ライフサイエンスコーパス: spasticity

1 ceptor 2C (5-HT2CR) contributing to post-SCI spasticity.

2 inoids for the treatment of chronic pain and spasticity.

3 ongenital cataracts, growth retardation, and spasticity.

4 but urinary symptoms were rare, despite the spasticity.

5 s of the nervous system such as seizures and spasticity.

6 flexes and/or diffuse tendon reflexes and/or spasticity.

7 y result in a reduction of hyperreflexia and spasticity.

8 s are a novel class of therapeutic agent for spasticity.

9 mplicated in epilepsy, neuropathic pain, and spasticity.

10 h increased tone and some of which have limb spasticity.

11 s the other 33.3% showed no or low levels of spasticity.

12 in subjects with motor disorders affected by spasticity.

13 d provide insight into mechanisms underlying spasticity.

14 pathic pain, but also epilepsy, tremors, and spasticity.

15 jerks, inability to initiate movements, and spasticity.

16 rticospinal tract and progressive lower limb spasticity.

17 Hypotonia gives way in adult life to spasticity.

18 ew perspective in the clinical evaluation of spasticity.

19 sample of people with multiple sclerosis and spasticity.

20 orm 2 (KCC2) was not changed in animals with spasticity.

21 ts with stable multiple sclerosis and muscle spasticity.

22 by progressive lower-extremity weakness and spasticity.

23 e clear ability of botulinum toxin to reduce spasticity.

24 onically active in the control of tremor and spasticity.

25 dren with perinatal brain damage who develop spasticity.

26 ma, stimulation of appetite, and spinal cord spasticity.

27 ncement of stretch reflexes is suggestive of spasticity.

28 sly progressive lower extremity weakness and spasticity.

29 amyloidosis, producing dementia, ataxia, and spasticity.

30 ficantly up-regulated in mice that exhibited spasticity.

31 ition of motoneurons, and the development of spasticity.

32 njury leads to an instantaneous reduction of spasticity.

33 and MEP size correlated with the severity of spasticity.

34 ized I(NaP) and KCC2 function, and curtailed spasticity.

35 d direct current stimulation (tsDCS) reduces spasticity.

36 nerve hyperactivity, for example in pain and spasticity.

37 nsitization and chronic pain associated with spasticity.

38 ally characterised by progressive lower limb spasticity.

39 for a role of brainstem serotonin neurons in spasticity.

40 lly-feasible time-point after injury reduced spasticity.

41 tor processing in the spinal cord leading to spasticity.

42 l symptoms, including movement disorders and spasticity.

43 d axial hypotonia with variable appendicular spasticity.

44 esent, including intellectual disability and spasticity.

45 seizures, irritability, ataxia, and extreme spasticity.

46 tnatal microcephaly and epilepsy and develop spasticity.

47 ed by intellectual disability, seizures, and spasticity.

48 ression - an indication of hyperreflexia and spasticity - 1 month following SCI as compared with base

49 the published data cohort for myoclonus and spasticity (19.4%, 16.6-22.2 and 15.0%, 12.5-17.6, respe

50 all patients associated with lower-extremity spasticity (6), cardiac abnormalities or cardiomyopathy

51 onia (91%) was seen, followed by progressive spasticity (82%, median onset = 15 months) and dystonia

52 -OBS cohort was low, including myoclonus and spasticity (9.3%, 95% CI 3.8-15.0), and seizures (2.8%,

53 However, both lines developed spasticity (a "clasping" phenotype) at a median age of 2

54 inal cord injury (SCI) is the development of spasticity, a clinical symptom of hyperexcitability with

55 Spasticity, a common complication after spinal cord inju

56 rlying spinal hyperreflexia with SCI-induced spasticity, a feasible druggable target has not been val

57 ctual disabilities, poor speech development, spasticity, a wide-based gait or an inability to walk an

58 on in the upper limb muscles on muscle tone, spasticity, active movement, and function.

59 l delay/intellectual disability, progressive spasticity affecting the upper and lower limbs, and corp

60 Muscle spasticity after nervous system injuries and painful low

61 h restores endogenous inhibition and reduces spasticity after SCI in rats.

