Spinal cord gray matter demyelination in multiple sclerosis -: A novel pattern of residual plaque morphology

被引:105
作者
Gilmore, Christopher P.
Bo, Lars
Owens, Trudy
Lowe, James
Esiri, Margaret M.
Evangelou, Nikos
机构
[1] Queens Med Ctr NHS Trust, Dept Neurol, Nottingham, England
[2] Vrije Univ Amsterdam Med Ctr, Dept Neuropathol, Amsterdam, Netherlands
[3] Haukeland Hosp, Dept Neurol, Natl Competence Ctr MS, Bergen, Norway
[4] Univ Nottingham, Dept Econ, Nottingham, England
[5] Univ Nottingham, Dept Neuropathol, Nottingham, England
[6] Oxford Radcliffe NHS Trust, Dept Neuropathol, Oxford, England
关键词
D O I
10.1111/j.1750-3639.2006.00018.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The extent and pattern of gray matter (GM) demyelination in the spinal cord in multiple sclerosis (MS) has not been examined in detail. Human autopsy material was obtained from 36 MS cases and 12 controls. Transverse sections were taken from five levels of the spinal cord (upper cervical, lower cervical, upper thoracic, lower thoracic and lumbar levels) and the extent of GM and white matter (WM) demyelination evaluated using proteolipid protein immunohistochemistry (IHC). The proportion of the GM that was demyelinated (33%) was significantly greater than the proportion of demyelinated WM (20%) (P < 0.0001). Similarly, demyelination was more extensive in the GM than in the WM at each of the five cord levels. The extent of GM demyelination was not significantly different between the five cord levels while WM demyelination was greatest at the upper cervical level. Morphologically, the borders of a proportion of the GM plaques show a strict respect for the GM/WM boundary. We demonstrate that extensive demyelination occurs in the GM of the spinal cord in MS. Myelin protein IHC reveals a novel pattern of residual plaque morphology challenging previous work suggesting that MS plaques display a total disregard for anatomical boundaries.
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页码:202 / 208
页数:7
相关论文
共 38 条
[1]  
Berger T, 1997, LAB INVEST, V76, P355
[2]   Efficient central nervous system remyelination requires T cells [J].
Bieber, AJ ;
Kerr, S ;
Rodriguez, M .
ANNALS OF NEUROLOGY, 2003, 53 (05) :680-684
[3]   Intracortical multiple sclerosis lesions are not associated with increased lymphocyte infiltration [J].
Bo, L ;
Vedeler, CA ;
Nyland, H ;
Trapp, BD ;
Mork, SJ .
MULTIPLE SCLEROSIS, 2003, 9 (04) :323-331
[4]  
BO ZL, 2003, J NEUROPATHOL EXP NE, V62, P723
[5]   The pathology of multiple sclerosis is location-dependent:: No significant complement activation is detected in purely cortical lesions [J].
Brink, BP ;
Veerhuis, R ;
Breij, ECW ;
van der Valk, P ;
Dijkstra, CD ;
Bö, L .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2005, 64 (02) :147-155
[6]   The longitudinal relation between brain lesion load and atrophy in multiple sclerosis: a 14 year follow up study [J].
Chard, DT ;
Brex, PA ;
Ciccarelli, O ;
Griffin, CM ;
Parker, GJM ;
Dalton, C ;
Altmann, DR ;
Thompson, AJ ;
Miller, DH .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 2003, 74 (11) :1551-1554
[7]   The contribution of demyelination to axonal loss in multiple sclerosis [J].
DeLuca, G. C. ;
Williams, K. ;
Evangelou, N. ;
Ebers, G. C. ;
Esiri, M. M. .
BRAIN, 2006, 129 :1507-1516
[8]   Axonal loss in multiple sclerosis: a pathological survey of the corticospinal and sensory tracts [J].
DeLuca, GC ;
Ebers, GC ;
Esiri, MM .
BRAIN, 2004, 127 :1009-1018
[9]   Pathological study of spinal cord atrophy in multiple sclerosis suggests limited role of local lesions [J].
Evangelou, N ;
DeLuca, GC ;
Owens, T ;
Esiri, MM .
BRAIN, 2005, 128 :29-34
[10]   Structural brain abnormalities in multiple sclerosis patients with major depression [J].
Feinstein, A ;
Roy, P ;
Lobaugh, N ;
Feinstein, K ;
O'Connor, P ;
Black, S .
NEUROLOGY, 2004, 62 (04) :586-590