ライフサイエンスコーパス: dysphagia

1 (heartburn and/or acid regurgitation and/or dysphagia).

2 stoperative complications (eg, postoperative dysphagia).

3 ild dysphagia) to 4.1 +/- 0.9 (mild/moderate dysphagia).

4 14.0-24.0]) were screened for postextubation dysphagia.

5 equire reoperation for recurrent GERD and/or dysphagia.

6 llowing pathways as a prelude to therapy for dysphagia.

7 blets for 5 years presented with progressive dysphagia.

8 a trend for improved symptoms, particularly dysphagia.

9 translation in future studies of neurogenic dysphagia.

10 observed association between mast cells and dysphagia.

11 roenterology for evaluation of dyspepsia and dysphagia.

12 amel hypoplasia, oral hyperpigmentation, and dysphagia.

13 to future clinical application in neurogenic dysphagia.

14 ocess might contribute to the development of dysphagia.

15 s a differential diagnosis in a patient with dysphagia.

16 h increased risk for wound complications and dysphagia.

17 l tool for understanding the neural basis of dysphagia.

18 eal stricture who have recurrent symptoms of dysphagia.

19 w insights into its clinical application for dysphagia.

20 yopathy, areflexia, respiratory distress and dysphagia.

21 issen group required intervention for severe dysphagia.

22 r gaze palsy, symmetric motor disability and dysphagia.

23 eakness, areflexia, respiratory distress and dysphagia.

24 in this group of subjects with oropharyngeal dysphagia.

25 associated with role functioning, pain, and dysphagia.

26 V) in subjects with neurogenic oropharyngeal dysphagia.

27 l, person-centered dining for residents with dysphagia.

28 bellar rTMS into a treatment for post-stroke dysphagia.

29 ief, with no differences in GERD symptoms or dysphagia.

30 hagia to be identified, including functional dysphagia.

31 mpared with SWS, especially in patients with dysphagia.

32 ement strategies and outcomes for functional dysphagia.

33 xia (20%), dehydration (16%), diarrhea (8%), dysphagia (10%), esophagitis (20%), fatigue (12%), hyper

34 most frequent grade 3-4 adverse events were dysphagia (17 [27%] of 63 patients in the chemoradiother

35 rm tube feeding-dependency because of severe dysphagia (2 patients) and chronic aspiration (2 patient

36 - 1.5 vs LNF 3.7 +/- 1.6; P = 0.031) but not dysphagia (2.8 +/- 1.9 vs 2.3 +/- 1.7; P = 0.302) and qu

37 in the radiotherapy plus panitumumab group), dysphagia (20 [32%] vs 36 [40%]), and radiation skin inj

38 Distal weakness (26 [41%]), dysphagia (22 [35%]), and dyspnea (23 [37%]) were common

39 e increase was most evident in patients with dysphagia (241 [67%] of 360 patients on STM vs 125 [35%]

40 2.69, 95% CI -2.33 to 7.72, n=231, p=0.293), dysphagia (-3.18, 95% CI -8.36 to 2.00, n=231, p=0.228),

41 In patients with T2D compared to controls, dysphagia (32.3% vs. 13.1%; p = 0.001) and globus sensat

42 [19%]), fatigue (26 [20%] vs 25 [19%]), and dysphagia (35 [27%] vs 37 [29%]).

43 5% CI 74%-81%] to 62% [56%-68%], p < 0.001), dysphagia (37% [33%-41%] to 15% [12%-20%], p < 0.001), a

44 cation (Nissen to partial fundoplication for dysphagia - 5; redo Nissen for reflux - 1; paraesophagea

45 st commonly reported signs and symptoms were dysphagia (53%), dysarthria (39%), and generalized weakn

46 Common symptoms of EoE included dysphagia (96%), food impaction (74%), and heartburn (94

47 axis for reducing pneumonia in patients with dysphagia after acute stroke.