62 erexcitability of motoneurons which leads to spasticity after SCI.

63 the potassium/chloride extruder KCC2 lead to spasticity after spinal cord injury (SCI).

64 5-HT2B/C is required for the development of spasticity after spinal cord injury and during amyotroph

65 has been associated with mood disorders and spasticity after spinal cord injury, whether and to what

66 No spasticity, albinism, or hematological symptoms were rep

67 major syndromic categories: (1) ataxia, (2) spasticity and (3) global neurodevelopmental impairment.

68 n includes early-onset nystagmus, ataxia and spasticity and a wide range of severity.

69 me characterized by intellectual disability, spasticity and absent speech.

70 t with movement deficits including weakness, spasticity and an inability to isolate movement to one o

71 Abnormal spasticity and associated synergistic patterns are the m

72 ve gait and movement, it remains unknown how spasticity and associated synergistic patterns change af

73 displayed a neurodegenerative phenotype with spasticity and ataxia by 15 mo.

74 ring cerebellar neurodegeneration leading to spasticity and ataxia.

75 Progressive limb spasticity and cerebellar ataxia are frequently found to

76 Prominent features include pyramidal spasticity and cerebellar ataxia, but the underlying pat

77 by nystagmus, psychomotor delay, progressive spasticity and cerebellar signs.

78 of several neurological disorders, including spasticity and chronic pain following spinal cord injury

79 ct compared with participants with no or low spasticity and control subjects.

80 in compared with participants with no or low spasticity and control subjects.

81 with early onset, characterized by seizures, spasticity and developmental delays, ultimately leading

82 inal tracts and dorsal columns, resulting in spasticity and difficulty walking.

83 ommon early comorbidities included seizures, spasticity and disordered sleep.

84 Supportive treatment focused on spasticity and drooling, and was effective in the indivi

85 G35) and leukodystrophy (leukodystrophy with spasticity and dystonia) spectrum.

86 ith signs of white matter dysfunction (i.e., spasticity and hyperreflexia).

87 the distal upper and lower limbs, lower limb spasticity and hyperreflexia, with onset in the first de

88 isorder characterized by mental retardation, spasticity and ichthyosis.

89 ulates activity in spinal pathways to reduce spasticity and improve functional recovery are poorly un

90 ts with upper motor neurone syndrome, reduce spasticity and improve voluntary movement and active fun

91 t syndrome, X-linked myoclonic epilepsy with spasticity and intellectual disability, Partington syndr

92 sorder manifested by lower limb weakness and spasticity and length-dependent axonopathy of corticospi

93 We found a correlation between signs of spasticity and long-interval intracortical inhibition in

94 e devastating neurological disorders such as spasticity and mental retardation.

95 ological techniques was used to characterize spasticity and motor phenotype.

96 l nervous-system-independent option to treat spasticity and muscle stiffness.

97 caudal to hemisection had significantly less spasticity and muscle wasting and greater mobility at th

98 therapy that treats the underlying causes of spasticity and not only its symptoms.

99 Clinical features included severe spasticity and nystagmus.

100 hat cannabinoids have a beneficial effect on spasticity and other symptoms related to multiple sclero

101 ce of a treatment effect on patient-reported spasticity and pain (p=0.003), with improvement in spast

102 ic areas such as the role of cannabinoids in spasticity and pain and new treatments for cognitive imp

103 ated in disorders such as multiple sclerosis spasticity and pain, basic research is discovering inter

104 Spasticity and paralysis were observed in chronically in

105 n mice, manifested clinically by progressive spasticity and paralysis.

106 Both patients developed spasticity and parkinsonism in their mid-60s, with the f

107 ns causes neuropathy that leads to hind limb spasticity and premature death.

108 e mental impairment, growth retardation, and spasticity and punctuated by sometimes fatal episodes of

109 l AMPA receptors and their role in mediating spasticity and rigidity.

110 ensation also contributed significantly, but spasticity and strength were not significant in the mode

111 oids are useful for symptomatic treatment of spasticity and tremor in chronic-relapsing experimental

112 myelin antigens Biozzi ABH mice also develop spasticity and tremor.

