Movement Disorders 13th Meet World Soc Stereotact Funct Neurosurg, Adelaide 2001 Stereotact Funct Neurosurg 2001;77:87–90 DOI: 10.1159/000064602 Targeting the Subthalamic Nucleus T.Z. Aziz a, b, d D. Nandi a S. Parkin c X. Liu a N. Giladi a P. Bain d R.G. Gregory c C. Joint b R.B. Scott b J.F. Stein a a University Laboratory of Physiology; Departments of b Neurosurgery, and Radcliffe Infirmary, Oxford, and d Department of Neurology, Charing Cross Hospital, London, UK c Neurology, Key Words Subthalamic nucleus W Targeting W Lesions W Stimulation W Parkinson’s disease Abstract The small size and surrounding neuronal structures and fibre tracts make the STN a difficult stereotactic target. In this article we present the technique used by us to target the STN. Our combined experience from two centres comprises 18 lesions and 27 stimulator implants in the STN. Our criteria for patient selection and the use of MRI, frame-on CT and volumetric image fusion are presented. The role of a movement disorder specialist neurologist in the operating theatre, local field potential recording, impedance monitoring, macrostimulation, post-operative CT/MRI and test stimulation are detailed. Copyright © 2002 S. Karger AG, Basel Introduction Since the demonstration in parkinsonian sub-human primates that lesioning the subthalamic nucleus (STN) could alleviate the cardinal signs of Parkinson’s disease [1–3], the STN has been adopted by many groups as the target of choice. ABC © 2002 S. Karger AG, Basel 1011–6125/01/0774–0087$18.50/0 Fax + 41 61 306 12 34 E-Mail karger@karger.ch Accessible online at: www.karger.com/journals/sfn www.karger.com Dr. T.Z. Aziz Department of Neurosurgery, Radcliffe Infirmary Woodstock Road, Oxford OX2 6HE (UK) Tel. +44 1865 228 425, Fax +44 1865 224 898 E-Mail tipuaziz@btinternet.com Given the small size of the target and the fact that it is encased in critical fibre tracts, many techniques have been adopted to safely approach this region. We present the technique used in the Radcliffe Infirmary, Oxford, and Charing Cross Hospital, London. We have experience of 18 STN lesions and 27 STN stimulator implants between the two sites from March 1998 to the present. Minimal Requirements For imaging, the basic requirements are an MRI scanner, a CT scanner and a CT compatible stereotactic frame (we use the Radionics CRW frame). We also routinely use software to volumetrically fuse MRI scans to the stereotactic scan which is very useful, but not critical. Personnel at each centre consists of an experienced stereotactic neurosurgeon, a neurologist experienced in movement disorders, a neuroanaesthetist, a neurophysiologist, a neuropsychologist and a specialist movement disorders nurse. Patient Selection The best outcomes will be obtained only if the right patients are offered surgery, and here the experience of the neurologist is critical. We offer surgery to patients with true idiopathic Parkinson’s disease who are very L-Dopa responsive, with no drug-resistant symptoms of ‘on’ freezing, frequents falls, poor balance, bulbar symptoms of low speech volume and poor swallowing, cognitive impairment, hallucinations on medication and unreal expectations of surgery. Although drug reduction is claimed to be one of the major advantages of STN surgery [4–6], we do not routinely pursue this goal unless the patient is young with early complications of L-Dopa therapy. Surgical Technique Pre-operatively patients undergo a T2 weighted axial MRI scan, parallel to the AC-PC plane in 3.0 mm contiguous slices. Patients may need intravenous sedation or even a general anaesthetic for this scan depending on the predominant symptomatology. Surgery is performed with the patient off all medications overnight. Given their disabilities, these cases are always first on the operating list. The base ring of the stereotactic frame is fitted to the skull under general anaesthesia and a stereotactic CT scan of the whole head aligned parallel to the orbito-meatal line and in 3.0 mm contiguous slices is obtained. The patient is then transferred back to the 88 Stereotact Funct Neurosurg 2001;77:87–90 Aziz/Nandi/Parkin/Liu/Giladi/Bain/Gregory/ Joint/Scott/Stein theatre, positioned supine on the table with the base ring fixed to the table and woken up after insertion of an arterial line to monitor blood pressure, which is maintained at normal pre-operative levels with hypotensives if necessary. When awake the attending neurologist confirms the patient is fully co-operative and the physical signs are present. Using Image Fusion and Stereoplan, the coordinates of the subthalamic nucleus are calculated. To do so we draw an imaginary line across the anterior limits of the red nucleus and choose as the target the hypointense