ライフサイエンスコーパス: spasm

1 ies, recurrent fever episodes, and infantile spasms .

2 ctrocardiographic changes, and no epicardial spasm).

3 had superior mesenteric artery stricture or spasm.

4 ocation testing in the diagnosis of coronary spasm.

5 in the targeted area, suggestive of coronary spasm.

6 le for the crotamine-induced skeletal muscle spasm.

7 d convergence spasm and 2=marked convergence spasm.

8 gger of a severe and diffuse coronary artery spasm.

9 duced hypothermia and acute diffuse coronary spasm.

10 a clinical syndrome suggestive of esophageal spasm.

11 line provocation was performed, had coronary spasm.

12 phy during the provocation test for coronary spasm.

13 e sensitive than TCD in the detection of MCA spasm.

14 eminal inputs in diseases such as hemifacial spasm.

15 h muscle was responsible for coronary artery spasm.

16 ers such as achalasia and diffuse esophageal spasm.

17 ect one side of the face, such as hemifacial spasm.

18 iomyocytes can feed back to produce vascular spasm.

19 h muscle providing a molecular mechanism for spasm.

20 s an approved drug used for managing biliary spasm.

21 cular dysfunction (CMD) due to microvascular spasm.

22 phalopathy, Ohtahara syndrome, and infantile spasms.

23 ic spasms but not in BSP patients with tonic spasms.

24 toration of neuronal excitability and muscle spasms.

25 s recorded immediately prior to the onset of spasms.

26 patients with a recent history of infantile spasms.

27 lonic spasms, but not in patients with tonic spasms.

28 rhythmia pattern characteristic of infantile spasms.

29 complex partial, focal clonic, and infantile spasms.

30 of neocortical pyramidal cells in generating spasms.

31 infancy and subsequently developed infantile spasms.

32 twork may contribute to the dyskinetic motor spasms.

33 nt of TSC brain disease, including infantile spasms.

34 tures involved in the development of flexion spasms.

35 uctures involved in the induction of flexion spasms.

36 l layers and a positive history of infantile spasms.

37 tetracosactide in the treatment of infantile spasms.

38 loss of coordination, paralysis, and violent spasms.

39 on is believed to cause muscle stiffness and spasms.

40 al activity in neocortex and thalamus during spasms.

41 ling infants with new diagnosis of infantile spasms.

42 d occasionally appear sufficient to initiate spasms.

43 re observed after the administration of NTG (spasm 0.13 +/- 0.03 mm vs. nonspasm 0.13 +/- 0.02 mm, p

44 onstrated a thicker maximum media thickness (spasm 0.24 +/- 0.04 mm vs. nonspasm 0.12 +/- 0.03 mm, p

45 lesion (spasm 80% vs. nonspasm 0%, p < 0.01, spasm 100% vs. nonspasm 0%, p < 0.01, respectively).

46 elated adverse effects, most commonly muscle spasms (12 patients), weight loss (10), dysgeusia (9), a

47 ents receiving etelcalcetide had more muscle spasms (12.0% and 11.1% vs 7.1% and 6.2% with placebo),

48 nces between arms (PAG v AG) included muscle spasms (13% v 1%), neutropenia (29% v 18%), and myalgia

49 ] years); of the 56 patients with hemifacial spasm, 25 (44.6%) used alleviating maneuvers (mean [SD]

50 (98%) patients; the most common were muscle spasms (317 [64%]), alopecia (307 [62%]), dysgeusia (269

51 d adverse events with bimagrumab were muscle spasms (32 [51%] in the bimagrumab 10 mg/kg group, 43 [6

52 Seven patients had hemifacial spasm, 4 Meige syndrome, and 26 benign essential blephar

53 any grade were diarrhoea (48 [66%]), muscle spasms (45 [62%]), and fatigue (41 [56%]).

54 ommon grade 1 or 2 complications were muscle spasm (76%), followed by dysgeusia (57%), alopecia (47%)

55 50 mg and one on seladelpar 200 mg), muscle spasms (8%; three patients on seladelpar 200 mg), myalgi

56 ing spasm compared with the nonspasm lesion (spasm 80% vs. nonspasm 0%, p < 0.01, spasm 100% vs. nons

57 Infantile spasms (a catastrophic epileptic syndrome of childhood)

58 transit in patients with diffuse esophageal spasm, achalasia and patients with normal manometry.

