ライフサイエンスコーパス: corticospinal tract

1 ent distal axonopathy of nerve fibers in the corticospinal tract.

2 otor output in motor disorders affecting the corticospinal tract.

3 h-dependent degeneration of the axons of the corticospinal tract.

4 to influence spinal circuits solely via the corticospinal tract.

5 neration of anterior horn cells but a normal corticospinal tract.

6 ic EPSP after stimulation of the ipsilateral corticospinal tract.

7 cesses that suppress excitability within the corticospinal tract.

8 orpus callosum and instead descend along the corticospinal tract.

9 ment as a midline repellant for axons of the corticospinal tract.

10 many studies have used probes reliant on the corticospinal tract.

11 assessed independent of the stroke-affected corticospinal tract.

12 e cerebellar hemisphere opposite the injured corticospinal tract.

13 growth after a unilateral transection of the corticospinal tract.

14 , anterior thalamic radiation, cingulum, and corticospinal tract.

15 rity of the primary sensorimotor network and corticospinal tract.

16 s early damage and lack of maturation of the corticospinal tract.

17 to execute the ipsilateral extension of the corticospinal tract.

18 nt of long intrahemispheric, commissural and corticospinal tracts.

19 genu and splenium of the corpus callosum and corticospinal tracts.

20 he corpus callosum, anterior commissure, and corticospinal tracts.

21 degenerative disease that afflicts the adult corticospinal tracts.

22 atistics, and tractography-based analysis on corticospinal tracts.

23 mmunohistochemically in ALS ventral horn and corticospinal tracts.

24 amidal neurons from the cerebral cortex, and corticospinal tracts.

25 etries in the structural connectivity of the corticospinal tracts.

26 -based analysis confirmed the results within corticospinal tracts.

27 s its adult onset or its specificity for the corticospinal tracts.

28 hange, and atrophy and hyperintensity of the corticospinal tracts.

29 l CST misprojections, resulting in bilateral corticospinal tracts.

30 1, contributes to axonal degeneration in the corticospinal tracts.

31 ngitudinal fasciculi, uncinate fasciculi and corticospinal tracts.

32 Corticospinal tract abnormalities could reflect a centri

33 ophy, parkinsonism, autonomic dysfunction or corticospinal tract abnormalities suggests a diagnosis o

34 day 0 netrin 1 mutant mice also demonstrate corticospinal tract abnormalities.

35 quantitation of myelin loss of fibres of the corticospinal tract and associated macrophage burden, as

36 e white matter integrity in the ipsilesional corticospinal tract and bilateral corpus callosum was in

37 te matter pathology was confirmed within the corticospinal tract and callosal body, and linked strong

38 AD or CJD cases, CHIT1 was expressed in the corticospinal tract and CHIT1 staining colocalised with

39 network was defined based upon the prominent corticospinal tract and corpus callosum involvement demo

40 nt in the L1 knockout mice, such as abnormal corticospinal tract and corpus callosum, were not observ

41 ide quantification of the involvement of the corticospinal tract and extramotor areas is inadequate a

42 L1CAM knock-out mice show hypoplasia of the corticospinal tract and failure of corticospinal axonal

43 alization, limited only to the corticobulbar/corticospinal tract and its main input/output structures

44 's stage correlated with DTI measures of the corticospinal tract and mid-callosum.

45 ailure or degeneration of motor axons in the corticospinal tract and progressive lower limb spasticit

46 ranscranial magnetic stimulation excited the corticospinal tract and responses were recorded in bicep

47 otal plaque load and axonal loss in both the corticospinal tract and sensory tracts were weak or abse

48 lly there was increased sprouting of injured corticospinal tract and serotonergic projections after h

49 that give rise to the crossing axons of the corticospinal tract and superior cerebellar peduncles.

50 sation (crossing in the brain) affecting the corticospinal tract and superior cerebellar peduncles.

51 Tractography of the corticospinal tract and the medial lemniscus was perform

52 anatomical relationship between the lesioned corticospinal tract and the wide distribution of activat

53 reconstruct the intracranial portion of the corticospinal tract and three regions of the corpus call

54 imaging (n = 10) evidence of disease in the corticospinal tract and white matter projections involvi

55 terized by the degeneration of long axons in corticospinal tracts and dorsal columns, resulting in sp

56 haracterized by selective axonal loss in the corticospinal tracts and dorsal columns.

