ライフサイエンスコーパス: polyneuropathy

1 peripheral neuropathy (familial amyloidotic polyneuropathy).

2 ch as L55P (associated with familial amyloid polyneuropathy).

3 physiological findings of peripheral sensory polyneuropathy.

4 idant that is used in patients with diabetic polyneuropathy.

5 onduction parameters in participants without polyneuropathy.

6 ic syndrome and its separate components with polyneuropathy.

7 th gangliosides at peripheral nerves causing polyneuropathy.

8 evelopment of vincristine-induced peripheral polyneuropathy.

9 ) is an acute postinfectious immune-mediated polyneuropathy.

10 ay reduce the prevalence of critical illness polyneuropathy.

11 es: Toronto consensus definition of probable polyneuropathy.

12 tosomal dominant distal symmetric peripheral polyneuropathy.

13 gth-dependent mixed demyelinating and axonal polyneuropathy.

14 ic testing showed a motor and sensory axonal polyneuropathy.

15 nt testing in patients with distal symmetric polyneuropathy.

16 ry testing in patients with distal symmetric polyneuropathy.

17 development of dysphagia in critical illness polyneuropathy.

18 d induced a sensory and predominantly axonal polyneuropathy.

19 while undergoing prospective assessments for polyneuropathy.

20 he TTR gene are involved in familial amyloid polyneuropathy.

21 ere most and least susceptible to paclitaxel polyneuropathy.

22 n implicated in the pathogenesis of diabetic polyneuropathy.

23 of familial chylomicronemia and TTR-mediated polyneuropathy.

24 e from measured data to predict the onset of polyneuropathy.

25 enes are the cause of rare familial forms of polyneuropathy.

26 nd Parkinson's diseases and familial amyloid polyneuropathy.

27 tic marker in transthyretin familial amyloid polyneuropathy.

28 ing amyloid fibril formation, known to cause polyneuropathy.

29 BG imaging in transthyretin familial amyloid polyneuropathy.

30 delayed gross motor development, ataxia, and polyneuropathy.

31 ation approved to treat TTR familial amyloid polyneuropathy.

32 l TTR mutants are linked to familial amyloid polyneuropathy.

33 ysis, and/or later-onset axonal sensorimotor polyneuropathy.

34 inct from chronic inflammatory demyelinating polyneuropathy.

35 drome and chronic inflammatory demyelinating polyneuropathy.

36 elial growth factor (VEGF) to treat diabetic polyneuropathy.

37 At baseline, 20% of patients had sensory polyneuropathy.

38 sociated glycoprotein antibody demyelinating polyneuropathy.

39 r detecting loss in sensitivity and onset of polyneuropathy.

40 e a diagnosis of a superimposed inflammatory polyneuropathy.

41 ritical in the development of distal sensory polyneuropathy.

42 verity of neuropathic pain in distal sensory polyneuropathy.

43 e detection and monitoring of distal sensory polyneuropathy.

44 tolerance is being explored as it relates to polyneuropathy.

45 ndrome or chronic inflammatory demyelinating polyneuropathy.

46 on distal symmetric sensory and sensorimotor polyneuropathy.

47 dose, and time-dependent axonal sensorimotor polyneuropathy.

48 develops a spontaneous autoimmune peripheral polyneuropathy.

49 le systemic amyloidosis and familial amyloid polyneuropathy.

50 weakness separately from overall severity of polyneuropathy.

51 ile systemic amyloidosis or familial amyloid polyneuropathy.

52 pathological changes typical of diphtheritic polyneuropathy.

53 icant beneficial effect of rhNGF on diabetic polyneuropathy.

54 te-onset autosomal-dominant parkinsonism and polyneuropathy.

55 tion of painful sensory symptoms in diabetic polyneuropathy.

56 tary transthyretin-mediated amyloidosis with polyneuropathy.

57 tary transthyretin-mediated amyloidosis with polyneuropathy.

58 may be beneficial in human diabetic sensory polyneuropathy.

59 disease that presents with cardiomyopathy or polyneuropathy.

60 uropathy and to detect the onset of diabetic polyneuropathy.

61 and 1 had chronic inflammatory demyelinating polyneuropathy.

62 diagnosed chronic inflammatory demyelinating polyneuropathy.

63 th impaired nerve function in people without polyneuropathy.

64 ctions in the course of familial amyloidotic polyneuropathy.

65 ecific components of metabolic syndrome with polyneuropathy.

