综述

皮质脊髓束与脑卒中患者运动功能预后的相关研究进展

  • 王瑜元 ,
  • 白玉龙
展开
  • 复旦大学附属华山医院北院康复医学科,上海市 201907
王瑜元(1984-),女,汉族,浙江绍兴市人,硕士研究生,主治医师,主要研究方向:脑卒中康复的临床研究。

收稿日期: 2018-07-23

  修回日期: 2018-08-06

  网络出版日期: 2018-12-26

基金资助

1.国家自然科学基金项目(No. 81572225); 2.上海市卫计委青年科研项目(No. 20154Y0047; No. 20164Y0235)

Advance in Corticospinal Tract and Motor Recovery after Stroke (review)

  • WANG Yu-yuan ,
  • BAI Yu-long
Expand
  • Department of Rehabilitation Medicine, Huashan Hospital of North, Fudan University, Shanghai 201907, China

Received date: 2018-07-23

  Revised date: 2018-08-06

  Online published: 2018-12-26

Supported by

Supported by National Natural Science Foundation of China (No. 81572225) and Shanghai Municipal Commission of Health and Family Planning Research Preject (Youth) (No. 20154Y0047; No. 20164Y0235)

摘要

皮质脊髓束(CST)是重要的随意运动传导通路。CST损伤影响脑卒中患者运动功能,尤其是上肢运动功能恢复,并与患者长期运动功能预后相关。CST在脑卒中后可发生皮质水平和皮质下重塑,从而促进运动功能恢复。CST重塑机制复杂,需要进一步研究。

本文引用格式

王瑜元 , 白玉龙 . 皮质脊髓束与脑卒中患者运动功能预后的相关研究进展[J]. 中国康复理论与实践, 2018 , 24(11) : 1280 -1283 . DOI: 10.3969/j.issn.1006-9771.2018.11.007

Abstract

Corticospinal tract (CST) is the major neuronal pathway that mediates voluntary movements, and the severity of injury may influence the recovery of motor function, especially that of the upper limbs, and involve to the long-term outcome. Axonal remodeling may happen in the CST after stroke, at the levels of spine and brain, which promotes the recovery of motor function. The mechanism of remodeling is complicated, and need more researched.

