ライフサイエンスコーパス: spastic

1 al: 6.02 +/- 0.49 mm, p = 0.038; compliance: spastic: 1.79 +/- 0.12 mm/N, contralateral: 2.21 +/- 0.1

2 the contralateral side (muscle displacement: spastic: 4.84 +/- 0.33 mm, contralateral: 6.02 +/- 0.49

3 24; 2.2% overall) were ultimately managed as spastic achalasia or DES.

4 pathophysiology: DES with short latency and spastic achalasia.

5 At the opposite extreme is type III (spastic) achalasia, which has no demonstrated neuronal l

6 Thus, the spastic allele of the murine glycine receptor beta subun

7 d/or non-febrile seizures, and a wide-based, spastic, and/or stiff-legged gait.

8 n patients show a combination of adult-onset spastic ataxia and a thin corpus callosum.

9 considered in the differential diagnosis of spastic ataxia and hypomyelination.

10 ests GBA2 mutations are a cause of recessive spastic ataxia and responsible for a form of glucosylcer

11 ole-exome sequencing findings in a recessive spastic ataxia family turned our attention to intronic v

12 ochondrial DNA maintenance is suspected when spastic ataxia is prominent.

13 eurodegenerative disease autosomal recessive spastic ataxia of Charlevoix Saguenay (ARSACS) is caused

14 Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a chil

15 Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is caused

16 Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS) is caused

17 n sacsin responsible for autosomal recessive spastic ataxia of Charlevoix-Saguenay, a degenerative di

18 nt with the diagnosis of autosomal recessive spastic ataxia of Charlevoix-Saguenay.

19 in three, with genomic re-diagnosis of SCA3, spastic ataxia of the Charlevoix-Saguenay type, and SCA4

20 tidomain protein, causes autosomal recessive spastic ataxia of the Charlevoix-Saguenay, one of the mo

21 disorders that are classified either as pure spastic ataxia or as complex spastic ataxia with additio

22 the differential diagnosis of patients with spastic ataxia phenotype.

23 A total of 321 index patients with spastic ataxia selected from the SPATAX network were ana

24 either as pure spastic ataxia or as complex spastic ataxia with additional neurological signs.

25 haracterized by adolescent-onset progressive spastic ataxia with frequent occurrence of tremor, invol

26 d MARS2 to be mutated in Autosomal Recessive Spastic Ataxia with Leukoencephalopathy (ARSAL) patients

27 ular investigation of an autosomal-recessive spastic ataxia with optic atrophy, present among the Old

28 has previously been implicated in a form of spastic ataxia with optic atrophy.

29 ting features on MRI are sometimes seen with spastic ataxia, but this is usually mild in adults and s

30 gressive external ophthalmoplegia/ptosis and spastic ataxia, or a progressive ataxic disorder.

31 linked to spinocerebellar ataxia type 28 and spastic ataxia-neuropathy syndrome in humans; however, t

32 as significantly enriched in 1139 cases with spastic ataxia-related phenotypes as compared to unrelat

33 report seven individuals with an early-onset spastic-ataxia phenotype.

34 in POLR3A are a frequent cause of hereditary spastic ataxias, accounting for about 3% of hitherto gen

35 gnosed in 22% of infants; half of these were spastic bilateral.

36 The glycine receptor-deficient mutant mouse spastic carries a full-length long interspersed nuclear

37 ypical development and in children with mild spastic cerebral palsy (CP; n = 15/group; 4-11 y).

38 Forty-nine children aged 3 to 8 years with spastic cerebral palsy were randomized to 40 treatments

39 The resistance due to spastic co-contraction might be reduced by botulinum tox

40 I (absent peristalsis with distal esophageal spastic contractions) is a spastic variant with less fav

41 ssociated with both unilateral and bilateral spastic CP subphenotypes.

42 range; mild hypotonia in infancy followed by spastic diplegia (mean age: 8.4 +/- 5.1 years, SD) and l

43 ted for evaluation and further management of spastic diplegia cerebral palsy.

44 ncy include elevated plasma arginine levels, spastic diplegia, intellectual disability, seizures and

45 e disorder associated with hyperargininemia, spastic diplegia, loss of ambulation, intellectual disab

46 clinically notable for developmental delays, spastic diplegia, psychomotor function loss, and (uncomm

47 perform SDR on children aged 3-9 years with spastic diplegic cerebral palsy.