48 Dysphagia after extubation was common in ICU patients, s

49 Dysphagia after mechanical ventilation may be an overloo

50 essment of patients older than 18 years with dysphagia after new stroke recruited from 48 stroke unit

51 on of post-stroke pneumonia in patients with dysphagia after stroke managed in stroke units.

52 Delays in screening for and assessing dysphagia after stroke, are associated with higher risk

53 pital mortality were higher in patients with dysphagia (all p < 0.001).

54 bronchoconstriction, airway mucus secretion, dysphagia, altered gastrointestinal motility, and itchy

55 by progressive eyelid drooping (ptosis) and dysphagia although muscles of the limbs can also be affe

56 resent a 62-year-old woman who suffered from dysphagia, an inability to tolerate a regular diet, and

57 al stimulation in acute stroke patients with dysphagia, an individual patient data meta-analysis and

58 ted of 221 patients, including 98 (44%) with dysphagia and 123 (56%) with reflux symptoms.

59 included 750 patients of whom 360 (48%) had dysphagia and 390 (52%) had reflux or other symptoms.

60 nts between the ages of 11 and 40 years with dysphagia and active esophageal eosinophilia were random

61 d were recurrent or persistent postoperative dysphagia and an abnormal 24-hour pH test result.

62 However, dysphagia and aspiration remain serious complications, d

63 Gastroesophageal reflux/dysphagia and asthma/rhinitis represent a risk factor fo

64 case series described adults suffering from dysphagia and children with refractory reflux symptoms,

65 but less common symptoms and signs, such as dysphagia and chronic cough, may occur.

66 ly plays an important role in the genesis of dysphagia and delayed esophageal emptying.

67 henotype than those with EA-EoE+ in terms of dysphagia and dilation need.

68 Dysphagia and dysarthria were the most commonly reported

69 variate HR 2.53; 95% CI 1.69 to 3.78), early dysphagia and early cognitive symptoms.

70 in esophageal eosinophil counts and improved dysphagia and endoscopic features.

71 Treatment-related grade >=3 dysphagia and esophagitis occurred in 3.2% and 5.0% of p

72 s but has been associated with postoperative dysphagia and esophagitis.

73 ssociated with a low prevalence of new-onset dysphagia and esophagitis.

74 le system atrophy developed ataxia, stridor, dysphagia and falls than patients with Lewy body disease

75 lic esophagitis (EoE) typically present with dysphagia and food impaction.

76 At 1 and 5 years, dysphagia and gas-related symptoms are lower after 180-d

77 e LAF has been alleged to reduce troublesome dysphagia and gas-related symptoms, with similar reflux

78 diaphragmatic pacing, secretions, nutrition, dysphagia and gastrostomy, communication problems, mobil

79 Dysphagia and GERD symptoms are common indications for e

80 wing impairment in patients with post stroke dysphagia and is appropriate for use in clinical researc

81 specification, and neurite growth, prefigure dysphagia and may then compromise circuits for additiona

82 n clinical and histologic factors, including dysphagia and odynophagia severity <=2 on a scale of 0-1

83 ate onset genetic disease leading to ptosis, dysphagia and proximal limb muscles at later stages.

84 dult-onset disorder characterized by ptosis, dysphagia and proximal limb weakness.

85 Dysphagia and proximal myopathy were common, but urinary

86 Many patients with persistent dysphagia and regurgitation after therapy have low or no

87 a case of a 84-year-old woman with anorexia, dysphagia and unintentional weight loss initially diagno

88 o underwent gastrostomy insertion for severe dysphagia and/or weight loss, were included.