59 nervous system injuries and painful low back spasm affect more than 10% of global population.

60 acterised by progressive rigidity and muscle spasms affecting the axial and limb muscles.

61 ecule and markedly suppressed basilar artery spasm after subarachnoid hemorrhage.

62 with type 3 achalasia had distal esophageal spasm after treatment.

63 ening up new targets for treatment of muscle spasms after SCI.

64 Spasms after spinal cord injury (SCI) are debilitating i

65 used for treating anxiety, epilepsy, muscle spasm, alcohol withdrawal, palliation, insomnia, and sed

66 ing in more than 30% of patients were muscle spasms, alopecia, dysgeusia (taste disturbance), weight

67 s on a scale of 0=normal, 1=mild convergence spasm and 2=marked convergence spasm.

68 We assessed 19 coronary arteries (10 spasm and 9 nonspasm lesions) with optical coherence tom

69 ould create a prolonged inhibition of muscle spasm and postoperative pain, facilitating tissue expand

70 bleeding complications such as radial artery spasm and radial artery occlusion are typically less mor

71 ated with increased risk for cerebrovascular spasm and stroke.

72 muscle develop spontaneous coronary vascular spasm and sudden death.

73 ded during a manoeuvre to elicit convergence spasm and the videotapes were rated by two blinded rater

74 19 patients had tonic orbicularis oculi (OO) spasms and 18 patients had clonic OO spasms) and 8 patie

75 ts who had a clinical diagnosis of infantile spasms and a hypsarrhythmic (or similar) EEG no more tha

76 ificant differences were found for abdominal spasms and abdominal distension.

77 r day [0.0-14.8]; p=0.005) to control muscle spasms and associated tachycardia.

78 l ventilation and improves control of muscle spasms and autonomic instability.

79 ridium tetani and is characterised by muscle spasms and autonomic nervous system dysfunction.

80 d ventilation and of drugs to control muscle spasms and cardiovascular instability within the 7-day s

81 equirement for other drugs to control muscle spasms and cardiovascular instability.

82 imination of C. tetani infection, control of spasms and convulsions, maintenance of the airway, and m

83 discomfort, recurrent episodes of carpopedal spasms and crampy abdominal pains.

84 ds impairs locomotion and leads to increased spasms and excessive mono- and polysynaptic low threshol

85 tient exhibits unusual signs, such as muscle spasms and fever.

86 of a child with ISOD who developed infantile spasms and hyperekplexia.

87 rx(E)), a mutation associated with infantile spasms and intellectual disabilities in humans.

88 with symptoms of muscle weakness, carpopedal spasms and limitation of movement which gradually progre

89 200Ala, previously associated with infantile spasms and microcephaly, is also pathogenic.

90 z correlated with the strength of the muscle spasms and preceded them by approximately 320 ms.

91 Treatment for tetanus aims to control spasms and reduce cardiovascular instability, and consis

92 drug (Sabril) for the treatment of infantile spasms and refractory adult epilepsy.

93 -AT) inactivator, is used to treat infantile spasms and refractory complex partial seizures and is in

94 of ARX mutations in patients with infantile spasms and related disorders, our data unveil a new mode

95 communication and motor skills and infantile spasms and seizures in predominantly females.

96 ated with intellectual disability, infantile spasms and seizures.

97 Further CRSs assessed body pain, spasms and sleep quality.

98 er characterized by sudden onset of dystonic spasms and slow movements.

99 nsitizes rats to development of NMDA-induced spasms and, most importantly, renders the spasms sensiti

100 der that manifests as repetitive involuntary spasms and/or aberrant postures of the affected body par

101 li (OO) spasms and 18 patients had clonic OO spasms) and 8 patients with IB were included in this cas

102 ng hypsarrhythmia (associated with infantile spasms) and burst suppression.

103 f focal dystonias: blepharospasm, hemifacial spasm, and apraxia of eyelid opening.

104 such as strabismus, blepharospam, hemificial spasm, and cervical dystonia, because of the toxin's tro

105 crovascular coronary vasoconstriction and/or spasm, and increased cardiac workload, to myocardial dam

106 Achalasia, diffuse esophageal spasm, and nutcracker esophagus are associated with hype

107 igue, two with hyponatremia, one with muscle spasm, and one with atrial fibrillation.

