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Current Neurovascular Research

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ISSN (Print): 1567-2026
ISSN (Online): 1875-5739

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Research Article

Risk Factors and Metabolism of Different Brain Regions by Positron Emission Tomography in Parkinson Disease with Disabling Dyskinesia

Author(s): Huan Wei, Yongtao Zhou *, Junwu Zhao and Liping Zhan

Volume 16, Issue 4, 2019

Page: [310 - 320] Pages: 11

DOI: 10.2174/1567202616666191009102112

Price: $65

Abstract

Objective: Dyskinesia is the most common motor complication in advanced Parkinson’s Disease (PD) and has a severe impact on daily life. But the mechanism of dyskinesia is still poorly understood. This study aims to explore risk factors for disabling dyskinesia in PD and further analyze the Vesicular Monoamine Transporter 2 (VMAT2) distribution (labeled with 18F-AV133) in the corpus striatum and the 18F-fluorodeoxyglucose (18F-FDG) metabolism of different brain regions by PET-CT.

Methods: This is a cross-sectional study involving 135 PD patients. They were divided into disabling dyskinesia group (DD group, N=22) and non-dyskinesia group (ND group, N=113). All the patients were agreed to undergo PET-CT scans. Clinical data were analyzed between two groups by using multivariate logistic regression analysis, and risk factors for disabling dyskinesia were then determined. The standard uptake value ratios (SUVr) of 18F-AV133 in the corpus striatum and the 18F-FDG metabolism of different brain regions were identified and calculated by the software.

Results: 16.3% patients have disabling dyskinesia. DD group were more likely to have longer Disease Duration, higher Hoehn-Yahr degree, more severe clinic symptoms, more frequent sleep behavior disorder, and higher levodopa dose equivalency than ND group (P < 0.05). After adjusting confounding factors by multivariate logistic regression, DD group had longer PD duration and high levodopa dose equivalency compared with ND group (P < 0.05). There is no significant difference between the VMAT2 distribution (labeled with 18F- AV133) in the putamen and caudate between two groups. And the 18F-FDG metabolic changes in cortical and subcortical regions did not show a significant difference between the two groups either (P > 0.05).

Conclusion: Long PD duration and high levodopa dose equivalency were two independent risk factors for disabling dyskinesia in PD patients. Compared to non-dyskinesia PD patients, there was no significant dopamine decline of the nigrostriatal system in disabling dyskinesia PD patients. Activities of different brain regions were not different between the two groups by 18F-FDG PETCT.

Keywords: Dyskinesia, Parkinson's disease, risk factors, metabolism, Positron Emission Tomography (PET), levodopainduced dyskinesia.

