Professional Documents
Culture Documents
eep brain stimulation is used for the treatment of patients with neurologic disorders who have an alteration of function that is not usually accompanied by gross structural or anatomical changes, such as Parkinson disease, essential tremors, dystonia, and certain psychiatric conditions.1,2 The aim of this procedure is to improve the quality of life of the patient. The insertion of the deep brain stimulator (DBS) is a minimally invasive procedure that includes the placement of electrodes into deep brain structures for microelectrode recordings (MERs) and macrostimulation for clinically testing the patient and connection of the DBS to an implanted pacemaker. The anesthesiologist plays a key role in the management of patients for the insertion of a DBS. The anesthetic technique varies depending on the traditions and requirements of each institution performing these procedures and has included monitored care under local anesthesia, conscious sedation, and general anesthesia.37 There are many challenges and demands for the anesthesiologist in the care of these patients, whichever anesthetic technique is used. The purpose of this article is to familiarize anesthesiologists with the surgery of DBS insertion, the influences of anesthesia on the procedure, and to describe the anesthetic management of patients undergoing DBS insertion.
lesion in deep brain structures with procedures such as thalamotomy, pallidotomy, and cingulotomy. Lesioning procedures were irreversible and were associated with several permanent side effects.8 After the discovery of the beneficial effects of intraoperative electrical stimulation, deep brain stimulation was first described in 1987 as an alternative treatment to ablative procedures to reduce the symptoms of Parkinson disease.9,10 Reversibility and the option of bilateral stimulation along with the ability to titrate the stimulation have revolutionized the use of the DBS for functional neurosurgery. The safety and long-term benefits of the DBS are well documented.11 After its initial success in patients with Parkinson disease, the indications and applications have now expanded to include many other disorders such as dystonia, other tremors, obsessivecompulsive disorder, epilepsy, chronic pain, Alzheimer disease, and multiple sclerosis.1,2,12 The exact mechanism of deep brain stimulation is incompletely understood and may differ depending on the site of stimulation. The primary target sites vary with the patients symptoms and include the subthalamic nuclei (STN), globus pallidus pars internal (GPi), and the ventralis intermedius nucleus of the thalamus (Vim)13 (Fig. 1). The effects of stimulation on the various nuclei differ. For example, stimulation of the STN causes hyperpolarization or neuronal jamming, and this consequentially results in the inhibition of its activity.14,15 In addition, STN inhibition decreases the production of glutamate, and this has been suggested as a mechanism of neuroprotection in patients with Parkinson disease after insertion of a DBS.16 Stimulation of the GPi nuclei may result in activation of -aminobutyric acid (GABA)ergic axons, which in turn inhibits GPi neurons.15 In contrast, stimulation of the Vim nucleus of the thalamus activates output to the neurons in the reticular nucleus, which then sends inhibitory efferents back to the thalamic nuclei.14 The inhibition of these targeted nuclei will then result in improvements of the patients symptoms. The effects of a
April 2010 Volume 110 Number 4
1138
www.anesthesia-analgesia.org
DBS are also shown to be frequency dependent, with the greatest relief of symptoms at 100 Hz and no therapeutic effect at 50 Hz.13 The DBS system consists of 3 components: the intracranial electrode, an extension cable, and an implanted pulse generator. The electrode is a coiled wire insulated in polyurethane with 4 platinum iridium electrodes for implantation in the target neural tissue. The lead is connected by an extension cable to the implanted pulse generator that is a battery-powered neurostimulator encased in titanium housing, which sends electrical pulses to stimulate the target site. It is placed subcutaneously below the clavicle or in the abdomen and can be programmed to optimize symptom suppression and control side effects.
