Annals of Clinical and Experimental NeurologyAnnals of Clinical and Experimental Neurology2075-54732409-2533Research Center of Neurology1610.17816/psaic16UnknownThe features of sensorimotor integration in patients with levodopa-induced dyskinesia in Parkinson’s diseaseAlenikovaOlga A.71alenicovaolga@tut.byLikhachevS. A.71alenicovaolga@tut.bySvinkovskayaT. V.71alenicovaolga@tut.byRepublican Research and Clinical Center of Neurology and Neurosurgery, the Ministry of Healthcare of the Republic of Belarus02122016104202530012017Copyright © 2016, Alenikova O.A., Likhachev S.A., Svinkovskaya T.V.2016<p><strong>Introduction.</strong>Parkinsons disease (PD) is characterized not onlyby motor but also by a number of nonmotor symptoms, such assensory, vegetative, and psycho-emotional disorders.<br /><strong>Objective.</strong>To study the states of the somatosensory system andthe sensorimotor integration in patients with levodopa-induceddyskinesia (LID).<br /><strong>Materials and methods.</strong>Fifty-two patients with LID associatedwith PD (Hoehn and Yahr stage IIIIV) and 29 patients free ofdyskinesia were examined. The somatosensory evoked potentials(SSEPs) and blink reflex (BR) were studied.<br /><strong>Results.</strong>LID in PD were observed significantly more often amongfemales than among males. No differences in disease durationand duration of levodopa administration were observed amongpatients free of dyskinesia and patients with LID. In the groupof patients with LID, MRI examination showed increased brainstemreflex excitability. The acceleration of signal passing fromthe medulla oblongata to the cortex revealed according to theSSEP data in this group of patients is indicative of the increasedreflex excitability at the spinal cord and brainstem, thalamic, andcortical levels. Significant differences in passage of sensory informationwere found between the two patient groups. Hence, inpatients with LID, the latency N20 was 20 (19.6; 21.3) ms; P18,16.0 (15.1; 16.6) ms; and N13, 13.7 (13.1; 14.8) and was reliablyshorter than in the group of patients free of LID, where the latencyN20 was 20.9 (20; 21.4) ms; Р18, 16.9 (16.2; 17.6); and N13,14.2 (13.5; 15.2) ms.<br /><strong>Conclusions.</strong>The revealed alterations in parameters of blinkreflex and SSEPs are hypothetically genetically determinedin patients with LID. Objectification of these disorders at theearliest stages of the disease can help in assessing their role aspredictor factors for development of LID. Allowance for thesefactors will make it possible to choose an appropriate treatmentstrategy and reduce the risk of complications associated withdrug therapy.</p>Parkinson’s diseaselevodopa-induced dyskinesiasblink reflexsomatosensory evoked potentialssensorimotor integrationболезнь Паркинсоналеводопа-индуцированные дискинезиимигательный рефлекссоматосенсорные вызванные потенциалысенсорно-моторная интеграция[Defazio G., Berardelli A., Fabbrini G., et al. Pain as a non motor symptom of parkinson disease: evidence from a case-control study. Arch. Neurol. 2008; 65(9): 1191–1194. DOI: 10.1001/archneurol.2008.2.][Illarioshkin S.N. [Treatment of Parkinson’s disease: possibilities and prospects]. Nevrologiya i revmatologiya. Prilozhenie k zhurnalu Consilium Medicum [Neurology and Rheumatology. Supplement to the journal Consilium Medicum]. 2009; 1: 35–40. (In Russ.).][DelSorbo F., Albanese A. Levodopa-induced dyskinesias and their management. J. Neurol. 2008; 255 [Suppl 4]: 32–41. DOI: 10.1007/s00415-008-4006-5.][Fabbrini G., Brotchie J.M., Grandas F. et al. Levodopa-Induced Dyskinesias. Mov. Disord. 2007; 22 (10):1379–1389. PMID: 17427940. DOI: 10.1002/mds.21475.][Guridi J., González-Redondo R., Obeso J.A. Clinical Features, Pathophysiology, and Treatment of Levodopa-Induced Dyskinesias in Parkinson’s Disease. Hindawi Publishing Corporation Parkinson’s Disease. 