ライフサイエンスコーパス: neuropathy

1 neuropathy, for example, cardiomyopathy and neuropathy.

2 of H3K36 is linked to the pathogenesis of a neuropathy.

3 any sensory disorders such as pain, itch and neuropathy.

4 es with therapeutic value against this toxic neuropathy.

5 cular with the development of Parkinson-like neuropathy.

6 t epiretinal membrane and glaucomatous optic neuropathy.

7 inc finger) domain in Schwann cells causes a neuropathy.

8 of bioenergetic loss in cell models of optic neuropathy.

9 ard an antigen-specific therapy for anti-MAG neuropathy.

10 outcomes were nephropathy, retinopathy, and neuropathy.

11 has been associated with hereditary sensory neuropathy.

12 ncers, thromboembolic events, and peripheral neuropathy.

13 minimize adverse events, such as peripheral neuropathy.

14 n-induced retinopathy, maculopathy, or optic neuropathy.

15 drug which induces a serious and intractable neuropathy.

16 and is the most common hereditary peripheral neuropathy.

17 rs, and in patients with painful small-fibre neuropathy.

18 were related to the presence and severity of neuropathy.

19 mbranes, with and without glaucomatous optic neuropathy.

20 gnaling can contribute to the development of neuropathy.

21 bitory dysfunction in human painful diabetic neuropathy.

22 subjects and patients with painless diabetic neuropathy.

23 sting of mild cytopenias with no significant neuropathy.

24 er acute or chronic demyelinating autoimmune neuropathy.

25 clinical syndromes in addition to peripheral neuropathy.

26 3 patients developed an EVD-associated optic neuropathy.

27 of disease severity in subjects with amyloid neuropathy.

28 to myelinate, resulting in severe peripheral neuropathy.

29 o the clinical phenotype in painful diabetic neuropathy.

30 insight into such disease states as diabetic neuropathy.

31 ic testing in patients with this acute optic neuropathy.

32 ent, cardiac and GI symptoms, and peripheral neuropathy.

33 nsory testing were consistent with a sensory neuropathy.

34 n ulcers, glomerulonephritis, and peripheral neuropathy.

35 siological and structural indices of sensory neuropathy.

36 nhibits macrophage activation and attenuates neuropathy.

37 drome (GBS) is an immune-mediated peripheral neuropathy.

38 esent in the SN, the region most affected by neuropathy.

39 inase elevation, and 1 (4.8%) ischemic optic neuropathy.

40 ical histories spanning narcolepsy to axonal neuropathy.

41 c and develop insulin resistance and sensory neuropathy.

42 drugs to treat tactile-driven pain following neuropathy.

43 g neuropathic pain disorder due to a sensory neuropathy.

44 development of bilateral glaucomatous optic neuropathy.

45 to fully counteract the oxaliplatin-induced neuropathy.

46 ve fibre density consistent with small fibre neuropathy.

47 insights into the pathogenesis of peripheral neuropathy.

48 ered for the novel indication of human optic neuropathy.

49 cobacterial diseases in producing peripheral neuropathy.

50 aocular pressure regulation and glaucomatous neuropathy.

51 lopment of therapies for peripheral diabetic neuropathy.

52 ry spastic paraplegia and hereditary sensory neuropathy.

53 ical features of copper-deficient peripheral neuropathy.

54 nderstanding and treating sensory peripheral neuropathies.

55 f cell-based therapies and models of enteric neuropathies.

56 neurotrophic support in models of peripheral neuropathies.

57 linked to phenotypically distinct peripheral neuropathies.

58 ontribute to a better understanding of these neuropathies.

59 fy axonal degeneration in several peripheral neuropathies.

60 esult in an increased risk for developmental neuropathies.

61 ations of SLC25A46 in patients with multiple neuropathies.

62 enetically heterogeneous group of peripheral neuropathies.

63 in the CNS and in the context of peripheral neuropathies.

64 oreover, in hereditary sensory and autonomic neuropathies.

65 c-Jun as a potential player in demyelinating neuropathies.

66 es, and has been implicated in demyelinating neuropathies.

67 emia (7% v 15%), leukopenia (26% v 25%), and neuropathy (1% v 5%).

68 edian age, 65 years), 18 patients with motor neuropathies (14 men [8.0%] and 4 women [2.3%]; median a

69 ic optic neuropathy (25%), compressive optic neuropathy (18.7%) and hereditary optic neuropathy (18.7

70 ptic neuropathy (18.7%) and hereditary optic neuropathy (18.7%).

