ライフサイエンスコーパス: secondary progressive

1 n be preceded by a relapsing disease course (secondary progressive).

2 ing-remitting, 28 primary progressive and 36 secondary progressive.

3 benign, 14 with relapsing-remitting, 10 with secondary progressive, 16 with primary progressive and t

4 olated syndrome, 198 relapsing remitting, 39 secondary progressive, 31 primary progressive multiple s

5 osis [94 (57%) relapsing-remitting, 25 (15%) secondary progressive], 45 (27%) remained clinically iso

6 6 +/- 2.89 versus 47.44 +/- 2.70, P < 0.01), secondary-progressive (46.33 +/- 2.84 versus 44.75 +/- 3

7 was observed in T(1) hypointense lesions in secondary-progressive (49.0 +/- 7.0 mM) and primary-prog

8 psing/remitting disease (EDSS > 3), 13 (24%) secondary progressive and 21 (39%) benign (relapsing/rem

9 ty-nine multiple sclerosis patients (21 with secondary progressive and 28 with relapsing-remitting mu

10 6+/-10 years; 67.8% relapsing-remitting, 28% secondary progressive and 4.2% primary progressive MS) a

11 from 54 patients (17 primary progressive, 30 secondary progressive and 7 controls).

12 llidum of patients with relapsing-remitting, secondary progressive and primary progressive multiple s

13 s and were divided into relapsing-remitting, secondary progressive and primary progressive subgroups.

14 ally isolated syndrome, relapsing-remitting, secondary progressive and primary progressive.

15 aging and compares the abnormalities between secondary progressive and relapsing remitting multiple s

16 7 patients with relapsing-remitting, 23 with secondary-progressive and 20 with primary-progressive mu

17 ndrome, 29 with relapsing-remitting, 28 with secondary-progressive and 28 with primary-progressive mu

18 tients with MS (27 relapsing-remitting, nine secondary progressive) and in 20 control subjects to qua

19 ed syndrome, and 416 relapsing-remitting, 84 secondary progressive, and 73 primary progressive multip

20 ct clinical descriptors-relapsing-remitting, secondary progressive, and primary progressive-for patie

21 ient may prevent recurrence, reoperation and secondary progressive aortic valve disease.

22 A phase 3 trial [the International MS Secondary Progressive Avonex Controlled Trial (IMPACT)]

23 e Sclerosis [SENTINEL], and International MS Secondary Progressive Avonex Controlled Trial [IMPACT])

24 nearer the outer subpial surface compared to secondary progressive cases.

25 g-remitting (coefficient = -0.48, P < 0.01), secondary-progressive (coefficient = -0.51, P < 0.01) an

26 ent = -0.28, P = 0.02), and both primary and secondary-progressive compared to relapsing-remitting mu

27 Sodium concentrations were higher in secondary-progressive compared with relapsing-remitting

28 Disability progression and secondary progressive conversion were defined by using s

29 a relapsing-remitting clinical course into a secondary progressive course.

30 , one a primary progressive course and one a secondary progressive course.

31 rse and 58 of 66 (87.8%) patients who became secondary progressive (cross-validated error rate = 7.2%

32 POMS patients also took longer to develop secondary progressive disease (32 vs 18 years, p=0.0001)

33 se duration particularly in patients who had secondary progressive disease (P (CSF) < 4 x 10(-5), P (

34 patients with multiple sclerosis (seven with secondary progressive disease and 14 with a relapsing re

35 m MRI natural history in a large cohort with secondary progressive disease and to ascertain its relat

36 s with progressive, and 12% of patients with secondary progressive disease course (2% of eyes).

37 disability progression and conversion into a secondary progressive disease course.

38 is associated with greater brain atrophy in secondary progressive disease over a period of short ter

39 cumulation of disability in MS patients with secondary progressive disease regardless of the severity

40 d WM abnormalities was weaker in primary and secondary progressive disease than in relapsing-remittin

41 short-term MRI activity is generally high in secondary progressive disease, confirming a useful role

42 ent outcome in early relapsing-remitting and secondary progressive disease.