2012; PMID 943159. DOI:10.1155/2012/943159.][Obeso J.A., Rodriguez-Oroz M.C., Rodriguez M. et al. Pathophysiology of levodopa-induced dyskinesias in Parkinson’s disease: problems with the current model. Annals of Neurology. 2000; 47 (4): 22–34. PMID: 10762129.][Shtok V.N., Fedorova N.V. Parkinson’s disease. In: Shtok V.N., Ivanova- Smolenskaya I.A., Levin O.S. Ekstrapiramidnye rasstroystva: Rukovodstvo po diagnostike i lecheniyu. [Extrapyramidal disorders: diagnosis and treatment Guide]. М.: Moscow. MEDpress-inform, 2002: 87–124 (In Russ.).][Vidailhet M., Bonnet A.M., Marconi R. The phenomenology of L-dopa-induced dyskinesias in Parkinson’s disease. Mov. Disord. 1999; 14 (Suppl 1): 13–18.][Albin R. L. The pathophysiology of chorea/ballism and Parkinsonism. Parkinsonism and Related Disorders. 1995; 1 (1): 3–11.][Bezard E., Brotchie J.M., Gross C.E. Pathophysiology of levodopa-induced dyskinesia: potential or new therapies. Nat. Rev. Neurosci. 2001; 2: 577–588. PMID: 11484001. DOI: 10.1038/35086062.][Gerfen C.R., Engber T.M., Mahan L.C. et al. D1 and D2 dopamine receptor-regulated gene expression of striato-nigral and striatopallidal neurons. Science. 1990; 250: 1429–1432. PMID: 2147780.][Olanow C.W., Obeso J.A., Stocchi F. Continuous dopamine-receptor treatment of Parkinson’s disease: scientific rationale and clinical implications. Lancet Neurol. 2006; 5: 677–687. PMID: 16857573. DOI: 10.1016/S1474-4422(06)70521-X.][Albin R.L., Young A.B. Somatosensory phenomena in Huntington’s disease. Mov. Disord.1988; 3: 343-346. PMID: 2974928. DOI: 10.1002/mds.870030411.][Beniczky S., Kéri S., Antal A. Somatosensory evoked potentials correlate with genetics in Huntington’s disease. Neuroreport. 2002; 3(13): 2295–2298.][Boecker H., Ceballos-Baumann A., Bartenstein P. et al. Sensory processing in Parkinson’s and Huntington’s disease: investigations with 3D H(2)(15)O-PET. Brain. 1999; 122: 1651–1665. PMID: 10468505.][Lefaucheur J.P., Bachoud-Levi A.C., Bourdet C. Clinical relevance of electrophysiological Tests in the assessment of patients with Huntington’s disease. Mov. Disord. 2002; 176: 1294–1301.][Yamada T., Rodnitzky R.L., Kameyama S. et al. Alteration of SEP topography in Huntington’s patients and their relatives at risk. Electroencephalog. Clin. Neurophysiol. 1991; 80(4): 251–261. PMID: 1713835.][Abbruzzese G., Berardelli A. Sensorimotor integration in movement disorders. Mov. Disord. 2003; 18: 231–240. PMID: 12621626. DOI: 10.1002/mds.10327.][Kaji R. Basal ganglia as a sensory gating devise for motor control. J. Med. Invest. 2001; 48(3–4): 142–146.][Valls-Sole J. Neurophysiological assessment of trigeminal nerve reflexes in disorders of central and peripheral nervous system. Clinical Neurophysiology. 2005; 116: 2255–2265. PMID: 16005260. DOI: 10.1016/j.clinph.2005.04.020.][Alenikova O.A., Likhachev S.A. [Blink reflex parameters in periods of motor fluctuations in Parkinson’s disease]. Mezhdunarodnyy Nevrologicheskiy zhurnal [International Neurological Journal].2013; 4 (58): 25–30. (In Russ.).][Calabresi P., Filippo M.D., Ghiglieri V., N. et al. Levodopa-induced dyskinesias in patients with Parkinson’s disease: filling the benchto-bedside gap. Lancet Neurology. 2010; 9 (11): 1106–1117. DOI: 10.1016/S1474-4422(10)70218-0.][Zappia M., Annesi G., Nicoletti G. et al. Sex differences in clinical and genetic determinants of levodopa peak-dose dyskinesias in Parkinson disease: an exploratorystudy. Arch. Neurol. 2005; 62: 601–605. PMID: 15824260. DOI: 10.1001/archneur.62.4.601][Illarioshkin S.N. [Parkinsonism with early onset]. Nervnye bolezni [Neural Disease]. 2006; 3: 14–20. (In Russ.).][Illarioshkin S.N., Zagorovskaya T.B., Markova E.D. et al. Mutation analysis of the parkin gene in Russian families with autosomal recessive juvenile parkinsonism. Mov. Disord. 2003; 18: 914–919.]