参考文献

[1] Jang SH.The corticospinal tract from the view point of brain rehabilitation[J]. J Rehabil Med, 2014, 46(3): 193-199.
[2] Seo JP, Jang SH.Different characteristics of the corticospinal tract according to the cerebral origin: DTI study[J]. Am J Neuroradiol, 2013, 34(7): 1359-1363.
[3] Lemon RN, Griffiths J.Comparing the function of the corticospinal system in different species: organizational differences for motor specialization?[J]. Muscle Nerve, 2005, 32(3): 261-279.
[4] Ahn YH, Ahn SH, Kim H, et al.Can stroke patients walk after complete lateral corticospinal tract injury of affected hemisphere?[J]. Neuroreport, 2006, 17(10): 987-990.
[5] Jang SH, You SH, Kwon YH, et al.Cortical reorganization associated lower extremity motor recovery as evidenced by functional MRI and diffusion tensor tractography in a stroke patient[J]. Restor Neurol Neurosci, 2005, 23(5-6): 325-329.
[6] Cramer SC, Moore CI, Finklestein SP, et al.A pilot study of somatotopic mapping after cortical infarct[J]. Stroke, 2000, 31(3): 668-671.
[7] Sawlani V, Gupta RK, Singh MK, et al.MRI demonstration of Wallerian degeneration in various intracranial lesions and its clinical implications[J]. J Neurol Sci, 1997, 146: 103-108.
[8] Watanabe H, Tashiro K.Brunnstrom stages and Wallerian degenerations: a study using MRI[J]. Tohoku J Exp Med, 1992, 166(4): 471-473.
[9] Lindenberg R, Renga V, Zhu LL, et al.Structural integrity of corticospinal motor fibers predicts motor impairment inchronic stroke[J]. Neurology, 2010, 74(4): 280-287.
[10] Koyama T, Tsuji M, Nishimura H, et al.Diffusion tensor imaging for intracerebral hemorrhage outcome prediction: comparison using data from the corona radiata/internal capsule and the cerebral peduncle[J]. J Stroke Cerebrovasc Dis, 2013, 22(1): 72-79.
[11] Jayaram G, Stagg CJ, Esser P, et al.Relationships between functional and structural corticospinal tract integrity and walking post stroke[J]. Clin Neurophysiol, 2012, 123(12): 2422-2428.
[12] Schaechter JD, Perdue KL, Wang R.Structural damage to the corticospinal tract correlates with bilateral sensorimotor cortex reorganization in stroke patients[J]. Neuroimage, 2008, 39(3): 1370-1382.
[13] Yu C, Zhu C, Zhang Y, et al.A longitudinal diffusion tensor imaging study on Wallerian degeneration of corticospinal tract after motor pathway stroke[J]. Neuroimage, 2009, 47(2): 451-458.
[14] Liu X, Tian W, Qiu X, et al.Correlation analysis of quantitative diffusion parameters in ipsilateral cerebral peduncle during Wallerian degeneration with motor function outcome after cerebral ischemic stroke[J]. J Neuroimaging, 2012, 22(3): 255-260.
[15] Jang SH, Kim K, Kim SH, et al. The relation between motor function of stroke patients and diffusion tensor imaging findings for the corticospinal tract [J]. Neurosci Lett, 2014, 572: l-6.
[16] Jang SH, Kim SH, Cho SH, et al.Demonstration of motor recovery process in a patient with intracerebral hemorrhage[J]. NeuroRehabilitation, 2007, 22(2): 141-145.
[17] Liu Z, Zhang RL, Li Y, et al.Remodeling of the corticospinal innervation and spontaneous behavioral recovery after ischemic stroke in adult mice[J]. Stroke, 2009, 40(7): 2546-2551.
[18] Ueno M, Hayano Y, Nakagawa H, et al.Intraspinal rewiring of the corticospinal tract requires target-derived brain-derived neurotrophic factor and compensates lost function after brain injury[J]. Brain, 2007, 135(Pt4): 1253-1267.
[19] Starkey ML, Bleul C, Zorner B, et al.Back seat driving: hindlimb corticospinal neurons assume forelimb control following ischaemic stroke[J]. Brain, 2012, 135(Pt11): 3265-3281.
[20] Okabe N, Shiromoto T, Himi N, et al.Neural network remodeling under lying motor map reorganization induced by rehabilitative training after ischemic stroke[J]. Neuroscience, 2016, 339: 338-362.
[21] Chisari C, Fanciullacci C, Lamola G, et al.NIBS-driven brain plasticity[J]. Arch Ital Biol, 2014, 152(4): 247-258.
[22] Grefkes C, Ward NS.Cortical reorganization after stroke: how much and how functional?[J]. Neuroscientist, 2014, 20(1): 56-70.
[23] Stinear CM, Barber PA, Smale PR, et al.Functional potential in chronic stroke patients depends on corticospinal tract integrity[J]. Brain, 2007, 130(Pt1): 170-180.
[24] Schulz R, Braass H, Liuzzi G, et al.White matter integrity of premotor-motor connections is associated with motor output in chronic stroke patients[J]. Neuroimag Clin, 2014, 18(7): 82-86.
[25] Wang KC, Kim JA, Sivasankaran R, et al.P75 interacts with the Nogo receptor as a co-receptor for Nogo, MAG and OMgp[J]. Nature, 2002, 420(6911): 74-78.
[26] Domeniconi M, Cao Z, Spencer T, et al.Myelin-associated glycoprotein interacts with the Nogo66 receptor to inhibit neurite out growth[J]. Neuron, 2002, 35(2): 283-290.
[27] Fournier AE, GrandPre T, Strittmatter SM. Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration[J]. Nature, 2001, 409(68): 341-346.
[28] Fouad K, Klusman I, Schwab ME.Regenerating corticospinal fibers in the Marmoset (Callitrix jacchus) after spinal cord lesion and treatment with the anti-Nogo-A antibody IN-l[J]. Eur J Neuorsci, 2004, 20(9): 2479-2482.
[29] Liebscher T, Schnell L, Schnell D, et al.Nogo-A antibody improves regeneration and locomotion of spinal cord-injuried rats[J]. Ann Neuor, 2005, 58(5): 706-719.
[30] Lee JK, Kim JE, Sivula M, et al.Nogo receptor antagonism promotes stroke recovery by enhancing axonal plasticity[J]. J Neurosci, 2004, 24(27): 6209-6217.
[31] Lindau NT, Banninger BJ, Gullo M, et al.Rewiring of the corticospinal tract in the adult rat after unilateral stroke and anti-Nogo-A therapy[J]. Brain, 2014, 137(Pt3): 739-756.
[32] Wahl AS, Omlor W, Rubio JC, et al.Neuronal repair. Asynchronous therapy restores motor control by rewiring of the rat corticospinal tract after stroke[J]. Science, 2014, 344(6189): 1250-1255.
[33] Chen K, Marsh BC, Cowan M, et al.Sequential therapy of anti-Nogo-A antibody treatment and treadmill training leads to cumulative improvements after spinal cord injury in rats[J]. Exp Neurol, 2017, 292: 135-144.
[34] Wong EV, David S, Jacob MH, et al.Inactivation of myelin-associated glycoprotein enhances optic nerve regeneration[J]. J Neurosci, 2003, 23(8): 3112-3117.
[35] Habib AA, Gulcher JR, Högnason T, et al.The OMgp gene, a second growth suppressor within the NF1 gene[J]. Oncogene, 1998, 16(12): 1525-1531.
[36] Ji B, Case LC, Liu K, et al.Assessment of functional recovery and axonal sprouting in oligodendrocyte-myelin glycoprotein (OMgp) null mice after spinal cord injury[J]. Mol Cell Neurosci, 2008, 39(2): 258-267.
文章导航

/