43 The cohort had clinical features typical of secondary progressive disease: thus, all had moderate or

44 nd cognitive speed deficits were observed in secondary-progressive disease.

45 5-HC) in patients with SPMS and in mice with secondary progressive experimental autoimmune encephalom

46 ctor H levels were capable of distinguishing secondary progressive from relapsing remitting disease (

47 or disability in the primary progressive and secondary progressive groups was similar preceding death

48 e sclerosis (MS) from relapsing-remitting to secondary progressive have not been clarified yet.

49 Secondary progressive is associated with more widespread

50 en men, 21 women; 18 relapsing remitting, 10 secondary progressive; mean age 42 years).

51 ssion, relapse, and chronic progression in a secondary progressive model of demyelinating disease.

52 gnificantly higher in the caudate nucleus in secondary progressive MS (12.9/s vs 10.9/s, p=0.03).

53 had RRMS and EDSS scores >3.5, 26 (34%) had secondary progressive MS (all had EDSS scores >3.5), and

54 ort of patients with relapsing-remitting and secondary progressive MS (n = 189), with validation on a

55 -remitting MS (P < 0.01), only marginally in secondary progressive MS (P < 0.05), and not at all in p

56 y Status Scale (EDSS) score in patients with secondary progressive MS (r = -0.69, P = .004) and no co

57 Among secondary progressive MS (SPMS) cases with attacks, all

58 y and mtDNA deletions in single neurons from secondary progressive MS (SPMS) cases.

59 essing from Relapsing-Remitting MS (RRMS) to Secondary Progressive MS (SPMS) in many cases.

60 volumes in relapsing remitting MS (RRMS) and secondary progressive MS (SPMS) patients and controls.

61 10 relapsing-remitting MS (RRMS) patients, 9 secondary progressive MS (SPMS) patients, and 9 healthy

62 psing-remitting multiple sclerosis (RRMS) to secondary progressive MS (SPMS) represents a huge clinic

63 colour vision in relapsing-remitting MS and secondary progressive MS (SPMS) than clinically isolated

64 pwPMS with primary progressive MS (PPMS) or secondary progressive MS (SPMS) with at least one GFAP v

65 ng-remitting MS (RRMS), and 27 patients with secondary progressive MS (SPMS).

66 ppressive therapies show limited efficacy in secondary progressive MS (SPMS).

67 easures as biomarkers of disease severity in secondary progressive MS (SPMS).

68 er (GM) volumes predict future disability in secondary progressive MS (SPMS).

69 s with active relapsing remitting (RRMS) and secondary progressive MS (SPMS).

70 classified as CIS, relapsing-remitting MS or secondary progressive MS (SPMS).

71 isability progression (DP) and conversion to secondary progressive MS (SPMS).

72 se, these therapies show limited efficacy in secondary progressive MS (SPMS).

73 I = 13.5-22.5%) evolved from relapsing MS to secondary progressive MS (SPMS).

74 ary progressive MS multiple sclerosis ( SPMS secondary progressive MS ) patients provided written inf

75 Thirty-four MS patients (7 with secondary progressive MS [SPMS], 27 with relapsing remit

76 AM/TSP, 74 relapsing-remitting MS [RRMS], 17 secondary progressive MS [SPMS], and 40 primary progress

77 4 converted to relapsing remitting MS, 26 to secondary progressive MS and 16 had died due to MS.

78 retina, and by inference the optic nerve, in secondary progressive MS and primary progressive MS.

79 e cellular microenvironment of MS lesions in secondary progressive MS and primary progressive MS.

80 edictors (within 5 years of presentation) of secondary progressive MS at 30 years were presence of ba

81 could differentiate primary progressive from secondary progressive MS better than random guessing.