108 used treatment for blepharospasm, hemifacial spasm, and other focal dystonias.

109 atency in the diagnosis of distal esophageal spasm, and the development of diagnoses including esopha

110 e, adrenocorticotropic hormone for infantile spasms, and enzyme replacement therapy with alglucosidas

111 teau potentials in motor neurons to generate spasms, and inhibitory interneurons to curtail them.

112 were back pain, arthralgia, headache, muscle spasms, and pain in extremity (all <2%).

113 arrhea, peripheral edema, hemorrhage, muscle spasms, and pneumonia, as well as adverse events leading

114 ctroencephalographically resembles infantile spasms, and show evolution through development.

115 s were greater than 15% regardless of delay, spasms, and young age.

116 , and the overall frequency of microvascular spasm (angina and ischemic ECG shifts without epicardial

117 Epicardial and microvascular spasm are frequently found in white patients with unobst

118 benign essential blepharospasm or hemifacial spasm are known to use botulinum toxin injections and al

119 Epileptic spasms are a hallmark of severe seizure disorders.

120 y analyses indicate that the ictal events of spasms are initiated in infragranular cortical layers.

121 Infantile spasms are seizures associated with a severe epileptic e

122 Epileptic seizures, particularly infantile spasms, are often seen in infants with tuberous sclerosi

123 In the CASPAR (Coronary Artery Spasm as a Frequent Cause for Acute Coronary Syndrome) s

124 In addition, acute muscle spasms associated with oxaliplatin were significantly re

125 useful for treatment of spasticity or muscle spasms associated with several clinical conditions.

126 Absence of spasms at final clinical assessment (hormone 41/55 [75%]

127 Here we develop a new model of flexion spasms based on prenatal exposure to betamethasone combi

128 Hormone treatment controls spasms better than does vigabatrin initially, but not at

129 ith 9 patients (36%) starting with epileptic spasms between 3 and 18 months of age.

130 ents with IB and in BSP patients with clonic spasms but not in BSP patients with tonic spasms.

131 patients with IB and in patients with clonic spasms, but not in patients with tonic spasms.

132 Better initial control of spasms by hormone treatment in those with no identified

133 Definitive diagnosis of coronary spasm can at times be difficult, given the transience of

134 Coronary spasm can cause myocardial ischemia and angina in patien

135 Our findings provide evidence that epileptic spasms can arise from the neocortex and reveal a previou

136 positive clinical signs such as convergence spasms can be triggered by the clinical examination.

137 ism, whereby tissue damage leads to vascular spasm, can be partially corrected by NO synthase inhibit

138 th some characteristics resembling infantile spasms, caused by mutations in a known infantile spasms

139 The 4 week period of spasm cessation required to achieve a primary clinical r

140 seizure-like responses (hyperactivity bouts, spasms, circular and corkscrew swimming) accompanied by

141 he following: nonwhite race/ethnicity; tonic spasms; coexisting autoimmunity; magnetic resonance imag

142 ump at baseline and intimal gathering during spasm compared with the nonspasm lesion (spasm 80% vs. n

143 ession studies in zebrafish that resulted in spasms, confirming a functional link with disruption of

144 The National Infantile Spasms Consortium established a multicenter, prospective

145 Infantile spasms constitutes a severe infantile epilepsy syndrome

146 The first structure of a SPASM-containing enzyme, anaerobic sulfatase-maturating

147 hecal antitoxin administration as methods of spasm control that can avoid the need for ventilatory su

148 benign essential blepharospasm or hemifacial spasm correlates with disease severity or botulinum toxi

149 ready an approved drug used to treat biliary spasm, could be repurposed to prevent, and possibly trea

150 not result in a significant change in daily spasm count.