113 is a genetic disorder that causes lower limb spasticity and weakness and intellectual disability.

114 characterized principally by lower extremity spasticity and weakness due to a length-dependent, retro

115 are characterised clinically by progressive spasticity and weakness of the lower limbs, and patholog

116 t not exclusively, by progressive lower limb spasticity and weakness resulting from distal degenerati

117 e disorders characterized by lower-extremity spasticity and weakness, are most commonly caused by mut

118 ease characterized by progressive lower-limb spasticity and weakness, as well as frequent bladder dys

119 s syndromes characterized by lower extremity spasticity and weakness, with distal axonal degeneration

120 ders characterized by progressive lower-limb spasticity and weakness.

121 orticospinal tracts, resulting in lower limb spasticity and weakness.

122 l disorders characterized by lower extremity spasticity and weakness.

123 ypically experience ataxia, bulbar signs and spasticity, and a more slowly progressive course.

124 rigin characterized by progressive dementia, spasticity, and cerebellar ataxia, with onset at around

125 vere disability, microcephaly, hearing loss, spasticity, and characteristic brain imaging findings.

126 icial tool for the treatment of cancer pain, spasticity, and chronic nonmalignant pain.

127 hite matter vacuolation that lead to ataxia, spasticity, and cognitive decline.

128 tor coordination and develop slurred speech, spasticity, and cognitive impairments.

129 disease characterized by mental retardation, spasticity, and congenital ichthyosis.

130 acterized by ichthyosis, mental retardation, spasticity, and deficient activity of fatty aldehyde deh

131 IFN-gamma(-/-) mice characterized by ataxia, spasticity, and dystonia, hallmarks of brain-specific di

132 ve cognitive decline associated with ataxia, spasticity, and eventually seizures.

133 eral extensor plantar reflexes, occasionally spasticity, and frequently psychiatric symptoms.

134 enesis, mental retardation, adducted thumbs, spasticity, and hydrocephalus.

135 Seizures, spasticity, and intellectual disability can be present,

136 EPs were only present in individuals who had spasticity, and MEP size correlated with the severity of

137 the immune response, appetite, reproduction, spasticity, and pain.

138 osis, facial wrinkles, migraine prophylaxis, spasticity, and spasms, had a significantly lower number

139 s ADNFLE), a syndrome of mental retardation, spasticity, and tapetoretinal degeneration (MRST); and a

140 pmental delay, epileptic encephalopathy, and spasticity, and ten individuals with de novo heterozygou

141 ogliosis, loss of descending inhibition, and spasticity are responsible for approximately 40% of case

142 n of antagonist muscles is characteristic of spasticity arising from perinatal brain damage but not i

143 ceps brachii) motor neurons in subjects with spasticity arising from perinatal brain damage.

144 manifestation of traditional post-traumatic spasticity as a basis for this activity.

145 ne dystonia with or without parkinsonism and spasticity as part of a mixed neurodegenerative disorder

146 d balance in the rotarod test, and increased spasticity as shown by a clasping phenotype.

147 s seen in those with unilateral or bilateral spasticity, as in those with a dyskinetic or ataxic disa

148 IDD for cancer pain, nonmalignant pain, and spasticity, as well as a new study of cerebrospinal flui

149 rious disease models and alleviates pain and spasticity associated with multiple sclerosis in humans.

150 tients suffer from extrapyramidal movements, spasticity, ataxia, and cognitive deficits.

151 developmental delay, acquired microcephaly, spasticity, ataxia, and hypoglycorrhachia.

152 ed of extrapyramidal movement abnormalities, spasticity, ataxia, cognitive deficit and sometimes epil

153 s, unilateral DLF lesions provide a model of spasticity but produce only several components of a more

154 Thus, long lasting reduction of spasticity by a-tsDCS via downregulation of NKCC1 may co

155 Since 1980, modification of spasticity by means of orally administered drugs, intram

156 t baclofen is taken daily as a treatment for spasticity by millions of stroke, brain injury and multi

157 definitive evidence for the tonic control of spasticity by the endocannabinoid system and open new ho

158 from other genetic diseases associated with spasticity can be challenging.