82 Forty-eight ROIs from 4 secondary progressive MS brains were analyzed.

83 pinal fluid (CSF) samples from 41 postmortem secondary progressive MS cases compared with 5 non-neuro

84 dorsomedial thalamic nuclei from postmortem secondary progressive MS cases in combination with detai

85 Patients with primary/secondary progressive MS from seven AHSCT MS centres and

86 Two-thirds of patients with secondary progressive MS had elevated anti-SNO-cysteine

87 duals suffering from relapsing-remitting and secondary progressive MS had significantly higher prothr

88 Increased caudate R(2)' in patients with secondary progressive MS is consistent with increased ir

89 RMS relaxing-remitting MS ) patients, and 12 secondary progressive MS multiple sclerosis ( SPMS secon

90 0, HD n = 110; primary progressive MS n = 9; secondary progressive MS n = 10; neuromyelitis optica sp

91 hin the first 5 years increased the risk for secondary progressive MS or MS related death by 30 years

92 that memory and naive B cells from RRMS and secondary progressive MS patients exhibited a significan

93 s in RNFLT and macular volume in the eyes of secondary progressive MS patients not previously affecte

94 hfield phase imaging of highly active and of secondary progressive MS patients.

95 y and EDSS score was better in patients with secondary progressive MS than in those with relapsing-re

96 ron beta had a lower hazard of conversion to secondary progressive MS than matched untreated patients

97 ion accrual was greater in participants with secondary progressive MS than with relapsing-remitting M

98 ssociated with a lower risk of conversion to secondary progressive MS vs initial treatment with glati

99 MPF macromolecular proton fraction in SPMS secondary progressive MS was reduced relative to RRMS re

100 Within each gender, men and women with secondary progressive MS were more depressed than men or

101 neurologic disability between episodes, and secondary progressive MS with activity, defined as stead

102 no disability and a half will have developed secondary progressive MS with increasing disability.

103 th secondary progressive multiple sclerosis (secondary progressive MS) (8 male; 19 female; mean age 5

104 ents (73 RRMS, 12 primary progressive MS, 20 secondary progressive MS) and 23 healthy controls (HCs).

105 progressive MS, relapsing-remitting MS, and secondary progressive MS) and disease severity levels.

106 essive MS, and intravenous immunoglobulin in secondary progressive MS).

107 Of the patients with secondary progressive MS, 14 had clinical history of opt

108 ants with relapsing-remitting MS and 13 with secondary progressive MS, along with 10 age-matched heal

109 macular volume were significantly reduced in secondary progressive MS, but not in primary progressive

110 39 patients treated with AHSCT (37 with secondary progressive MS, mean age 37 years, EDSS 5.7, 2

111 ue from MS patients, particularly those with secondary progressive MS, showed decreased mitochondrial

112 in patients with active relapsing than with secondary progressive MS.

113 ice, a model which resembles some aspects of secondary progressive MS.

114 ppear to be at increased risk for developing secondary progressive MS.

115 rate a partial effect on disease activity in secondary progressive MS.

116 itting MS and 23.6 mL per year in those with secondary progressive MS.

117 mulation of new inflammatory disease foci in secondary progressive MS.

118 rior to TN symptom onset; 57% had primary or secondary progressive MS.

119 rum and cerebrospinal fluid of patients with secondary progressive MS.

120 se of irreversible disability accrual termed secondary progressive MS.

121 Conversion to objectively defined secondary progressive MS.

122 pairments were most prevalent in people with secondary progressive MS.

123 The highest brain-PADs were in secondary-progressive MS (+13.3 years; 95% CI = 11.3-15.

124 me (n = 9); relapsing-remitting MS (n = 20); secondary-progressive MS (n = 22); and age-matched, heal

125 nts with relapsing-remitting MS (n = 123) or secondary-progressive MS (n = 28) (mean age, 36 years; r

126 Fifteen secondary-progressive MS (SPMS) patients, 12 relapsing-r

127 btypes, i.e., relapsing-remitting MS (RRMS), secondary-progressive MS (SPMS), and primary-progressive

128 and EDSS <4 or <6, and time to conversion to secondary-progressive MS (SPMS).