« Previous Next »
[1]
Horstink M, Tolosa E, Bonuccelli U, et al. European Federation of Neurological Societies Movement Disorder Society-European Section. Review of the therapeutic management of Parkinson’s disease. Report of a joint task force of the European Federation of Neurological Societies (EFNS) and the Movement Disorder Society-European Section (MDS-ES). Part II: Late (complicated) Parkinson’s disease. Eur J Neurol 2006; 13(11): 1186-202.
[http://dx.doi.org/10.1111/j.1468-1331.2006.01548.x] [PMID: 17038032]
[2]
Haaxma CA, Horstink MW, Zijlmans JC, Lemmens WA, Bloem BR, Borm GF. Risk of disabling response fluctuations and dyskinesias for dopamine agonists versus levodopa in parkinson’s disease. J Parkinsons Dis 2015; 5(4): 847-53.
[http://dx.doi.org/10.3233/JPD-150532] [PMID: 26444087]
[3]
Carta AR, Mulas G, Bortolanza M, et al. l-DOPA-induced dyskinesia and neuroinflammation: Do microglia and astrocytes play a role? Eur J Neurosci 2017; 45(1): 73-91.
[http://dx.doi.org/10.1111/ejn.13482] [PMID: 27859864]
[4]
Cerasa A, Koch G, Donzuso G, et al. A network centred on the inferior frontal cortex is critically involved in levodopa-induced dyskinesias. Brain 2015; 138(Pt 2): 414-27.
[http://dx.doi.org/10.1093/brain/awu329] [PMID: 25414038]
[5]
Cenci MA, Jörntell H, Petersson P. On the neuronal circuitry mediating L-DOPA-induced dyskinesia. J Neural Transm (Vienna) 2018; 125(8): 1157-69.
[http://dx.doi.org/10.1007/s00702-018-1886-0] [PMID: 29704061]
[6]
Brooks DJ, Pavese N. Imaging biomarkers in Parkinson’s disease. Prog Neurobiol 2011; 95(4): 614-28.
[http://dx.doi.org/10.1016/j.pneurobio.2011.08.009] [PMID: 21896306]
[7]
Tripathi M, Dhawan V, Peng S, et al. Differential diagnosis of parkinsonian syndromes using F-18 fluorodeoxyglucose positron emission tomography. Neuroradiology 2013; 55(4): 483-92.
[http://dx.doi.org/10.1007/s00234-012-1132-7] [PMID: 23314836]
[8]
Niethammer M, Eidelberg D. Metabolic brain networks in translational neurology: Concepts and applications. Ann Neurol 2012; 72(5): 635-47.
[http://dx.doi.org/10.1002/ana.23631] [PMID: 22941893]
[9]
Postuma RB, Berg D, Stern M, et al. MDS clinical diagnostic criteria for Parkinson’s disease. Mov Disord 2015; 30(12): 1591-601.
[http://dx.doi.org/10.1002/mds.26424] [PMID: 26474316]
[10]
Hoehn MM, Yahr MD. Parkinsonism: Onset, progression and mortality. Neurology 1967; 17(5): 427-42.
[http://dx.doi.org/10.1212/WNL.17.5.427] [PMID: 6067254]
[11]
Fahn S, Elton RL. Members of the UPDRS Development Committee. Unified Parkinson’s disease rating scale Recent developmentsin Parkinson’s disease. Florham Park: Macmillan Healthcare Information 1987; pp. 153-63.
[12]
Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975; 12(3): 189-98.
[http://dx.doi.org/10.1016/0022-3956(75)90026-6] [PMID: 1202204]
[13]
Kandiah N, Zhang A, Cenina AR, Au WL, Nadkarni N, Tan LC. Montreal Cognitive Assessment for the screening and prediction of cognitive decline in early Parkinson’s disease. Parkinsonism Relat Disord 2014; 20(11): 1145-8.
[http://dx.doi.org/10.1016/j.parkreldis.2014.08.002] [PMID: 25176439]
[14]
Li SX, Wing YK, Lam SP, et al. Validation of a new REM sleep behavior disorder questionnaire (RBDQ-HK). Sleep Med 2010; 11(1): 43-8.
[http://dx.doi.org/10.1016/j.sleep.2009.06.008] [PMID: 19945912]
[15]
Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep 1991; 14(6): 540-5.
[http://dx.doi.org/10.1093/sleep/14.6.540] [PMID: 1798888]