159 Spasticity can cause pain, fatigue and sleep disturbance

160 Spasticity can, therefore, be measured through electroph

161 l recessive neurodevelopmental disorder with spasticity, cataracts and cerebellar hypoplasia.

162 microcephaly, facial dysmorphism, epilepsy, spasticity, cerebellar ataxia and nystagmus, sensorineur

163 Abnormal vision and/or hearing, progressive spasticity, choreoathetoid movements, refractory epileps

164 l nervous system resulting primarily in limb spasticity, cognitive impairment, nystagmus, and spastic

165 Spasticity comorbidity was present in 79/230 (34.3%) chi

166 Diffuse spasticity, dementia, vegetative state, or death ensues.

167 spasticity, whereas the other 40% showed no spasticity, demonstrating the presence of 2 clear subgro

168 trophy gene at 12p13; 4) the choreoathetosis/spasticity disease locus on 1p that lies in a region con

169 uana for chronic pain, neuropathic pain, and spasticity due to multiple sclerosis is supported by hig

170 ts to test the hypothesis that inhibition of spasticity, due to CNS autoimmunity, could be controlled

171 functional involvement by weakness, wasting, spasticity, dysarthria or dysphagia of one central nervo

172 childhood, followed by progressive dystonia, spasticity, dysphagia, mental deterioration, paranoia an

173 Spasticity, dystonia, tremor and migraine were variably

174 The short-term benefits of baclofen on spasticity (e.g. management of muscle spasms that may ot

175 y spastic paraplegias represents progressive spasticity, exaggerated reflexes and muscular weakness.

176 nset bilateral optic atrophy and later-onset spasticity, extrapyramidal dysfunction, and cognitive de

177 t onset Parkinson's disease or earlier onset spasticity followed by parkinsonism.

178 of NKCC1 may constitute a novel therapy for spasticity following spinal cord injury.

179 Subjects with spasticity, from brain damage acquired in adulthood were

180 We found that participants with spasticity had smaller MEPs and MVCs and larger StartRea

181 or(B) agonist, is used to reduce symptoms of spasticity (hyperreflexia, increases in muscle tone, inv

182 re used to develop a conceptual framework of spasticity impact, and to generate a pool of items with

183 s a re-analysis of the basic assumption that spasticity impairs voluntary movement and a review of th

184 We measured spasticity in 33 individuals with motor complete SCI (de

185 3 quantitatively ameliorated both tremor and spasticity in diseased mice.

186 activity of 5-HT2B/C receptors and abolished spasticity in end-stage mice.

187 tion of descending motor pathways influences spasticity in humans with motor complete SCI; this knowl

188 nce of residual descending motor pathways on spasticity in humans with SCI.

189 eticulospinal tract has been associated with spasticity in humans with upper motor neuron lesions.

190 with upper motor neuron defects that lead to spasticity in humans.

191 rrently in clinical use for the treatment of spasticity in multiple sclerosis (MS) patients and to al

192 sed, interval-level measure of the impact of spasticity in multiple sclerosis.

193 lated to chemotherapy, neuropathic pain, and spasticity in multiple sclerosis.

194 serotonergic system could be useful to treat spasticity in neurological diseases.

195 Cannabis-based treatments for pain and spasticity in patients with multiple sclerosis have been

196 diazepines are commonly used to treat muscle spasticity in spinal cord injured subjects and the gamma

197 ABA(B) agonist prescribed as a treatment for spasticity in stroke, brain injury and multiple sclerosi

198 e and its high sensitivity in examination of spasticity in stroke.

199 baclofen, a drug prescribed specifically for spasticity in Sweden, of which many patients had relapsi

200 mode of exclusion; induction and control of spasticity in the ABH mouse model of multiple sclerosis;

201 araplegia (HSP), a disorder characterized by spasticity in the lower limbs.

202 underlie the neuroregression and progressive spasticity in these affected individuals.