71 daemia (21 [39%] of 54 patients), peripheral neuropathy (21 [39%] of 54 patients), and peripheral oed

72 ing neutropenia (57.5% vs 53.3%), peripheral neuropathy (23.1% vs 24.8%), and diarrhea (20.6% vs 20.7

73 he most common diagnoses were ischemic optic neuropathy (25%), compressive optic neuropathy (18.7%) a

74 nomenon (11.6% v 21.4%; P < .01), peripheral neuropathy (29.2% v 21.4%; P = .02), and obesity (25.5%

75 s were (in decreasing frequency): peripheral neuropathy, 53%; cerebellar ataxia, dysmetria, or dysart

76 sory predominant length-dependent peripheral neuropathy (71%).

77 ho experienced treatment-emergent peripheral neuropathy, 88% experienced either resolution (73%) or i

78 In the absence of neuropathy, a bortezomib-rituximab-based option is reaso

79 type 1A (CMT1A) is the most common inherited neuropathy, a debilitating disease without known cure.

80 (eg, amblyopia, nystagmus, foveopathy, optic neuropathy) accounted for residual postoperative subnorm

81 elopment in addition to optic and peripheral neuropathy across the life span.

82 tween groups; only grade 2 or higher sensory neuropathy adverse events persisted at 24 months (25 [10

83 unnel syndrome is the most common entrapment neuropathy, affecting the median nerve at the wrist.

84 Sensory and autonomic neuropathy affects the majority of type II diabetic pati

85 Sensory neuropathy (all grade 1-3) was recorded in 17 (94%) of t

86 findings compatible with acute motor axonal neuropathy (AMAN) type, and had rapid evolution of disea

87 Thirty-three patients experienced peripheral neuropathy, among whom, the majority (30 of 33, 91%) had

88 tional 79 Taiwanese pedigrees with inherited neuropathies and 163 index cases from Australian, Europe

89 e ALS and FTD groups compared with the motor neuropathies and control groups (hazard ratio [HR], 2.45

90 Fluoroquinolone-induced peripheral neuropathies and tendinopathies are well documented, but

91 misdiagnosed as glaucoma (two ischemic optic neuropathies and two congenital optic disc anomalies).

92 nd acute CF, 11 T2D patients with equivalent neuropathy and 11 non-diabetic controls.

93 ealthy controls and absent in 77 small fibre neuropathy and 167 JHS/EDS-HT patients without itch.

94 mutations may cause distal hereditary motor neuropathy and alter canonical and non-canonical functio

95 tus or chemotherapy resulting in small fibre neuropathy and associated neuropathic pain.

96 oradic patient with type 1 painless diabetic neuropathy and chronic itch.

97 nt in the WD with respect to driving enteric neuropathy and colonic dysmotility.

98 where it remains a major cause of peripheral neuropathy and disability.

99 nt models of chemotherapy-induced peripheral neuropathy and explored its mechanism of action.

100 in (PJVK) gene are thought to cause auditory neuropathy and hearing loss of cochlear origin by affect

101 al muscular atrophy, distal hereditary motor neuropathy and LMN variants of familial motor neuron dis

102 eficiency definitively proved to cause optic neuropathy and loss of vision.

103 cers are deemed neuroischaemic if peripheral neuropathy and peripheral artery disease are both presen

104 T1A) is the most common heritable peripheral neuropathy and results from a duplication on chromosome

105 These descending pathways are altered in neuropathy and the effects of excess serotonin may now b

106 opathy, for example, spasticity, the type of neuropathy and the other neurological and non-neurologic

107 betic rodents exhibiting features of painful neuropathy and the translational potential of this marke

108 ing patients for the presence of small fibre neuropathy and to assess disease progression.

109 conditions that may mimic glaucomatous optic neuropathy and to determine which most often lead to mis

110 diated disorders, including multifocal motor neuropathy and variants of chronic inflammatory demyelin

111 fferences were identified between those with neuropathy and without neuropathy (corneal nerve branch

112 nc18-1, or SNAP-25, modulate alpha-synuclein neuropathy and/or are dysregulated in Alzheimer's diseas

113 h, enucleation, radiation retinopathy, optic neuropathy, and best-corrected visual acuity (BCVA).

114 ivative (ADM_12) reverts in vivo OXA-induced neuropathy, and it is an effective antagonist of the noc

115 associated with ocular motor apraxia, axonal neuropathy, and progressive cerebellar ataxia.

116 stem-most commonly causing axonal peripheral neuropathy-and usually manifest later in life.

117 and mortality; retinopathy, nephropathy, and neuropathy; and harms.

118 Small fibre neuropathies are a heterogeneous group of disorders affe

119 Optic neuropathies are associated with death of retinal gangli

120 These neuropathies are linked to heterozygosity for missense m

121 pathogenic mechanism of the SLC25A46-related neuropathies are not fully understood.

122 ipheral neuropathy, cardiovascular autonomic neuropathy, arterial stiffness, and hypertension.