references to external coordinates for accurate insertion of the electrode into the target areas for stimulation. Depending on the institutional preference, different head frames are used. In a survey of North American centers performing DBS operations, the Cosman-Roberts-Wells frame was the most frequently used frame followed by the Leksell G.18 Both of these frames may restrict access to the patients airway in varying degrees. There are also reports of the use of frameless navigation systems for a DBS.19 After imaging, the patient is transferred to the operating room where he or she is positioned in a supine or semisitting position on the operating room table with the stereotactic frame fixed to the bed. A bur hole is made in the cranium for electrode insertion. To localize the target area for stimulation (STN, GPi, and Vim), the neurophysiology team will obtain MERs that are used to detect and amplify the activity of individual neurons. The electrode is usually inserted 10 to 15 mm above the target site and is advanced 0.5 to 1 mm along its trajectory toward the target nuclei while spontaneous neuronal discharges are recorded. The neurophysiologists use the variations in spontaneous firing rates between specific nuclei (GPi and globus pallidus external) and movement-related changes in the firing rates to localize the specific brain target (Fig 2). Macrostimulation, which involves the clinical testing of the patients movements, is then used to verify that the stimulation of the electrode at this location will improve their symptoms and not cause any side effects. After radiologic confirmation, the electrode is secured, and the wound is closed. If bilateral DBS insertions are planned, a second incision will be made on the other side and the procedure is repeated. The second stage, the internalization, is performed by tunneling the electrode(s) and connecting the extension cable through the scalp and subcutaneously on the side of the neck to an infraclavicular area where it is connected to the generator pacemaker.
Surgical Technique
The overall surgical procedure involves 2 stages: insertion of the electrode(s) into the target area of the brain, and the internalization of the lead(s) and implantation of the programmable pulse generator. The nuclei that are targeted are deep and small in size, requiring a variety of methods to increase the accuracy of targeting. This includes the use of frame-based imaging to visualize brain structures and to establish coordinates, electrophysiologic guidance with MER, and macrostimulation testing of an awake patient. The whole procedure may be completed on the same day or as a 2-staged procedure with the internalization of the electrode(s) and generator on a different day, typically 3 days to 2 weeks after the procedure. Currently, there is no evidence favoring the best timing of the second stage. The timing depends on many factors including duration of the procedure and patient cooperation. Another reason for delaying of the internalization is the microlesion effect caused by edema around the freshly implanted electrode. This effect may cause improvement of the patients symptoms without any stimulation, and this impairs the ability to check for stimulation-induced benefits.17 The procedure begins with the placement of a rigid head frame to the patients skull and magnetic resonance imaging (MRI) to visualize brain structures and to establish
www.anesthesia-analgesia.org
1139
REVIEW ARTICLE
Figure 2. A typical microelectrode recording during mapping of the globus pallidus internal (GPi) neurons. Changes in neuronal ring are shown as the electrode travels from globus pallidus external (Gpe) to GPi. Movement-related (exion and extension) changes in neuronal ring are also shown.
firing rates in dystonia. The effects of general anesthesia with desflurane were studied by Sanghera et al.24 in 11 patients with dystonia and 6 patients with Parkinson disease. There were no differences between awake and anesthetized patients with respect to GPi nuclei firing rates for the dystonia group, but there was a significant decrease in GPi nuclei firing rates in the Parkinson group. Thus, there were differences in GPi neuronal firing rates between the patients with dystonia and Parkinson disease, and the effect of anesthesia may be more pronounced in Parkinson disease. The ability to obtain MERs from the STN nuclei during anesthesia has been more successful.4,2529 The anesthetic techniques used have varied from conscious sedation with propofol and dexmedetomidine with no airway manipulation to general anesthesia with endotracheal intubation with either IV or inhaled techniques. The differences in the anesthetic effects on the various target nuclei (STN versus GPi) may be explained by the amount of their GABA input. The GPi neurons have a higher GABA input compared with the STN neurons and, therefore, are more suppressed by most anesthetic drugs.30 There is limited information regarding the effects of anesthetics on the Vim nuclei.