203 is was found to cause long-term reduction in spasticity, increased rate-dependent depression in spina

204 rojections simply become unmasked as part of spasticity, independent of the age of occurrence of the

205 s positively correlated with the severity of spasticity, indicating preservation of white matter rela

206 Spasticity is a complicating sign in multiple sclerosis

207 Spasticity is a disabling complication of stroke, and it

208 Spasticity is a disorder of muscle tone that is associat

209 Spasticity is a painful symptom and can severely restric

210 Spasticity is associated with the DH hyperexcitability r

211 Spasticity is most commonly defined as an inappropriate,

212 tor recovery.SIGNIFICANCE STATEMENT Although spasticity is one of the most common symptoms manifested

213 Spasticity is one of the most common symptoms manifested

214 Secondary to the UMNl esion,which causes spasticity, is a pathological response by muscle - namel

215 aracterized by weakness, muscle atrophy, and spasticity, is the most common adult-onset motor neuron

216 294/315 assessable children, 15/294 had pure spasticity, leaving 279/294 with dystonia classified as

217 smorphism, congenital cataracts, ichthyosis, spasticity, microcephaly, and mental disability.

218 Consistent with spasticity mitigating motor symptoms, selective deletion

219 selective death of motor neurons leading to spasticity, muscle atrophy and paralysis.

220 selective death of motor neurons leading to spasticity, muscle wasting and paralysis.

221 Thus, spasticity negatively influences an individual's quality

222 niques incorporate the patient experience of spasticity, nor how it affects people's daily lives.

223 ising from perinatal brain damage but not in spasticity occurring after brain damage in adulthood.

224 Spasticity occurs in a wide range of neurological diseas

225 disability, childhood hypotonia, progressive spasticity of lower limbs, and abnormal craniofacial fea

226 Thirty-eight subjects, aged 8-30 years, with spasticity of perinatal origin (11 hemiplegic, 11 quadri

227 rn was observed in older subject groups with spasticity of perinatal origin.

228 Physical activity, including the chronic spasticity of SQCP, was estimated from the ratio of TEE

229 Spasticity of the biceps brachii muscle was assessed usi

230 In post-stroke patients with spasticity of the biceps brachii, we found involuntary m

231 stic paraplegias (HSPs) are characterized by spasticity of the leg muscles due to axonal degeneration

232 ive' neurological syndromes characterized by spasticity of the legs.

233 that are characterized by abnormal gait and spasticity of the lower limbs.

234 d primarily by hyperreflexia and progressive spasticity of the lower limbs.

235 rative diseases characterised by progressive spasticity of the lower limbs.

236 corticospinal motor neurons and progressive spasticity of the lower limbs.

237 cular injections of botulinum toxin A reduce spasticity of the wrist and finger muscles and associate

238 xin type A reduce disability in persons with spasticity of the wrist and fingers after a stroke.

239 penditure, such as for physical activity and spasticity, of children with SQCP was low.

240 o quantify the perspectives of the impact of spasticity on people with multiple sclerosis.

241 c features, hypotonia, feeding difficulties, spasticity or ataxic gait, and abnormal brain MRI.

242 mia (MH) and is also useful for treatment of spasticity or muscle spasms associated with several clin

243 c pain states, including disorders involving spasticity or myofascial pain, neuropathic pain, and chr

244 d as either pure with predominant lower limb spasticity, or complex where spastic paraplegia is compl

245 l delay but without macrocephaly, hypotonia, spasticity, or seizures.

246 nifying feature of prominent lower extremity spasticity, owing to a length-dependent axonopathy of co

247 y of WM damage correlated with the degree of spasticity (P < .05, family-wise error corrected) and co

248 in BFMDRS-M at last FU, and the presence of spasticity (p = 0.027) and fixed skeletal deformities (p

249 strostomy, communication problems, mobility, spasticity, pain, cognition, depression and emotional la

250 tness, ataxia, fatigue, bladder dysfunction, spasticity, pain, cognitive deficits, depression, and ps

251 eported outcome measures assessed aspects of spasticity, physical and psychological impact, and walki

252 All affected individuals developed spasticity predominantly of the lower limbs over the cou

253 corticospinal tract degeneration, and motor spasticity recapitulating key aspects of FTLD and primar

254 ent consists of orthotics, physical therapy, spasticity reduction treatment and surgical correction.

