Annals of Clinical and Experimental NeurologyAnnals of Clinical and Experimental NeurologyАнналы клинической и экспериментальной неврологии2075-54732409-2533Eco-Vector1610.17816/psaic16Original articlesОригинальные статьиUnknownThe features of sensorimotor integration in patients with levodopa-induced dyskinesia in Parkinson’s diseaseОсобенности сенсорно-моторной интеграции у пациентов с леводопа-индуцированными дискинезиями при болезни ПаркинсонаAlenikovaOlga A.АлениковаОльга Анатольевна
Belarus
71alenicovaolga@tut.byLikhachevS. A.ЛихачевС. A.
Belarus
71alenicovaolga@tut.bySvinkovskayaT. V.СвинковскаяT. В.
Belarus
71alenicovaolga@tut.byRepublican Research and Clinical Center of Neurology and Neurosurgery, the Ministry of Healthcare of the Republic of BelarusГУ «Республиканский научно-практический центр неврологии и нейрохирургии» Министерства здравоохранения Республики Беларусь02122016104202530012017Copyright ©; 2016, Alenikova O.A., Likhachev S.A., Svinkovskaya T.V.Copyright ©; 2016, Alenikova O.A., Likhachev S.A., Svinkovskaya T.V.2016Alenikova O.A., Likhachev S.A., Svinkovskaya T.V.Alenikova O.A., Likhachev S.A., Svinkovskaya T.V.https://creativecommons.org/licenses/by/4.0https://annaly-nevrologii.com/pathID/article/view/16

Introduction. Parkinson’s disease (PD) is characterized not only by motor but also by a number of nonmotor symptoms, such as sensory, vegetative, and psycho-emotional disorders.Objective. To study the states of the somatosensory system and the sensorimotor integration in patients with levodopa-induced dyskinesia (LID).Materials and methods. Fifty-two patients with LID associated with PD (Hoehn and Yahr stage III–IV) and 29 patients free of dyskinesia were examined. The somatosensory evoked potentials (SSEPs) and blink reflex (BR) were studied.Results. LID in PD were observed significantly more often among females than among males. No differences in disease duration and duration of levodopa administration were observed among patients free of dyskinesia and patients with LID. In the group of patients with LID, MRI examination showed increased brainstem reflex excitability. The acceleration of signal passing from the medulla oblongata to the cortex revealed according to the SSEP data in this group of patients is indicative of the increased reflex excitability at the spinal cord and brainstem, thalamic, and cortical levels. Significant differences in passage of sensory information were found between the two patient groups. Hence, in patients 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 reliably shorter than in the group of patients free of LID, where the latency N20 was 20.9 (20; 21.4) ms; Р18, 16.9 (16.2; 17.6); and N13, 14.2 (13.5; 15.2) ms.Conclusions. The revealed alterations in parameters of blink reflex and SSEPs are hypothetically genetically determined in patients with LID. Objectification of these disorders at the earliest stages of the disease can help in assessing their role as predictor factors for development of LID. Allowance for these factors will make it possible to choose an appropriate treatment strategy and reduce the risk of complications associated with drug therapy.

Введение. Болезнь Паркинсона (БП) характеризуется не только двигательными симптомами, но и целым рядом немоторных нарушений: сенсорных, вегетативных, психоэмоциональных.Цель работы. Изучение состояния соматосенсорной системы и сенсорно-моторной интеграции у пациентов с леводопа-индуцированными дискинезиями (ЛИД).Материалы и методы. Обследовано 52 пациента с ЛИД при БП в стадии 3–4 по функциональной шкале Хен–Яра и 29 пациентов без дискинезий. Исследовались соматосенсорные вызванные потенциалы (ССВП) и мигательный рефлекс (МР).Результаты. ЛИД при БП встречались достоверно чаще у женщин, чем у мужчин. Различия по продолжительности заболевания и длительности приема леводопы между пациентами без дискинезий и с ЛИД отсутствовали. В группе пациентов с ЛИД исследование МР показало повышение рефлекторной возбудимости на стволовом уровне. Выявленное ускорение прохождения сигнала от уровня продолговатого мозга к коре, по данным ССВП, у данной категории больных указывает на повышение рефлекторной возбудимости на спинально-стволовом, таламическом и кортикальном уровнях. Между двумя группами пациентов установлены значимые различия в проведении сенсорной информации. Так, у лиц с ЛИД латентное время N20 составило 20 (19,6; 21,3) мс, Р18 – 16,0 (15,1; 16,6) мс, N13 – 13,7 (13,1; 14,8) мс и было достоверно короче, чем в группе пациентов без ЛИД, где латентность N20 – 20,9 (20; 21,4) мс, Р18 – 16,9 (16,2; 17,6) и N13 – 14,2 (13,5; 15,2) мс.Заключение. Можно предположить, что выявленные изменения в параметрах МР и ССВП у пациентов с ЛИД генетически детерминированы. Объективизация этих нарушений на самых ранних стадиях заболевания может помочь оценить их роль в качестве предикторных факторов развития ЛИД, учет которых позволит выбрать правильную тактику лечения и снизить риск осложнений медикаментозной терапии.

Parkinson’s diseaselevodopa-induced dyskinesiasblink reflexsomatosensory evoked potentialssensorimotor integrationболезнь Паркинсоналеводопа-индуцированные дискинезиимигательный рефлекссоматосенсорные вызванные потенциалысенсорно-моторная интеграцияDefazio 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.62.4.601Illarioshkin 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.