The features of sensorimotor integration in patients with levodopa-induced dyskinesia in Parkinson’s disease
Introduction.Parkinsons disease (PD) is characterized not onlyby motor but also by a number of nonmotor symptoms, such assensory, vegetative, and psycho-emotional disorders. Objective.To study the states of the somatosensory system andthe sensorimotor integration in patients with levodopa-induceddys...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Research Center of Neurology
2017-02-01
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| Series: | Анналы клинической и экспериментальной неврологии |
| Subjects: | |
| Online Access: | https://annaly-nevrologii.com/journal/pathID/article/viewFile/16/117 |
| Summary: | Introduction.Parkinsons disease (PD) is characterized not onlyby motor but also by a number of nonmotor symptoms, such assensory, vegetative, and psycho-emotional disorders.
Objective.To study the states of the somatosensory system andthe sensorimotor integration in patients with levodopa-induceddyskinesia (LID).
Materials and methods.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.
Results.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.
Conclusions.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. |
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| ISSN: | 2075-5473 2409-2533 |