48 otypes: without peristalsis, with premature (spastic) distal esophageal contractions, with panesophag

49 nt alternatives for patients with achalasia, spastic esophageal disorders and upper gastrointestinal

50 ia and 90% of patients with type 3 achalasia/spastic esophageal motility disorders, with a low rate o

51 presses neuronal excitability and results in spastic flies.

52 ond most common type of cerebral palsy after spastic forms.

53 lthough more than 50 genetic loci are known [spastic gait (SPG)1 to -57], over half of hereditary spa

54 out cardiovascular side effects and improved spastic gait disorders after brain injury in a disease m

55 n disorders with the hallmark of progressive spastic gait disturbance.

56 tics, we demonstrate that all but one of the spastic gait locus #46 (SPG46)-connected mutations cause

57 acterized by neurogenic bladder, progressive spastic gait, and peripheral neuropathy.

58 ith multiorgan IgG4-RD developed progressive spastic hemiparesis and dementia.

59 ) on the reflex and non-reflex components of spastic hypertonia and intramuscular blood perfusion amo

60 sults, WBV had an acute effect on modulating spastic hypertonia dominated by hyperreflexia in people

61 e previously demonstrated that for long-term spastic limb paralysis, transferring the seventh cervica

62 (DeltaNLS-FUS), which developed progressive spastic motor deficits and neuronal loss in the motor co

63 ul long-lasting muscle relaxation effects on spastic motor disorders.

64 to its treatment) remains unknown, although spastic motor dysfunction has been related to the hypere

65 as a cause of a progressive, pediatric-onset spastic movement disorder with variable clinical present

66 clinically variable form of pediatric-onset spastic movement disorder.

67 ortical motor neurons degenerate and cause a spastic movement disorder.

68 spinal and reticulospinal tract to control a spastic muscle in humans with chronic incomplete SCI.

69 ys distinctly contribute to the control of a spastic muscle in humans with incomplete spinal cord inj

70 of muscle displacement and compliance in the spastic muscles as compared to the contralateral side (m

71 inal and larger reticulospinal influences to spastic muscles in humans with SCI and suggest that thes

72 e maturational arrest, interneuron loss, and spastic neuromotor dysfunction.

73 global developmental delay with regression, spastic para- or tetraparesis, epilepsy and progressive

74 PZQ causes Ca(2+) influx and spastic paralysis of adult worms and rapid vacuolization

75 They are characterized by progressive spastic paralysis of the legs as a result of selective,

76 evere clinical dysfunction with an ascending spastic paralysis ultimately resulting in fatal respirat

77 eoathetoid movements, dysarthria, dysphagia, spastic paralysis, and behavioral dementia in descendant

78 n the central nervous system (CNS) to elicit spastic paralysis.

79 neurons and protected mice from TeNT-induced spastic paralysis.

80 e BoNTs cause flaccid paralysis, TeNT causes spastic paralysis.

81 isease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T cell leukemia/

82 pe 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS

83 us 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS

84 pe I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) are known to be caused by

85 pe 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a progressive inflammat

86 ent of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), observed in up to 5% of i

87 ing in HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), or adult T cell leukemia/

88 L) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

89 termed HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

90 L) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

91 We studied a case of Hereditary Spastic Paraparesis (HSP) in a single inbred Palestinian

92 nia and parkinsonism (n = 1), and hereditary spastic paraparesis (n = 1).

93 eases: HTLV-1-associated myelopathy/tropical spastic paraparesis and adult T cell leukemia.

94 ed with a similar combination of progressive spastic paraparesis and polyneuropathy, variably associa

95 FR deficiency is a rare cause of complicated spastic paraparesis in adults, it should be considered i

96 a complicated form of adult-onset hereditary spastic paraparesis partially responsive to betaine ther

97 s with HTLV-1-associated myelopathy/tropical spastic paraparesis than in 29 asymptomatic carriers (80

98 sive neurodegenerative subtype of lower limb spastic paraparesis with additional diffuse skin and hai

99 t with HTLV-1-associated myelopathy/tropical spastic paraparesis), ongoing infectious spread during c

100 is mutated, patients frequently present with spastic paraparesis, a thin corpus callosum, and cogniti

101 kemia virus-1-associated myelopathy/tropical spastic paraparesis, A6 also recognizes a self peptide f

102 tive motor neuron disorders characterized by spastic paraparesis.

103 progressive gait ataxia with a superimposed spastic paraparesis.

104 in Reep1 null mice in addition to prominent spastic paraparesis.

105 result in debilitating leukodystrophies and spastic paraparesis.

106 ia and HTLV-1-associated myelopathy/tropical spastic paraparesis.

