech- Discussion nique that will minimally interfere with MER, and maintaining spontaneous ventilation and airway patency DBS involves the placement of wire electrodes into deep are crucial to a successful outcome in these cases. Finally, brain nuclei. For movement disorders, these deeper brain an appropriate blood pressure should be maintained in structures include the subthalamic nucleus, internal seg- order to minimize the risk of intracranial bleeding, a ment of the globus pallidus, and thalamic nucleus ventral- well-known complication in DBS procedures [4]. All of is intermedius. Electrical impulses are delivered to these these challenges are magnified in the younger or develop- structures with the objective of altering specific neural mentally delayed patient population. networks, resulting in a therapeutic effect. The electrodes The anesthetic management of an awake craniotomy are then connected to an implanted pacemaker that pro- has changed over the past 20 years in an attempt to duces high-frequency stimulations that help ameliorate address the aforementioned challenges. Currently, the the clinical manifestations of functional neurologic disor- most popular technique is the “asleep-awake-asleep” tech- ders, while having the added qualities of titratability and nique. This employs a heavier sedation or general anes- reversibility [3]. thesia during the initial stages, alternating with Targeting specific deep brain structures in DBS surgery consciousness using rapid-onset medications with a short is based on stereotactic principles that use advanced brain duration of action during brain mapping and neurocogni- imaging and atlases. The surgical trajectory is guided by tive testing [2]. After mapping is complete, deep sedation stereotactic platforms, which may be framed or frameless. or general anesthesia can be reestablished for surgical clo- The deep brain nuclei targets are verified by their electro- sure and removal of the pins. Propofol, remifentanil, and physiological signature using intraoperative neurophysio- dexmedetomidine are some of the anesthetics that have logic mapping. This presents several unique challenges to been used for awake craniotomy (Table 1). While propo- the anesthesiologist: providing patient reassurance and fol and remifentanil are short-acting, propofol can attenu- comfort, especially during head frame placement and Burr ate MER and remifentanil may cause muscle rigidity. Both drugs can result in respiratory depression, so they must be titrated carefully. While high doses of dexmede- tomidine can abolish MER, low dose infusion rates (0.3– 0.6 lg/kg/h) usually preserve MER integrity, while also providing analgesia and sedation without respiratory depression [1]. The a-2A receptors in the locus ceruleus are responsible for the sedative, analgesic, and sympatho- lytic effects of dexmedetomidine. This specific effect over a-2A receptors may allow cortical neurons to continue functioning upon stimulation in contrast to propofol or even barbiturates that produce generalized neuronal hyperpolarization. In a recent case study, 6 pediatric patients with severe dystonia successfully underwent DBS procedures with the use of low-dose dexmedetomidine as part of the anes- thetic technique with unimpaired neuroelectrophysiologi- cal signals [5]. Since it does not directly affect the activity of subthalamic neurons, dexmedetomidine may be an ideal sedative medication for neurophysiologic monitor- Figure 1. Head frame for stereotactic neurosurgery (courtesy of ing [6]. Low-dose dexmedetomidine (0.1–0.4 lg/kg/h) Elektaâ). infusion has been shown to produce MER from subtha- 2 ª 2015 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd. J. M. Jani et al. Anesthesia for DBS in TBI-induced Hemidystonia Table 1. Commonly used anesthetic agents in awake craniotomies and DBS. Anesthetic agent Advantages Disadvantages Effects on MER for DBS Benzodiazepines Sedation May induce dyskinesia Abolishes MER Anxiolysis Potentiate ventilatory depressant