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1.
Zh Nevrol Psikhiatr Im S S Korsakova ; 118(6. Vyp. 2): 95-98, 2018.
Article in Russian | MEDLINE | ID: mdl-30346441

ABSTRACT

AIM: To study the efficacy of replacement of the single daily dose of two-component levodopa by three-component levodopa in work capable patients with Parkinson's disease with motor fluctuations during the most active working hours. MATERIAL AND METHODS: The study included 157 patients from 19 Russian centers specialized in extrapyramidal pathology. The period of highest working activity was analyzed in all patients. In these patients, the previous treatment with two-component levodopa was replaced by three-component levodopa in the equivalent dose. Other antiparkinsonian treatment remained unchanged during the study period. The duration of the study was 1 month. RESULTS AND CONCLUSION: The single replacement of two-component levodopa by stalevo allows increasing the optimal working activity by 19% and improving patient's state.


Subject(s)
Parkinson Disease , Antiparkinson Agents , Humans , Levodopa , Russia
2.
Klin Med (Mosk) ; 93(1): 18-22, 2015.
Article in Russian | MEDLINE | ID: mdl-26031144

ABSTRACT

Polyneuropathy of thin fibers (PTF) is a disorder with selective damage of Aδ- and C-fibers. Having a skin biopsy the SFN became visible. In the article there are data on the pathogenesis, clinics and diagnostics of the PTF. The skin biopsy, the quantitative sensory testing, the corneal confocal microscopy, nociceptive evoked potentials, the microneurography and the autonomic testing are described in detail. New diagnostic criteria ofthe PTF are given. Main directions in the management of the PTF are the treatment of systemic diseases and the neuropathic pain relief.


Subject(s)
Nerve Fibers, Myelinated/pathology , Nerve Fibers, Unmyelinated/pathology , Polyneuropathies , Humans , Polyneuropathies/diagnosis , Polyneuropathies/pathology , Polyneuropathies/physiopathology
3.
Vestn Oftalmol ; 131(5): 82-86, 2015.
Article in Russian | MEDLINE | ID: mdl-26845877

ABSTRACT

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a mutation in the huntingtin gene. The whole nervous system, including visual analyzer, is involved in the pathogenesis of the disease. Various ocular sings can be found in both preclinical and clinical stages of HD. Specific retinal damage, namely, abnormal proteins formation, photoreceptor degeneration and retinal remodeling, has been studied in animal models. Functional changes in occipital lobe activity and its atrophy as well as degeneration of visual pathways can already be present in the early stages of the disease. Oculomotor symptoms of HD include disturbed visual fixation, slower tracking eye movements and saccades, and suppressed vestibulo-ocular reflex. Visual perceptual disorders, such as visuospatial difficulties, problems of stimulus identification and motion perception, along with decreased contrast sensitivity, have also been described. The possibility of using certain ophthalmic parameters as biomarkers of HD is being discussed.


Subject(s)
Contrast Sensitivity/physiology , Eye Movements/physiology , Huntington Disease , Vision, Low , Visual Pathways/physiopathology , Fixation, Ocular , Humans , Huntington Disease/complications , Huntington Disease/metabolism , Huntington Disease/physiopathology , Vision, Low/diagnosis , Vision, Low/etiology , Vision, Low/physiopathology
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