66 polyneuropathy and possibly other peripheral polyneuropathies.

67 e disease characterized by sensory and motor polyneuropathies.

68 various peripheral nerve antigens and immune polyneuropathies.

69 It is also the target of autoantibodies in polyneuropathies.

70 ween CD and acute inflammatory demyelinating polyneuropathy (0.8; 0.3-2.1; P = .68).

71 Among the 2892 patients with polyneuropathy (1364 women and 1528 men; mean [SD] age,

72 ; multiple sclerosis, 2 (CI: 2, 3); diabetic polyneuropathy, 2 (CI: 1, 3); compressive mononeuropathi

73 due to muscle weakness and not to worsening polyneuropathy; (2) in multivariate analysis, duration o

74 230); shingles, 140 (CI: 104, 184); diabetic polyneuropathy, 54 (CI: 33, 83); compressive neuropathie

75 imab in patients with anti-MAG demyelinating polyneuropathy (A-MAG-DP).

76 y-somatic nervous system underlie peripheral polyneuropathy, a common complication of diabetes.

77 gy to halt neurodegeneration associated with polyneuropathy, according to recent placebo-controlled c

78 riants of chronic inflammatory demyelinating polyneuropathy, account for a proportion of LMN presenta

79 teria, with acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy

80 ntly in the acute inflammatory demyelinating polyneuropathy (AIDP) type of GBS or in central nervous

81 ents with chronic inflammatory demyelinating polyneuropathy, an autoimmune disease of the peripheral

82 tment-related serious AEs included 2 grade 3 polyneuropathies and 1 grade 3 edema.

83 The evaluation of demyelinating polyneuropathies and the data for treatment of inflammat

84 tor deficient mouse (dbdb) model of diabetic polyneuropathy and 2) superoxide dismutase 1 knockout (S

85 aluable both for diagnosis of distal sensory polyneuropathy and as a predictor of the condition occur

86 In conclusion, axonal sensory-motor polyneuropathy and autonomic neuropathy are commonly see

87 to provide a therapeutic effect in models of polyneuropathy and chronic regional pain.

88 for a patient presenting with demyelinating polyneuropathy and concurrent papilledema.

89 long-term opioid therapy among patients with polyneuropathy and controls.

90 ogenesis of the most common familial amyloid polyneuropathy and familial amyloid cardiomyopathy mutat

91 TTR mutants lead to familial amyloidotic polyneuropathy and familial amyloid cardiomyopathy, with

92 mbalance toward inflammation predisposing to polyneuropathy and foot ulcers.

93 homechanisms underlying chemotherapy-induced polyneuropathy and for the development of novel therapeu

94 t reported in HSAN IE-large and small fibres polyneuropathy and lower limbs oedema.

95 zing the prevalence and severity of diabetic polyneuropathy and makes research into the deleterious e

96 has been shown to have beneficial effects on polyneuropathy and on the parameters of oxidative stress

97 rom 2 unrelated families with primary axonal polyneuropathy and optic atrophy.

98 a rare plasma cell dyscrasia presenting with polyneuropathy and other systemic findings.

99 on to prevent vincristine-induced peripheral polyneuropathy and possibly other peripheral polyneuropa

100 hown the relationship between distal sensory polyneuropathy and the use of neurotoxic antiretroviral

101 of long-term opioid use among patients with polyneuropathy and to assess the association of long-ter

102 cted of prescriptions given to patients with polyneuropathy and to controls in ambulatory practice be

103 sed framework to identify the probability of polyneuropathy and to detect the onset of diabetic polyn

104 nd a discharge diagnosis of critical illness polyneuropathy and/or myopathy along with adult ICU prop

105 of a discharge diagnosis of critical illness polyneuropathy and/or myopathy and the need for effectiv

106 th a discharge diagnosis of critical illness polyneuropathy and/or myopathy had fewer 28-day hospital

107 e, a discharge diagnosis of critical illness polyneuropathy and/or myopathy is strongly associated wi

108 ut a discharge diagnosis of critical illness polyneuropathy and/or myopathy, patients with a discharg

109 th a discharge diagnosis of critical illness polyneuropathy and/or myopathy, we matched 3,436 of thes

110 ve a discharge diagnosis of critical illness polyneuropathy and/or myopathy.