89 reased orodental disease, speech impairment, dysphagia, and a significant negative effect on quality

90 % of patients with premature contraction had dysphagia, and all (n = 24; 2.2% overall) were ultimatel

91 progression with disequilibrium, dysarthria, dysphagia, and central hypoventilation, and died 2 month

92 e-threatening, causing pulmonary aspiration, dysphagia, and choking, yet relevant sensory pathways re

93 te impairments, of which limb motor deficit, dysphagia, and incontinence have declined between 2001 a

94 hagia, behavioral adaptations to living with dysphagia, and pain while swallowing accounted for 67% o

95 and these were followed by muscle weakness, dysphagia, and spino-cerebellar signs with impaired gait

96 opy and other symptoms measured by the GSRS, dysphagia, and the Gastrointestinal Quality of Life Inde

97 with an exudative tonsillitis, sore throat, dysphagia, and unilateral neck pain.

98 k or arm or shoulder pain, arm paraesthesia, dysphagia, and worsening of myelopathy.

99 Palifermin appeared to reduce mucositis, dysphagia, and xerostomia during hyperfractionated radio

100 e gender, allergic rhinitis, the presence of dysphagia, and younger age were independently associated

101 ze, slowed horizontal and vertical saccades, dysphagia, apathy, and progressive cognitive decline, wh

102 lonus, hypotonia, optic nerve abnormalities, dysphagia, apnea, and early developmental arrest.

103 Many modalities of palliation of dysphagia are available, but the procedure with least mo

104 ed to the pathophysiologic basis of neonatal dysphagia as well as potential opportunities to improve

105 We investigated mechanisms of dysphagia, assessing the response of human esophageal fi

106 ile adjusted OR 1.14, 1.03 to 1.24) and SALT dysphagia assessment (4th quartile adjusted OR 2.01, 1.7

107 auses of mortality after acute stroke, early dysphagia assessment may contribute to preventing deaths

108 n a dose-response manner with delays in SALT dysphagia assessment, with an absolute increase of pneum

109 a screen, and (2) admission to comprehensive dysphagia assessment.

110 gia screen, and 24 542 (39%) a comprehensive dysphagia assessment.

111 edside dysphagia screening and comprehensive dysphagia assessments by a speech and language therapist

112 adiotherapy alone for treatment of malignant dysphagia at 22 hospitals in Australia, Canada, New Zeal

113 Spinal onset patients with dysphagia at diagnosis had a median survival similar to

114 a subgroup of spinal onset patients without dysphagia at diagnosis had a severe weight loss and an o

115 About 20% of spinal onset patients without dysphagia at diagnosis had severe weight loss and initia

116 d be stratified according to the presence of dysphagia at the time of enrolment and not by site of on

117 by gait instability followed by dysarthria, dysphagia, ataxia, or chorea.

118 esthesias and progressed to fever, seizures, dysphagia, autonomic dysfunction, and brain death) was c

119 s that are used to assess characteristics of dysphagia, behavioral adaptations to living with dysphag

120 and women with heartburn and alarm symptoms (dysphagia, bleeding, anemia, weight loss, and recurrent

121 e reduction of nutritional intake related to dysphagia, but a subgroup of spinal onset patients witho

122 Almost all patients (93%) reported some dysphagia, but dysphagia scores remained significantly l

123 n, stinging pain, foreign body sensation and dysphagia can be observed with this syndrome.

124 Chemoradiotherapy with IMRT aiming to reduce dysphagia can be performed safely for OPC and has high l

125 paresis and truncal instability, dysarthria, dysphagia, cerebellar ataxia, and cognitive deficits, of

126 uld be considered when patients present with dysphagia, chest pain, and refractory reflux symptoms af

127 geal symptoms found in those with GERD were, dysphagia, coated tongue, nocturnal cough, xerostomia, l

128 6 areas: timing and approach; motor therapy; dysphagia; cognitive, speech, and sensory therapy; menta

129 come of the stents as evaluated by recurrent dysphagia, complications and reinterventions.

