Subthalamotomy for Parkinson’s Disease

  1. Obeso, J. A.
  2. Alvarez, L.
  3. Macias, R.
  4. Pavon, N.
  5. Lopez, G.
  6. Rodriguez-Rojas, R.
  7. Rodriguez-Oroz, M. C.
  8. Guridi, J.
Book:
Textbook of Stereotactic and Functional Neurosurgery

ISBN: 9783540699590,  9783540699606

Year of publication: 2009

Pages: 1569-1576

Type: Book chapter

DOI: 10.1007/978-3-540-69960-6_94 GOOGLE SCHOLAR lock_openOpen access editor

Abstract

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) or the globus pallidus pars interna (GPi) has become a standard treatment of motor complications in Parkinson¿s disease (PD). Compared with classic ablative surgery, DBS offers the advantage of some degree of reversibility and adaptability, avoids causing new lesions in a brain undergoing a progressive neurodegenerative process and may be less hazardous to undertake in surgical practice. Altogether, the general medical and public opinion has evolved towards favoring DBS over potentially damaging procedures. On the other hand, ablative surgery may be the only or best option on some occasions. This may occur when, for instance, a previously implanted device for DBS has to be removed due to persistent infection or some other technical problem. In addition, DBS may not be easily applied to patients living in remote regions or may be contraindicated for patients suffering from immune deficiency or personality disorders. It should be noted that the cost of DBS and its associated consumables is not affordable for many patients in countries where medical care is not guaranteed by public institutions. Finally, there is a small proportion of PD patients with severe parkinsonian features confined to one hemisphere in whom unilateral surgery may be a reasonable therapeutic option. In such cases, a unilateral lesion may have many practical advantages over DBS.