111 increase the diagnostic yield in late-onset polyneuropathies, and it will be tempting to explore whe

112 V30M mutant associated with familial amyloid polyneuropathy, and Abeta42 associated with Alzheimer's

113 utants exhibit hyperexcitability, peripheral polyneuropathy, and axonal degeneration reminiscent of C

114 and ICU-acquired weakness, critical illness polyneuropathy, and critical illness myopathy.

115 enile systemic amyloidosis, familial amyloid polyneuropathy, and familial amyloid cardiomyopathy.

116 enile systemic amyloidosis, familial amyloid polyneuropathy, and familial amyloid cardiomyopathy.

117 revalence of baseline and treatment-emergent polyneuropathy, and identify molecular markers associate

118 syndrome, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy and as s

119 c therapies for neuropathic pain in diabetic polyneuropathy appear promising.

120 Axonal polyneuropathies are a frequent cause of progressive dis

121 Sensory polyneuropathies are the most frequent neurological comp

122 sible for chronic inflammatory demyelination polyneuropathy are broad and may include dysfunctions at

123 s of and differential diagnosis for diabetic polyneuropathy are reviewed herein.

124 ion was used to model the primary outcome of polyneuropathy as a function of the components of metabo

125 ur single-center study shows genetic sensory polyneuropathies associated with progressive neurodegene

126 y is that of a symmetrical, length-dependent polyneuropathy associated with sensory or autonomic symp

127 splantation is effective in familial amyloid polyneuropathy associated with variant transthyretin, be

128 he L55P transthyretin (TTR) familial amyloid polyneuropathy-associated variant is distinct from the o

129 rade 3 cytokine release syndrome and grade 3 polyneuropathy, both of which resolved.

130 ariant of chronic inflammatory demyelinating polyneuropathy but that multifocal motor neuropathy is d

131 idney disease prevents worsening of diabetic polyneuropathy, but neuropathic improvement is delayed a

132 n association between metabolic syndrome and polyneuropathy, but the precise components that drive th

133 Diabetes mellitus is a known risk factor for polyneuropathy, but the role of pre-diabetes and metabol

134 Indeed, small-fiber-predominant polyneuropathies cause CRPS-like abnormalities, and path

135 abnormal neonatal cry, hypotonia, epilepsy, polyneuropathy, cerebral gray matter atrophy), visual im

136 Chronic inflammatory axonal polyneuropathy (CIAP) is defined on the basis of the cli

137 e the aetiology of chronic idiopathic axonal polyneuropathy (CIAP), 50 consecutive patients were comp

138 n between chronic inflammatory demyelinating polyneuropathy (CIDP) and diabetes is uncertain despite

139 (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) are conditions that affect periphe

140 atures of chronic inflammatory demyelinating polyneuropathy (CIDP) except 'motor neuropathy subtype'.

141 Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated neuropathy t

142 ents with chronic inflammatory demyelinating polyneuropathy (CIDP) need long-term intravenous immunog

143 ents with chronic inflammatory demyelinating polyneuropathy (CIDP) were compared with 10 healthy subj

144 ents with chronic inflammatory demyelinating polyneuropathy (CIDP), CIDP associated with human immuno

145 trophy in chronic inflammatory demyelinating polyneuropathy (CIDP), magnetic resonance neurography wi

146 mimicking chronic inflammatory demyelinating polyneuropathy (CIDP).

147 n disease chronic inflammatory demyelinating polyneuropathy (CIDP).

148 disease, chronic inflammatory demyelinating polyneuropathy (CIDP).

149 enesis of chronic inflammatory demyelinating polyneuropathy (CIDP).

150 weakness and atrophy due to critical illness polyneuropathy (CIP), an axonal neuropathy associated wi

151 d in the etiology of the symmetrical sensory polyneuropathy commonly associated with diabetes.

152 enes is also associated with common forms of polyneuropathy-considered "acquired" in medical parlance

153 outcomes, and mortality among patients with polyneuropathy could influence disease-specific decision

154 ortionate contribution from critical illness polyneuropathy/critical illness myopathy and severe seps

155 dies examining patients for critical illness polyneuropathy/critical illness myopathy and those with

156 Sensory polyneuropathy developed during treatment in 64% of pati

157 esembling chronic inflammatory demyelinating polyneuropathy develops spontaneously in NOD mice with a

158 l contact for head injury, stroke, epilepsy, polyneuropathy, diseases of myoneural junction, Parkinso

159 n may contribute to nerve damage in diabetic polyneuropathy (DN).