1140
www.anesthesia-analgesia.org
procedures are performed with local anesthesia and monitored care or with conscious sedation during parts of the procedure when testing is not performed. However, general anesthesia may be needed for specific groups of patients who have an irrational fear of awake surgery, chronic pain syndromes, severe off-medication movements, severe dystonia or choreoathetosis, and the young pediatric population. The second stage of the procedure (internalization) is usually performed with general anesthesia. The airway may be secured with an endotracheal tube, because access to the airway is restricted with tunneling of the cable on the side of the neck. During this procedure, there are no concerns with specific anesthetic drugs because no testing is performed. The stereotactic frame is usually placed on the patients skull with the use of local anesthesia for the pin sites, which is followed by MRI for localization and tabulating of the variables for DBS insertion. Some patients may require sedation for frame placement and/or for MRI. If conscious sedation or general anesthesia is to be started in the radiology suite, the anesthesiologist must have adequate equipment and support to care for the patient in this potentially remote site. Also, if anesthesia is required for MRI, all safety concerns for anesthesia in an MRI suite must be adhered to. Ideally, airway management (endotracheal tube and laryngeal mask airway [LMA]) should precede placement of the stereotactic frame. However, if general anesthesia needs to be induced with the frame in place, conventional laryngoscopy may be difficult. Other options of securing the airway such as fiberoptic endotracheal intubation or an LMA may be used. If an LMA is used, one needs to be aware of the increased risk of regurgitation and aspiration, especially in patients with Parkinson disease.
clinical testing. This poses additional challenges to the perioperative care because the drug-off state may worsen the patients symptoms, especially in Parkinson disease and dystonia (Table 2). If the symptoms are severe, a reduced dose of the patients regular medication can be administered after discussion with the neurosurgical team.
Anesthetic Techniques
To facilitate the intraoperative neurophysiologic mapping (MER) and/or clinical testing of the patient, most DBS
www.anesthesia-analgesia.org
1141
REVIEW ARTICLE
Propofol
? Minimal effect on MER Short acting Non-GABA-mediated action Less effect on MER Anxiolysis and analgesic effects6,25,26 Sedationeasily arousable Does not ameliorate clinical signs of Parkinsonism Maintains hemodynamic stability Preserves respiration
-aminobutyric acid.
MER
important step to ensure maximal comfort and cooperativeness, especially for awake patients. The head and neck should be positioned with some degree of flexion at the lower cervical spine and extension at the atlantooccipital junction. This helps to make the patients airway patent and make it possible for the anesthesiologist to secure the airway in an emergency. The legs should be flexed and supported under the knees to maintain stability when the head and back are elevated to a sitting position. To aid in positioning, special treatment modalities have been used such as physiotherapy, small doses of levodopa, and intrathecal hydromorphone.47,48 Patients with obstructive sleep apnea may need continuous positive airway pressure therapy intraoperatively. In these patients, the facemask needs to be placed before the head frame, and the patients continuous positive airway pressure machine should be readily available. The use of clear plastic drapes will make it easy for the anesthesiologist to maintain verbal and eye contact with the patient throughout the case.
Conscious Sedation
In some institutions and/or for some patients, conscious sedation is used for DBS insertion, especially during the opening and closure of the procedure. Frequently used drugs include midazolam, propofol, opioids such as fentanyl or remifentanil, and dexmedetomidine.57,25,26,49,50 However, there are concerns with the use of all these drugs as discussed above. The advantages and disadvantages of various drugs used for conscious sedation are shown in Table 3. Generally, the use of benzodiazepines is discouraged.51 Propofol has been widely used, most frequently as a continuous infusion, alone, or combined with remifentanil. The mean infusion rates of propofol reported in the literature are approximately 50 g/kg/min.7,48,52 However, one needs to be aware, if using target-controlled infusion devices, that the pharmacokinetic behavior of propofol in patients with Parkinson disease may differ from the general population for which the model was
developed.53 Dexmedetomidine with low-dose infusion rates (0.3 0.6 g/kg/h) may be a better choice because of its nonGABA-mediated mechanism of action allowing for MER, hemodynamic stability, and analgesic properties.6,25,26 Optimal conditions for MER or stimulation testing can be obtained with the use of conscious sedation as long as short-acting drugs are used and stopped before the recordings and testing. The use of depth of anesthesia monitors to titrate sedation and the state of arousal during DBS insertion would be ideal; however, studies have shown conflicting results. The reliability of bispectral index (BIS) monitoring during MER is questionable because the effects of anesthetics are heterogeneous across the different regions of the brain, and there is dissociation between the neocortical and subcortical effects of IV and inhaled drugs.20 Schulz et al.54 found that the use of BIS did not offer any advantages regarding the time to arousal, total propofol consumption, and cardiopulmonary stability. However, they did not study the effect of the anesthetics on MER. A study by Elias et al.26 showed a positive result for the use of BIS monitoring for titrating dexmedetomidine sedation. They found that the subthalamic MER signals were equivalent to the awake state when sedation was titrated to an easily arousable state (BIS value 80) in patients with Parkinson disease. However, deep sedation (BIS 80) suppressed MER signals.