151 he manometric diagnosis of distal esophageal spasm (DES) uses "simultaneous contractions" as a defini

152 ng of 47 patients with unexplained infantile spasms did not reveal additional de novo mutations, but

153 Importantly, one [4Fe-4S] cluster in the SPASM domain exhibits an open coordination site in absen

154 study suggests novel mechanistic links among SPASM domain radical SAM enzymes and supports the involv

155 at RumMC2 is a member of the large family of SPASM domain radical SAM enzymes characterized by the pr

156 enzyme, belonging to the emerging family of SPASM domain radical SAM enzymes, likely contains three

157 radical SAM enzymes, as well as a C-terminal SPASM domain that contains two auxiliary [4Fe-4S] cluste

158 sylmethionine (RS) protein with a C-terminal SPASM domain, and is proposed to catalyze the formation

159 served cysteine residues, present within the SPASM domain, are critical for enzyme activity.

160 One extension, termed a SPASM domain, binds two auxiliary [4Fe-4S] clusters and

161 in a cysteine-rich C-terminal domain, termed SPASM domain, that contains homology to ~1,400 other uni

162 The former implicated a new SPASM-domain-containing radical SAM enzyme StrB, while t

163 without culprit lesion and proof of coronary spasm during 3 years of follow-up.

164 euvers used for blepharospasm and hemifacial spasm, dystonia severity, and dose and frequency of botu

165 logram results correspond to human infantile spasms: electrodecrement or afterdischarges were observe

166 PqqD orthologues are associated with the RS-SPASM family of proteins (subtilosin, pyrroloquinoline q

167 Moreover, vascular spasm feeds forward to produce additional cardiac damage

168 re for Precise Analysis of Single Molecules (SPASM), for generating ensemble averages of single-molec

169 treatment-related adverse events were muscle spasms (four [4%] patients in treatment group A vs 12 [1

170 entification of achalasia, distal esophageal spasm, functional obstruction, and subtypes thereof.

171 ms, caused by mutations in a known infantile spasms gene.

172 interplay between brain state physiology and spasm generation.

173 SPASM GPCR sensors serve the dual purpose of detecting a

174 -10 to 70 units]; P = .15) or the hemifacial spasm group (58 vs 60 units; Hodges-Lehmann median diffe

175 nts (62%), 35 patients (45%) with epicardial spasm (>/=75% diameter reduction with reproduction of th

176 The overall frequency of epicardial spasm (>75% diameter reduction with angina and ischemic

177 and strokes with anastrozole and more muscle spasm, gynaecological cancers and symptoms, vasomotor sy

178 nkles, migraine prophylaxis, spasticity, and spasms, had a significantly lower number of depression r

179 Coronary artery spasm has been identified as an alternative cause for ac

180 without culprit lesion and proof of coronary spasm have an excellent prognosis for survival and coron

181 and from a group of patients with hemifacial spasm (HFS).

182 is characterized by rigidity, painful muscle spasms, hyperekplexia, and brainstem signs.

183 model correlates well with current infantile spasm hypotheses and opens an opportunity for developmen

184 oline (ACH) testing, which elicited coronary spasm in 77 patients (62%), 35 patients (45%) with epica

185 mecromone, that is approved to treat biliary spasm in humans, we propose that it could be repurposed

186 iggered epicardial or microvascular coronary spasm in nearly two-thirds of these patients.

187 nce of epicardial and microvascular coronary spasm in patients with anginal symptoms, despite angiogr

188 interneurons as well as motor neurons during spasms in a mouse model of chronic SCI.

189 peutic target for the treatment of infantile spasms in DS.

190 plus developmental syndrome after infantile spasms in others.

191 focal dystonia characterized by involuntary spasms in the laryngeal muscles during speech production

192 ogical disorder characterized by involuntary spasms in the laryngeal muscles during speech production

193 onsidered as initial treatment for infantile spasms, including those with impaired development or kno

194 xiety, mood swings, severe headaches, muscle spasms, interphalangeal joint stiffness, decreased perip

195 However, whether spasms involve activation of premotor spinal excitatory

196 taracts, severe epilepsy including infantile spasms, irritability, failure to thrive, and stereotypic

197 Vascular spasm is a poorly understood but critical biomedical pro

198 Coronary spasm is an important and often overlooked etiology of c

199 Luminal narrowing during spasm is associated with intimal gathering without alter

200 t much of what was labeled distal esophageal spasm is in fact achalasia with esophageal compression a

201 Epicardial spasm is most often diffuse and located in the distal co

202 on remain largely unknown, although coronary spasm is suspected.