160 rophysiology that a progressive sensorimotor polyneuropathy does indeed segregate with the mutation,

161 isms underlying painful symptoms in diabetic polyneuropathy (DPN) are poorly understood.

162 erations of nerve microstructure in diabetic polyneuropathy (DPN) by magnetic resonance (MR) neurogra

163 etic resonance neurography (MRN) in diabetic polyneuropathy (DPN) have found proximal sciatic nerve l

164 tabolic syndrome that contribute to diabetic polyneuropathy (DPN) in type 2 diabetes mellitus (T2DM),

165 BackgroundDiabetic polyneuropathy (DPN) is associated with loss of muscle s

166 Large-fiber diabetic polyneuropathy (DPN) leads to balance and gait abnormali

167 Distal symmetric polyneuropathy (DSP) is a prevalent condition that resul

168 Diabetic distal symmetrical peripheral polyneuropathy (DSP) results in decreased somatosensory

169 Distal symmetric polyneuropathy (DSP), associated with HIV infection, is

170 t common manifestation is distal symmetrical polyneuropathy (DSP), but many patterns of nerve injury

171 herapy increased the risk for distal sensory polyneuropathy (DSPN) in subjects with human immunodefic

172 diabetes, in particular distal sensorimotor polyneuropathy (DSPN), is unclear.

173 measures are lower in diabetic sensorimotor polyneuropathy (DSPN).

174 Familial amyloid polyneuropathy (FAP) associated with mutations in the ge

175 tetramers including two familial amyloidotic polyneuropathy (FAP) causing variants (V30M and L55P), a

176 thy is a major component of familial amyloid polyneuropathy (FAP) due to mutated transthyretin, with

177 Familial amyloidotic polyneuropathy (FAP) has a high prevalence in Portugal,

178 Familial amyloid polyneuropathy (FAP) is a neurodegenerative disorder ass

179 Transthyretin (TTR)-related familial amyloid polyneuropathy (FAP) is an autosomal dominant neurologic

180 TR) in Indian patients with familial amyloid polyneuropathy (FAP) is described.

181 DLT using livers from familial amyloidotic polyneuropathy (FAP) patients is a well-described techni

182 are early presentations of familial amyloid polyneuropathy (FAP) with transthyretin (TTR) mutations.

183 tations associated with familial amyloidotic polyneuropathy (FAP), a neurodegenerative disease charac

184 In the most common familial amyloid polyneuropathy (FAP), transthyretin (TTR) displays this

185 (1) transthyretin (TTR) familial amyloidotic polyneuropathy (FAP; n = 20), (2) TTR mutation carriers

186 ve regeneration, early diagnosis of diabetic polyneuropathy, followed by tight glycemic control with

187 ion is neuropathy, of which distal symmetric polyneuropathy (for the purpose of this Primer, referred

188 the human neurodegenerative disorder PHARC (polyneuropathy, hearing loss, ataxia, retinosis pigmento

189 1487 showed clearly symptoms associated with polyneuropathy, hearing loss, cerebellar ataxia, RP, and

190 drome, a neurodegenerative disease including polyneuropathy, hearing loss, cerebellar ataxia, RP, and

191 le systemic amyloidosis and familial amyloid polyneuropathy), immunoglobulin light chains (light-chai

192 nerve conduction studies indicated an axonal polyneuropathy in 14 percent.

193 a is a risk factor for development of axonal polyneuropathy in critically ill patients and since insu

194 the most prevalent cause of familial amyloid polyneuropathy in heterozygotes, whereas a Thr119 --> Me

195 y that mimics vincristine-induced peripheral polyneuropathy in humans.

196 evelopment of vincristine-induced peripheral polyneuropathy in mice.

197 ly reduces the incidence of distal symmetric polyneuropathy in patients with type 1 diabetes but not

198 electrodiagnostic data of confirmed sensory polyneuropathy in subjects at a tertiary-care Children's

199 a 52-year-old woman who has had progressive polyneuropathy in the setting of diabetes for the past 8

200 Grade </=2 polyneuropathy increased from 19% at baseline to 52% at

201 Polyneuropathy increased the likelihood of long-term opi

202 sease and chronic inflammatory demyelinating polyneuropathy indicate that the association is more fre

203 of 'immunotherapy responding chronic axonal polyneuropathy (IR-CAP)'.