[16]
Tomlinson CL, Stowe R, Patel S, Rick C, Gray R, Clarke CE. Systematic review of levodopa dose equivalency reporting in Parkinson’s disease. Mov Disord 2010; 25(15): 2649-53.
[http://dx.doi.org/10.1002/mds.23429] [PMID: 21069833]
[17]
Zhou Y, Su Y, Xu W, et al. constipation increases disability and decreases dopamine levels in the nigrostriatal system through gastric inflammatory factors in parkinson’s disease. Curr Neurovasc Res 2019. [Epub ahead of print]
[18]
Bjornestad A, Forsaa EB, Pedersen KF, Tysnes OB, Larsen JP, Alves G. Risk and course of motor complications in a population-based incident Parkinson’s disease cohort. Parkinsonism Relat Disord 2016; 22: 48-53.
[http://dx.doi.org/10.1016/j.parkreldis.2015.11.007] [PMID: 26585090]
[19]
de la Fuente-Fernández R, Lu JQ, Sossi V, et al. Biochemical variations in the synaptic level of dopamine precede motor fluctuations in Parkinson’s disease: PET evidence of increased dopamine turnover. Ann Neurol 2001; 49(3): 298-303.
[http://dx.doi.org/10.1002/ana.65] [PMID: 11261503]
[20]
de La Fuente-Fernández R, Lim AS, Sossi V, et al. Apomorphine-induced changes in synaptic dopamine levels: Positron emission tomography evidence for presynaptic inhibition. J Cereb Blood Flow Metab 2001; 21(10): 1151-9.
[http://dx.doi.org/10.1097/00004647-200110000-00003] [PMID: 11598492]
[21]
de la Fuente-Fernández R, Sossi V, Huang Z, et al. Levodopa-induced changes in synaptic dopamine levels increase with progression of Parkinson’s disease: Implications for dyskinesias. Brain 2004; 127(Pt 12): 2747-54.
[http://dx.doi.org/10.1093/brain/awh290] [PMID: 15329355]
[22]
Lewitt PA, Mouradian MM. Predicting the development of levodopa-induced dyskinesias: A presynaptic mechanism? Neurology 2014; 82(18): 1574-5.
[http://dx.doi.org/10.1212/WNL.0000000000000390] [PMID: 24719487]
[23]
Pagano G, Niccolini F, Politis M. Current status of PET imaging in Huntington’s disease. Eur J Nucl Med Mol Imaging 2016; 43(6): 1171-82.
[http://dx.doi.org/10.1007/s00259-016-3324-6] [PMID: 26899245]
[24]
Politis M, Piccini P. Positron emission tomography imaging in neurological disorders. J Neurol 2012; 259(9): 1769-80.
[http://dx.doi.org/10.1007/s00415-012-6428-3] [PMID: 22297461]
[25]
Niccolini F, Su P, Politis M. Dopamine receptor mapping with PET imaging in Parkinson’s disease. J Neurol 2014; 261(12): 2251-63.
[http://dx.doi.org/10.1007/s00415-014-7302-2] [PMID: 24627109]
[26]
Kum WF, Gao J, Durairajan SS, et al. Risk factors in development of motor complications in Chinese patients with idiopathic Parkinson’s disease. J Clin Neurosci 2009; 16(8): 1034-7.
[http://dx.doi.org/10.1016/j.jocn.2008.10.015] [PMID: 19428256]
[27]
Zhang ZX, Chen H, Chen SD, et al. Chinese culture permeation in the treatment of Parkinson disease: A cross-sectional study in four regions of China. BMC Res Notes 2014; 7: 65.
[http://dx.doi.org/10.1186/1756-0500-7-65] [PMID: 24476129]
[28]
Ahlskog JE, Muenter MD. Frequency of 1evodopa-related dyskinesia and motor fluctuations as estimated from the cumulative literature. Mov Disord 2001; 16: 48-458.
[http://dx.doi.org/10.1002/mds.1090]
[29]
Warren Olanow C, Kieburtz K, Rascol O, et al. Stalevo Reduction in Dyskinesia Evaluation in Parkinson’s Disease (STRIDE-PD) Investigators. Factors predictive of the development of Levodopainduced dyskinesia and wearing-off in Parkinson’s disease. Mov Disord 2013; 28(8): 1064-71.
