ライフサイエンスコーパス: corticospinal tract

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

2 to execute the ipsilateral extension of the corticospinal tract.

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

4 otor output in motor disorders affecting the corticospinal tract.

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

6 e spinal branching compared to contralateral corticospinal tract.

7 to influence spinal circuits solely via the corticospinal tract.

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

9 ic EPSP after stimulation of the ipsilateral corticospinal tract.

10 orpus callosum and instead descend along the corticospinal tract.

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

12 disorders resulting from degeneration of the corticospinal tract.

13 spinal neurons, the cells that originate the corticospinal tract.

14 rity of the primary sensorimotor network and corticospinal tract.

15 cesses that suppress excitability within the corticospinal tract.

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

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

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

19 l CST misprojections, resulting in bilateral corticospinal tracts.

20 1, contributes to axonal degeneration in the corticospinal tracts.

21 ngitudinal fasciculi, uncinate fasciculi and corticospinal tracts.

22 nt of long intrahemispheric, commissural and corticospinal tracts.

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

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

25 degenerative disease that afflicts the adult corticospinal tracts.

26 er and pathological involvement (2/2) of the corticospinal tracts.

27 mmunohistochemically in ALS ventral horn and corticospinal tracts.

28 0001) and spinal cord (r = 0.57, P < 0.0001) corticospinal tracts.

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

30 diata, superior longitudinal fasciculus, and corticospinal tracts.

31 etries in the structural connectivity of the corticospinal tracts.

32 -based analysis confirmed the results within corticospinal tracts.

33 % large hemispheric, 6.0% diencephalic, 4.3% corticospinal tract), 72.2% had spinal cord lesions (46.

34 Corticospinal tract abnormalities could reflect a centri

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

36 st a cumulative effect of lesions within the corticospinal tracts along the brain, brainstem and spin

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

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

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

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

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

42 are the archetypal projection neurons of the corticospinal tract and corpus callosum, respectively.

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

44 erves or central nervous system axons of the corticospinal tract and dorsal columns, respectively.

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

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

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

48 ue properties and their variations along the corticospinal tract and optic radiation.

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

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

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

52 nce molecule EphA4, axonal misrouting of the corticospinal tract and spinal interneurons is manifeste

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 link between lesion load and location within corticospinal tracts, and disability at baseline and 2-y

74 in motor regions (bilateral precentral gyri, corticospinal tracts, and the corpus callosum) of partic

75 Corticospinal tracts, and the thalamic radiation and cal

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

77 al cord target tissue of the stroke-affected corticospinal tract are mainly defined by two phases: an

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

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

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

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

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

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

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

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

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

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

88 rcuits including descending serotonergic and corticospinal tract axons and afferents from muscle and

89 Corticospinal tract axons did not regrow beyond the lesi

90 Adult corticospinal tract axons do not regenerate because they

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

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

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

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

95 Optogenetic stimulation of host corticospinal tract axons regenerating into grafts elici

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

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

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

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

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

101 akness resulting from distal degeneration of corticospinal tract axons.

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

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

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

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

106 Following damage to the corticospinal tract, both the move and hold period comma

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

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

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

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

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

112 Corticospinal tracts correlated with patients' self-rati

113 ephalic-mesencephalic junction with abnormal corticospinal tract course.

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

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

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

117 ionship between RT and microstructure of the corticospinal tract (CST) and the optic radiation (OR),

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Corticospinal tract (CST) connections to spinal interneu

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

135 Corticospinal tract (CST) degeneration and cortical atro

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

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

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

139 p, WM atrophy was accompanied by significant corticospinal tract (CST) fractional anisotropy (FA) red

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

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

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

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

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

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

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

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

148 The corticospinal tract (CST) is the major descending pathwa

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

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

151 form translational profiling specifically of corticospinal tract (CST) motor neurons in mice, to iden

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 timulation of the primary motor cortex (M1), corticospinal tract (CST), and reticulospinal tract (RST

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

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

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

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

172 CREB-mediated transcription maintain nascent corticospinal tract (CST)-relay neuron contacts.

173 en with unilateral cerebral palsy (uCP), the corticospinal tract (CST)-wiring patterns may differ (co

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

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

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

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

178 fasciculus (SLF), corpus callosum (CC), and corticospinal tract (CST).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 n response to cortical stroke and unilateral corticospinal tract degeneration, compensatory sprouting

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

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

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

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

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

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

200 likelihood that a given measurement reflects corticospinal tract degeneration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 scribe the distribution of lesions along the corticospinal tracts from the cortex to the cervical spi

216 CC mRNA expression, a functional ipsilateral corticospinal tract, greater "mirroring" motor represent

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

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

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

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

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 Moreover, decreases in ipsi-lesional corticospinal tract integrity and increases in contra-le

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

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

241 The corticospinal tract is a predominantly crossed pathway.

242 The corticospinal tract is an important target for motor rec

243 The corticospinal tract is unique to mammals and the corpus

244 Damage to the corticospinal tract is widely studied following unilater

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

246 The spinal cord corticospinal tracts lesion volume fraction remained the

247 Baseline spinal cord corticospinal tracts lesion volume fraction was also ass

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

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

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

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

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

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

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

258 ficant bilateral clusters in the spinal cord corticospinal tracts (P < 0.01).

259 hypothesis could be that lesion location in corticospinal tracts plays a key role in explaining moto

260 turally altered pathways, in addition to the corticospinal tract, post stroke.

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

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

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

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

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

266 ut via the somatosensory subcomponent of the corticospinal tract (S1 CST), and is critically importan

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

268 Corticospinal tract signs were frequent, including exten

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

270 known to strengthen following damage to the corticospinal tract, such as after stroke, partially con

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

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

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

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

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

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

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

283 The corticospinal tract was affected, as reflected by delaye

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

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

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

287 The lesion volume fraction in the corticospinal tracts was higher in secondary and primary

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

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

290 n, brainstem and spinal cord portions of the corticospinal tracts were identified using probabilistic

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

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

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

294 stroke axonal sprouting of corticobulbar and corticospinal tracts, which might have contributed to re

295 were not homogeneously distributed along the corticospinal tracts, with the highest lesion frequency

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