General Anesthesia
General anesthesia may provide a higher level of acceptance for DBS surgery by some patients and a possible enlargement of the group of patients that can be treated. Intraoperative mapping and stimulation testing will be difficult under general anesthesia. There are no prospective, randomized, blinded studies to compare the clinical outcome with that of an awake technique. There are few reports in the literature on the use of general anesthesia for DBS insertion.4,27,28,29,55 Yamada et al.27 found that general
1142
www.anesthesia-analgesia.org
anesthesia in 15 patients with Parkinson disease did not adversely affect postoperative improvements in motor and daily activity scores, except for off-medication bradykinesia, when compared with 10 patients under local anesthesia. In another study with 10 patients, Lin et al.29 found that desflurane anesthesia allowed for adequate MERs for successful DBS insertion. Thus, DBS insertion under general anesthesia is possible with careful titration of anesthetics and with the use of limited electrophysiologic mapping. Randomized controlled studies are needed to compare the long-term clinical benefits of patients undergoing DBS insertion under general anesthesia with that of local anesthesia.
COMPLICATIONS
The insertion of a DBS is not without the potential for perioperative complications, which demands vigilance in rapid recognition and treatment of these events by the anesthesiologist. Overall, intraprocedure complications have been reported to occur in 12% to 16% of patients.5,7 Intraoperative respiratory complications are of great concern, occurring in 1.6% to 2.2% of patients.5,7 In the awake patient, they may result from oversedation or intracranial events such as seizures or hemorrhage leading to a decreased level of consciousness. Acute airway obstruction may occur in a restless awake patient as the body shifts but the head remains fixed to the bed.5 All appropriate airway equipment should be readily available because managing the airway in a patient with a rigid head frame poses a great challenge. The frame restricts neck movement and covers some or all the patients mouth and nose. Ideally, if possible, one should attempt to secure the airway without the removal of the patients head frame, so the surgery could be continued if indicated. Releasing the frame from the table may take time, and in an emergency securing, the airway with an LMA may be the most appropriate option. Other respiratory complications relate to the patients diseases. Patients with Parkinson disease may have restrictive pulmonary dysfunction from poor respiratory muscle function resulting in reduced forced vital capacity and reduced baseline arterial oxygen saturation, upper airway obstruction, dysarthria, and obstructive sleep apnea.7,38,51,56,57 Respiratory insufficiency caused by the absence of anti-Parkinson medications in the postoperative period may also occur. Cardiovascular complications can lead to devastating outcomes. Hypertension has been associated with increased risk of intracerebral hemorrhages.58,59 This may be more problematic in the awake patient who becomes agitated and anxious. Arterial blood pressure must be controlled before the insertion of the electrode to prevent intracranial hemorrhages. Frequently used drugs include labetalol, hydralazine, nitroglycerine, sodium nitroprusside, and esmolol. The optimal level of blood pressure is not well defined; one may use a systolic blood pressure of 140 mm Hg or a 20% increase of the patients usual range.59 Orthostatic hypotension may result from antiParkinson medications or might be further aggravated by the vasodilating effects of anesthetics, perioperative hypovolemia, and autonomic dysfunction. Glossop and Dobbs60
reported on 2 patients who experienced chest pain, tachycardia, hypertension, and oxygen desaturation during insertion of a DBS under local anesthesia. This was accompanied with ST segment changes and increased troponins, although further testing showed normal coronary arteries. They attributed the symptoms to abnormal vasoactive responses resulting in coronary vasospasm. Animal studies have shown that stimulation of the paraventricular region in the hypothalamus can cause either hypertension or hypotension.61 Other less common complications include venous air embolism.62 65 Semisitting position in a hypovolemic patient increases the risk. During creation of the bur hole in awake patients, sudden vigorous coughing may be a sign of venous air embolism. Other signs are unexplained hypoxia and hypotension. Early detection may be possible with precordial Doppler monitoring. The incidence of venous air embolism as detected by a precordial Doppler ultrasound has been reported to be 4.5%. Hooper et al.65 in their small study of 21 patients noted 1 venous air embolism (1 of 22 lead insertions), and the important predictors were patient positioning and the occurrence of coughing. There are no reports of whether the precordial Doppler interferes with MER. Tension pneumocephalus has also been reported during DBS insertion.66 Neurologic complications may occur during or after the procedure.67,68 Focal deficits such as extremity weakness or confusion may not require any acute treatment by the anesthesiologist. Seizures have been reported to occur in 0.8% to 4.5% of patients and often occur during stimulation testing.5,7 Most seizures were focal and did not require treatment. Small doses of midazolam and/or propofol may initially be used, and the procedure resumed after control of the seizure. A sudden loss of consciousness resulting from an intracranial bleed or neurologic injury will require rapid and more aggressive treatment.