[http://dx.doi.org/10.1002/mds.25364] [PMID: 23630119]
[30]
Hinkle JT, Perepezko K, Rosenthal LS, et al. Markers of impaired motor and cognitive volition in Parkinson’s disease: Correlates of dopamine dysregulation syndrome, impulse control disorder, and dyskinesias. Parkinsonism Relat Disord 2018; 47: 50-6.
[http://dx.doi.org/10.1016/j.parkreldis.2017.11.338] [PMID: 29198499]
[31]
Grandas F, Galiano ML, Tabernero C. Risk factors for levodopa-induced dyskinesias in Parkinson’s disease. J Neurol 1999; 246(12): 1127-33.
[http://dx.doi.org/10.1007/s004150050530] [PMID: 10653303]
[32]
Rajput AH. Factors predictive of the development of levodopa-induced dyskinesia and wearing-off in Parkinson’s disease. Mov Disord 2014; 29(3): 429.
[http://dx.doi.org/10.1002/mds.25800] [PMID: 24375668]
[33]
Hashim HZ, Norlinah MI, Nafisah WY, Tan HJ, Raymond AA, Tamil AM. Risk factors and predictors of levodopa-induced dyskinesia among multiethnic Malaysians with Parkinson’s disease. Int J Neurosci 2014; 124(3): 187-91.
[http://dx.doi.org/10.3109/00207454.2013.833511] [PMID: 23952588]
[34]
Chen HM, Feng T, Ma HZ. Risk factors for dyskinesia and levodopa safe dosage for Parkinson’s disease based on data-mining analysis. Chin J Geriatr Heart Brain Vessel Dis 2017; 8: 789-92.
[35]
Shen SS, Shen Y, Xiong KP, et al. Validation study of REM sleep behavior disorder questionnaire-Hong Kong (RBDQ-HK) in east China. Sleep Med 2014; 15(8): 952-8.
[http://dx.doi.org/10.1016/j.sleep.2014.03.020] [PMID: 24938584]
[36]
Postuma RB, Gagnon JF, Vendette M, Charland K, Montplaisir J. REM sleep behaviour disorder in Parkinson’s disease is associated with specific motor features. J Neurol Neurosurg Psychiatry 2008; 79(10): 1117-21.
[http://dx.doi.org/10.1136/jnnp.2008.149195] [PMID: 18682443]
[37]
Putterman DB, Munhall AC, Kozell LB, Belknap JK, Johnson SW. Evaluation of levodopa dose and magnitude of dopamine depletion as risk factors for levodopa-induced dyskinesia in a rat model of Parkinson’s disease. J Pharmacol Exp Ther 2007; 323(1): 277-84.
[http://dx.doi.org/10.1124/jpet.107.126219] [PMID: 17660384]
[38]
Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi B. Levodopa-induced dyskinesias in patients with Parkinson’s disease: Filling the bench-to-bedside gap. Lancet Neurol 2010; 9(11): 1106-17.
[http://dx.doi.org/10.1016/S1474-4422(10)70218-0] [PMID: 20880751]
[39]
de la Fuente-Fernández R, Pal PK, Vingerhoets FJ, et al. Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations. J Neural Transm (Vienna) 2000; 107(1): 49-57.
[http://dx.doi.org/10.1007/s007020050004] [PMID: 10809403]
[40]
Hong JY, Oh JS, Lee I, et al. Presynaptic dopamine depletion predicts levodopa-induced dyskinesia in de novo Parkinson disease. Neurology 2014; 82(18): 1597-604.
[http://dx.doi.org/10.1212/WNL.0000000000000385] [PMID: 24719485]
[41]
Hsiao IT, Weng YH, Hsieh CJ, et al. Correlation of Parkinson disease severity and 18F-DTBZ positron emission tomography. JAMA Neurol 2014; 71(6): 758-66.
[http://dx.doi.org/10.1001/jamaneurol.2014.290] [PMID: 24756323]
[42]
Linazasoro G, Van Blercom N, Bergaretxe A, Iñaki FM, Laborda E, Ruiz Ortega JA. Levodopa-induced dyskinesias in Parkinson disease are independent of the extent of striatal dopaminergic denervation: a pharmacological and SPECT study. Clin Neuropharmacol 2009; 32(6): 326-9.
[http://dx.doi.org/10.1097/WNF.0b013e3181b52792] [PMID: 19855268]
[43]