130 Dysphagia correlated most strongly with overall histopat

131 ve disability, unintelligible speech, severe dysphagia, dependence on wheelchair for mobility, the us

132 New-onset dysphagia developed in only 2 patients.

133 The dysphagia domain correlated most with esophageal gene tr

134 y captures symptoms; (3) determined that the dysphagia domain most closely aligns with symptoms and t

135 e two patients who presented with refractory dysphagia due to malignant proximal oesophageal strictur

136 All patients had relief of dysphagia [dysphagia score </= 1 ("rare")].

137 atio, 1.1:1), ENT symptoms (eg, odynophagia, dysphagia, dysphonia, dyspnea, earache, nasal obstructio

138 suitable for curative treatment, symptomatic dysphagia, Eastern Cooperative Oncology Group performanc

139 opathy, areflexia, respiratory distress, and dysphagia (EMARDD), a rare congenital muscle disease, bu

140 opathy, areflexia, respiratory distress, and dysphagia (EMARDD).

141 cation and treatment of an uncommon cause of dysphagia, esophageal intramural pseudodiverticulosis.

142 This is a very infrequent cause of dysphagia following prone-position ventilation.

143 7.1%, p = 0.023) were higher, offset by less dysphagia for solids (mean score 1.8 vs 3.3, p = 0.015),

144 ve [11%]), and during chemoradiotherapy were dysphagia (four [9%]) and mucositis (four [9%]).

145 A total of 8/30 patients (26.6%) were dysphagia-free after the end of follow-up: 1 (10%) in th

146 with some featuring in multiple categories: dysphagia frequency (n = 38), swallowing physiology (n =

147 h tracheostomy) ranged from 10 to 3,320, and dysphagia frequency ranged from 11% to 93% in studies wi

148 t patients with EAC present with symptoms of dysphagia from late-stage tumors; only a small number of

149 is vital for distinguishing true oesophageal dysphagia from oropharyngeal dysphagia or other causes.

150 technique to 6 patients with severe, chronic dysphagia from stroke (mean of 38.8 +/- 24.4 weeks posts

151 ion in healthy individuals and patients with dysphagia from stroke.

152 a rehabilitative approach for patients with dysphagia from stroke.

153 different clinical symptoms, with increased dysphagia, gagging, cough, and poor appetite compared to

154 However, whether patient-identified domains (dysphagia, gastroesophageal reflux disease [GERD], nause

155 e following terms: heartburn, regurgitation, dysphagia, gastroesophageal reflux disease, cough, aspir

156 ere the following: heartburn, regurgitation, dysphagia, gastroesophageal reflux disease, cough, aspir

157 s in the gastrointestinal tract that include dysphagia, gastroparesis, prolonged gastrointestinal tra

158 a regarding the presence of reflux symptoms, dysphagia, general health, PPI use, and need for surgica

159 n-free administration, assists patients with dysphagia, has increased patient compliance, can be self

160 Such proposed therapies for post-stroke dysphagia have required confirmation of physiological ef

161 patients with active EoE, dupilumab reduced dysphagia, histologic features of disease (including eos

162 ts with RBES may lead to long-term relief of dysphagia in 30 and 40% of patients, respectively.

163 the most suitable therapy for palliation of dysphagia in a given patient.

164 5 and 2015 on various modes of palliation of dysphagia in carcinoma esophagus were studied, which wer

165 The prevalence of dysphagia in critical illness polyneuropathy is not know

166 this study was to evaluate the prevalence of dysphagia in critical illness polyneuropathy using fiber

167 contributing factors for the development of dysphagia in critical illness polyneuropathy.

168 rescribed for palliative relief of malignant dysphagia in patients with incurable oesophageal cancer.

169 The increased odds of postoperative dysphagia in the group undergoing myotomy with anterior

170 e and well tolerated treatment for malignant dysphagia in the palliative setting.