129 Patients had secondary-progressive MS and an Expanded Disability Stat

130 This analysis also determined that secondary-progressive MS patients are immunologically cl

131 clinical trials (primary-progressive MS and secondary-progressive MS trials) and a routine-care MS d

132 ignificantly more GM, but not WM atrophy, in secondary-progressive MS versus relapsing-remitting MS (

133 ch as multiple sclerosis (MS), especially in secondary-progressive MS which follows relapsing-remitti

134 ith relapsing-remitting MS and 16 (28%) with secondary-progressive MS, and 21 HC subjects were imaged

135 whom developed relapsing-remitting MS and 11 secondary-progressive MS, with the rest experiencing no

136 people with SPMS from the Multiple Sclerosis-Secondary Progressive Multi-Arm Randomisation Trial OCT

137 Rates of worsening and evolution to secondary progressive multiple sclerosis (MS) may be sub

138 tex of patients with relapsing-remitting and secondary progressive multiple sclerosis (p<=0.026), but

139 Some studies comparing primary and secondary progressive multiple sclerosis (PPMS, SPMS) re

140 ase duration 11 years), and 27 patients with secondary progressive multiple sclerosis (secondary prog

141 rferon beta-1b (IFNbeta-1b) in patients with secondary progressive multiple sclerosis (SP multiple sc

142 te that grossly unaffected white matter from secondary progressive multiple sclerosis (SP-MS) patient

143 Patients with secondary progressive multiple sclerosis (SPMS) are lack

144 n effects on brain atrophy and disability in secondary progressive multiple sclerosis (SPMS) are medi

145 of relapsing-remitting multiple sclerosis to secondary progressive multiple sclerosis (SPMS), charact

146 ial of simvastatin (80 mg) versus placebo in secondary progressive multiple sclerosis (SPMS), the adj

147 sing-remitting multiple sclerosis (RRMS) and secondary progressive multiple sclerosis (SPMS), which i

148 psing-remitting multiple sclerosis (RRMS) or secondary progressive multiple sclerosis (SPMS).

149 rate of whole brain atrophy in patients with secondary progressive multiple sclerosis (SPMS).

150 therapy substantially reduced the hazard of secondary progressive multiple sclerosis [0.76 (0.73, 0.

151 vival time from relapsing-remitting phase to secondary progressive multiple sclerosis among all patie

152 Thirty patients with secondary progressive multiple sclerosis and 17 healthy

153 els identified independent MRI predictors of secondary progressive multiple sclerosis and Expanded Di

154 post-mortem brain tissue from 20 cases with secondary progressive multiple sclerosis and five age-ma

155 nges has been identified as a key feature of secondary progressive multiple sclerosis and may contrib

156 lyses used the operationalized definition of secondary progressive multiple sclerosis and the Swedish

157 P < 0.01) were independently associated with secondary progressive multiple sclerosis at 15 years.

158 Significantly, analysis of secondary progressive multiple sclerosis brain tissue al

159 was used to estimate the cumulative risk of secondary progressive multiple sclerosis by country of r

160 cent subpial cortical lesions of post-mortem secondary progressive multiple sclerosis cases relative

161 cid levels (i) are abnormal in patients with secondary progressive multiple sclerosis compared with h

162 etization transfer ratio were greater in the secondary progressive multiple sclerosis compared with r

163 otrigine on cerebral volume of patients with secondary progressive multiple sclerosis did not differ

164 amma was found in the meninges of cases with secondary progressive multiple sclerosis exhibiting tert

165 ed patients aged 18-65 years with primary or secondary progressive multiple sclerosis from 27 UK neur

166 d 18-65 years, had a diagnosis of primary or secondary progressive multiple sclerosis fulfilling the

167 s was equally low in primary progressive and secondary progressive multiple sclerosis groups versus c

168 ntricles in both the relapsing remitting and secondary progressive multiple sclerosis groups.

169 A substantial proportion of cases with secondary progressive multiple sclerosis have extensive

170 xonal damage between primary progressive and secondary progressive multiple sclerosis have not been r

171 tem cells were safely given to patients with secondary progressive multiple sclerosis in our study.

172 We evaluated differences in the risk of secondary progressive multiple sclerosis in relation to

173 Patients with secondary progressive multiple sclerosis involving the v

174 ects of axonal pathobiology in patients with secondary progressive multiple sclerosis is insufficient

175 ctively recruited 20 relapsing-remitting, 15 secondary progressive multiple sclerosis participants an

176 Secondary progressive multiple sclerosis patients showed

177 e and efficacious in relapsing-remitting and secondary progressive multiple sclerosis patients.