Tanaka H, Kannari K, Maeda T, Tomiyama M, Suda T, Matsunaga M. Role of serotonergic neurons in L-DOPA-derived extracellular dopamine in the striatum of 6-OHDA-lesioned rats. Neuroreport 1999; 10(3): 631-4.
[http://dx.doi.org/10.1097/00001756-199902250-00034] [PMID: 10208602]
[44]
Niccolini F, Rocchi L, Politis M. Molecular imaging of levodopa-induced dyskinesias. Cell Mol Life Sci 2015; 72(11): 2107-17.
[http://dx.doi.org/10.1007/s00018-015-1854-x] [PMID: 25681866]
[45]
Pagano G, Yousaf T, Politis M. PET molecular imaging research of levodopa-induced dyskinesias in Parkinson’s disease. Curr Neurol Neurosci Rep 2017; 17(11): 90.
[http://dx.doi.org/10.1007/s11910-017-0794-2] [PMID: 28975571]
[46]
Attwell D, Iadecola C. The neural basis of functional brain imaging signals. Trends Neurosci 2002; 25(12): 621-5.
[http://dx.doi.org/10.1016/S0166-2236(02)02264-6] [PMID: 12446129]
[47]
Attwell D, Iadecola C. The neural basis of functional brain imaging signals. Trends Neurosci 2002; 25(12): 621-5.
[48]
Heeger DJ, Ress D. What does fMRI tell us about neuronal activity? Nat Rev Neurosci 2002; 3(2): 142-51.
[http://dx.doi.org/10.1038/nrn730] [PMID: 11836522]
[49]
Wu P, Wang J, Peng S, et al. Metabolic brain network in the Chinese patients with Parkinson’s disease based on 18F-FDG PET imaging. Parkinsonism Relat Disord 2013; 19(6): 622-7.
[http://dx.doi.org/10.1016/j.parkreldis.2013.02.013] [PMID: 23529021]
[50]
Ma Y, Tang C, Spetsieris PG, Dhawan V, Eidelberg D. Abnormal metabolic network activity in Parkinson’s disease: Test-retest reproducibility. J Cereb Blood Flow Metab 2007; 27(3): 597-605.
[http://dx.doi.org/10.1038/sj.jcbfm.9600358] [PMID: 16804550]
[51]
Spetsieris PG, Eidelberg D. Scaled subprofile modeling of resting state imaging data in Parkinson’s disease: Methodological issues. Neuroimage 2011; 54(4): 2899-914.
[http://dx.doi.org/10.1016/j.neuroimage.2010.10.025] [PMID: 20969965]
[52]
Hirano S, Asanuma K, Ma Y, et al. Dissociation of metabolic and neurovascular responses to levodopa in the treatment of Parkinson’s disease. J Neurosci 2008; 28(16): 4201-9.
[http://dx.doi.org/10.1523/JNEUROSCI.0582-08.2008] [PMID: 18417699]
[53]
Lozza C, Baron JC, Eidelberg D, Mentis MJ, Carbon M, Marié RM. Executive processes in Parkinson’s disease: FDG-PET and network analysis. Hum Brain Mapp 2004; 22(3): 236-45.
[http://dx.doi.org/10.1002/hbm.20033] [PMID: 15195290]
[54]
Brooks DJ, Piccini P, Turjanski N, Samuel M. Neuroimaging of dyskinesia. Ann Neurol 2000; 47(4): S154-8.
[PMID: 10762143]
[55]
Kuriakose R, Stoessl AJ. Imaging the nigrostriatal system to monitor disease progression and treatment-induced complications.Prog Brain Res. 2010; 184: pp. 177-92.
[http://dx.doi.org/ 10.1016/S0079-6123(10)84009-9] [PMID: 20887875]
[56]
Kogan RV, de Jong BA, Renken RJ, et al. Factors affecting the harmonization of disease-related metabolic brain pattern expression quantification in [18F]FDG-PET (PETMETPAT). Alzheimers Dement (Amst) 2019; 11: 472-82.
[57]
Musafargani S, Ghosh KK, Mishra S, Mahalakshmi P, Padmanabhan P, Gulyás B. PET/MRI: A frontier in era of complementary hybrid imaging. Eur J Hybrid Imaging 2018; 2(1): 12.
[http://dx.doi.org/10.1186/s41824-018-0030-6] [PMID: 29998214]
[58]
Zhang XY, Yang ZL, Lu GM, Yang GF, Zhang LJ. PET/MR imaging: New frontier in Alzheimer’s disease and other dementias. Front Mol Neurosci 2017; 10: 343.
[http://dx.doi.org/10.3389/fnmol.2017.00343] [PMID: 29163024]

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