107 ma and HTLV-1-associated myelopathy/tropical spastic paraparesis.

108 luding HTLV-1-associated myelopathy/tropical spastic paraparesis.

109 and the neurodegenerative disorder tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HA

110 adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-1-associated myelopathy in abou

111 4 (AP-4) leads to childhood-onset hereditary spastic paraplegia (AP-4-HSP): SPG47 (AP4B1), SPG50 (AP4

112 ociated neurodegeneration, FAHN), hereditary spastic paraplegia (HSP type SPG35) and leukodystrophy (

113 RLIN1, ERLIN2) are known to cause hereditary spastic paraplegia (HSP) and cerebellar ataxia.

114 lt in similar problems that cause hereditary spastic paraplegia (HSP) and Charcot-Marie-Tooth type 2

115 of upper and lower motor neurons, hereditary spastic paraplegia (HSP) and distal hereditary motor neu

116 autosomal recessive (AR) complex hereditary spastic paraplegia (HSP) and juvenile onset amyotrophic

117 Two syndromes - hereditary spastic paraplegia (HSP) and mycobacterial disease - thu

118 itary cerebellar ataxia (HCA) and hereditary spastic paraplegia (HSP) are scarce.

119 yndrome is an autosomal recessive hereditary spastic paraplegia (HSP) caused by frameshift mutations

120 cot-Marie-Tooth type 2 (CMT2) and Hereditary Spastic Paraplegia (HSP) depending on the affected neuro

121 Hereditary spastic paraplegia (HSP) describes a heterogeneous group

122 of an autosomal-dominant gene for hereditary spastic paraplegia (HSP) in 10 families that are of dive

123 Complex hereditary spastic paraplegia (HSP) is a genetic disorder that caus

124 Hereditary spastic paraplegia (HSP) is a neurological syndrome char

125 nt alleles of Atlastin-1 found in Hereditary Spastic Paraplegia (HSP) patients show similar ER phenot

126 Hereditary spastic paraplegia (HSP) type 2 is a proteolipid protein

127 IAA0196) cause autosomal dominant hereditary spastic paraplegia (HSP) type SPG8.

128 its four subunits cause a form of hereditary spastic paraplegia (HSP) with intellectual disability.

129 stin, strumpellin, or REEP1 cause hereditary spastic paraplegia (HSP), a disease characterized by axo

130 odegenerative diseases, including hereditary spastic paraplegia (HSP), a disorder characterized by sp

131 in an autosomal dominant form of hereditary spastic paraplegia (HSP), a motor-neurological disorder

132 e an unbranched ER morphology and hereditary spastic paraplegia (HSP), a neurodegenerative disease ch

133 tified in patients suffering from hereditary spastic paraplegia (HSP), a neurodegenerative disorder a

134 Mutations of various genes cause hereditary spastic paraplegia (HSP), a neurological disease involvi

135 plex, have been reported to cause hereditary spastic paraplegia (HSP), although their impact at the c

136 hy (SMA), Multiple Sclerosis (MS) Hereditary Spastic Paraplegia (HSP), and Huntington's Disease (HD).

137 A2 gene have been associated with hereditary spastic paraplegia (HSP), autosomal-recessive cerebellar

138 cot-Marie-Tooth disease (CMT) and Hereditary Spastic Paraplegia (HSP), but the mechanism of its invol

139 In hereditary spastic paraplegia (HSP), the axons of cortical motor ne

140 ing spastin and atlastin, lead to hereditary spastic paraplegia (HSP).

141 tReact effect in humans with pure hereditary spastic paraplegia (HSP).

142 tin, are the most common cause of hereditary spastic paraplegia (HSP).

143 use an axon degenerative disease, hereditary spastic paraplegia (HSP).

144 in produces similar phenotypes of hereditary spastic paraplegia (mitochondrial dysfunction and defect

145 HD2 genes cause specific types of hereditary spastic paraplegia (SPG28 and SPG54, respectively), and

146 ns in kinesin family member 5A (KIF5A) cause spastic paraplegia 10.

147 otypic ER-shaping proteins, in families with spastic paraplegia 12 (SPG12).

148 (mutations in which cause autosomal-dominant spastic paraplegia 4 [SPG4]) have been described, their

149 diverse cellular activities (m-AAA) protease spastic paraplegia 7 (SPG7) has been recently implicated

150 dentified a necessary and conserved role for spastic paraplegia 7 (SPG7) in Ca(2+)- and ROS-induced P

151 encoding a later step, result in hereditary spastic paraplegia accompanied by intellectual deficits.