255 BAB receptor agonist commonly used to relief spasticity related to motor disorders.

256 city and pain (p=0.003), with improvement in spasticity reported in 61% (n=121, 95% CI 54.6-68.2), 60

257 can represent a novel therapy in modulating spasticity/rigidity of spinal origin and that astrocytes

258 Spasticity/rigidity were identified by simultaneous meas

259 The 88-item Multiple Sclerosis Spasticity Scale (MSSS-88) is a reliable and valid, pati

260 ials), and average reduction in the Ashworth spasticity scale (WMD, -0.36 [95% CI, -0.69 to -0.05]; 7

261 rimary outcome measure was change in overall spasticity scores, using the Ashworth scale.

262 l delay, intellectual disability, hypotonia, spasticity, seizures, sensorineural hearing loss, cortic

263 nistered endocannabinoids and PEA ameliorate spasticity, selective inhibitors of endocannabinoid re-u

264 um and white matter abnormalities, seizures, spasticity, short stature, muscle fatigability and weakn

265 We found that participants with SCI with spasticity showed small corticospinal responses and maxi

266 rols and mice with spinal cord injuries with spasticity, spinal-to-sciatic DCS reduced transit and st

267 ty involvement and recent methods to control spasticity, such as selective dorsal rhizotomy and admin

268 ction model, ephrinB3(-/-) mice show greater spasticity than wild-type mice for 2 mo, with slightly g

269 o investigate the severe muscle weakness and spasticity that precede the death of these animals near

270 associated with the neuropathy, for example, spasticity, the type of neuropathy and the other neurolo

271 only in the quadriceps in participants with spasticity, thoracic MEPs were present in both muscles w

272 tients had microcephaly, short stature, mild spasticity, thoracic scoliosis, hyperextendable MCP join

273 of serotonin neurons is necessary to trigger spasticity through the 5-HT2B/C receptor.

274 chidonoyl glycerol-significantly ameliorated spasticity to an extent comparable with that observed pr

275 greatly to include numerous focal dystonias, spasticity, tremors, cosmetic applications, migraine and

276 migraine/facial and head muscles, spasms and spasticity/upper and lower limbs, torticollis and neck p

277 g various pathological conditions underlying spasticity, upregulated expression of 5-HT receptors (5-

278 severely delayed speech, varying degrees of spasticity, ventriculomegaly, and ICH/cerebral calcifica

279 378 and SAD448) were identified that control spasticity via action on the peripheral nerve CB1 recept

280 A 4 week reduction in spasticity was associated with an increase in rate-depen

281 racic MEPs were present in both muscles when spasticity was present.

282 of white matter related to motor tracts when spasticity was present.

283 Spasticity was quantified by muscle displacements and co

284 natal (dpn) and are characterized by ataxia, spasticity, weight loss and hypercholesterolemia.

285 Hyper-reflexia and spasticity were monitored using electromyographic record

286 Clinical scores of spasticity were negatively correlated with MEP-max and M

287 abinoids did not have a beneficial effect on spasticity when assessed with the Ashworth scale.

288 from Conus textile, causes hyperactivity and spasticity when injected intracerebral ventricularly int

289 % of the SCI participants showed symptoms of spasticity, whereas the other 33.3% showed no or low lev

290 that 60% of participants showed symptoms of spasticity, whereas the other 40% showed no spasticity,

291 s with neurological diseases associated with spasticity, who had IDDS system implanted and were unabl

292 t of patients also exhibited dystonia and/or spasticity with impaired ambulation.

293 n most cases, characterized by a progressive spasticity with neuropathy, cognitive impairment and a t

294 neonatal rats developed behavioral signs of spasticity with the emergence of both hyperreflexia and

295 ia, nystagmus, dorsal column dysfuction, and spasticity with upper motor neuron dysfunction.

296 zures, encephalopathy, myoclonus, tremor and spasticity, with immunotherapy responsiveness.

297 o use pharmacological strategies to decrease spasticity without hindering the recovery of motor funct

298 was identified in a male with hypertonia and spasticity without syndromic features.

299 worsened after partial cervical lesions and spasticity worsened after complete transection.

300 X-linked parkinsonism with spasticity (XPDS) presents either as typical adult onset