178 ients with primary progressive compared with secondary progressive multiple sclerosis raise the quest

179 Tunisia, Iran and Canada had higher risks of secondary progressive multiple sclerosis relative to the

180 tients with relapsing-remitting or relapsing secondary progressive multiple sclerosis to receive 3 mg

181 Secondary progressive multiple sclerosis was identified

182 One hundred and twenty three cases with secondary progressive multiple sclerosis were examined f

183 Patients aged 18-65 years with secondary progressive multiple sclerosis were randomly a

184 Twenty-four patients with secondary progressive multiple sclerosis were studied ps

185 Patients with secondary progressive multiple sclerosis who attended th

186 We report the findings in 60 patients with secondary progressive multiple sclerosis who had monthly

187 e recruited patients (aged 25-65 years) with secondary progressive multiple sclerosis who were not on

188 e disability in both primary progressive and secondary progressive multiple sclerosis with a common p

189 res in an extensive collection of cases with secondary progressive multiple sclerosis with a wide age

190 on-beta1b was performed on 718 patients with secondary progressive multiple sclerosis with follow-up

191 (relapsing-remitting multiple sclerosis and secondary progressive multiple sclerosis with relapses)

192 ressive multiple sclerosis or a diagnosis of secondary progressive multiple sclerosis without relapse

193 ver time may evolve to a progressive course (secondary progressive multiple sclerosis) or as having a

194 sis (either relapsing-remitting or relapsing secondary progressive multiple sclerosis), and one or mo

195 se, and 2.89 cm3/year in those who developed secondary progressive multiple sclerosis, a difference o

196 from 23 patients with relapsing-remitting or secondary progressive multiple sclerosis, all of whom we

197 luated geographical variation in the risk of secondary progressive multiple sclerosis, an advanced fo

198 atients with relapsing remitting and 28 with secondary progressive multiple sclerosis, and 38 healthy

199 4 years disease duration), 13 subjects with secondary progressive multiple sclerosis, and in 17 age-

200 ) stimulation was lower in the patients with secondary progressive multiple sclerosis, compared with

201 Secondary progressive multiple sclerosis, for which no s

202 omly assigned participants with nonrelapsing secondary progressive multiple sclerosis, in a 2:1 ratio

203 edictors of key long-term outcomes including secondary progressive multiple sclerosis, physical disab

204 In secondary progressive multiple sclerosis, T2* in normal-

205 We conclude that for relapsing-remitting and secondary progressive multiple sclerosis, the combinatio

206 In participants with nonrelapsing secondary progressive multiple sclerosis, the risk of di

207 s to disability accrual and earlier onset of secondary progressive multiple sclerosis.

208 al substrate that causes major disability in secondary progressive multiple sclerosis.

209 as a potential neuroprotective treatment for secondary progressive multiple sclerosis.

210 ferent pathogenetic mechanisms compared with secondary progressive multiple sclerosis.

211 ine is also neuroprotective in patients with secondary progressive multiple sclerosis.

212 cal spinal cord in patients with primary and secondary progressive multiple sclerosis.

213 tic neuritis, and chronically in primary and secondary progressive multiple sclerosis.

214 EAE) and in brain samples from patients with secondary progressive multiple sclerosis.

215 ications for the axonal loss associated with secondary progressive multiple sclerosis.

216 ng tissue loss in both arms of this study of secondary progressive multiple sclerosis.

217 ing-remitting multiple sclerosis and 20 with secondary progressive multiple sclerosis.

218 -beta-1b was also shown to be efficacious in secondary progressive multiple sclerosis.

219 carried out in 20 patients with primary and secondary progressive multiple sclerosis.

220 cord lesions over time were associated with secondary progressive multiple sclerosis.

221 ion were associated with increased hazard of secondary progressive multiple sclerosis.

222 ated with a higher probability of developing secondary progressive multiple sclerosis.

223 ically distinct from relapsing-remitting and secondary progressive multiple sclerosis.

224 are no approved treatments for nonrelapsing secondary progressive multiple sclerosis.

225 elapsing multiple sclerosis including active secondary progressive multiple sclerosis.

226 m that was most evident in participants with secondary progressive multiple sclerosis.

