ライフサイエンスコーパス: spasm

1 ctrocardiographic changes, and no epicardial spasm).

2 in the targeted area, suggestive of coronary spasm.

3 le for the crotamine-induced skeletal muscle spasm.

4 d convergence spasm and 2=marked convergence spasm.

5 gger of a severe and diffuse coronary artery spasm.

6 duced hypothermia and acute diffuse coronary spasm.

7 a clinical syndrome suggestive of esophageal spasm.

8 line provocation was performed, had coronary spasm.

9 phy during the provocation test for coronary spasm.

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

11 eminal inputs in diseases such as hemifacial spasm.

12 h muscle was responsible for coronary artery spasm.

13 ers such as achalasia and diffuse esophageal spasm.

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

15 iomyocytes can feed back to produce vascular spasm.

16 h muscle providing a molecular mechanism for spasm.

17 inue to focus on the alleviation of vascular spasm.

18 t in Sur2(-/-) mice consistent with vascular spasm.

19 l treatment for blepharospasm and hemifacial spasm.

20 cular dysfunction (CMD) due to microvascular spasm.

21 had superior mesenteric artery stricture or spasm.

22 ocation testing in the diagnosis of coronary spasm.

23 rhythmia pattern characteristic of infantile spasms.

24 complex partial, focal clonic, and infantile spasms.

25 infancy and subsequently developed infantile spasms.

26 twork may contribute to the dyskinetic motor spasms.

27 nt of TSC brain disease, including infantile spasms.

28 tures involved in the development of flexion spasms.

29 uctures involved in the induction of flexion spasms.

30 l layers and a positive history of infantile spasms.

31 tetracosactide in the treatment of infantile spasms.

32 t 3 years of life and a history of infantile spasms.

33 patients did not have a history of infantile spasms.

34 loss of coordination, paralysis, and violent spasms.

35 itions characterized by chronic rigidity and spasms.

36 d in patients with unexplained stiffness and spasms.

37 on is believed to cause muscle stiffness and spasms.

38 ling infants with new diagnosis of infantile spasms.

39 phalopathy, Ohtahara syndrome, and infantile spasms.

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

41 toration of neuronal excitability and muscle spasms.

42 patients with a recent history of infantile spasms.

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

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

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

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

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

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

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

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

51 (98%) patients; the most common were muscle spasms (317 [64%]), alopecia (307 [62%]), dysgeusia (269

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

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

56 Infantile spasms (a catastrophic epileptic syndrome of childhood)

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

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

59 ascular regulation and the cause of coronary spasm after cardiac surgery.

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

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

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

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

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

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

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

67 There were 2 operative deaths due to ductal spasm and 4 late deaths, 1 due to duct thrombosis, 1 due

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

69 Other disorders, such as diffuse oesophageal spasm and hypercontracting oesophagus, have no well defi

70 ting capacity and increased risk of coronary spasm and myocardial ischemia in older people.

71 ning to minimize the degree of smooth-muscle spasm and peristalsis and to reduce the patient's discom

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

73 ated with increased risk for cerebrovascular spasm and stroke.

74 muscle develop spontaneous coronary vascular spasm and sudden death.

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

76 19 patients had tonic orbicularis oculi (OO) spasms and 18 patients had clonic OO spasms) and 8 patie

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

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

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

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

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

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

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

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

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

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

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

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

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

90 the pathogenesis of the associated infantile spasms and mental retardation.

91 ified in a subset of patients with infantile spasms and mental retardation.

92 cannabis in the treatment of painful muscle spasms and other symptoms of multiple sclerosis are curr

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

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

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

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

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

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

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

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

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

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

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

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

105 e pathogenesis of hypertension, blood vessel spasm, and atherosclerosis.

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

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

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

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

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

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

112 , benign essential blepharospasm, hemifacial spasm, and Tourette syndrome.

113 tem (CNS) characterized by chronic rigidity, spasms, and autoimmunity directed against synaptic antig

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

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

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

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

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

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

120 ssue-protective cytokine preventing vascular spasm, apoptosis, and inflammatory responses.

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

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

123 Infantile spasms are seizures associated with a severe epileptic e

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

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

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

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

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

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

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

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

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

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

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

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

136 Coronary spasm can cause myocardial ischemia and angina in patien

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

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

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

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

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

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

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

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

145 The National Infantile Spasms Consortium established a multicenter, prospective

146 Infantile spasms constitutes a severe infantile epilepsy syndrome

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 d single instances of distal coronary artery spasm, fistula dissection and unretrieved coil embolizat

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

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

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

170 SPASM GPCR sensors serve the dual purpose of detecting a

171 -10 to 70 units]; P = .15) or the hemifacial spasm group (58 vs 60 units; Hodges-Lehmann median diffe

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

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

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

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

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

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

178 cterized by muscle rigidity, episodic muscle spasms, high titers of antibodies against glutamic acid

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

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

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

182 gnosed in three patients, diffuse esophageal spasm in five, "nutcracker" esophagus in two, and a nons

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

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

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

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

187 ee doxorubicin injections in reducing muscle spasms in blepharospasm patients but with increased safe

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

189 plus developmental syndrome after infantile spasms in others.

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

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

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

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

194 ire consists of initial and delayed bouts of spasm interposed with paralysis and followed by recovery

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 CCK-induced cystic duct spasm is the etiology for low EF in both CAC and CCC.

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

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

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

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

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

210 The spasm lesion demonstrated a thicker maximum media thickn

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

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

213 iform discharges and early-onset, persistent spasm-like seizures.

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

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

216 Convergence spasm may provide benefit in the clinical examination of

217 Infantile spasms, mental retardation, autism, and dystonia represe

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

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

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

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

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

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

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

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

226 nd the rat's lower portal blood flow induces spasm of the intrahepatic portal system resulting in hyp

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

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

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

230 The primary outcome was cessation of spasms on days 13 and 14.

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

232 ause of poor control over secretions, airway spasm, or hypoventilation.

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 lerosis is associated with muscle stiffness, spasms, pain, and tremor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 0.23; P = .049) and patients with hemifacial spasm (r = 0.45; P = .001).

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

253 Convergence spasm refers to transient ocular convergence, miosis and

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

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

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

257 t-line treatment for patients suffering from spasms secondary to facial dystonias.

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

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

260 SPASM sensors also retain signaling through the endogeno

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

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

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

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

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

266 ematic Protein Affinity Strength Modulation (SPASM) technique.

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

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

269 Acute panic can evoke coronary spasm that is associated with sympathoneural and adrenom

270 haracterized by muscle rigidity and episodic spasms that involve axial and limb musculature.

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

272 s (strabismus, blepharospasm, and hemifacial spasm), the number of indications being treated has incr

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

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

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

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

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

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

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

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

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

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

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

284 Cessation of spasms was more likely in infants given hormonal treatme

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

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

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

288 Dystonic involuntary muscle spasms were specifically associated with increased theta

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

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

291 Infantile spasms, which comprise a severe infantile seizure disord

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

293 lex also eliminated coronary artery vascular spasm, while restoration of smooth muscle sarcoglycan in

294 0-1]; P = .03) than patients with hemifacial spasm who did not use alleviating maneuver.

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

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

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

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

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

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