203 CCK-induced cystic duct spasm is the cause of low GBEF in CAC and CCC, and the s

204 Infantile spasms is a severe infantile seizure disorder that is di

205 We sought to assess whether early control of spasms is associated with improved developmental or epil

206 Infantile spasms (IS) and Lennox-Gastaut syndrome (LGS) are epilep

207 Infantile spasms (IS) is an early-onset epileptic encephalopathy o

208 ) Lennox-Gastaut syndrome (LGS) or infantile spasms (IS).

209 The spasm lesion demonstrated a thicker maximum media thickn

210 The spasm lesion more frequently showed an intimal bump at b

211 G)10+7) ("Arx plus 7") pups display abnormal spasm-like myoclonus and other key EEG features, includi

212 ned three principal regions involved in NMDA spasms: limbic areas (except the dorsal hippocampus), hy

213 ) or more frequent (e.g., migraine, coronary spasm, lupus, vasculitis, Raynaud's phenomenon, etc.) in

214 Convergence spasm may provide benefit in the clinical examination of

215 on of an inflammatory cascade, microvascular spasm, microthrombosis, cortical spreading depolarisatio

216 Such events may arise from spasm, microvascular disease, or other pathways.

217 such as convergence and unilateral platysmal spasm might lend diagnostic weight to a suspected functi

218 one auxiliary cluster and exhibit a partial SPASM motif, coined a Twitch domain.

219 n as first-line therapy, including infantile spasms, myoclonic-astatic epilepsy (Doose syndrome), Dra

220 ruction (n = 1), transient ophthalmic artery spasm (n = 1), central retinal artery obstruction (n = 1

221 atic bradycardia [n=6], and catheter-induced spasm [n=1]).

222 dverse events were fatigue, diarrhea, muscle spasms, nausea, and bruising.

223 tions, as it increased slow oscillations and spasm numbers and clustering.

224 of spasms, which was defined as no witnessed spasms on and between day 14 and day 42 from trial entry

225 Absence of spasms on days 13 and 14 after randomisation is more com

226 Proportions with no spasms on days 13 and 14 were: 40 (73%) of 55 infants as

227 phate (n = 6); (ii) a patient with infantile spasms (onset 5 months) responsive to pyridoxal 5'-phosp

228 enerator pocket pain (five [4%]), and muscle spasm or cramp (three [2%]).

229 st suggests that the headaches are caused by spasm or tension of scalp, shoulders, and neck muscles i

230 onth of life, mainly consisting of epileptic spasms or myoclonic seizures.

231 ilepsy (OR = 0.23, p = 0.022), and infantile spasms (OR = 0, p < 0.001).

232 pathy, non-ischemic cardiomyopathy, coronary spasm, or nonspecific myocardial injury, and the prevale

233 Although coronary spasm, or Prinzmetal's angina, has been thought of as be

234 y represent dissection, intramural hematoma, spasm, or tortuosity.

235 hronic symptoms, including muscle stiffness, spasms, pain and insomnia.

236 e placebo group), with hypocalcaemia, muscle spasm, paraesthesias, headache, and nausea being the mos

237 isons were made to recordings from infantile spasm patients.

238 spasms, which was also observed in infantile spasm patients.

239 a catastrophic pediatric epilepsy with motor spasms, persistent seizures, mental retardation, and in

240 ry for the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse and may represent a nov

241 n upon the GABAB R agonist-induced infantile spasms phenotype in the Ts mouse model of DS.

242 escued the GABAB R agonist-induced infantile spasms phenotype in Ts mutants.

243 ry for the GABAB R agonist-induced infantile spasms phenotype in Ts.

244 DS) is exquisitely sensitive to an infantile spasms phenotype induced by gamma-aminobutyric acidB rec

245 escued the GABAB R agonist-induced infantile spasms phenotype.

246 le stiffness, pain and discomfort and muscle spasms,), physical impact (activities of daily living, w

247 es were not indicative of recurrent coronary spasm playing a major role in the genesis of transient l

248 Coronary artery spasm plays an important role in the pathogenesis of isc

249 peptide modification pathways that use an RS-SPASM protein.

250 revealed unexpected similarities to two non-SPASM proteins, butirosin biosynthetic enzyme 2-deoxy-sc

251 uvers scored higher on the 7-item Hemifacial Spasm Quality of Life scale (median score, 7 vs 3; Hodge

252 0.23; P = .049) and patients with hemifacial spasm (r = 0.45; P = .001).

