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Динамика нейрофизиологических показателей сегментарного и надсегментарного моторного проведения у пациентов с миелопатиями и церебральным инсультом
Динамика нейрофизиологических показателей сегментарного и надсегментарного моторного проведения у пациентов с миелопатиями и церебральным инсультом
Ковражкина Е.А., Стаховская Л.В., Разинская О.Д. Динамика нейрофизиологических показателей сегментарного и надсегментарного моторного проведения у пациентов с миелопатиями и церебральным инсультом. Consilium Medicum. 2016; 18 (2): 37–43. DOI: 10.26442/2075-1753_2016.2.37-43
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Аннотация
Введение: повреждения аксонов центральной нервной системы (ЦНС) взрослого субъекта вызывают серьезные и малообратимые функциональные нарушения, что является следствием неспособности ЦНС в отличие от периферической нервной системы восстанавливать поврежденные нервные волокна. Зародышевые аксоны ЦНС восстанавливаются, но регенераторный ответ взрослых нейронов становится несостоятельным. Миелин и вырабатывающие миелин олигодендроциты ЦНС способны ингибировать рост аксонов, соответственно, длительное сохранение миелина в области повреждения может препятствовать регенерации аксонов.
Цель: изучить динамику аксонального повреждения и миелинопатии на сегментарном и надсегментарном уровнях у пациентов с миелопатиями и церебральным инсультом.
Методы: обследованы 340 пациентов с миелопатиями разного уровня (70% с последствиями позвоночно-спинномозговых травм и 30% с миелопатиями нетравматического генеза) – основная группа, группу сравнения составили 30 пациентов с церебральным полушарным инсультом. Состояние сегментарного проведения оценивалось методом электронейромиографии, надсегментарного – транскраниальной магнитной стимуляции. Пациенты обследовались дважды: при поступлении на курс реабилитации и в динамике через 2–3 мес.
Результаты: первичное обследование в основной группе не показало достоверных различий в выраженности аксоно- и миелинопатии при разной тяжести неврологического дефицита. При обследовании в динамике у пациентов с улучшением функционального статуса (по шкале FIM) была выявлена достоверно (p<0,05) большая выраженность миелинопатии на сегментарном и надсегментарном уровнях, сохраняющаяся при повторных исследованиях (у больных без динамики по шкале FIM выраженность миелинопатии при повторных обследованиях уменьшалась). У пациентов с функциональным ухудшением выявлена достоверно большая (p<0,05) выраженность аксонопатии и достоверно (p<0,05) меньшая выраженность миелинопатических изменений. Аналогичные изменения были обнаружены у пациентов с инсультом: при обследовании в динамике у больных с лучшим восстановлением (по шкале Рэнкина) обнаружены меньшая выраженность аксональных и большая – миелинопатических изменений.
Заключение: при повреждениях ЦНС обнаружено нарастание миелинопатических изменений на сегментарном и надсегментарном уровне при повторном обследовании у пациентов с улучшением функционального статуса, а у больных с ухудшением функциональных возможностей, наоборот, – уменьшение выраженности миелинопатии.
Ключевые слова: регенерация аксонов, ингибиторы аксонального роста, миелин, миелопатии, инсульт.
Objective: To study the dynamics of axonal damage and mielinopatii on segmental and suprasegmental levels in patients with myelopathy and cerebral stroke.
Methods: The study involved 340 patients with myelopathy of different levels (70% of the effects of spinal spinal injuries and 30% of nontraumatic myelopathy origin) – the main group, the comparison group consisted of 30 patients with cerebral hemispheric stroke. Status of segmental evaluated by electromyographic, suprasegmental – transcranial magnetic stimulation. The patients were examined twice: when applying for a rehabilitation course in the dynamics of 2–3 months.
Results: Initial examination in the study group showed no significant differences in the severity and axon- myelinopathy with varying severity of neurological deficit. In a study in dynamics in patients with improvement in functional status (for FIM scale) was found, significant (p<0.05) myelopathy of great severity at the segmental and suprasegmental levels of persisting in repeated studies (in patients without the dynamics on the scale of severity of FIM myelopathy with repeated surveys decreased). For patients with functional impairment revealed significantly greater (p<0.05) axonopathy severity and significantly (p<0.05) lower severity myelopathic changes. Similar changes were found in patients with stroke: when examining the dynamics in patients with a better recovery (Rankin Scale) found lower severity of axonal and large – myelopathic changes.