171 The most frequent adverse event was dysphagia (in 68% of patients postoperatively, in 11% at

172 The dysphagia incidence at ICU discharge was 10.3% (n = 96/9

173 monias, venous thromboembolism, fever, pain, dysphagia, incontinence, and depression are particularly

174 with stroke experience swallowing problems (dysphagia); increased risk of aspiration pneumonia, maln

175 change from baseline to week 10 in Straumann Dysphagia Instrument (SDI) patient-reported outcome (PRO

176 QOL was evaluated using the MD Anderson Dysphagia Inventory and the University of Michigan patie

177 Dysphagia is a common symptom in the general population.

178 Considering that neurogenic oropharyngeal dysphagia is a prevalent condition with or without cardi

179 Oesophageal dysphagia is a so-called red flag alarm symptom requirin

180 The onset of dysphagia is associated with advanced disease, which has

181 Rating Scale (DSRS), which grades how severe dysphagia is based on fluid and diet modification and su

182 Coexistent dysphagia is considered an alarm symptom, prompting eval

183 Dysphagia is frequent among patients with critical illne

184 Achalasia should be considered when dysphagia is present and not explained by an obstruction

185 Dysphagia is the main symptom of adult eosinophilic esop

186 -ecological model for successful dining with dysphagia is ultimately proposed: optimizing health and

187 Dysphagia is well known to deteriorate outcome in the IC

188 yopathy, areflexia, respiratory distress and dysphagia, is severe and immediately life-threatening.

189 , and swallowing from birth onward-perinatal dysphagia-is often associated with several neurodevelopm

190 However, for residents with dysphagia, it is unclear how to best support this enhanc

191 lation (rTMS) can be used as a treatment for dysphagia, its efficacy varies across individuals.

192 We investigated the incidence of dysphagia, its time course, and association with clinica

193 egree partial fundoplication, offset by less dysphagia, leading to a clinical outcome that is equival

194 ogressive limb weakness, muscle atrophy, and dysphagia, making them vulnerable to insufficient energy

195 Thus, perinatal dysphagia may be an early indicator of disrupted genetic

196 Dysphagia may develop in or after the fourth decade of l

197 esophagitis, heartburn score, dilatation for dysphagia, modified Dakkak dysphagia score (0-45), and r

198 gurgitation in 5 patients (46%), followed by dysphagia (n = 4, 37%) and chest pain (n = 2, 18%).

199 mptoms may include heartburn, regurgitation, dysphagia, nausea, or vague epigastric pain depending on

200 dity, mortality, and long-term palliation of dysphagia needs to be chosen for the patient.

201 Based on evidence from the post-stroke dysphagia neurostimulation literature, these changes may

202 n unpleasant/painful sensation, unrelated to dysphagia, occurring immediately after esophageal contac

203 y healthy female presented with intermittent dysphagia, odynophagia and loss of weight of 3 months du

204 (4% versus 4%) and 8 weeks (11% versus 9%), dysphagia/odynophagia/chest pain (9% versus 2%), strictu

205 weakness, wasting, spasticity, dysarthria or dysphagia of one central nervous system region defined a

206 Tracheostomy and dysphagia often coexist during critical illness; however

207 iting (one), diarrhoea (one), fatigue (one), dysphagia (one), neck pain (one), and diaphoresis (one);

208 ogressive ataxia, tremor, cognitive decline, dysphagia, optic atrophy, dysarthria, as well as urinary

209 ars of age or older, choking or pill-induced dysphagia or globus caused 37.6% (95% CI, 29.1 to 46.2)

210 ; adjusted OR, 1.67; 95% CI, 1.10- 2.53) and dysphagia or hoarseness (4.35% with BMP vs 2.45% without

211 nd had a higher incidence of post-procedural dysphagia or odynophagia (40% vs. 10%; p = 0.02).

212 rue oesophageal dysphagia from oropharyngeal dysphagia or other causes.

213 ignificantly more likely to have symptoms of dysphagia (OR=10.67; p=0.03) and reduced forced vital ca

214 Neonatal dysphagia, or abnormalities of swallowing, represent a m

215 ntraindications to antibiotics, pre-existing dysphagia, or known infections, or who were not expected

216 skin reaction, pneumonitis, dyspnea, cough, dysphagia, or neutropenia.