253 lysis for the presence of marked convergence spasm (rating 2) yielded agreement in 32/36 (88.9%) exam

254 Convergence spasm refers to transient ocular convergence, miosis and

255 in the absence of mechanical ventilation is spasm-related respiratory failure, whereas in ventilated

256 mber of injections needed for patient muscle spasm relief, decreasing the risk of negative side effec

257 nt) and 42 patients (55%) with microvascular spasm (reproduction of symptoms, ischemic electrocardiog

258 associated with schizophrenia and infantile spasms, respectively.

259 ed spasms and, most importantly, renders the spasms sensitive to adrenocorticotropin therapy.

260 reshold of 200 cm/sec used for more advanced spasm, sensitivities and specificities of both methods w

261 SPASM sensors also retain signaling through the endogeno

262 SPASM sensors are tested for the beta2-, alpha1-, and al

263 xperienced malignant diffuse coronary artery spasm, so-called Prinzmetal's angina, leading to myocard

264 nts enrolled in the United Kingdom Infantile Spasms Study (UKISS) were randomly assigned hormone trea

265 The United Kingdom Infantile Spasms Study assessed these treatments in a multicentre,

266 Infantile spasms syndrome (ISS) is a catastrophic pediatric epilep

267 ematic Protein Affinity Strength Modulation (SPASM) technique.

268 icantly more effective at stopping infantile spasms than hormonal therapy alone.

269 icantly more effective at stopping infantile spasms than hormonal therapy alone.

270 fen on spasticity (e.g. management of muscle spasms that may otherwise hinder movement or social inte

271 Muscle spasms, the most frequent adverse event in the bardoxolo

272 a potential mechanism for the propagation of spasms throughout the limb.

273 hageal compression (type II), achalasia with spasm (type III), and functional obstruction with some p

274 s in the detection of mild and more advanced spasm using 120 cm/sec and 200 cm/sec thresholds, respec

275 Coronary artery spasm was inducible in 27% of MINOCA patients, and throm

276 Spasm was mild in 17, moderate in 16, and severe in only

277 Epicardial spasm was most often diffuse and located in the distal c

278 Acute coronary occlusion or spasm was not observed at a median separation distance o

279 Supporting this notion, vascular spasm was noted in coronary arteries, and disruption of

280 Convergence spasm was present in 9/13 (69%) psychogenic movement dis

281 ation, and it was hypothesized that vascular spasm was responsible for this focal necrosis.

282 hreshold of 120 cm/sec for less advanced MCA spasm was significantly better than that of TCD at simil

283 a and ischemic ECG shifts without epicardial spasm) was 24.2%.

284 guineous families of children with infantile spasms were analysed for linkage to the phospholipase C-

285 y on the development of age-specific flexion spasms were determined and electroencephalographic corre

286 Dystonic involuntary muscle spasms were specifically associated with increased theta

287 Between days 14 and 42 inclusive no spasms were witnessed in 133 (72%) of 186 patients on ho

288 ons mirrors the extensor weakness and flexor spasm which in neurological experience is a common limit

289 Infantile spasms, which comprise a severe infantile seizure disord

290 r of neocortical slow oscillations preceding spasms, which was also observed in infantile spasm patie

291 The primary outcome was cessation of spasms, which was defined as no witnessed spasms on and

292 0-1]; P = .03) than patients with hemifacial spasm who did not use alleviating maneuver.

293 Patients with hemifacial spasm who used alleviating maneuvers scored higher on th

294 lepharospasm and 56 patients with hemifacial spasm who were consecutively recruited from adnexal clin

295 a mechanism capable of initiating epileptic spasms will likely provide new targets for interventiona

296 mprovement of muscle weakness and carpopedal spasm with near-normal biochemical parameters.

297 l artery obstruction (1%), ophthalmic artery spasm with reperfusion (2%), ophthalmic artery obstructi

298 h ISOD; however, to our knowledge, infantile spasms with a corresponding hypsarrhythmia pattern on el

299 ted with cranial asymmetry, severe infantile spasms with hypsarrhythmia, and dysproportionate dwarfis

300 taut syndrome, Dravet syndrome and infantile spasms with intellectual disability as well as relativel