Conclusion: The CNS lesions observed increase in myelopathic changes in segmental and suprasegmental level, the re-testing of patients with improvement in functional status, and in patients with deterioration of functional capacity, on the contrary, – reduced severity of myelopathy.
Key words: axon regeneration, inhibitors of axonal growth, myelin, myelopathy, stroke.
Цель: изучить динамику аксонального повреждения и миелинопатии на сегментарном и надсегментарном уровнях у пациентов с миелопатиями и церебральным инсультом.
Методы: обследованы 340 пациентов с миелопатиями разного уровня (70% с последствиями позвоночно-спинномозговых травм и 30% с миелопатиями нетравматического генеза) – основная группа, группу сравнения составили 30 пациентов с церебральным полушарным инсультом. Состояние сегментарного проведения оценивалось методом электронейромиографии, надсегментарного – транскраниальной магнитной стимуляции. Пациенты обследовались дважды: при поступлении на курс реабилитации и в динамике через 2–3 мес.
Результаты: первичное обследование в основной группе не показало достоверных различий в выраженности аксоно- и миелинопатии при разной тяжести неврологического дефицита. При обследовании в динамике у пациентов с улучшением функционального статуса (по шкале FIM) была выявлена достоверно (p<0,05) большая выраженность миелинопатии на сегментарном и надсегментарном уровнях, сохраняющаяся при повторных исследованиях (у больных без динамики по шкале FIM выраженность миелинопатии при повторных обследованиях уменьшалась). У пациентов с функциональным ухудшением выявлена достоверно большая (p<0,05) выраженность аксонопатии и достоверно (p<0,05) меньшая выраженность миелинопатических изменений. Аналогичные изменения были обнаружены у пациентов с инсультом: при обследовании в динамике у больных с лучшим восстановлением (по шкале Рэнкина) обнаружены меньшая выраженность аксональных и большая – миелинопатических изменений.
Заключение: при повреждениях ЦНС обнаружено нарастание миелинопатических изменений на сегментарном и надсегментарном уровне при повторном обследовании у пациентов с улучшением функционального статуса, а у больных с ухудшением функциональных возможностей, наоборот, – уменьшение выраженности миелинопатии.
Ключевые слова: регенерация аксонов, ингибиторы аксонального роста, миелин, миелопатии, инсульт.
________________________________________________
Objective: To study the dynamics of axonal damage and mielinopatii on segmental and suprasegmental levels in patients with myelopathy and cerebral stroke.
Methods: The study involved 340 patients with myelopathy of different levels (70% of the effects of spinal spinal injuries and 30% of nontraumatic myelopathy origin) – the main group, the comparison group consisted of 30 patients with cerebral hemispheric stroke. Status of segmental evaluated by electromyographic, suprasegmental – transcranial magnetic stimulation. The patients were examined twice: when applying for a rehabilitation course in the dynamics of 2–3 months.
Results: Initial examination in the study group showed no significant differences in the severity and axon- myelinopathy with varying severity of neurological deficit. In a study in dynamics in patients with improvement in functional status (for FIM scale) was found, significant (p<0.05) myelopathy of great severity at the segmental and suprasegmental levels of persisting in repeated studies (in patients without the dynamics on the scale of severity of FIM myelopathy with repeated surveys decreased). For patients with functional impairment revealed significantly greater (p<0.05) axonopathy severity and significantly (p<0.05) lower severity myelopathic changes. Similar changes were found in patients with stroke: when examining the dynamics in patients with a better recovery (Rankin Scale) found lower severity of axonal and large – myelopathic changes.
Conclusion: The CNS lesions observed increase in myelopathic changes in segmental and suprasegmental level, the re-testing of patients with improvement in functional status, and in patients with deterioration of functional capacity, on the contrary, – reduced severity of myelopathy.
Key words: axon regeneration, inhibitors of axonal growth, myelin, myelopathy, stroke.
Полный текст
Список литературы
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16. Shamash S, Reichert F, Rotshenker S. The cytokine network of Wallerian degeneration: tumor necrosis facror-alpha, interleukin-1alpha and interleukin-1beta. J Neurosci 2002; 22: 3052–60.
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18. George R, Griffin J. Delayed macrophage responses and myelin clearance during Wallerian degeneration in the central neurous system: the dorsal radiculotomi model. Exp Neurol 1994; 129: 225–36.
19. Bandlow C, Loschinger J. Developmental changes in neuronal responsiveness to CNS myelin-associated neurite grown ingiditor NI-35/250. Eur J Neurosci 1997; 9: 2743–52.
20. Caroni P, Schwab M. Two membrane protein fractions from rat central myelin with ingiitory properties for neurite growth and fibroblast spreading. J Cell Biol 1988; 106: 1281–8.