217 of mild hoarseness, with no associated pain, dysphagia, or stridor.

218 elated to specific parent-reported symptoms: dysphagia (P = .0012), GERD (P = .0001), and nausea/vomi

219 ts with intracerebral haemorrhage (p=0.014), dysphagia (p=0.003) and urinary incontinence/catheterisa

220 so showed benefits for docetaxel in reducing dysphagia (p=0.02) and abdominal pain (p=0.01).

221 ion, institution accrual volume, esophagitis/dysphagia, planning target volume and heart V5.

222 eks later), and key secondary endpoints were dysphagia progression-free survival (defined as a worsen

223 iotherapy alone, with minimal improvement in dysphagia progression-free survival and overall survival

224 Median dysphagia progression-free survival was 4.1 months (95%

225 eactivity was predictive for muscle atrophy, dysphagia, pronounced muscle fiber damage, and vasculiti

226 Post stroke dysphagia (PSD) is common and associated with poor outco

227 ssociated with pain (r = 0.27, P = .06) than dysphagia (r = 0.24, P = .13).

228 In patients with chronic dysphagia, real PAS induced short-term bilateral changes

229 Dysphagia, recurrence and need for redo fundoplication w

230 hat screening patients with acute stroke for dysphagia reduces the risk of stroke-associated pneumoni

231 75 years old] with neurogenic oropharyngeal dysphagia regardless of gender.

232 ingested food not only leads to symptoms of dysphagia, regurgitation, chest pain, and weight loss, b

233 ation," "any re-operation/re-intervention," "dysphagia/regurgitation," and "micronutrient status." Th

234 interaction (HCI) for swallowing training in dysphagia rehabilitation.

235 ndividuals and has therapeutic potential for dysphagia rehabilitation.

236 The primary endpoint was dysphagia relief (defined as >/=1 point reduction on the

237 %, 26-44) in the radiotherapy group obtained dysphagia relief (difference 10.6%, 95% CI -2 to 23; p=0

238 t not statistically significant, increase in dysphagia relief compared with radiotherapy alone, with

239 hemoradiotherapy with radiotherapy alone for dysphagia relief in the palliative setting.

240 At a mean follow-up of 11.4 months, dysphagia relief persisted for all patients.

241 All patients had dysphagia relief, 83% having relief of noncardiac chest

242 -term follow-up, showed excellent results on dysphagia relief.

243 verity and length of mechanical ventilation, dysphagia remained an independent predictor for 28-day a

244 However, severe dysphagia requiring endoscopy +/- dilatation was signifi

245 ligible speech, cognitive impairment, severe dysphagia, residential care).

246 Symptoms (weight loss, dysphagia, retrosternal pain, and regurgitation) were as

247 All patients had relief of dysphagia [dysphagia score </= 1 ("rare")].

248 e, dilatation for dysphagia, modified Dakkak dysphagia score (0-45), and reoperation rate.

249 r high-power field (eos/hpf) and a validated dysphagia score (dysphagia symptom questionnaire [DSQ])

250 Patients were stratified by hospital, dysphagia score (Mellow scale 1-4), and presence of meta

251 At 1 year, the Dakkak dysphagia score [2.8 vs 4.8; weighted mean difference: -

252 At 5 years, the Dakkak dysphagia score, flatulence, inability to belch, and ina

253 Mean dysphagia scores improved from 3.3 (SD 0.6) pre-SEMS (n=

254 patients (93%) reported some dysphagia, but dysphagia scores remained significantly lower than preop

255 Dysphagia scores, morbidity, mortality, and survival wer

256 fundoplication, which was reflected by lower dysphagia scores.