204 dyslipidaemia, are strongly associated with polyneuropathy, irrespective of the presence of diabetes

205 Peripheral polyneuropathy is a common and dose-limiting side effect

206 Critical illness polyneuropathy is a common disorder in the neurological

207 Chronic inflammatory demyelinating polyneuropathy is a debilitating autoimmune disease char

208 Polyneuropathy is a frequent and potentially severe side

209 Transthyretin familial amyloid polyneuropathy is a hereditary form of amyloidosis chara

210 Chronic inflammatory demyelination polyneuropathy is a heterogeneous and treatable immune-m

211 le consistent with previous critical illness polyneuropathy is almost invariable and can be found up

212 Diabetic peripheral polyneuropathy is associated with decrements in motor/se

213 Familial amyloidotic polyneuropathy is characterized by poor functional recov

214 Conclusions and Relevance: The prevalence of polyneuropathy is high in obese individuals, even those

215 prevalence of dysphagia in critical illness polyneuropathy is not known.

216 Polyneuropathy is one of the most common painful conditi

217 e incidence of HIV-associated distal sensory polyneuropathy is reduced.

218 Distal symmetrical polyneuropathy is the most common form of HIV infection-

219 eady in clinical trials for familial amyloid polyneuropathy, is a strong candidate for therapeutic in

220 cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzym

221 gs raise the possibility that other acquired polyneuropathies may also be codetermined by genetic eti

222 h severe polyneuropathy (sDPN), 13 with mild polyneuropathy (mDPN), and 25 without polyneuropathy (nD

223 In participants without polyneuropathy, metabolic syndrome associated with lower

224 Efficacy assessments included measures of polyneuropathy (modified Neuropathy Impairment Score +7

225 syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and amyotro

226 syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and some pa

227 s of amyloid fibrils of familial amyloidotic polyneuropathy mutant TTR suggest a structure similar to

228 west incidence of confirmed distal symmetric polyneuropathy (n = 123), confirmed distal symmetric pol

229 = 20; 48%) included infections (n = 14) and polyneuropathy (n = 2); treatment-related serious AEs in

230 polyradiculoneuropathy (CIDP: N=20); amyloid polyneuropathy (N=20); intraneural B-cell lymphoma (N=20

231 h mild polyneuropathy (mDPN), and 25 without polyneuropathy (nDPN)-along with 30 healthy control subj

232 e major expressions of varieties of diabetic polyneuropathies needing improved assessments for clinic

233 OLT was uneventful, and he developed neither polyneuropathy nor exacerbation of photosensitivity.

234 th painful mononeuropathies or an asymmetric polyneuropathy of acute or subacute onset.

235 Pure sensory polyneuropathy of genetic origin is rare in childhood an

236 The polyneuropathy of the GBS affects one to four humans per

237 t common example is that of familial amyloid polyneuropathy, of particular concern for the clinician

238 Inherited polyneuropathies often go undiagnosed.

239 thy was seen more commonly than motor axonal polyneuropathy on nerve conduction studies.

240 itive Romberg's test and large fiber sensory polyneuropathy on sensory nerve conduction studies in al

241 19 index case subjects diagnosed with axonal polyneuropathies or neurodegenerative conditions involvi

242 the 4 affected members of the RP-1292 had no polyneuropathy or ataxia, and the sensorineural hearing

243 Metabolic syndrome was associated with polyneuropathy (OR 1.92, 95% CI 1.09 to 3.38), with a st

244 Diabetes was associated with polyneuropathy (OR 3.01, 95% CI 1.60 to 5.65), while imp

245 s and early treatment prevents disability in Polyneuropathy Organomegaly Endocrinopathy Monoclonal-pr

246 The POEMS syndrome (coined to refer to polyneuropathy, organomegaly, endocrinopathy, M protein,

247 Polyneuropathy, organomegaly, endocrinopathy, monoclonal

248 e (the acronym reflects the common features: Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal

249 uncommon syndromic disorder characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal

250 irus-8 (HHV8)-associated MCD (HHV8-MCD), and polyneuropathy, organomegaly, endocrinopathy, monoclonal

251 ng complications (confirmed distal symmetric polyneuropathy, overt nephropathy, or coronary artery di

252 ients were identified from the 2 ends of the polyneuropathy phenotype distribution: patients that wer

253 ns and caused a more severe distal symmetric polyneuropathy phenotype.