21. Bernstein-Goral H, Bregman B. Spinal cord transplants support the regeneration of axonotomized neurons after spinal cord lessions at birth: a quantitative doublelabeling study. Exp Neurol 1993; 123: 118–32.
22. Kalil K, Reh T. A light and electron microscopic study of regrowing pyramidal tract fibers. J Comp Neurol 1982; 211: 265–75.
23. Saunders N., Kitchener P., Knott G et al. Development of walking, swimming and neuronal connections after complete spinal cord transection in neonatal opossum, Monodelphisdomestica. J Neurosci 1998; 18: 339–55.
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2. Mironov E.M. Analiz pervichnoi invalidnosti sredi bol'nykh s posledstviiami pozvonochno-spinnomozgovoi travmy. Mediko-sotsial'naia ekspertiza i reabilitatsiia. M.: Meditsina, 2004; 1: 33–4. [in Russian]
3. Kondakov E.N., Simonova I.A., Poliakov I.V. Epidemiologiia tpavm pozvonochnika i spinnogo mozga v Sankt-Petepbupge. Vopr. neirokhirurgii im. N.N.Burdenko. 2002; 2: 34. [in Russian]
4. Akshulakov S.K., Kerimbaev T.T. Epidemiologiia travm pozvonochnika i spinnogo mozga. Materialy III s"ezda neirokhirurgov Rossii. SPb., 2002; s. 182. [in Russian]
5. Ivanova G.E., Krylov V.V., Tsikunov M.B. i dr. Reabilitatsiia bol'nykh s travmaticheskoi bolezn'iu spinnogo mozga. M., 2010. [in Russian]
6. Stoporov A.G. Nekotorye aspekty integral'noi otsenki obshchei kompensatsii bol'nykh, perenesshikh pozvonochno-spinomozgovuiu travmu. Vestn. fizioterapii i kurortologii. 2007; 2: 172–7. [in Russian]
7. Shevelev I.N., Baskov A.V., Iarikov D.E., Borshchenko I.A. Vosstanovlenie funktsii spinnogo mozga: sovremennye vozmozhnosti i perspektivy issledovaniia. Vopr. neirokhirurgii. 2000; 3. [in Russian]
8. Borshchenko I.A., Baskov A.V., Korshunov A.G., Satanova F.S. Nekotorye aspekty patofiziologii travmaticheskogo povrezhdeniia i regeneratsii spinnogo mozga. Vopr. neirokhirurgii. 2000; 2. [in Russian]
9. Goldberg J, Barres B. The relationship between neuronal survival and regeneration. Annu Rev Neurosci 2000; 23: 579–612.
10. Stoll G, Jander S, Myers R. Degeneration and regeneration on the peripheral nervous system: from Augustus Waller’s observations to neuroinglammation. J Peripher Nevr Syst 2002; 7: 13–27.
11. Broude E, McAtee M, Kelley M, Bregman B. c-Jun expression in adult rat dorsal root ganglion neurons: differential response after central or peripheral axonotomy. Exp Neurol 1997; 148: 367–77.
12. Schwaiger F, Hager G, Schmitt A et al. Peripheral but not central axonotomy induces changes in Janus kinases (JAK) and signal transduces and activators of transcription (STAT). Eur J Neurosci 2000; 12: 1165–76.
13. Dusart L, Airaksinen M, Sotelo C. Purkinje cell survival and axonal regeneration are age dependent: an in vitro study. J Neurosci 1997; 17: 3710–26.
14. Gianola S, Rossi F. Evolution of the Purkije cell rwsronse to injuri and regenerative potential during postnatal development of the rat cerebellum. J Comp Neurol 2001; 430: 101–17.
15. Steeves J, Keirstead H, Ethell D et al. Permissive and restrictive periods for brainstem-spinal regeneration in the chick. Prog Brain Res 1994; 103: 243–62.
16. Shamash S, Reichert F, Rotshenker S. The cytokine network of Wallerian degeneration: tumor necrosis facror-alpha, interleukin-1alpha and interleukin-1beta. J Neurosci 2002; 22: 3052–60.
17. Stoll G, Jander S. The role of microglia and macrophages in the pathophysiology of the CNS. Prog Neurobiol 1999; 58: 233–47.
18. George R, Griffin J. Delayed macrophage responses and myelin clearance during Wallerian degeneration in the central neurous system: the dorsal radiculotomi model. Exp Neurol 1994; 129: 225–36.