152 sense mutations in AP5Z1 and presenting with spastic paraplegia accompanied by neuropathy, parkinsoni

153 cular features of AP-4-associated hereditary spastic paraplegia across the age spectrum our results w

154 eration: many candidate genes for hereditary spastic paraplegia also have central roles in lipid-drop

155 tified in genes usually associated with pure spastic paraplegia and also in the Parkinson's disease-a

156 Next, we screened a cohort of hereditary spastic paraplegia and cerebellar ataxia cases (n = 618)

157 in genetic neurological diseases (hereditary spastic paraplegia and cerebellar ataxia).

158 POLR3A to be a frequent cause of hereditary spastic paraplegia and cerebellar ataxia.

159 a disease gene for a new complex hereditary spastic paraplegia and confirm that etherlipid homeostas

160 e fusion gene data could explain a report of spastic paraplegia and dementia cosegregating in a famil

161 patients suffering from SPG4-type hereditary spastic paraplegia and explain why single amino acid exc

162 in neurological disorders such as hereditary spastic paraplegia and hereditary sensory neuropathy.

163 erosis, infantile-onset ascending hereditary spastic paraplegia and juvenile primary lateral sclerosi

164 milies with an autosomal dominant hereditary spastic paraplegia and lacking mutations in known heredi

165 ns with intellectual disability, progressive spastic paraplegia and short stature, born to a consangu

166 fficking is a common theme between heritable spastic paraplegia and some inherited epilepsies.

167 e: amyotrophic lateral sclerosis, hereditary spastic paraplegia and spinal muscular atrophy.

168 l longer axons, and support a model in which spastic paraplegia can be caused by impairment of axonal

169 gait (SPG)1 to -57], over half of hereditary spastic paraplegia cases are caused by pathogenic mutati

170 broad pools of previously unknown hereditary spastic paraplegia causative genes and subtypes, we perf

171 Mutations in PNPLA6 also cause human spastic paraplegia characterized by motor neuron degener

172 Several causative genes for hereditary spastic paraplegia encode proteins with intramembrane ha

173 Spastic paraplegia gene 11(SPG11)-linked hereditary spas

174 o most common autosomal recessive hereditary spastic paraplegia gene products, the SPG15 protein spas

175 Mutations in the Spastic Paraplegia Gene11 (SPG11), encoding spatacsin, c

176 ns in several loci known collectively as the spastic paraplegia genes (SPGs).

177 variants in a number of other known complex spastic paraplegia genes, including five in SPG7 (5/97),

178 ia and lacking mutations in known hereditary spastic paraplegia implicated genes.

179 and by far the most common cause of complex spastic paraplegia in the UK, with severe and progressiv

180 paraplegia gene 11(SPG11)-linked hereditary spastic paraplegia is a complex monogenic neurodegenerat

181 Hereditary spastic paraplegia is a highly heterogeneous group of ne

182 Clinical data showed that spastic paraplegia is accompanied by a number of other f

183 form of pure, autosomal dominant hereditary spastic paraplegia is caused by mutation in the ATL1 gen

184 ommon form of autosomal recessive hereditary spastic paraplegia is caused by mutations in the SPG11/K

185 eurodegenerative disease that in addition to spastic paraplegia is characterized by childhood onset c

186 nant lower limb spasticity, or complex where spastic paraplegia is complicated with additional neurol

187 assified as either 'pure' or 'complex' where spastic paraplegia is complicated with additional neurol

188 tion is the main regulator of the hereditary spastic paraplegia microtubule severing enzyme spastin.

189 functional defects of an atypical hereditary spastic paraplegia mutant, ATL1-F151S, that is impaired

190 h the microtubule cytoskeleton in hereditary spastic paraplegia pathogenesis.

191 Here, we show that the hereditary spastic paraplegia protein M1 Spastin, a membrane-bound

192 ional progression rate of 0.56 points on the Spastic Paraplegia Rating Scale per year was slightly lo

193 Clinical severity was assessed by the Spastic Paraplegia Rating Scale.

194 ated a series of 97 index cases with complex spastic paraplegia referred to a tertiary referral neuro

195 e cause Troyer syndrome, a recessive form of spastic paraplegia resulting in muscle weakness, short s

196 cated form of autosomal-recessive hereditary spastic paraplegia termed AP-4-deficiency syndrome.