region lying between the red nucleus and the cerebral peduncle. In relation to the mid-commissural point this lies usually 4.0 mm posterior, 10–12 mm lateral and 5 mm below it. A trajectory is planned to avoid transgressing the lateral ventricles. We do not shave the patient’s head but wash the hair with aqueous and then alcoholic chlorhexidine and infiltrate the line of incision with 0.25% bupivacaine. The co-ordinates are transferred to the frame and checked against the phantom and fixed to the base ring. Through a linear scalp incision for neurostimulation or a punctate incision for lesioning, a 2.7 mm twist drill is performed just anterior to the coronal suture and lateral enough to avoid the lateral ventricle. The initial exploration is made with a Radionics TM electrode with a 2.0-mm-exposed tip and 1.8 mm diameter, both to confirm clinical effects prior to lesioning or to create a tract for the deep brain electrode for neuromodulation. In the region of the STN the impedance as measured by this electrode is 600–700 ø. Stimulation at 100 Hz, 1.0 ms pulse width and abolition of contralateral parkinsonian signs of rigidity, bradykinesia and tremor at 0.5–1.5 V and no capsular effects at 2.0 V and 2 Hz confirms it is safe to lesion. A temporary lesion is then made for 60 s at 45 C to confirm this. If so three lesions are placed for 60 s and at 75 C, 2.0 mm beyond, at and 2.0 mm above target. Lesions are always performed unilaterally at one sitting. Exploration for neurostimulation with the TM electrode is performed at 150–180 Hz, 0.1 ms pulse width with clinical effect observed at 1.5–2.0 V with no side effects at twice the clinically effective amplitude. The TM electrode is then replaced with the permanent DBS electrode and on table bipolar stimulation and field potential recording performed. Those set of electrodes with greatest coherence with EMG recordings are chosen to lie in the middle two of the four electrodes of the Medtronics 3389 electrode. The electrode is then gently fixed to the skull with a mini-plate and field potentials and effects of stimulation checked again to confirm identical effects and hence no shift in position. The electrode is then externalised to allow for a week of clinical assessment of effect. If confirmed and a postoperative CT scan shows good localisation, then the following week the patient is anaesthetised and full implantation of the extension cable and pacemaker is performed subcutaneously below the clavicle. Because of our experience of global confusion that can attend very occasionally patients with simultaneous Targeting the Subthalamic Nucleus Stereotact Funct Neurosurg 2001;77:87–90 89 bilateral STN implants, we usually implant one electrode initially but also pass a contralateral extension cable under the scalp to make contralateral surgery straightforward at a later date. Conclusions The technique presented is that practiced in our units and the conclusions drawn also are very personal. We have abandoned STN lesioning generally because of short-lived benefits. We have also noted that post-pallidotomy and thalamotomy patients do not benefit significantly from STN stimulation on the same side. Our clinical experience is that not all patients benefit from the STN as a target and therefore still offer thalamic and pallidal surgery, be it lesional or stimulation, as clinical and social reasons dictate. Acknowledgements D.N. is supported by the Norman Collisson Foundation and T.Z.A. by the Medical Research Council, UK. N.G. is a McDonal Pew fellow in Oxford University from the Movement Disorders Unit of Tel-Aviv Medical Centre in Israel. References 1 2 3 4 5 6 90 Aziz TZ, Peggs D, Sambrook MA, Crossman AR: Lesion of the subthalamic nucleus for the alleviation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism in the primate. Mov Disord 1991;6:288–292. Aziz TZ, Peggs D, Agarwal E, Sambrook MA, Crossman AR: Subthalamic nucleotomy alleviates parkinsonism in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-exposed primate. Br J Neurosurg 1992;6:575–582. Bergman H, Wichmann T, DeLong MR: Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science 1990;249:1436–1438. Limousin P, Krack P, Pollak P, et al.: Electrical stimulation of the subthalamic nucleus in advanced Parkinson’s disease. N Engl J Med 1998;339:1105–1111. Limousin P, Pollak P, Benazzouz A, et al.: Bilateral subthalamic nucleus stimulation for severe Parkinson’s disease. Mov Disord 1995;10:672–674. Benabid AL, Pollak P, Gross C, et al.: Acute and long-term effects of subthalamic nucleus stimulation in Parkinson’s disease. Stereotact Funct Neurosurg 1994;62:76–84. Stereotact Funct Neurosurg 2001;77:87–90 Aziz/Nandi/Parkin/Liu/Giladi/Bain/Gregory/ Joint/Scott/Stein