254 onic Coombs-negative hemolysis and relapsing polyneuropathy presenting as chronic inflammatory demyel

255 [SD] age, 67.5 [16.5] years), patients with polyneuropathy received long-term opioids more often tha

256 ortality were compared between patients with polyneuropathy receiving long-term opioid therapy (>/=90

257 utcomes were more common among patients with polyneuropathy receiving long-term opioids, including de

258 pioid therapy (>/=90 days) and patients with polyneuropathy receiving shorter durations of opioid the

259 In general, treatment options for diabetic polyneuropathy remain primarily symptomatic.

260 enesis of chronic inflammatory demyelinating polyneuropathy remain still fragmentary and insufficient

261 cdh10 overexpression in familial amyloidotic polyneuropathy represents a protective or deleterious re

262 ile systemic amyloidosis or familial amyloid polyneuropathy, respectively.

263 Chronic inflammatory demyelinating polyneuropathy results from autoimmune destruction of th

264 ican family with dominantly inherited axonal polyneuropathy reveals a phenotype similar to those in p

265 opathy (n = 123), confirmed distal symmetric polyneuropathy risk increased fivefold for those with th

266 the development of a spontaneous autoimmune polyneuropathy (SAP), which resembles the human disease

267 abetes (n = 49) were included-11 with severe polyneuropathy (sDPN), 13 with mild polyneuropathy (mDPN

268 An acute or subacute demyelinating polyneuropathy should be considered a potential adverse

269 istory of chronic inflammatory demyelinating polyneuropathy, Sjogren's syndrome, and systemic lupus e

270 Objectives: To determine the prevalence of polyneuropathy stratified by glycemic status in well-cha

271 nt with the acute inflammatory demyelinating polyneuropathy subtype of the Guillain-Barre syndrome.

272 e model of HIV-associated distal symmetrical polyneuropathy that can be used for investigating the ro

273 s on the mitochondrion may be related to the polyneuropathy that develops in these patients.

274 ment of a distal, sensory predominant axonal polyneuropathy that mimics vincristine-induced periphera

275 g of chronic symmetric sensorimotor diabetic polyneuropathy, the most common and problematic of chron

276 cy for the treatment of TTR familial amyloid polyneuropathy, the most common familial TTR amyloid dis

277 and therapeutic advances in distal symmetric polyneuropathy, the most common subtype of peripheral ne

278 rogression of transthyretin familial amyloid polyneuropathy, there are no approved pharmacologic ther

279 requent among patients with critical illness polyneuropathy treated in the ICU.

280 ress some of the challenges of past diabetic polyneuropathy trials.

281 tment of Transthyretin Type Familial Amyloid Polyneuropathy (TTR-FAP) and demonstrated a slowing of d

282 nt feature of transthyretin familial amyloid polyneuropathy (TTR-FAP).

283 Familial amyloid polyneuropathy type I is an autosomal dominant disorder

284 om patients with MS, Parkinson, Epilepsy and Polyneuropathy using both the aptasensor and commercial

285 prevalence of dysphagia in critical illness polyneuropathy using fiberoptic endoscopic evaluation of

286 ation of progressive spastic paraparesis and polyneuropathy, variably associated with behavioral chan

287 The prevalence of polyneuropathy was 3.8% in lean controls (n = 2), 11.1%

288 ointestinal (12%), and skin disorders (10%); polyneuropathy was infrequent (1%).

289 ities, an independent measure of severity of polyneuropathy, was not significantly worse and, in fact

290 Diabetic patients with polyneuropathy were randomized to receive a VEGF-to-plac

291 ents, and often favour a diagnosis of axonal polyneuropathy, whereas muscle histology, where availabl

292 s, including retinopathy, renal disease, and polyneuropathy, which are the topics of this review.

293 the disease: transthyretin familial amyloid polyneuropathy, which primarily affects the peripheral n

294 Patients with polyneuropathy who were receiving long-term opioids had

295 n age 70.0, 54.5% females) were screened for polyneuropathy with a questionnaire, neurological examin

296 nt axonal, predominantly sensory, peripheral polyneuropathy with an onset in early adulthood.

297 el to investigate the association of non-CMT polyneuropathy with CMT genes.

298 ive or relapsing symmetrical or asymmetrical polyneuropathy with duration of progression >2 months; (

299 genetic causes of diverse forms of inherited polyneuropathies without genetic diagnosis.

300 ter LTx, as reported to the Familial Amyloid Polyneuropathy World Transplant Registry (FAPWTR).