197 greatly, ranging from muscular dystrophy to spastic paraplegia to a childhood blinding disorder to b

198 Motor signs developed ascending from spastic paraplegia to tetraplegia and pseudobulbar palsy

199 Using spastic paraplegia type 4 (SPG4, the most frequent HSP s

200 Spastic paraplegia type 5 (SPG5) is a rare subtype of he

201 Spastic paraplegia types 4 (prevalence, 0.91 per 100,000

202 patients with adult onset leukodystrophy or spastic paraplegia with early onset of urinary symptoms

203 utations, and predominant complex hereditary spastic paraplegia with marked cognitive impairment, wit

204 es related to autosomal recessive hereditary spastic paraplegia with thin corpus callosum and axonal

205 uent cause of autosomal recessive hereditary spastic paraplegia with thin corpus callosum and periphe

206 cal findings were neurogenic bladder (100%), spastic paraplegia with vibration loss (90%), and axonal

207 ity Gene2) and Bhlhb5 (mutated in Hereditary Spastic Paraplegia), providing a molecular handle to inv

208 sociated with various subtypes of hereditary spastic paraplegia, a highly heterogeneous group of neur

209 ype 5 (SPG5) is a rare subtype of hereditary spastic paraplegia, a highly heterogeneous group of neur

210 bone and frontotemporal dementia, hereditary spastic paraplegia, and 1-2% of familial amyotrophic lat

211 ase, hypoxia, multiple sclerosis, hereditary spastic paraplegia, and others.

212 autonomic neuropathy, complicated hereditary spastic paraplegia, and select hereditary metabolic neur

213 ions were found in patients with ichthyosis, spastic paraplegia, and severe neurodevelopmental defect

214 utosomal dominant pure or complex hereditary spastic paraplegia, as well as in two sporadic patients.

215 assified as a complicated form of hereditary spastic paraplegia, associated with mutation in the etha

216 ven to these patients included dementia with spastic paraplegia, corticobasal degeneration syndrome,

217 ave been linked to diseases such as familial spastic paraplegia, developmental delay with premature d

218 bellar ataxia type 2, ataxia telangiectasia, spastic paraplegia, giant axonal neuropathy, and fumarat

219 neuromuscular diseases including hereditary spastic paraplegia, hereditary sensory neuropathy type 1

220 set seizures, severe developmental delay and spastic paraplegia, in whom whole-genome sequencing reve

221 INS220/ARMS in three unrelated patients with spastic paraplegia, intellectual disability, nystagmus,

222 ghter, muscular hypotonia that progressed to spastic paraplegia, microcephaly, foot deformity, decrea

223 egenerative disorder mainly characterized by spastic paraplegia, optic atrophy and neuropathy (SPOAN)

224 have the unusual combination of early-onset spastic paraplegia, optic atrophy, and neuropathy.

225 in the clinico-genetic work-up of hereditary spastic paraplegia, particularly in dominant cases, as t

226 , parkinsonism, muscle weakness, neuropathy, spastic paraplegia, personality/behavioral problems, and

227 y classified as a complex form of hereditary spastic paraplegia, present in families from Kuwait, Ita

228 that are mutated in patients with hereditary spastic paraplegia, SPG11 and SPG15.

229 lity syndrome, and three forms of hereditary spastic paraplegia, SPG11, SPG15 and SPG49 caused by SPG

230 had normal development with childhood-onset spastic paraplegia, spinal lesion, and optic atrophy.

231 ly progressive type of cerebellar ataxia and spastic paraplegia, without intellectual disability.

232 irst causal treatment strategy in hereditary spastic paraplegia.

233 tin, is the chief gene mutated in hereditary spastic paraplegia.

234 over time show progressive motor symptoms, a spastic paraplegia.

235 od model system for understanding hereditary spastic paraplegia.

236 dered the most frequent metabolic hereditary spastic paraplegia.

237 e, highlighting the genetic heterogeneity of spastic paraplegia.

238 s, consistent with a diagnosis of hereditary spastic paraplegia.

239 to motor neuron diseases, such as hereditary spastic paraplegia.

240 uting factor to early autonomic symptoms and spastic paraplegia.

241 developmental defects and a familial form of spastic paraplegia.

242 ion of adolescent-onset, isolated hereditary spastic paraplegia.

243 has been associated with a familial form of spastic paraplegia.

244 stin are the most common cause of hereditary spastic paraplegia.

245 s been linked to SPG13, a form of hereditary spastic paraplegia.

246 e human gene mutated in a form of hereditary spastic paraplegia.

247 stin is mutated in the axonopathy hereditary spastic paraplegia.