Bibliographic References

  • Mitchell IJ, Clarke CE, Boyce S, Robertson RG, Peggs D, Sdambrook MA, Crossman AR. Neural mechanism underlying parkinsonian symptoms based upon regional uptake of 2-deoxiglucose in monkeys exposed to 1-methyl-4phenyl-1,2,3,6-tretrahydropyridine. Neuroscience 1989;32:213–26.
  • Miller WC, DeLong MR. Altered tonic activity of neurons in the globus pallidus and subthalamic nucleus in the primate model of parkinsonism. In: Carpenter MB, Jayaraman A, editors. The basal ganglia II. Structure and function. New York: Plenum; p. 415–27; 1987.
  • Levy R, Herrero MT, Ruberg M, Villares J, Faucheux B, Guridi J, Guillen J, Luquin MR, Javoy-Agid F, Obeso JA, et al. Effects of nigrostriatal denervation and L-dopa therapy on the GABAergic neurons in the striatum, in MPTP-treated monkeys and Parkinson’s disease: an in situ hybridization study of GAD67 mRNA. Eur J Neurosci 1995;7:1199–209.
  • Smith Y, Parent A. Neurons of the subthalamic nucleus in primates diplay glutamate but not GABA immunoreactivity. Brain Res 1988;453:353–6.
  • Crossman AR, Peggs D, Boyce S, Luquin MR, Sambrook MA. Effecto of NMDA antagonist MK-801 on MPTP-induced parkinsonism in the monkey. Neuropharmacology 1989;28:1271–3.
  • Bergman H, Wichmann T, DeLong MR. Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science 1990;249:1436–8.
  • 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 tetrahydropiridine (MPTP)-induced parkinsonism in the primate. Mov Disord 1991;6:288–92.
  • Guridi J, Herrero MT, Luquin MR, Guillén J, Ruberg M, Laguna J et al. Subthalamotomy in parkinsonian monkeys. Behavioural and biochemical analysis. Brain 1996;119:1717–27.
  • Laitinen LV, Bergenheim AT, Hariz MI. Leksell’s posteroventral pallidotomy in the treatment of Parkinson’s disease. J Neurosurg 1992;76:53–61.
  • Whittier JR, Mettler FA. Studies on subthalamus of rhesus monkey: hyperkinesia and other physiologic effects of subthalamic lesions, with special reference to the subthalamic nucleus of Luys. J Com Neurol 1949;90:319–72.
  • Carpenter MB, Whittier JR, Mettler FA. Analysis of choreoid hyperkinesia in the rhesus monkey. J Comp Neurol 1950;92:293–322.
  • Purdon Martin J, Alcock NS. Hemichorea associated with a lesion of the corpus Luysii. Brain 1934;57:504–16.
  • Marsden CD and Obeso JA. The functions of the basal ganglia and the paradox of stereotaxic surgery in Parkinson’s disease. Brain 1994;117:877–97.
  • Obeso JA, Rodriguez MC, DeLong MR. Basal ganglia pathophysiology: a critical review. Adv Neurol 1997;74:3–18.
  • Guridi J, Herrero MT, Luquin MR, Obeso JA. The subthalamic nucleus: a new possible stereotaxic target for Parkinson’s disease. Mov Disord 1993;8:421–9.
  • Guridi J, Obeso JA. The subthalamic nucleus, hemiballismus and Parkinson’s disease: reappraisal of a neurosurgical dogma. Brain 2001;124:5–19.
  • Dierssen G, Bergmann L, Gioino L, Cooper IS. Hemiballism following surgery for Parkinson’s disease. Arch Neurol 1961;5:627–37.
  • Andy OJ, Jurko MF, Sias FR. Subthalamotomy in treatment of parkinsonian tremor. J Neurosurg 1963;20:860–70.
  • Fager CA. Evaluation of thalamic and subthalamic surgical lesions in the alleviation of Parkinson’s disease. J Neurosurg 1963;28:145–9.
  • Lopez G, Morales J, Tejeiro J, Vitek JL, Perez-Paara S, Fernandez R, Maragoto C, et al. Anatomic and neurophysiological methods for the targeting and lesioning of the subthalamic nucleus. Cuban experience and review. Neurosurgery 2003;52:817–31.
  • Obeso JA, Alvarez L, Macias R, Guridi J, Juncos JL, Tejeiro J, et al. 1997;Neurology 48 Suppl 3:A138.
  • Gill SS, Heywood P. Bilateral dorsolateral subthalamotomy for advanced Parkinson’s disease. Lancet 1997;350:1224.
  • Alvarez L, Macias R, Guridi J, Lopez G, Alvarez E, Maragoto CT, et al. Dorsal subthalamotomy for Parkinson’s disease. Mov Disord 2001;16:72–8.
  • Patel NK, Heywood P, O’Sullivan K, McCarter R, Love S, Gill SS. Unilateral subthalamotomy in the treatment of Parkinson’s disease. Brain 2003;126:1136–45.
  • Su PC, Tseng HM, Liu HM, Yen RF, Liou HH. Subthalamotomy for advanced Parkinson disease. J. Neurosurg 2002;97:598–606.
  • Vilela F, da Silva DJ. Unilateral subthalamic nucleus lesioning: a safe and effective treatment for Parkinson’s disease. Arq. Neuropsiquiatr 2002;60:935–48.
  • Alvarez L, Macias R, Lopez G, Alvarez E, Pavon N, Rodriguez-Oroz MC, Juncos JL, Maragoto C, Guridi J, Litvan I, Tolosa ES, Koller W, Vitek J, DeLong MR, Obeso JA. Bilateral subthalamotomy in Parkinson’s disease: initial and long-term response. Brain 2005;128:570–83.
  • Lang AE, Lozano AM, Montgomery E, Duff J, Tasker R, Hutchison W. Posteroventral pallidotomy in advanced Parkinson’s disease. N Engl J Med 1997;337:1036–42.
  • Baron MS, Vitek JL, Bakay RAE, Kaneoke Y, Hashimoto T, Turner RS, et al. Treatment of advanced Parkinson’s disease by posterior GPi pallidotomy: 1-year results of a pilot study. Ann Neurol 1996;40:355–66.
  • Suarez JI, Metman LV, Reich SG, Dougherty PM, Hallet M, Lenz FA. Pallidotomy for hemiballismus efficacy and characteristics of neuronal activity. Ann Neurol 1997;42:807–11.
  • Vitek JL, Chockkan V, Zhang JY, Kaneoke Y, Evatt M, DeLOng MR, et al. Neuronal activity in the basal ganglia in patients with generalized dystonia and hemiballismus. Ann Neurol 1999;46:22–35.
  • Lozano AM. The subthalamic nucleus: myth and opportunities. Mov Disord 2001;16:183–4.
  • Merello M, Perez-Lloret S, Antico J, Obeso JA. Dyskinesias induced by subthalamotomy in Parkinson’s disease are unresponsive to amantadine. J Neurol Neurosurg Psychiatry 2006;77:172–4.
  • McCarter RJ, Walton NH, Rowan AF, Gill SS, Palomo M. Cognitive functioning after subthalamic nucleotomy for refractory Parkinson’s disease. J Neurol Neurosurg Psychiatry 2000;69:60–6.
  • Baunez C, Nieoullon A, Amalric M. In a rat model of parkinsonism, lesions of the subthalamic nucleus reverse increases of reaction time but induce a dramatic premature responding deficit. J Neurosci 1995;15:6531–41.
  • Frank MJ, Samanta J, Moustafa AA, Sherman SJ. Hold your horses: impulsivity, deep brain stimulation, and medication in parkinsonism. Science 2007;23318(5854):1309–12.
  • Wichmann T, Bergman H, DeLong MR. The primate subthalamic nucleus. III. Changes in motor behavior and neuronal activity in the internal pallidum induced by subthalamic inactivation in the MPTP model of parkinsonism. J Neurophysiol 1994;72:521–30.
  • Blandini F, Garcia-Osuna M, Greenamyre JT. Subthalamic ablation reverses changes in the basal ganglia oxidative metabolism and motor response to apomorphine induced by nigrostriatal lesion in rats. Eur J Neurosci 1997;9:1407–13.
  • Trost M, Su PC, Barnes A, Su SL, Yen RF, Tseng HM, Ma Y, Eidelberg D. Evolving metabolic changes during the first postoperative year after subthalamotomy. J Neurosurg 2003;99:872–8.
  • Asanuma K, Tang C, Ma Y, Dhawan V, Mattis P, Edwards C, Kaplitt MG, et al. Network modulation in the treatment of Parkinson’s disease. Brain 2006;129:2667–78.
  • Obeso JA, Rodriguez-Oroz MC, Marin C, Alonso F, Zamarbide I, Lanciego JL, Rodriguez-Diaz M. The origin of motor fluctuations in Parkinson’s disease: importance of dopaminergic innervation and basal ganglia circuits. Neurology 2004;62 Suppl 1:17–30.
  • Piallat B, Benazzouz A, Benabid AL. Subthalamic nucleus lesion in rats prevents dopaminergic nigral neuron degeneration after striatal 6-OHDA injection behavioural and immunohistochemical studies. Eur J Neurosc 1996;8:1408–14.