19. Bandlow C, Loschinger J. Developmental changes in neuronal responsiveness to CNS myelin-associated neurite grown ingiditor NI-35/250. Eur J Neurosci 1997; 9: 2743–52.
20. Caroni P, Schwab M. Two membrane protein fractions from rat central myelin with ingiitory properties for neurite growth and fibroblast spreading. J Cell Biol 1988; 106: 1281–8.
21. Bernstein-Goral H, Bregman B. Spinal cord transplants support the regeneration of axonotomized neurons after spinal cord lessions at birth: a quantitative doublelabeling study. Exp Neurol 1993; 123: 118–32.
22. Kalil K, Reh T. A light and electron microscopic study of regrowing pyramidal tract fibers. J Comp Neurol 1982; 211: 265–75.
23. Saunders N., Kitchener P., Knott G et al. Development of walking, swimming and neuronal connections after complete spinal cord transection in neonatal opossum, Monodelphisdomestica. J Neurosci 1998; 18: 339–55.
24. Young W. Strategies for the development of new and better farmacogical treatment for acute spinal cord injury. In: F.G.Seil. Advances in neurology. New York: Raven Press, 1993; p. 249–56.
25. Yao L, Moody C, Schonherr E et al. Indentification of the proteoglycan versican in aorta and smoth musle cells by DNA sequence analysis, in situ hybridization and immunohistochemistry. Mattrix Biol 1994; 14: 213–25.
26. Sugiura Y, Mori N. SCG10 exppresses growth-associated manner in developing rat brain, but shows a different pattern to p19/stathmin or GAP-43. Brain Res Dev Brain Res 1995; 90: 73–91.
27. Mori N, Morii H. SCGIO-related neuronal growth-associated proteins in neural development, plasticity, degeneration and aging. J Neurosci Res 2002; 70: 264–73.
28. Bandlow C, Zachleder T, Schwab M. Oligodendrocytes arrest neurite grown by contact ingibition. J Neurosci 1990; 10: 3837–48.
29. Bouslama-Oueghlani L, Wehrle R, Sotelo C, Dusart I. The developmental loss of the ability of Purkinje cells to regenerate their axons occurs in the absence of myelin: an in vitro model to prevent myelination. J Neurosci 2003; 23: 8318–29.
30. Colemann M, Perry V. Axon pathology in neurological disease: a neglected therapeutic target. Trends Neurocsci 2002; 25: 532–7.
31. Kottis V, Thibaut P, Micol D. Oligodendrocyte-myelin glycoprotein (OMgp) is an inhibitor of neurite outgrowth. J Neurochem 2002; 82: 1566–9.
32. Fujita Y, Yamashita T. Axon growth inhibition by RhoA/ROCK in the central nervous system. Front Neurosci 2014; 8: 338.
33. Chelyshev Iu.L., Viktorov I.V. Kletochnye tekhnologii remielinizatsii pri travme spinnogo mozga. Nevrol. vestn. 2009; XLI (1): 49–55. [in Russian]
34. Baldwin K, Giger R. Insights into the physiological role of CNS regeneration inhibitors. Front Mol Neurosci 2015; 11; 8: 23.
35. Barbay S, Plautz E, Zoubina et al. Effects of postinfarct myelin-associated glycoprotein antibody treatment on motor recovery and motor map plasticity in squirrel monkeys. Stroke 2015; 46 (6): 1620–5.
36. Fagoe N, Van Heest J, Verhaagen J. Spinal cord injury and the neuron-intrinsic regeneration-associated gene program. Neuromolecular Med 2014; 16 (4): 799–813.
37. Geoffroy C, Lorenzana AO, Kwan J et al. Effects of PTEN and NogoCodeletion on Corticospinal Axon Sprouting and Regeneration in Mice. J Neurosci 2015; 35 (16): 6413–28.
38. Goldshmit Y, Frisca F, Kaslin J. et al. Decreased anti-regenerative effects after spinal cord injury in spry4-/- mice. Neuroscience 2015; 287C: 104–12.
39. Vajda F, Jordi W, Dalkara D. Cell type-specific Nogo-A gene ablation promotes axonal regeneration in the injured adult optic nerve. Cell Death Differ 2015; 22 (2): 323–35.
