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1 tion of a cohort of injured CST axons past a spinal cord lesion.
2 in and the sensory and motor neurons below a spinal cord lesion.
3 can be accurately quantified within a single spinal cord lesion.
4 , or (3) four to eight brain lesions and one spinal cord lesion.
5 nsplantation of OECs into a demyelinated rat spinal cord lesion.
6 D is related to the craniocaudal location of spinal cord lesions.
7 ught to restore neurological function across spinal cord lesions.
8 o the uncertainties about axon sparing after spinal cord lesions.
9 set significantly reduced clinical signs and spinal cord lesions.
10 ents with neurogenic bladder overactivity or spinal cord lesions.
11 vide information on the level and density of spinal cord lesions.
12 l regeneration and functional recovery after spinal cord lesions.
13 zed fibers from regenerating after adult rat spinal cord lesions.
14  large F4/80(+) macrophages/microglia in the spinal cord lesions.
15 rier (BSCB) breakdown, causing microvascular spinal-cord lesions.
16        Subjects who evolved to PPMS had more spinal cord lesions (100%) before symptomatic evolution
17 ed increased sensory axon turning within the spinal cord lesion after SCI with peripheral conditionin
18 afferent axon dynamics after a laser-induced spinal cord lesion and observed massive microglia infilt
19  they first present with clinically isolated spinal cord lesions and before they have developed sympt
20         Besides age, unequivocal presence of spinal cord lesions and being male predicted evolution t
21 elination in lysolecithin-induced rat dorsal spinal cord lesions and in slice cultures.
22 gether does not result in regeneration after spinal cord lesion, and the minimal sprouting that occur
23 y matter and white matter lesions, including spinal cord lesions, and global and regional cortical th
24     Adult Fischer 344 rats were subjected to spinal cord lesions, and the temporal and spatial expres
25       Three-day-old rats received a cervical spinal cord lesion at C3, with or without a transplant o
26 ]; GBD 2013 0.215 [0.144-0.307]) and treated spinal cord lesions (below the neck: GBD 2010 0.047 [0.0
27 iated with central pain, such as strokes and spinal cord lesions, but also disorders such as fibromya
28 ower limb motor function be improved after a spinal cord lesion by re-engaging functional activity of
29 al areas 3b and 1 occur contralateral to the spinal cord lesion, even when <1% of labeled dorsal colu
30 of this study was to quantify axonal loss in spinal cord lesions from 5 paralyzed (Expanded Disabilit
31 ructural analyses of individual demyelinated spinal cord lesions from chronically infected mice to de
32 male preponderance, longitudinally extensive spinal cord lesions (&gt;3 vertebral segments), and absence
33  large numbers of injured CST axons beyond a spinal cord lesion has never been achieved.
34 eas involvement of the brainstem was common; spinal cord lesions, hemisphere lesions and meningoencep
35 ter by surface tension, and deposited onto a spinal cord lesion in glial fibrillary acidic protein-lu
36 g DRG axons that grew toward the center of a spinal cord lesion in rats.
37 idges at the epicenter of traumatic cervical spinal cord lesions in 24 subacute tetraplegic patients.
38   Increased (18)F-FDG uptake was observed in spinal cord lesions in all diseased rats.
39 quency and characteristics of ring-enhancing spinal cord lesions in neuromyelitis optica spectrum dis
40 nal growth and functional recovery following spinal cord lesions in rodents.
41 ensory cortex after sensory loss produced by spinal cord lesions in the common marmoset (Callithrix j
42 , CO, USA) with acute flaccid paralysis with spinal-cord lesions involving mainly grey matter on imag
43 ts suggest that prolonged CMCT is related to spinal cord lesion load and that, over time, changes in
44 er time, changes in the CMCT occur only when spinal cord lesion load increases.
45 hown to occur largely independently of focal spinal cord lesion load, which emphasises their relevanc
46  cord cross-sectional area (UCCA), brain and spinal cord lesion loads, and brain atrophy were measure
47 nd experimental autoimmune encephalomyelitis spinal cord lesions, more specifically in reactive astro
48  also measured brain lesion volume, cervical spinal cord lesion number and cross-sectional area, vibr
49                        Evaluation of CSF and spinal cord lesions of HAM/TSP patients revealed the pre
50 dren had confluent, longitudinally extensive spinal-cord lesions of the central grey matter, with pre
51            The injured axons regrow into the spinal cord lesion, often traversing the injury site.
52 e presence of important risk factors for MS (spinal cord lesions, oligoclonal bands, and disseminatio
53 I model, we analyzed the effects of complete spinal cord lesions on the intrinsic electrophysiologica
54 st occur months or years following a stroke, spinal cord lesion or amputation of a limb; a previously
55 is required: (1) nine brain lesions, (2) two spinal cord lesions, or (3) four to eight brain lesions
56 pplication of the GSK-3 inhibitor lithium to spinal cord-lesioned rats suppresses the activity of thi
57 onance imaging of the brainstem and cervical spinal cord lesions resulting from damage to LMNs has pr
58      Systemic administration of ibuprofen to spinal cord-lesioned rodents reverses the active RhoA si
59 resence of a cellular fibroblast bridge in a spinal cord lesion site and after a growth factor stimul
60 rophin-3 (NT-3) within and beyond a cervical spinal cord lesion site grafted with autologous bone mar
61  dorsal column sensory axons extend across a spinal cord lesion site if axons are guided by a gradien
62  cellular profiles in close proximity to the spinal cord lesion site, peaking 3 d after injury.
63 prostaglandin E2 are elevated in the chronic spinal cord lesion site.
64 f other myelin-associated inhibitors, within spinal cord lesion sites in vivo.
65 e corticospinal projection within and beyond spinal cord lesion sites, achieving a major unmet goal o
66 ated axons for prolonged time periods within spinal cord lesion sites.
67  first myelitis episode was accompanied by a spinal cord lesion spanning >/=3 vertebral segments.
68 AT2 in AQP4-deficient regions of NMO patient spinal cord lesions supports our immunocytochemical and
69  (whole brain and gray matter), and cervical spinal cord lesions (T2LV) and atrophy.
70 Adult rats underwent bilateral dorsal column spinal cord lesions that remove the dorsal corticospinal
71 those which had previously been subjected to spinal cord lesions that transected the axons of the bul
72        However, there is little evidence for spinal cord lesions that would account for alterations i
73                               Ring-enhancing spinal cord lesions were more common in NMOSD than other
74 cterized by both focal and spatially diffuse spinal cord lesions with heterogeneous pathologies that
75 ntifies patients with severe optic nerve and spinal cord lesions with specific pathological features

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