57 anisotropy and increased trace in bilateral corticospinal tracts and genu of corpus callosum (p < 0.

58 essed atrophy in white matter in the cranial corticospinal tracts and grey matter in sensorimotor cor

59 atter and corpus callosum in addition to the corticospinal tracts and mean diffusivity measures in th

60 controls in the diffusion properties of the corticospinal tracts and motor fibres of the callosum.

61 es in several white matter tracts, including corticospinal tracts and optic radiations, indicating pr

62 lly by retrograde axonal degeneration of the corticospinal tracts and posterior columns.

63 uals had signal abnormalities in the central corticospinal tracts and spinal cord where imaging was a

64 , encompassing parts of the corpus callosum, corticospinal tracts and superior longitudinal fasciculu

65 e degeneration of long spinal neurons in the corticospinal tracts and the dorsal columns.

66 y relevant white matter (corpus callosum and corticospinal tract) and deep grey matter (thalamus) str

67 on results in significant axon growth of the corticospinal tract, and improves functional recovery.

68 ndle, splenium of the corpus callosum, right corticospinal tract, and left inferior fronto-occipital

69 ter abnormalities in the corpus callosum and corticospinal tract, and reduced thalamic and globus pal

70 rmed the most significant alterations in the corticospinal tracts, and captured additional significan

71 t, certain supraspinal pathways, such as the corticospinal tract, appear to be completely abolished,

72 to forelimb motoneurons from the ipsilateral corticospinal tract are weak and indirect and that modul

73 ding corpus callosum, cingulum, uncinate and corticospinal tracts) as well as globally in a voxel-by-

74 white matter volume change encompassing the corticospinal tract at the level of the right internal c

75 olume decline of white matter in the cranial corticospinal tracts at the level of the internal capsul

76 ion coefficient (ADC) were measured from the corticospinal tracts at the level of the internal capsul

77 .004) and reduced white matter volume of the corticospinal tracts at the level of the right internal

78 Competitive interactions are known to shape corticospinal tract axon outgrowth and withdrawal during

79 treatment, a substantial portion of severed corticospinal tract axon processes were able to grow thr

80 city of descending serotonergic pathways and corticospinal tract axonal regeneration.

81 n-1-null mutant (knock-out) mice, dieback of corticospinal tract axons also is reduced after SCI.

82 Corticospinal tract axons did not regrow beyond the lesi

83 Adult corticospinal tract axons do not regenerate because they

84 acent to the forward processes of transected corticospinal tract axons in a spatial profile that coul

85 ficient mice showed enhanced regeneration of corticospinal tract axons in comparison with wild-type c

86 pression of Sox11 to stimulate the growth of corticospinal tract axons in the cervical spinal cord an

87 Sprouting of spared corticospinal tract axons in the contralesional spinal c

88 include the sprouting patterns of descending corticospinal tract axons into spinal gray matter after

89 that the regenerative capacity of transected corticospinal tract axons persists for weeks after injur

90 able for the robust spontaneous sprouting of corticospinal tract axons seen after pyramidotomy in pos

91 to the lesion level, and greater numbers of corticospinal tract axons sprout rostral to the lesion.

92 , we show that inosine triples the number of corticospinal tract axons that project from the unaffect

93 cterized by distal axonopathy of the longest corticospinal tract axons, and so their study provides a

94 ndent degeneration of the distal ends of the corticospinal tract axons, resulting in spastic paralysi

95 bilaterally symmetric loss of small-diameter corticospinal tract axons.

96 ascending sensory projections and descending corticospinal tract axons.

97 akness resulting from distal degeneration of corticospinal tract axons.

98 ed to determine: (i) the number of surviving corticospinal tract axons; (ii) the extent of grey and w

99 was predicted by axial diffusivity along the corticospinal tract (beta = 4.6 x 10(3); P < .001), Symb

100 s (P < 0.01) were significantly smaller; and corticospinal tract (bilaterally; P < 0.045, P < 0.05) a

101 use weakness, including many strokes, injure corticospinal tract but leave motor cortex intact.