2. Миронов Е.М. Анализ первичной инвалидности среди больных с последствиями позвоночно-спинномозговой травмы. Медико-социальная экспертиза и реабилитация. М.: Медицина, 2004; 1: 33–4. / Mironov E.M. Analiz pervichnoi invalidnosti sredi bol'nykh s posledstviiami pozvonochno-spinnomozgovoi travmy. Mediko-sotsial'naia ekspertiza i reabilitatsiia. M.: Meditsina, 2004; 1: 33–4. [in Russian]
3. Кондаков Е.Н., Симонова И.А., Поляков И.В. Эпидемиология тpавм позвоночника и спинного мозга в Санкт-Петеpбуpге. Вопр. нейрохирургии им. Н.Н.Бурденко. 2002; 2: 34. / Kondakov E.N., Simonova I.A., Poliakov I.V. Epidemiologiia tpavm pozvonochnika i spinnogo mozga v Sankt-Petepbupge. Vopr. neirokhirurgii im. N.N.Burdenko. 2002; 2: 34. [in Russian]
4. Акшулаков С.К., Керимбаев Т.Т. Эпидемиология травм позвоночника и спинного мозга. Материалы III съезда нейрохирургов России. СПб., 2002; с. 182. / Akshulakov S.K., Kerimbaev T.T. Epidemiologiia travm pozvonochnika i spinnogo mozga. Materialy III s"ezda neirokhirurgov Rossii. SPb., 2002; s. 182. [in Russian]
5. Иванова Г.Е., Крылов В.В., Цикунов М.Б. и др. Реабилитация больных с травматической болезнью спинного мозга. М., 2010. / Ivanova G.E., Krylov V.V., Tsikunov M.B. i dr. Reabilitatsiia bol'nykh s travmaticheskoi bolezn'iu spinnogo mozga. M., 2010. [in Russian]
6. Стопоров А.Г. Некоторые аспекты интегральной оценки общей компенсации больных, перенесших позвоночно-спинномозговую травму. Вестн. физиотерапии и курортологии. 2007; 2: 172–7. / Stoporov A.G. Nekotorye aspekty integral'noi otsenki obshchei kompensatsii bol'nykh, perenesshikh pozvonochno-spinomozgovuiu travmu. Vestn. fizioterapii i kurortologii. 2007; 2: 172–7. [in Russian]
7. Шевелев И.Н., Басков А.В., Яриков Д.Е., Борщенко И.А. Восстановление функции спинного мозга: современные возможности и перспективы исследования. Вопр. нейрохирургии. 2000; 3. / Shevelev I.N., Baskov A.V., Iarikov D.E., Borshchenko I.A. Vosstanovlenie funktsii spinnogo mozga: sovremennye vozmozhnosti i perspektivy issledovaniia. Vopr. neirokhirurgii. 2000; 3. [in Russian]
8. Борщенко И.А., Басков А.В., Коршунов А.Г., Сатанова Ф.С. Некоторые аспекты патофизиологии травматического повреждения и регенерации спинного мозга. Вопр. нейрохирургии. 2000; 2. / Borshchenko I.A., Baskov A.V., Korshunov A.G., Satanova F.S. Nekotorye aspekty patofiziologii travmaticheskogo povrezhdeniia i regeneratsii spinnogo mozga. Vopr. neirokhirurgii. 2000; 2. [in Russian]
9. Goldberg J, Barres B. The relationship between neuronal survival and regeneration. Annu Rev Neurosci 2000; 23: 579–612.
10. Stoll G, Jander S, Myers R. Degeneration and regeneration on the peripheral nervous system: from Augustus Waller’s observations to neuroinglammation. J Peripher Nevr Syst 2002; 7: 13–27.
11. Broude E, McAtee M, Kelley M, Bregman B. c-Jun expression in adult rat dorsal root ganglion neurons: differential response after central or peripheral axonotomy. Exp Neurol 1997; 148: 367–77.
12. Schwaiger F, Hager G, Schmitt A et al. Peripheral but not central axonotomy induces changes in Janus kinases (JAK) and signal transduces and activators of transcription (STAT). Eur J Neurosci 2000; 12: 1165–76.
13. Dusart L, Airaksinen M, Sotelo C. Purkinje cell survival and axonal regeneration are age dependent: an in vitro study. J Neurosci 1997; 17: 3710–26.
14. Gianola S, Rossi F. Evolution of the Purkije cell rwsronse to injuri and regenerative potential during postnatal development of the rat cerebellum. J Comp Neurol 2001; 430: 101–17.
15. Steeves J, Keirstead H, Ethell D et al. Permissive and restrictive periods for brainstem-spinal regeneration in the chick. Prog Brain Res 1994; 103: 243–62.
16. Shamash S, Reichert F, Rotshenker S. The cytokine network of Wallerian degeneration: tumor necrosis facror-alpha, interleukin-1alpha and interleukin-1beta. J Neurosci 2002; 22: 3052–60.