CONCLUSION
The use of a DBS has and will continue to increase in popularity for the treatment of many functional neurologic disorders. This is especially true for an increasing elderly population ratio within the rapidly changing population demographics worldwide. DBS use has been shown to be safe, and new indications will continue to emerge. The role of the anesthesiologist in the care of these patients will also continue to evolve. New developments in surgical and imaging technology and a better understanding of the effects of drugs on the MER will lessen the difficulties and complications of these procedures. Even though the anesthetic techniques will continue to differ among various centers and may include monitored anesthesia care, conscious sedation, and general anesthesia, the general principles of anesthesia care remain the same. The anesthesiologist needs to be aware of the unique requirements of these patients and of these procedures. Continuous monitoring and extreme vigilance are vital to early diagnosis and rapid treatment of complications.
REFERENCES 1. Pereira EA, Green AL, Nandi D. Deep brain stimulation: indications and evidence. Expert Rev Med Devices 2007;4:591 603
www.anesthesia-analgesia.org
1143
REVIEW ARTICLE
2. Halpern C, Hurtig H, Jaggi J, Grossman M, Won M, Baltuch G. Deep brain stimulation in neurologic disorders. Parkinsonism Relat Disord 2007;13:116 3. Ollinet C, Bedague D, Carcey J, Oddoux ME, Payen JF. Functional surgery for movement disorders: implications for anesthesia. Ann Fr Anesth Reanim 2004;23:428 32 4. Maltete D, Navarro S, Welter ML, Roche S, Bonnet AM, Houeto JL, Mesnage V, Pidoux B, Dormont D, Cornu P, Agid Y. Subthalamic stimulation in Parkinson disease: with or without anesthesia? Arch Neurol 2004;61:390 2 5. Venkatraghavan L, Manninen P, Mak P, Lukitto K, Hodaie M, Lozano A. Anesthesia for functional neurosurgery. Review of complications. J Neurosurg Anesthesiol 2006;18:64 7 6. Rozet I. Anesthesia for functional neurosurgery: the role of dexmedetomidine. Curr Opin Anaesthesiol 2008;21:537 43 7. Khatib R, Ebrahim Z, Rezai A, Cata JP, Boulis NM, John Doyle D, Schurigyn T, Farag E. Perioperative events during deep brain stimulation: the experience at Cleveland clinic. J Neurosurg Anesthesiol 2008;20:36 40 8. Lozano AM, Lang AE. Pallidotomy for Parkinsons disease. Arch Neurol 2005;62:1377 81 9. Benabid AL, Pollak P, Gervason C, Hoffmann D, Gao DM, Hommel M, Perret JE, de Rougemont J. Long term suppression of tremor by chronic electrical stimulation of the ventral intermediate thalamic nucleus. Lancet 1991;337:403 6 10. Benabid AL, Pollak P, Louveau A, et al. Henry S, de Rougemont J. Combined (thalamotomy and stimulation) stereotactic surgery of the VIM thalamic nucleus for bilateral Parkinson disease. Appl Neurophysiol 1987;50:344 6 11. Benabid AL, Chabardes S, Mitrofanis J, Pollak P. Deep brain stimulation of the subthalamic nucleus for the treatment of Parkinsons disease. Lancet Neurol 2009;8:67 81 12. Marangell LB, Martinez M, Jurdi RA, Zboyan H. Neurostimulation therapies in depression: a review of new modalities. Acta Psychiatr Scand 2007;116:174 81 13. Johnson MD, Miocinovic S, McIntyre CC, Vitek JL. Mechanisms and targets of deep brain stimulation in movement disorders. Neurotherapeutics 2008;5:294 308 14. Ashby P, Rothwell