102 the 15-30 Hz range is dependent on an intact corticospinal tract but persists in the face of selectiv

103 Combined lesions of both dorsal and ventral corticospinal tract components eliminated sprouting and

104 d in the distal portions of the intracranial corticospinal tract, consistent with a distal axonal deg

105 ABSTRACT: It is well accepted that the corticospinal tract contributes to the control of finger

106 KEY POINTS: The corticospinal tract contributes to the control of finger

107 the anterior commissure, cerebral peduncle (corticospinal tract), corpus callosum, fornix, internal

108 Corticospinal tracts correlated with patients' self-rati

109 mice showed a more pronounced dieback of the corticospinal tract (CST) and a decreased sprouting capa

110 (up to 180 days) protection for spinal cord corticospinal tract (CST) and dorsal column (DC) axons i

111 ed whether compensatory reinnervation in the corticospinal tract (CST) and the corticorubral tract (C

112 on forming specific connections between the corticospinal tract (CST) and the spinal cord.

113 quantify the axonal integrity of the cranial corticospinal tract (CST) and to establish how microstru

114 ty, resulting in significant regeneration of corticospinal tract (CST) axons after SCI.

115 genetic assessment of the role of Nogo-A in corticospinal tract (CST) axons after spinal cord dorsal

116 tex of neonatal mice enables regeneration of corticospinal tract (CST) axons after spinal cord injury

117 Eighty-seven percent of corticospinal tract (CST) axons decussated in the medull

118 otably, a mean of 10.1 +/- 0.6% (+/- SEM) of corticospinal tract (CST) axons descended in the lateral

119 In rodents, the main contingent of corticospinal tract (CST) axons descends in the ventral

120 Studies that have assessed regeneration of corticospinal tract (CST) axons in mice after genetic mo

121 Here we show that Wnt proteins repel corticospinal tract (CST) axons in the opposite directio

122 The growth of corticospinal tract (CST) axons was studied quantitative

123 the somato-motor cortex to trace descending corticospinal tract (CST) axons, into the midbrain to la

124 encoding potent repellents of the descending corticospinal tract (CST) axons, were robustly and acute

125 eotyped pruning in the CNS is the pruning of corticospinal tract (CST) axons.

126 Development of skilled movements and the corticospinal tract (CST) begin prenatally and continue

127 Partial injury to the corticospinal tract (CST) causes sprouting of intact axo

128 Corticospinal tract (CST) connections to spinal interneu

129 lumn SCI that bilaterally ablated the dorsal corticospinal tract (CST) containing approximately 96% o

130 tions and whether the RN/RST compensates for corticospinal tract (CST) developmental motor impairment

131 estion of whether the cells of origin of the corticospinal tract (CST) die following spinal cord inju

132 own to promote axon collateral growth in the corticospinal tract (CST) following stroke and focal TBI

133 The rodent corticospinal tract (CST) has been used extensively to i

134 The corticospinal tract (CST) has dense contralateral and sp

135 Despite the essential role of the corticospinal tract (CST) in controlling voluntary movem

136 aging (DTI), we assessed degeneration of the corticospinal tract (CST) in the cervical cord above a t

137 received a unilateral lesion of the lateral corticospinal tract (CST) in the thoracic spinal cord.

138 to investigate whether an imaging measure of corticospinal tract (CST) injury in the acute phase can

139 The corticospinal tract (CST) is a major descending pathway

140 aches, we discovered that the anatomy of the corticospinal tract (CST) is abnormal in patients with N

141 The corticospinal tract (CST) is the most important motor sy

142 Of descending pathways, the corticospinal tract (CST) is thought to be the most crit

143 it fails to promote neurite outgrowth after corticospinal tract (CST) lesions in the adult rat.

144 iption factor Sox11 increases axon growth by corticospinal tract (CST) neurons after spinal injury.

145 Adult corticospinal tract (CST) neurons failed to up-regulate

146 ggests that these connections come only from corticospinal tract (CST) neurons in the subdivision of

147 neurons in the adult mammalian CNS, notably corticospinal tract (CST) neurons, display a much lower

148 of the lesion cavity to identify transected corticospinal tract (CST) neurons.

149 neurones and their axonal projections in the corticospinal tract (CST) of the spinal cord.