17. Stoll G, Jander S. The role of microglia and macrophages in the pathophysiology of the CNS. Prog Neurobiol 1999; 58: 233–47.
18. George R, Griffin J. Delayed macrophage responses and myelin clearance during Wallerian degeneration in the central neurous system: the dorsal radiculotomi model. Exp Neurol 1994; 129: 225–36.
19. Bandlow C, Loschinger J. Developmental changes in neuronal responsiveness to CNS myelin-associated neurite grown ingiditor NI-35/250. Eur J Neurosci 1997; 9: 2743–52.
20. Caroni P, Schwab M. Two membrane protein fractions from rat central myelin with ingiitory properties for neurite growth and fibroblast spreading. J Cell Biol 1988; 106: 1281–8.
21. Bernstein-Goral H, Bregman B. Spinal cord transplants support the regeneration of axonotomized neurons after spinal cord lessions at birth: a quantitative doublelabeling study. Exp Neurol 1993; 123: 118–32.
22. Kalil K, Reh T. A light and electron microscopic study of regrowing pyramidal tract fibers. J Comp Neurol 1982; 211: 265–75.
23. Saunders N., Kitchener P., Knott G et al. Development of walking, swimming and neuronal connections after complete spinal cord transection in neonatal opossum, Monodelphisdomestica. J Neurosci 1998; 18: 339–55.
24. Young W. Strategies for the development of new and better farmacogical treatment for acute spinal cord injury. In: F.G.Seil. Advances in neurology. New York: Raven Press, 1993; p. 249–56.
25. Yao L, Moody C, Schonherr E et al. Indentification of the proteoglycan versican in aorta and smoth musle cells by DNA sequence analysis, in situ hybridization and immunohistochemistry. Mattrix Biol 1994; 14: 213–25.
26. Sugiura Y, Mori N. SCG10 exppresses growth-associated manner in developing rat brain, but shows a different pattern to p19/stathmin or GAP-43. Brain Res Dev Brain Res 1995; 90: 73–91.
27. Mori N, Morii H. SCGIO-related neuronal growth-associated proteins in neural development, plasticity, degeneration and aging. J Neurosci Res 2002; 70: 264–73.
28. Bandlow C, Zachleder T, Schwab M. Oligodendrocytes arrest neurite grown by contact ingibition. J Neurosci 1990; 10: 3837–48.
29. Bouslama-Oueghlani L, Wehrle R, Sotelo C, Dusart I. The developmental loss of the ability of Purkinje cells to regenerate their axons occurs in the absence of myelin: an in vitro model to prevent myelination. J Neurosci 2003; 23: 8318–29.
30. Colemann M, Perry V. Axon pathology in neurological disease: a neglected therapeutic target. Trends Neurocsci 2002; 25: 532–7.
31. Kottis V, Thibaut P, Micol D. Oligodendrocyte-myelin glycoprotein (OMgp) is an inhibitor of neurite outgrowth. J Neurochem 2002; 82: 1566–9.
32. Fujita Y, Yamashita T. Axon growth inhibition by RhoA/ROCK in the central nervous system. Front Neurosci 2014; 8: 338.
33. Челышев Ю.Л., Викторов И.В. Клеточные технологии ремиелинизации при травме спинного мозга. Неврол. вестн. 2009; XLI (1): 49–55. / Chelyshev Iu.L., Viktorov I.V. Kletochnye tekhnologii remielinizatsii pri travme spinnogo mozga. Nevrol. vestn. 2009; XLI (1): 49–55. [in Russian]
34. Baldwin K, Giger R. Insights into the physiological role of CNS regeneration inhibitors. Front Mol Neurosci 2015; 11; 8: 23.
35. Barbay S, Plautz E, Zoubina et al. Effects of postinfarct myelin-associated glycoprotein antibody treatment on motor recovery and motor map plasticity in squirrel monkeys. Stroke 2015; 46 (6): 1620–5.
36. Fagoe N, Van Heest J, Verhaagen J. Spinal cord injury and the neuron-intrinsic regeneration-associated gene program. Neuromolecular Med 2014; 16 (4): 799–813.
37. Geoffroy C, Lorenzana AO, Kwan J et al. Effects of PTEN and NogoCodeletion on Corticospinal Axon Sprouting and Regeneration in Mice. J Neurosci 2015; 35 (16): 6413–28.
38. Goldshmit Y, Frisca F, Kaslin J. et al. Decreased anti-regenerative effects after spinal cord injury in spry4-/- mice. Neuroscience 2015; 287C: 104–12.