JC. Neurophysiologic aspects of deep brain stimulation. Neurology 2000;55:1720 15. Benazzouz A, Hallett M. Mechanism of action of deep brain stimulation. Neurology 2000;55:13 6 16. Wamke PC. STN stimulation and neuroprotection in Parkinsons disease: when beautiful theories meet ugly facts. J Neurol Neurosurg Psychiatr 2005;76:1186 7 17. Rezai AR, Kopell BH, Gross RE, Vitek JL, Sharan AD, Limousin P, Benabid A. Deep brain stimulation for Parkinsons disease: surgical issues. Mov Disord 2006;21:S197218 18. Ondo WG, Bronte-stewart H. The North American survey of placement and adjustment strategies for deep brain stimulation. Stereotact Funct Neurosurg 2005;83:1427 19. Gumprechet H, Widenka D, Lumenta C. Brainlab VectorVision Neuronavigation System: technology and clinical experiences in 131 cases. Neurosurgery 1999;44:97105 20. Velly LJ, Rey MF, Bruder NJ, Gouvitsos FA, Witjas T, Regis JM, Peragut JC, Gouin F. Differential dynamic of action on cortical and subcortical structures of anesthetic agents during induction of anesthesia. Anesthesiology 2007;107:20212 21. Hutchison WD, Lang AE, Dostrovsky JO, Lozano AM. Pallidal neuronal activity: implications for models of dystonia. Ann Neurol 2003;53:480 8 22. Peduto VA, Concas A, Santoro G, Biggio G, Gessa GL. Biochemical and electrophysiologic evidence that propofol enhances GABAergic transmission in the rat brain. Anesthesiology 1991;75:1000 9 23. Steigerwald F, Hinz L, Pinsker MO, Herzog J, Stiller RU, Kopper F, Mehdorn HM, Deuschl G, Volkmann J. Effects of propofol anesthesia on pallidal neuronal discharges in generalized dystonia. Neurosci Lett 2005;386:156 9 24. Sanghera MK, Grossman RG, Kalhorn CG, Hamilton WJ, Ondo WG, Jankovic J. Basal ganglia neuronal discharge in primary and secondary dystonia in patients undergoing pallidotomy. Neurosurgery 2003;52:1358 73
25. Rozet I, Muangman S, Vavilala MS, Lee LA, Souter MJ, Domino KJ, Slimp JC, Goodkin R, Lam AM. Clinical experience with dexmedetomidine for implantation of deep brain stimulators in Parkinsons disease. Anesth Analg 2006;103:1224 8 26. Elias WJ, Durieux ME, Huss D, Frysinger RC. Dexmedetomidine and arousal affect of subthalamic neurons. Mov Disord 2008;23:131720 27. Yamada K, Goto S, Kuratsu J, Matsuzaki K, Tamura T, Nagahiro S, Murase N, Shimazu H, Kaji R. Stereotactic surgery for subthalamic nucleus stimulation under general anesthesia: a retrospective evaluation of Japanese patients with Parkinsons disease. Parkinsonism Relat Disord 2007;13:1017 28. Hertel F, Zuchner M, Weimar I, Gemmar P, Noll B, Bettag M, Decker C. Implantation of electrodes for deep brain stimulation of the subthalamic nucleus in advanced Parkinsons disease with the aid of intraoperative microrecording under general anesthesia. Neurosurgery 2006;59:1138 45 29. Lin SH, Chen TY, Lin SZ, Shyr MH, Chou YC, Hsieh WA, Tsai ST, Chen SY. Subthalamic deep brain stimulation after anesthetic inhalation in Parkinson disease: a preliminary study. J Neurosurg 2008;109:238 44 30. Benarroch EE. Subthalamic nucleus and its connections: anatomic substrate for the network effects of deep brain stimulation. Neurology 2008;70:19915 31. Anderson BJ, Marks PV, Futter ME. Propofol-contrasting effects in movement disorders. Br J Neurosurg 1994;8:387 8 32. Bohmdorfer W, Schwarzinger P, Binder S, Sporn P. Temporary suppression of tremor