APD  Vol.2 No.3 , August 2013
Factors affecting early decline of executive function after subthalamic nucleus stimulation in Parkinson’s disease
Subthalamic nucleus deep brain stimulation (STN DBS) is an effective treatment for medically refractory Parkinson’s disease (PD). However, a minority of patients develop cognitive problems, particularly a decline of executive function in the early period after STN DBS. Although this problem is usually transient, it may cause social maladjustment. We investigated factors affecting early decline of executive function after STN-DBS. Fifty-seven patients whose preoperative global cognitive screening was normal (MMSE score; 28 or more) were enrolled in this study. Executive function was evaluated with the Trail-Making Test (TMT) preoperatively and 1-month after surgery. We considered a patient to have decline in executive function if the TMT (B-A) was prolonged more than 30 seconds after STN DBS. Among 57 patients, 25 patients were categorized as having decline of executive function. Univariate analysis revealed that high preoperative UPDRS III motor score in the medication-off period and a depressive state evaluated with BDI-II correlated significantly with decline in executive function. Multiple logistic regression analysis revealed that the only significant independent variable related to early decline of executive function was the preoperative BDI-II score. Postoperative factors such as active contact location or dopaminergic medication reduction had no relation with the decline of executive function. Even in cognitively well-selected patients, STN DBS causes early decline in executive function in a significant number of patients. Preoperative simple cognitive screening alone could not predict early decline in executive function. More detailed neuropsychological evaluation, including mood status, should be undertaken before surgery.

Cite this paper
Umemura, A. , Oka, Y. , Tsuboi, R. , Fujii, S. , Shimizu, Y. , Okita, K. , Matsukawa, N. and Yamada, K. (2013) Factors affecting early decline of executive function after subthalamic nucleus stimulation in Parkinson’s disease. Advances in Parkinson's Disease, 2, 75-80. doi: 10.4236/apd.2013.23015.
[1]   Weaver, F.M., Follett, K., Stern, M., Hur, K., Harris, C., Marks Jr., W.J., et al. (2009) Bilateral deep brain stimulation vs best medical therapy for patients with advanced Parkinson disease: A randomized controlled trial. JAMA, 301, 63-73. doi:10.1001/jama.2008.929

[2]   Williams, A., Gill, S., Varma, T., Jenkinson, C., Quinn, N., Mitchell, R., et al. (2010) Deep brain stimulation plus best medical therapy versus best medical therapy alone for advanced Parkinson’s disease (PD SURG trial): A randomised, open-label trial. The Lancet Neurology, 9, 581-591. doi:10.1016/S1474-4422(10)70093-4

[3]   Parsons, T.D., Rogers, S.A., Braaten, A.J., Woods, S.P. and Tr?ster, A.I. (2006) Cognitive sequelae of subthalamic nucleus deep brain stimulation in Parkinson’s disease: A meta-analysis. The Lancet Neurology, 5, 578-588. doi:10.1016/S1474-4422(06)70475-6

[4]   Voon, V., Kubu, C., Krack, P., Houeto, J.L. and Tr?ster, A.I. (2006) Deep brain stimulation: Neuropsychological and neuropsychiatric issues. Movement Disorders, 21, S305-S327. doi:10.1002/mds.20963

[5]   Witt, K., Daniels, C., Reiff, J., Krack, P., Volkmann, J., Pinsker, M.O., et al. (2008) Neuropsychological and psychiatric changes after deep brain stimulation for Parkinson’s disease: A randomised, multicentre study. The Lancet Neurology, 7, 605-614. doi:10.1016/S1474-4422(08)70114-5

[6]   Stuss, D.T. and Levine, B. (2002) Adult clinical neuropsychology: Lessons from studies of the frontal lobes. Annual Review of Psychology, 53, 401-433. doi:10.1146/annurev.psych.53.100901.135220

[7]   Lezak, M.D., Howieson, D.B. and Loring, D.W. (2004) Neuropsychological assessment. 4th Edition, Oxford University Press, New York.

[8]   Zangaglia, R., Pacchetti, C., Pasotti, C., Mancini, F., Servello, D., Sinforiani, E., et al. (2009) Deep brain stimulation and cognitive functions in Parkinson’s disease: A three-year controlled study. Movement Disorders, 24, 1621-1628. doi:10.1002/mds.22603

[9]   Auclair-Ouellet, N., Chantal, S., Cantin, L., Prud’homme, M., Langlois, M. and Macoir, J. (2011) Transient executive dysfunction following STN-DBS in Parkinson’s disease. Canadian Journal of Neurological Sciences, 38, 360-363.

[10]   Yamanaka, T., Ishii, F., Umemura, A., Miyata, M., Horiba, M., Oka, Y., et al. (2012) Temporary deterioration of executive function after subthalamic deep brain stimulation in Parkinson’s disease. Clinical Neurology and Neurosurgery, 114, 347-351. doi:10.1016/j.clineuro.2011.11.009

[11]   Schüpbach, M., Gargiulo, M., Welter, M.L., Mallet, L., Béhar, C., Houeto, J.L., et al. (2006) Neurosurgery in Parkinson disease: A distressed mind in a repaired body? Neurology, 66, 1811-1816. doi:10.1212/01.wnl.0000234880.51322.16

[12]   Smeding, H.M., Speelman, J.D., Koning-Haanstra, M., Schuurman, P.R., Nijssen, P., van Laar, T., et al. (2006) Neuropsychological effects of bilateral STN stimulation in Parkinson disease: A controlled study. Neurology, 66, 1830-1836. doi:10.1212/01.wnl.0000234881.77830.66