39. Vajda F, Jordi W, Dalkara D. Cell type-specific Nogo-A gene ablation promotes axonal regeneration in the injured adult optic nerve. Cell Death Differ 2015; 22 (2): 323–35.
________________________________________________
2. Mironov E.M. Analiz pervichnoi invalidnosti sredi bol'nykh s posledstviiami pozvonochno-spinnomozgovoi travmy. Mediko-sotsial'naia ekspertiza i reabilitatsiia. M.: Meditsina, 2004; 1: 33–4. [in Russian]
3. Kondakov E.N., Simonova I.A., Poliakov I.V. Epidemiologiia tpavm pozvonochnika i spinnogo mozga v Sankt-Petepbupge. Vopr. neirokhirurgii im. N.N.Burdenko. 2002; 2: 34. [in Russian]
4. Akshulakov S.K., Kerimbaev T.T. Epidemiologiia travm pozvonochnika i spinnogo mozga. Materialy III s"ezda neirokhirurgov Rossii. SPb., 2002; s. 182. [in Russian]
5. Ivanova G.E., Krylov V.V., Tsikunov M.B. i dr. Reabilitatsiia bol'nykh s travmaticheskoi bolezn'iu spinnogo mozga. M., 2010. [in Russian]
6. Stoporov A.G. Nekotorye aspekty integral'noi otsenki obshchei kompensatsii bol'nykh, perenesshikh pozvonochno-spinomozgovuiu travmu. Vestn. fizioterapii i kurortologii. 2007; 2: 172–7. [in Russian]
7. Shevelev I.N., Baskov A.V., Iarikov D.E., Borshchenko I.A. Vosstanovlenie funktsii spinnogo mozga: sovremennye vozmozhnosti i perspektivy issledovaniia. Vopr. neirokhirurgii. 2000; 3. [in Russian]
8. Borshchenko I.A., Baskov A.V., Korshunov A.G., Satanova F.S. Nekotorye aspekty patofiziologii travmaticheskogo povrezhdeniia i regeneratsii spinnogo mozga. Vopr. neirokhirurgii. 2000; 2. [in Russian]
9. Goldberg J, Barres B. The relationship between neuronal survival and regeneration. Annu Rev Neurosci 2000; 23: 579–612.
10. Stoll G, Jander S, Myers R. Degeneration and regeneration on the peripheral nervous system: from Augustus Waller’s observations to neuroinglammation. J Peripher Nevr Syst 2002; 7: 13–27.
11. Broude E, McAtee M, Kelley M, Bregman B. c-Jun expression in adult rat dorsal root ganglion neurons: differential response after central or peripheral axonotomy. Exp Neurol 1997; 148: 367–77.
12. Schwaiger F, Hager G, Schmitt A et al. Peripheral but not central axonotomy induces changes in Janus kinases (JAK) and signal transduces and activators of transcription (STAT). Eur J Neurosci 2000; 12: 1165–76.
13. Dusart L, Airaksinen M, Sotelo C. Purkinje cell survival and axonal regeneration are age dependent: an in vitro study. J Neurosci 1997; 17: 3710–26.
14. Gianola S, Rossi F. Evolution of the Purkije cell rwsronse to injuri and regenerative potential during postnatal development of the rat cerebellum. J Comp Neurol 2001; 430: 101–17.
15. Steeves J, Keirstead H, Ethell D et al. Permissive and restrictive periods for brainstem-spinal regeneration in the chick. Prog Brain Res 1994; 103: 243–62.
16. Shamash S, Reichert F, Rotshenker S. The cytokine network of Wallerian degeneration: tumor necrosis facror-alpha, interleukin-1alpha and interleukin-1beta. J Neurosci 2002; 22: 3052–60.
17. Stoll G, Jander S. The role of microglia and macrophages in the pathophysiology of the CNS. Prog Neurobiol 1999; 58: 233–47.
18. George R, Griffin J. Delayed macrophage responses and myelin clearance during Wallerian degeneration in the central neurous system: the dorsal radiculotomi model. Exp Neurol 1994; 129: 225–36.
19. Bandlow C, Loschinger J. Developmental changes in neuronal responsiveness to CNS myelin-associated neurite grown ingiditor NI-35/250. Eur J Neurosci 1997; 9: 2743–52.
20. Caroni P, Schwab M. Two membrane protein fractions from rat central myelin with ingiitory properties for neurite growth and fibroblast spreading. J Cell Biol 1988; 106: 1281–8.