150 l cells are observed accompanying the entire corticospinal tract (CST) on the injured side, but not t

151 The limited rewiring of the corticospinal tract (CST) only partially compensates the

152 whether EPO treatment promotes contralateral corticospinal tract (CST) plasticity in the spinal cord

153 Two lines did not display enhanced corticospinal tract (CST) regeneration, and one displaye

154 tory bulb into unilateral lesions of the rat corticospinal tract (CST) restore function in a directed

155 is the limited regrowth of the axons in the corticospinal tract (CST) that originate in the motor co

156 g the contralateral spinal projection of the corticospinal tract (CST) to investigate the effects of

157 rsy about whether the cells of origin of the corticospinal tract (CST) undergo retrograde cell death

158 The corticospinal tract (CST) was cut unilaterally at the le

159 release of glutamate within the ipsilesional corticospinal tract (CST), and an enhanced NMDA-mediated

160 In the context of injury to the corticospinal tract (CST), brainstem-origin circuits may

161 scending motor pathway for motor skills, the corticospinal tract (CST), sprout after brain or spinal

162 The primate corticospinal tract (CST), the major descending pathway

163 niculus, the same location as the descending corticospinal tract (CST), which develops postnatally.

164 We observed enhanced regeneration of the corticospinal tract (CST).

165 vity measures along the tractography-derived corticospinal tract (CST).

166 , which is partly mediated by the descending corticospinal tract (CST).

167 spinal cord often assess regeneration of the corticospinal tract (CST).

168 tudy the primary descending motor tract, the corticospinal tract (CST).

169 d tract-specific integrity of PC and lateral corticospinal tracts (CST).

170 identified measures of brain injury (smaller corticospinal tract [CST] injury), cortical function (gr

171 g to define the location and organization of corticospinal tracts (CSTs) in the posterior limb of the

172 tical inhibitory circuits in the same way as corticospinal tract (CTS) projections to spinal motoneur

173 otor outcome after stroke, but assessment of corticospinal tract damage alone is unlikely to be suffi

174 r are not established although the extent of corticospinal tract damage is suggested to be a contribu

175 In addition, we observe corticospinal tract defects in mice homozygous for a spo

176 We aimed to assess the severity of corticospinal tract degeneration in a large cohort of ca

177 adjusting for disease duration, severity of corticospinal tract degeneration remained significantly

178 ; however, the cases with moderate to severe corticospinal tract degeneration showed right-sided temp

179 In contrast, the cases with no or equivocal corticospinal tract degeneration were more likely to sho

180 cases, however, had moderate to very severe corticospinal tract degeneration with myelin and axonal

181 cases, and only two cases showed evidence of corticospinal tract degeneration without lower motor neu

182 Eight cases had no corticospinal tract degeneration, and 14 cases had equiv

183 in selectively vulnerable forebrain regions, corticospinal tract degeneration, and motor spasticity r

184 Only one case, without corticospinal tract degeneration, was found to have a he

185 lobar degeneration with type C pathology and corticospinal tract degeneration, with this entity showi

186 neration, and 14 cases had equivocal to mild corticospinal tract degeneration.

187 ias (HSPs) are a group of diseases caused by corticospinal tract degeneration.

188 likelihood that a given measurement reflects corticospinal tract degeneration.

189 neuron involvement and FTD might reflect the corticospinal tract degeneration.

190 eneration; and (iii) moderate to very severe corticospinal tract degeneration.

191 currence of cases of type C pathology having corticospinal tract degeneration.

192 ded into three groups based on the degree of corticospinal tract degeneration: (i) no corticospinal t

193 of corticospinal tract degeneration: (i) no corticospinal tract degeneration; (ii) equivocal cortico

194 icospinal tract degeneration; (ii) equivocal corticospinal tract degeneration; and (iii) moderate to

195 ial magnetic stimulation (TMS) characterized corticospinal tract development from each hemisphere ove

196 These data support a role for L1CAM in corticospinal tract development in hemizygous males and

197 s in Thy1-YFP-H mice elicited alterations in corticospinal tract development.