[13]   Tomlinson, C.L., Stowe, R., Patel, S., Rick, C., Gray, R. and Clarke, C.E. (2010) Systematic review of levodopa dose equivalency reporting in Parkinson’s disease. Movement Disorders, 25, 2649-2653. doi:10.1002/mds.23429

[14]   Perriol, M.P., Krystkowiak, P., Defebvre, L., Blond, S., Destée, A. and Dujardin, K. (2006) Stimulation of the subthalamic nucleus in Parkinson’s disease: Cognitive and affective changes are not linked to the motor outcome. Parkinsonism & Related Disorders, 12, 205-210. doi:10.1016/j.parkreldis.2005.11.009

[15]   Benarroch, E.E. (2008) Subthalamic nucleus and its connections: Anatomic substrate for the network effects of deep brain stimulation. Neurology, 70, 1991-1995. doi:10.1212/01.wnl.0000313022.39329.65

[16]   Baláz, M., Rektor, I. and Pulkrábek, J. (2008) Participation of the subthalamic nucleus in executive functions: An intracerebral recording study. Movement Disorders, 23, 553-557. doi:10.1002/mds.21873

[17]   Cools, R., Stefanova, E., Barker, R.A., Robbins, T.W. and Owen, A.M. (2002) Dopaminergic modulation of highlevel cognition in Parkinson’s disease: The role of the prefrontal cortex revealed by PET. Brain, 125, 584-594. doi:10.1093/brain/awf052

[18]   Funkiewiez, A., Ardouin, C., Krack, P., Fraix, V., Van Blercom, N., Xie, J., et al. (2003) Acute psychotropic effects of bilateral subthalamic nucleus stimulation and levodopa in Parkinson’s disease. Movement Disorders, 18, 524-530. doi:10.1002/mds.10441

[19]   Dujardin, K., Sockeel, P., Delliaux, M., Destée, A. and Defebvre, L. (2009) Apathy may herald cognitive decline and dementia in Parkinson’s disease. 24, 2391-2397. doi:10.1002/mds.22843

[20]   Butterfield, L.C., Cimino, C.R., Oelke, L.E., Hauser, R.A. and Sanchez-Ramos, J. (2010) The independent influence of apathy and depression on cognitive functioning in Parkinson’s disease. Neuropsychology, 24, 721-730. doi:10.1037/a0019650

[21]   Smeding, H.M., Speelman, J.D., Huizenga, H.M., Schuurman, P.R. and Schmand B. (2011) Predictors of cognitive and psychosocial outcome after STN DBS in Parkinson’s disease. Journal of Neurology, Neurosurgery & Psychiatry, 82, 754-760. doi:10.1136/jnnp.2007.140012

[22]   Daniels, C., Krack, P., Volkmann, J., Pinsker, M.O., Krause, M., Tronnier, V., et al. (2010) Risk factors for executive dysfunction after subthalamic nucleus stimulation in Parkinson’s disease. Movement Disorders, 25, 1583-1589. doi:10.1002/mds.23078

[23]   Lang, A.E., Houeto, J.L., Krack, P., Kubu, C., Lyons, K.E., Moro, E., et al. (2006) Deep brain stimulation: Preoperative issues. Movement Disorders, 21, S171-196. doi:10.1002/mds.20955

[24]   Starkstein, S.E., Preziosi, T.J., Berthier, M.L., Bolduc, P.L., Mayberg, H.S., Robinson, R.G. (1989) Depression and cognitive impairment in Parkinson’s disease. Brain, 112, 1141-1153. doi:10.1093/brain/112.5.1141

[25]   Giladi, N., Treves, T.A., Paleacu, D., Shabtai, H., Orlov, Y., Kandinov, B., et al. (2000) Risk factors for dementia, depression and psychosis in long-standing Parkinson’s disease. Journal of Neural Transmission, 107, 59-71. doi:10.1007/s007020050005

[26]   Mayberg, H.S., Starkstein, S.E., Sadzot, B., Preziosi, T., Andrezejewski, P.L., Dannals, R.F., et al. (1990) Selective hypometabolism in the inferior frontal lobe in depressed patients with Parkinson’s disease. Annals of Neurology, 28, 57-64. doi:10.1002/ana.410280111

[27]   Mayberg, H.S. (1994) Frontal lobe dysfunction in secondary depression. The Journal of Neuropsychiatry and Clinical Neurosciences, 6, 428-442.

[28]   Smeding, H.M., van den Munckhof, P., Esselink, R.A., Schmand, B., Schuurman, P.R. and Speelman, J.D. (2007) Reversible cognitive decline after DBS STN in PD and displacement of electrodes. Neurology, 68, 1235-1236. doi:10.1212/01.wnl.0000259067.68691.87

[29]   Tsai, S.T., Lin, S.H., Lin, S.Z., Chen, J.Y., Lee, C.W. and Chen, S.Y. (2007) Neuropsychological effects after chronic subthalamic stimulation and the topography of the nucleus in Parkinson’s disease. Neurosurgery, 61, E1024-E1029. doi:10.1227/01.neu.0000303198.95296.6f

[30]   York, M.K., Wilde, E.A., Simpson, R. and Jankovic, J. (2009) Relationship between neuropsychological outcome and DBS surgical trajectory and electrode location. Journal of the Neurological Sciences, 287, 159-171. doi:10.1016/j.jns.2009.08.003