257 ures were time from (1) admission to bedside dysphagia screen, and (2) admission to comprehensive dys

258 mitted with acute stroke, 55 838 (88%) had a dysphagia screen, and 24 542 (39%) a comprehensive dysph

259 Patients with the longest delays in dysphagia screening (4th quartile adjusted OR 1.14, 1.03

260 n is a very promising noninvasive method for dysphagia screening and aspiration detection, as it does

261 We aimed to identify if delays in bedside dysphagia screening and comprehensive dysphagia assessme

262 spective observational trial with systematic dysphagia screening and follow-up until 90 days or death

263 Dysphagia screening was positive in 12.4% (n = 116/933)

264 ain scan within 12 h, brain scan within 1 h, dysphagia screening), a day of the week pattern (stroke

265 d 8 of the 13 QIs for performance reporting: dysphagia screening, National Institutes of Health Strok

266 The Dysphagia Severity Rating Scale (DSRS), which grades how

267 with AS (ataxia, action tremor, dysarthria, dysphagia, sialorrhea and excessive chewing/mouthing beh

268 -quarter of patients developed postoperative dysphagia similarly distributed between both groups.

269 essive choreoathetoid movements, dysarthria, dysphagia, spastic paralysis, and behavioral dementia in

270 ity (EPX) were significantly associated with dysphagia (strongest r = 0.37, P = .02).

271 iers to successful dining for residents with dysphagia such as the importance of positive social conn

272 had a numerical reduction in scores from the dysphagia symptom diary (P = .0733).

273 Patients completed a daily dysphagia symptom diary through week 16 and patient-repo

274 Co-primary outcomes were change in Dysphagia Symptom Questionnaire (DSQ) score from baselin

275 d (eos/hpf) and a validated dysphagia score (dysphagia symptom questionnaire [DSQ]) at week 8.

276 nly one phenotype of a broader 'inflammatory dysphagia syndrome' spectrum.

277 eyes and mouth, difficulty chewing, and mild dysphagia that worsened throughout the day.

278 Interestingly, dysphagia, the main symptom of adult EoE patients follow

279 ation to allow the causes of non-obstructive dysphagia to be identified, including functional dysphag

280 e of 1 to 7) worsened from 2.9 +/- 1.5 (mild dysphagia) to 4.1 +/- 0.9 (mild/moderate dysphagia).

281 Both patients exhibited dysarthria, dysphagia, tongue atrophy, neck extensor weakness, and w

282 ariate hazard ratio for 90-day mortality for dysphagia was 3.74 (95% CI, 2.01-6.95; p < 0.001).

283 At 1 year after therapy, observer-rated dysphagia was absent or minimal (scores 0 to 1) in all p

284 Dysphagia was diagnosed in 6 and mild voice abnormalitie

285 Bedside screening for dysphagia was performed within 3 hours after extubation

286 Dysphagia was seen to decrease over time (58% at <2 year

287 Dysphagia was significantly less common after surgery (p

288 The incidence of postoperative dysphagia was similar in the 2 groups, however, signific

289 udy of adults with active EoE (2 episodes of dysphagia/week with peak esophageal eosinophil density o

290 ned with warning symptoms of malignancy (eg, dysphagia, weight loss, bleeding) and those with other m

291 The odds of postoperative dysphagia were 0.06 (95% CI, 0.03-0.12) for myotomy only

292 onstrated therapeutic promise in post-stroke dysphagia when applied contralaterally.

293 With the exception of dysphagia, which improved over time, esophagectomy was a

294 lower reintervention rates for postoperative dysphagia, while providing similar reflux control compar

295 The most common presenting symptom is dysphagia with associated esophageal stricture formation

296 ination of severe parkinsonism, near mutism, dysphagia with choking, vertical supranuclear gaze palsy

297 or chemotherapy for long-term palliation of dysphagia with good quality of life.

298 o discuss the recent trends in palliation of dysphagia with promising results and the most suitable t

299 al swallowing neurophysiology in post-stroke dysphagia with therapeutic effects which are critically

300 All measures of dysphagia worsened soon after therapy; observer-rated an