248 amyotrophic lateral sclerosis and hereditary spastic paraplegia.

249 1 (UBAP1) gene, which co-segregated with the spastic paraplegia.

250 esentation was a pure lower limb predominant spastic paraplegia.

251 lly involved in MND, particularly hereditary spastic paraplegia.

252 s in UBAP1 can cause pure autosomal dominant spastic paraplegia.

253 ms of childhood-onset and complex hereditary spastic paraplegia: SPG47 (AP4B1), SPG50 (AP4M1), SPG51

254 r ataxias and autosomal recessive hereditary spastic paraplegias (ARHSPs) are clinically and genetica

255 ation is the most common cause of hereditary spastic paraplegias (HSP).

256 Hereditary spastic paraplegias (HSPs) are a group of diseases cause

257 Hereditary spastic paraplegias (HSPs) are a group of genetically he

258 Hereditary spastic paraplegias (HSPs) are a large, genetically dive

259 The hereditary spastic paraplegias (HSPs) are a rare and heterogeneous

260 The hereditary spastic paraplegias (HSPs) are characterized by spastici

261 Hereditary spastic paraplegias (HSPs) are clinically and geneticall

262 Hereditary spastic paraplegias (HSPs) are genetically driven disord

263 The hereditary spastic paraplegias (HSPs) are heterogeneous neurodegene

264 Hereditary spastic paraplegias (HSPs) are neurodegenerative motor n

265 The family of genes implicated in hereditary spastic paraplegias (HSPs) is quickly expanding, mostly

266 ein 1 (REEP1) are associated with hereditary spastic paraplegias (HSPs).

267 drome, one of several complicated hereditary spastic paraplegias (HSPs).

268 Hereditary spastic paraplegias (HSPs, SPG1-46) are inherited neurol

269 Hereditary spastic paraplegias (HSPs; SPG1-48) are inherited neurol

270 Hereditary spastic paraplegias (HSPs; SPG1-76 plus others) are leng

271 ng as a candidate key pathway for hereditary spastic paraplegias and cerebellar ataxias and thus prio

272 h rare movement disorders such as hereditary spastic paraplegias and cerebellar ataxias remain geneti

273 pedigrees with autosomal dominant hereditary spastic paraplegias and lacking mutations in known causa

274 ulation of disease progression in hereditary spastic paraplegias and other MNDs.

275 Hereditary spastic paraplegias are a clinically and genetically het

276 The hereditary spastic paraplegias are a heterogeneous group of degener

277 Hereditary spastic paraplegias are a large, diverse group of neurol

278 Hereditary spastic paraplegias are heterogeneous neurological disor

279 Hereditary spastic paraplegias are inherited neurological disorders

280 Complex recessive spastic paraplegias have in the past been frequently ass

281 Hereditary spastic paraplegias refer to a heterogeneous group of ne

282 characterization of patients with hereditary spastic paraplegias represents progressive spasticity, e

283 been identified in patients with hereditary spastic paraplegias, a diverse group of neurological dis

284 h define a diverse set of complex hereditary spastic paraplegias.

285 different neurological diseases, hereditary spastic paresis type 5 (SPG5) and cerebrotendinous xanth

286 Future research into the treatment of spastic paresis with botulinum toxin should use active m

287 SPG5 is characterized by spastic paresis, and similar symptoms may occur in CTX.

288 delay, microcephaly, sensorineural deafness, spastic quadriparesis and progressive cortical and cereb

289 2 to 4 months with progressive microcephaly, spastic quadriparesis, and global developmental delay.

290 stonia (DYT4), isolated hypomyelination with spastic quadriplegia, and an infantile onset encephalopa

291 was later diagnosed with diabetes insipidus, spastic quadriplegia, developmental delay, agenesis of t

292 ual disability, seizures, optic atrophy, and spastic quadriplegia.

293 nce); Ludvig and Sara Elsass Foundation, The Spastics Society and Vanforefonden (Denmark); Cooperativ

294 These results were consistently present in spastic subjects but not in the other populations.

295 ophy was greater in nonspastic compared with spastic subjects.

296 rly childhood onset predominantly lower limb spastic tetraparesis and truncal instability, dysarthria

297 lated children (both female) presenting with spastic tetraparesis, severe generalized dystonia and in

298 ticity, cognitive impairment, nystagmus, and spastic urinary bladder of varying severity.

299 distal esophageal spastic contractions) is a spastic variant with less favorable outcomes (66%) after

300 l disorders characterized by lower extremity spastic weakness.