21. Bernstein-Goral H, Bregman B. Spinal cord transplants support the regeneration of axonotomized neurons after spinal cord lessions at birth: a quantitative doublelabeling study. Exp Neurol 1993; 123: 118–32.
22. Kalil K, Reh T. A light and electron microscopic study of regrowing pyramidal tract fibers. J Comp Neurol 1982; 211: 265–75.
23. Saunders N., Kitchener P., Knott G et al. Development of walking, swimming and neuronal connections after complete spinal cord transection in neonatal opossum, Monodelphisdomestica. J Neurosci 1998; 18: 339–55.
24. Young W. Strategies for the development of new and better farmacogical treatment for acute spinal cord injury. In: F.G.Seil. Advances in neurology. New York: Raven Press, 1993; p. 249–56.
25. Yao L, Moody C, Schonherr E et al. Indentification of the proteoglycan versican in aorta and smoth musle cells by DNA sequence analysis, in situ hybridization and immunohistochemistry. Mattrix Biol 1994; 14: 213–25.
26. Sugiura Y, Mori N. SCG10 exppresses growth-associated manner in developing rat brain, but shows a different pattern to p19/stathmin or GAP-43. Brain Res Dev Brain Res 1995; 90: 73–91.
27. Mori N, Morii H. SCGIO-related neuronal growth-associated proteins in neural development, plasticity, degeneration and aging. J Neurosci Res 2002; 70: 264–73.
28. Bandlow C, Zachleder T, Schwab M. Oligodendrocytes arrest neurite grown by contact ingibition. J Neurosci 1990; 10: 3837–48.
29. Bouslama-Oueghlani L, Wehrle R, Sotelo C, Dusart I. The developmental loss of the ability of Purkinje cells to regenerate their axons occurs in the absence of myelin: an in vitro model to prevent myelination. J Neurosci 2003; 23: 8318–29.
30. Colemann M, Perry V. Axon pathology in neurological disease: a neglected therapeutic target. Trends Neurocsci 2002; 25: 532–7.
31. Kottis V, Thibaut P, Micol D. Oligodendrocyte-myelin glycoprotein (OMgp) is an inhibitor of neurite outgrowth. J Neurochem 2002; 82: 1566–9.
32. Fujita Y, Yamashita T. Axon growth inhibition by RhoA/ROCK in the central nervous system. Front Neurosci 2014; 8: 338.
33. Chelyshev Iu.L., Viktorov I.V. Kletochnye tekhnologii remielinizatsii pri travme spinnogo mozga. Nevrol. vestn. 2009; XLI (1): 49–55. [in Russian]
34. Baldwin K, Giger R. Insights into the physiological role of CNS regeneration inhibitors. Front Mol Neurosci 2015; 11; 8: 23.
35. Barbay S, Plautz E, Zoubina et al. Effects of postinfarct myelin-associated glycoprotein antibody treatment on motor recovery and motor map plasticity in squirrel monkeys. Stroke 2015; 46 (6): 1620–5.
36. Fagoe N, Van Heest J, Verhaagen J. Spinal cord injury and the neuron-intrinsic regeneration-associated gene program. Neuromolecular Med 2014; 16 (4): 799–813.
37. Geoffroy C, Lorenzana AO, Kwan J et al. Effects of PTEN and NogoCodeletion on Corticospinal Axon Sprouting and Regeneration in Mice. J Neurosci 2015; 35 (16): 6413–28.
38. Goldshmit Y, Frisca F, Kaslin J. et al. Decreased anti-regenerative effects after spinal cord injury in spry4-/- mice. Neuroscience 2015; 287C: 104–12.
39. Vajda F, Jordi W, Dalkara D. Cell type-specific Nogo-A gene ablation promotes axonal regeneration in the injured adult optic nerve. Cell Death Differ 2015; 22 (2): 323–35.
Авторы
Е.А.Ковражкина*, Л.В.Стаховская, О.Д.Разинская
ГБОУ ВПО Российский национальный исследовательский медицинский университет им. Н.И.Пирогова Минздрава России. 117997, Россия, Москва, ул. Островитянова, д. 1
*elekov2@yandex.ru
N.I.Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Ostrovitianova, d. 1
*elekov2@yandex.ru
ГБОУ ВПО Российский национальный исследовательский медицинский университет им. Н.И.Пирогова Минздрава России. 117997, Россия, Москва, ул. Островитянова, д. 1
*elekov2@yandex.ru
________________________________________________
N.I.Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Ostrovitianova, d. 1
*elekov2@yandex.ru
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