by remifentanil in a patient with Parkinsons disease during cataract extraction under local anesthesia. Anaesthesist 2003;52:7957 33. Lozano AM, Kumar R, Gross RE, Giladi N, Hutchison WD, Dostrovsky JO, Lang AE. Globus pallidus internus pallidotomy for generalized dystonia. Mov Disord 1997;12:86570 34. Krause M, Fogel W, Kloss M, Rasche D, Volkmann J, Tronnier V. Pallidal stimulation for dystonia. Neurosurgery 2004;55: 1361 8 35. Coubes P, Vayssiere N, El Fertit H, Hemm S, Cif L, Kienlen J, Bonafe A, Frerebeau P. Deep brain stimulation for dystonia. Surgical technique. Stereotact Funct Neurosurg 2002;78:18391 36. Rodriguez RL, Fernandez HH, Haq I, Okun MS. Pearls in patient selection for deep brain stimulation. Neurologist 2007;13:253 60 37. Poon CCM, Irvin MG. Anaesthesia for deep brain stimulation and in patients with implanted neurostimulator devices. Br J Anaesth 2009;103:152 65 38. Mason LJ, Cojocaru TT, Cole DJ. Surgical intervention and anesthetic management of the patient with Parkinsons disease. Int Anesthesiol Clin 1996;34:13350 39. Nicholson G, Pereira AC, Hall GM. Parkinsons disease and anesthesia. Br J Anaesth 2002;89:904 16 40. Fikkers BF, Zandstra DF. Primary Laryngospasm in a patient with Parkinsons disease: treatment with CPAP via a minitracheostomy following extubation. Intensive Care Med 1995;21:863 4 41. Frost EA, Osborn I. Deep brain stimulationsurgery for movement disorders and Parkinsons disease. Int Anesthesiol Clin 2009;47:57 68 42. Zanettini R, Antonini A, Gatto G. Valvular heart disease and the use of dopamine agonist for Parkinsons disease. N Engl J Med 2007;356:39 46 43. Gillman PK. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. Br J Anaesth 2005;95:434 41 44. Krauss JK, Akeyson EW, Giam P, Jankovic J. Propofol-induced dyskinesias in Parkinsons disease. Anesth Analg 1996;83:420 2 45. Watson R, Leslie K. Nerve blocks versus subcutaneous infiltration for stereotactic frame placement. Anesth Analg 2001;92:424 7 46. Heavner JE. Local anesthetics. Curr Opin Anaesthesiol 2007;20:336 42 47. Chevrier E, Fraix V, Krack P. Is there a role for physiotherapy during deep brain stimulation surgery in patients with Parkinsons disease? Eur J Neurol 2006;13:496 8 48. Lotto M, Boulis N. Intrathecal opiods for control of chronic low back pain during deep brain stimulation procedures. Anesth Anal 2007;105:1410 2
1144
www.anesthesia-analgesia.org
49. Fukuda M, Kameyama S, Noguchi R, Tanaka R. Intraoperative monitoring for functional neurosurgery during intravenous anesthesia with propofol. No Shinkei Geka 1997;25:2317 50. Murata J, Sawamura Y, Kitagawa M, Saito H, Kikuchi S, Tashiro K. Minimally invasive stereotactic functional surgery using an intravenous anesthetic propofol and applying image Fusion and AtlasPlan. No To Skinkei 2001;53:457 62 51. Davies A. Midazolam induced dyskinesias. Palliat med 2000;14:435 6 52. Deiner S, Hagen J. Parkinsons disease and deep brain stimulator placement. Anesthesiology Clin 2009;29:391 415 53. Fabregas N, Rapado J, Gambus PL, Valero R, Carrero E, ` Salvador L, Nalda-Felipe MA, Troconiz IF. Modeling of the sedative and airway obstruction effects of propofol in patients with Parkinsons disease undergoing stereotactic surgery. Anesthesiology 2002;97:1378 86 54. Schulz U, Keh D, Barner C, Kaiser U, Boemke W. Bispectral Index