198 neurite outgrowth assay in vitro, tracing of corticospinal tract fibers after dorsal hemisection of t

199 Tract tracing demonstrated corticospinal tract fibers passing through the injury ep

200 Furthermore, we show that corticospinal tract fibers respond differently to loss o

201 period where functional connections between corticospinal tract fibres and spinal motoneurones under

202 iod where the functional connections between corticospinal tract fibres and spinal motoneurones under

203 ked brainstem and cervical cord atrophy with corticospinal tract findings, but the typical olivary MR

204 Loss of Map2k1/2 (Mek1/2) led to deficits in corticospinal tract formation and subsequent corticospin

205 nal motor neurons, accompanied by failure of corticospinal tract formation.

206 of corpus callosum, anterior commissure, and corticospinal tract formation.

207 entricles and white matter (corpus callosum, corticospinal tract, fornix system) increase; in TASTPMs

208 Basal ganglia volumes and bilateral corticospinal tract fractional anisotropy correlated sig

209 omic studies demonstrated hypertrophy of the corticospinal tract from the noninfarcted hemisphere.

210 uantitatively the population of axons in the corticospinal tracts from the medulla to the lumbar spin

211 onance imaging and anatomic studies compared corticospinal tract growth in 13 patients with perinatal

212 orona radiata, higher FA and AD in bilateral corticospinal tracts (>/=164mul, p<.01), and lower MD in

213 The corticospinal tract has a key role in producing this pla

214 hemiparesis from a subcortical lesion of the corticospinal tract have a higher-order motor planning d

215 ns in all the white matter tracts except the corticospinal tracts; however, staining of sensory axons

216 MR images were evaluated for corticospinal tract hyperintensity and central sulcus di

217 Corticospinal tract hyperintensity, central sulcus enlar

218 s includes the distinct finding of brainstem corticospinal tract hypoplasia.

219 in the white matter along the corticobulbar/corticospinal tract in 20 spasmodic dysphonia patients c

220 After lesioning the corticospinal tract in adult rats, ECs were transplanted

221 Although clearly secondary to the corticospinal tract in healthy function, this could assu

222 tially used to evaluate the integrity of the corticospinal tract in humans non-invasively.

223 The corticospinal tract in Old World primates makes monosyna

224 In this study we examined the role of the corticospinal tract in pathway reorganization following

225 h reductions in fractional anisotropy in the corticospinal tract in patients with amyotrophic lateral

226 ased mean diffusivity and volume loss of the corticospinal tract in patients with primary lateral scl

227 also induced sprouting of the contralesional corticospinal tract in the aged treated hemicord.

228 ter in the hand knob area; the region of the corticospinal tract in the centrum semiovale, in the pos

229 had complete destruction of the main dorsal corticospinal tract in the dorsal columns and some damag

230 The corticospinal tract in the macaque and human forms the m

231 Strong experimental evidence implicates the corticospinal tract in voluntary control of the contrala

232 preservation or restoration of ipsilesional corticospinal tracts in combination with reinstatement o

233 uperior and inferior longitudinal fasciculi, corticospinal tract, inferior fronto-occipital tract, su

234 Baseline impairment also correlated with corticospinal tract injury (R(2) = 0.52), though not inf

235 ructural magnetic resonance imaging measured corticospinal tract injury and infarct volume.

236 ctivity with a structural measure of injury (corticospinal tract injury) performed better than either

237 with incomplete resection: corpus callosum, corticospinal tract, insular lobe, middle cerebral arter

238 complicated HSP suggests that the "primary" corticospinal tract involvement known to occur in these

239 Damage to the corticospinal tract is a leading cause of motor disabili

240 The corticospinal tract is a predominantly crossed pathway.

241 The corticospinal tract is an important target for motor rec

242 The corticospinal tract is strongly positive throughout its

243 with age was found in the internal capsule, corticospinal tract, left arcuate fasciculus, and right

244 ninjured) monkeys, we performed a unilateral corticospinal tract lesion at the thoracic level.

245 I, we created bilaterally complete medullary corticospinal tract lesions in adult mice, eliminating a

246 tional recovery was also abolished if dorsal corticospinal tract lesions were followed 5 weeks later

247 sions were followed 5 weeks later by ventral corticospinal tract lesions.

248 Results While considering damage within a corticospinal tract mask resulted in 73% classification

249 Abnormalities in the corpus callosum, corticospinal tract, medial lemniscus and cerebellar ped

250 ined by progressive neurodegeneration of the corticospinal tract motor neurons.