227 n appealing candidate drug for patients with secondary progressive multiple sclerosis.

228 patients with early relapsing-remitting and secondary progressive multiple sclerosis; (ii) assess th

229 esion development in relapsing-remitting and secondary progressive multiple, sclerosis, and this usua

230 sability Status Scale (EDSS), development of secondary-progressive multiple sclerosis (SPMS), brain T

231 clerosis, with higher concentrations seen in secondary-progressive multiple sclerosis and in patients

232 um concentrations were higher in primary and secondary-progressive multiple sclerosis.

233 n heterozytgotes was significantly higher in secondary progressive (P < 0.01) and primary progressive

234 Inversely, secondary progressive participants presented with more c

235 more extensive in primary progressive versus secondary progressive patients (33% reduction versus 16%

236 bal and local network properties differed in secondary progressive patients compared with the other g

237 m and putamen, and this was most apparent in secondary progressive patients with MS.

238 By contrast, in the subgroup of secondary progressive patients, microglial activation at

239 The secondary progressive phase is due to neurodegeneration

240 on in time from relapsing-remitting phase to secondary progressive phase of multiple sclerosis was mo

241 course during the study and entered into the secondary progressive phase.

242 nating MS subtypes (relapsing-remitting from secondary progressive), providing evidence about the und

243 MS while these measures were also reduced in secondary progressive relative to relapsing-remitting pa

244 e sclerosis [20 relapsing remitting (RR), 21 secondary progressive (SP) and 10 primary progressive (P

245 s and remissions and typically followed by a secondary progressive (SP) course.

246 in the disease course towards development of secondary progressive (SP) disease; (2) if so, when the

247 ses with relapsing-remitting (RR)-MS (n=81), secondary progressive (SP) MS (n=13) and primary progres

248 -remitting (RR), 17 with benign, and 23 with secondary progressive (SP) MS and 18 healthy control sub

249 edictors of clinical worsening, evolution to secondary progressive (SP) MS and reaching EDSS=3.0, 4.0

250 f relapse activity (PIRA), and transition to secondary progressive (SP) MS, and ACES and RAM rates un

251 itting (RR) MS who are at risk of developing secondary progressive (SP) MS.

252 in people with relapsing-remitting (RR) and secondary progressive (SP) MS.

253 syndrome (CIS), relapsing remitting (RR) and secondary progressive (SP) MS.

254 10 relapsing remitting (RR) and 11 secondary progressive (SP) patients with multiple sclero

255 relapsing-remitting (RR) stage followed by a secondary progressive (SP) phase.

256 iple sclerosis, primary progressive (PP) and secondary progressive (SP) versus relapsing-remitting (R

257 roteins differentiating the MS subtypes, and secondary progressive (SP)MS was the most different also

258 ients had relapsing-remitting (RR) (n=92) or secondary-progressive (SP) (n=49) MS; clinical course wa

259 ical outcomes: aggressive MS, benign MS, and secondary-progressive (SP)MS.

260 11 with relapsing-remitting [RR] MS, 92 with secondary-progressive [SP] MS, and 37 with primary-progr

261 (RRMS), 28 primary progressive MS (PPMS), 36 secondary progressive (SPMS) and 51 healthy controls (HC

262 sera with no significant difference between secondary progressive (SPMS) and relapsing-remitting (RR

263 s were validated in an independent cohort of secondary progressive (SPMS) patients, but not in a thir

264 toantibody patterns that distinguished RRMS, secondary progressive (SPMS), and primary progressive (P

265 n relapse and n = 11 in remission) patients, secondary progressive (SPMS, n = 6) MS patients, and non

266 lerosis determines when a patient enters the secondary progressive stage of the disease.

267 e initial relapsing-remitting and subsequent secondary-progressive stage.

268 ffectively treat patients in the primary and secondary progressive stages of the disease.

269 h is three times higher in those who develop secondary progressive than in those who remain relapsing

270 ople with multiple sclerosis, and more so in secondary progressive than relapsing remitting multiple

271 e range 1.5-6.5; 35 relapsing remitting, two secondary-progressive) underwent 3 T MRI including high-