Monitoring does not improve anesthesia performance in patients with movement disorders undergoing deep brain stimulating electrode implantation. Anesth Analg 2007;104: 14817 55. Lefaucheur JP, Gurruchaga JM, Pollin B, von Raison F, Mohsen N, Shin M, Menard-Lefaucheur I, Oshino S, Kishima H, Fenelon G, Remy P, Cesaro P, Gabriel I, Brugieres P, Keravel Y, ` Nguyen JP. Outcome of bilateral subthalamic nucleus stimulation in the treatment of Parkinsons disease: correlation with intraoperative multi-unit recordings but not with the type of anesthesia. Eur Neurol 2008;60:186 99 56. Santos P, Valero R, Arguis MJ, Carrero E, Salvador L, Rumia J, Valldeoriola F, Fabregas N. Preoperative adverse events during stereotactic microelectrode-guided deep brain surgery in Parkinsons disease. Rev Esp Anestesiol Reanim 2004;51:52330 57. Easdown LJ, Tessler MJ. Minuk J, Upper airway involvement in Parkinsons disease resulting in postoperative respiratory failure. Can J Anaesth 1995;42:344 7 58. Binder DK, Rau GM, Starr PA. Risk factors for hemorrhage during microelectrode-guided deep brain stimulator implantation for movement disorders. Neurosurgery 2005;56:72232
59. Gorgulho A, De Salles AA, Frighetto L, Behnke E. Incidence of hemorrhage associated with electrophysiological studies performed using macroelectrodes and microelectrodes in functional neurosurgery. J Neurosurg 2005;102:888 96 60. Glossop A, Dobbs P. Coronary artery vasospasm during awake deep brain stimulation surgery. Br J Anaesth 2008;101:222 4 61. Mack SO, Wu M, Kc P, Haxhiu M. Stimulation of the hypothalamic paraventricular nucleus modulates cardiorespiratory responses via oxytocinergic innervation of neurons in preBotzinger complex. J Appl Physiol 2007;102:779 83 62. Suarez S, Ornaque I, Fabregas N, Valero R, Carrero E. Venous air embolism during Parkinson surgery in patients with spontaneous ventilation. Anesth Analg 1999;88:793 4 63. Moitra V, Permut TA, Penn RM, Roth S. Venous air embolism in an awake patient undergoing placement of deep brain stimulators. J Neurosurg Anesthesiol 2004;16:3212 64. Deogaonkar A, Avitsian R, Henderson JM, Schubert A. Venous air embolism during deep brain stimulation surgery in an awake supine patient. Stereotact Funct Neurosurg 2005;83:325 65. Hooper AK, Okun MS, Foote KD, Haq IU, Fernandez HH, Hegland D, Robicsek SA. Venous air embolism in deep brain stimulation. Stereotact Funct Neurosurg 2008;87:2530 66. Jain V, Prabhakar H, Rath GP, Sharma D. Tension pneumocephalus following deep brain stimulation surgery with bispectral index monitoring. Eur J Anaesthesiol 2007;24:203 4 67. Beric A, Kelly PJ, Rezai A, Sterio D, Mogilner A, Zonenshayn M, Kopell B. Complications of deep brain stimulation surgery. Stereotact Funct Neurosurg 2001;77:73 8 68. Higuchi Y, Iacono RP. Surgical complications in patients with Parkinsons disease after posteroventral pallidotomy. Neurosurgery 2003;52:558 71 69. Tao J, Nunery W, Kresovsky S, Lister L, Mote T. Efficacy of fentanyl or alfentanil in suppressing reflex sneezing after propofol sedation and periocular injection. Ophthal Plast Reconstr Surg 2008;24:4657 70. Klausner JM, Caspi J, Lelcuk S, Khazam A, Marin G, Hechtman HB, Rozin RR. Delayed muscular rigidity and respiratory depression following fentanyl anesthesia. Arch Surg 1988;123:66 7
www.anesthesia-analgesia.org
1145