251 3% classification accuracy, using other (non-corticospinal tract) motor areas provided 87% accuracy,

252 After injury to the corticospinal tract, NgR1 limits axon collateral sprouti

253 xons, spontaneous sprouting from the ventral corticospinal tract occurred onto medial motoneuron pool

254 contrast, myelination of motor axons in the corticospinal tract of the spinal cord occurred normally

255 at, over time, truncated M1 could damage the corticospinal tracts of human patients.

256 athfinding and fasciculation are abnormal in corticospinal tracts of Scn1b null mice consistent with

257 , we failed to demonstrate anisotropy in the corticospinal tracts of the basis pontis in 4 affected b

258 spinal cord receive the synaptic inputs from corticospinal tract or serotonergic axons, limited bouto

259 n the dorsolateral column (the "dorsolateral corticospinal tract," or DLCST).

260 esection was due to tumor involvement of the corticospinal tract (P < .01), large tumor volume (P < .

261 uated using 3 probes independent of affected corticospinal tract: passive finger movement, a hand-rel

262 l diffusivity and disease duration along the corticospinal tracts (r = 0.806, P < 0.01) was found.

263 onal antibody recognizes Nogo-A and promotes corticospinal tract regeneration and locomotor recovery;

264 R in axonal growth inhibition in vitro or in corticospinal tract regeneration block in vivo.

265 that activation of ERK signaling can elicit corticospinal tract regeneration.

266 initially disrupted structural integrity in corticospinal tract regions, which correlated positively

267 a length-dependent distal axonopathy of the corticospinal tracts, resulting in lower limb spasticity

268 In addition to the corticospinal tracts, significant differences in fractio

269 Corticospinal tract signs were frequent, including exten

270 s the ability of a trophic factor to promote corticospinal tract sprouting.

271 ring of the outer blades, and involvement of corticospinal tracts, thalami, and spinal cord.

272 re more widespread and more prominent in the corticospinal tract than the decreases in fractional ani

273 recognized the additional involvement of the corticospinal tracts that distinguished this from progre

274 en for IIV in one or both trial types in the corticospinal tract, the left superior longitudinal fasc

275 n the extent of stroke-induced damage to the corticospinal tract, the major descending motor pathway

276 igrations, also controls the guidance of the corticospinal tract, the major tract responsible for coo

277 Our results indicate that in the corticospinal tracts there is a significant reduction of

278 in the transmission of information from the corticospinal tract to upper limb motoneurons.

279 ation for the selective sensitivity of adult corticospinal tracts to loss of spastin activity.

280 esions spread beyond precentral cortices and corticospinal tracts, to include the corpus callosum; fr

281 Corticospinal tract tracing reveals no abnormality in un

282 Denervation of neuron-astrocyte signaling by corticospinal tract transection, ricin-induced motor neu

283 and and forearm muscles from the ipsilateral corticospinal tract using multiple methods.

284 The corticospinal tract was absent in Fezl(-/-) mice, cortic

285 The corticospinal tract was affected, as reflected by delaye

286 For comparison, the corticospinal tract was assessed in 86 type A and B case

287 The corticospinal tract was defective as axons failed to res

288 The corticospinal tract was most likely to be damaged in bot

289 However, while damage in the corticospinal tract was the best indicator of motor defi

290 ion factor required for the formation of the corticospinal tract, was not expressed in the Fezl-defic

291 izophrenia in the sensori-motor cortices and corticospinal tract were less marked or even disappeared

292 DTI showed displacement of the ipsilateral corticospinal tract, whereas MR spectroscopy showed abse

293 who display mirror movements, have abnormal corticospinal tracts which innervate motoneurons of the

294 training may produce plastic changes in the corticospinal tract, which are responsible for improveme

295 This contrasts with the corticospinal tract, which is thought to be involved in

296 y) and of the structural connectivity of the corticospinal tracts within the brainstem (by magnetic r

297 ally when the structural connectivity of the corticospinal tracts within the brainstem is asymmetric.

298 ent and degenerative pathology in the distal corticospinal tracts without apparent motor neuron patho

299 V pyramidal neurons and degeneration of the corticospinal tract, without involvement of anterior hor

300 cISMS with stimulation of the contralateral corticospinal tract yielded no evidence of response occl