Neural plasticity after spinal cord injury

被引:94
作者
Ding, YM [1 ]
Kastin, AJ [1 ]
Pan, WH [1 ]
机构
[1] Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA
关键词
spinal cord injury; plasticity; reorganization; cortex; blood-brain barrier;
D O I
10.2174/1381612053507855
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Spinal cord injury (SCI) has devastating physical and socioeconomical impact. However, some degree of functional recovery is frequently observed in patients after SCI. There is considerable evidence that functional plasticity occurs in cerebral cortical maps of the body, which may account for functional recovery after injury. Additionally, these plasticity changes also occur at multiple levels including the brainstem, spinal cord, and peripheral nervous system. Although the interaction of plasticity changes at each level has been less well studied, it is likely that changes in subcortical levels contribute to cortical reorganization. Since the permeability of the blood-brain barrier (131313) is changed, SCI-induced factors, such as cytokines and growth factors, can be involved in the plasticity events, thus affecting the final functional recovery after SCI. The mechanism of plasticity probably differs depending on the time frame. The reorganization that is rapidly induced by acute injury is likely based on unmasking of latent synapses resulting from modulation of neurotransmitters, while the long-term changes after chronic injury involve changes of synaptic efficacy modulated by long-term potentiation and axonal regeneration and sprouting. The functional significance of neural plasticity after SCI remains unclear. It indicates that in some situations plasticity changes can result in functional improvement, while in other situations they may have harmful consequences. Thus, further understanding of the mechanisms of plasticity could lead to better ways of promoting useful reorganization and preventing undesirable consequences.
引用
收藏
页码:1441 / 1450
页数:10
相关论文
共 119 条
[1]  
Abraham J, 1985, Cent Nerv Syst Trauma, V2, P45
[2]   A role for the dorsal column in nociceptive visceral input into the thalamus of primates [J].
Al-Chaer, ED ;
Feng, Y ;
Willis, WD .
JOURNAL OF NEUROPHYSIOLOGY, 1998, 79 (06) :3143-3150
[3]   Pathogenesis and pharmacological strategies for mitigating secondary damage in acute spinal cord injury [J].
Amar, AP ;
Levy, ML .
NEUROSURGERY, 1999, 44 (05) :1027-1039
[4]   CEREBRAL UNITS ACTIVATED BY TACTILE STIMULI VIA A VENTRAL SPINAL PATHWAY IN MONKEYS [J].
ANDERSSON, SA ;
FINGER, S ;
NORRSELL, U .
ACTA PHYSIOLOGICA SCANDINAVICA, 1975, 93 (01) :119-128
[5]  
Asanuma H, 1997, NEUROREPORT, V8, pR1
[6]  
Beattie MS, 2000, PROG BRAIN RES, V128, P9
[7]   Review of current evidence for apoptosis after spinal cord injury [J].
Beattie, MS ;
Farooqui, AA ;
Bresnahan, JC .
JOURNAL OF NEUROTRAUMA, 2000, 17 (10) :915-925
[8]  
BECERRA JL, 1995, AM J NEURORADIOL, V16, P125
[9]   REGENERATION OF AXONS AND SYNAPTIC COMPLEX-FORMATION ROSTRAL TO SITE OF HEMISECTION IN SPINAL-CORD OF MONKEY [J].
BERNSTEIN, ME ;
BERNSTEIN, JJ .
INTERNATIONAL JOURNAL OF NEUROSCIENCE, 1973, 5 (01) :15-26
[10]  
BLIGHT AR, 1993, ADV NEUROL, V59, P91