123 These data may explain why hereditary neuropathies associated with decreased laminin function

124 tials in peripheral nerves showed peripheral neuropathy associated with degeneration and demyelinatio

125 The human, neuropathy-associated IgM antibody is also shown to indu

126 Furthermore, neuropathy-associated KIF1Bbeta mutations impede cargo t

127 mouse Schwann cells (Miz1DeltaPOZ) causes a neuropathy at 90 d after birth [postnatal day (P) 90], w

128 loss (HHL) is a recently described auditory neuropathy believed to contribute to speech discriminati

129 turbations.SIGNIFICANCE STATEMENT Peripheral neuropathies can result from damage or dysregulation of

130 etic kidney disease, retinopathy, peripheral neuropathy, cardiovascular autonomic neuropathy, arteria

131 he charts of consecutive patients with optic neuropathies caused by neurophthalmological conditions s

132 ropathy is a disabling autoimmune peripheral neuropathy caused by monoclonal IgM autoantibodies that

133 V) vaccine has been used for many years, the neuropathy caused by VZV infection is still a major heal

134 Enteric nervous system neuropathy causes a wide range of severe gut motility di

135 gth-dependent sensory predominant peripheral neuropathy causing sensory ataxia is characteristic of c

136 opathy is a heterogeneous group of inherited neuropathies characterized by distal limb muscle weaknes

137 Chemotherapy-induced peripheral neuropathy (CIPN) arises from collateral damage to perip

138 Chemotherapy-induced peripheral neuropathy (CIPN) is a common adverse effect experienced

139 Chemotherapy-induced peripheral neuropathy (CIPN) is a common dose-limiting side effect

140 Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect of many

141 Chemotherapy-induced peripheral neuropathy (CIPN) is a major cause of disability in canc

142 Purpose Chemotherapy-induced peripheral neuropathy (CIPN) may persist after treatment ends and m

143 cal model of chemotherapy-induced peripheral neuropathy (CIPN), the most common treatment-limiting si

144 Late-onset axonal Charcot-Marie-Tooth neuropathy (CMT2) is an autosomal-dominantly inherited c

145 aracterized by a progressive spasticity with neuropathy, cognitive impairment and a thin corpus callo

146 monstrated in patients with painful diabetic neuropathy compared with healthy control subjects and pa

147 aged 3 to 20 years enrolled in the Inherited Neuropathies Consortium were assessed at baseline and 2

148 ed between those with neuropathy and without neuropathy (corneal nerve branch density: 95.83/mm2 for

149 -MRN correlated closely with the severity of neuropathy, demonstrating strong associations with sciat

150 also developed bilateral glaucomatous optic neuropathy despite a well-controlled intraocular pressur

151 Anterior ischemic optic neuropathy developed in one patient in the group that re

152 se type 2 (CMT-2) or distal hereditary motor neuropathy (dHMN).

153 ions of retinopathy, nephropathy, peripheral neuropathy, diabetic foot, and ischemic heart disease we

154 (3) healthy controls (n = 20), (4) diabetic neuropathy disease controls (n = 20), and (5) patients w

155 nderstand the mechanisms underlying diabetic neuropathy (DN).

156 Dysthyroid optic neuropathy (DON) is the commonest cause of blindness in

157 SWE) in the detection of diabetic peripheral neuropathy (DPN) of the tibial nerve.

158 Diabetic peripheral neuropathy (DPN) often leads to neurotrophic ulcerations

159 apy, showed promising results without severe neuropathy emerging.

160 European, and Korean distal hereditary motor neuropathy families identified the same mutation in anot

161 e additional Belgian distal hereditary motor neuropathy family of Caucasian origin.

162 hypokalaemia (six [33%]), peripheral sensory neuropathy (five [28%]), diarrhoea (five [28%]), and abd

163 edominant system involved in addition to the neuropathy, for example, cardiomyopathy and neuropathy.

164 nt neurological syndrome associated with the neuropathy, for example, spasticity, the type of neuropa

165 device discriminated eyes with glaucomatous neuropathy from healthy eyes in a clinically based setti

166 basis of the presence of glaucomatous optic neuropathy (GON) and 24-2 visual field abnormalities: ea

167 AGES) with a diagnosis of glaucomatous optic neuropathy (GON) or ocular hypertension (OHT) and at lea

168 Concurrent peripheral neuropathy has been recognised in association with coppe

169 cardiac involvement is exceedingly rare and neuropathy has not been reported.

170 glycosylation site cause Charcot-Marie-Tooth neuropathy, has abundant GlcNAc-6-O-sulfated N-glycans.

171 Mouse models of Charcot-Marie-Tooth neuropathy have indicated that low-grade secondary infla

172 n of new target antigens in the inflammatory neuropathies heralds a revolution in diagnosis, and has

173 ese findings imply that ORF7 plays a role in neuropathy, highlighting a potential strategy to develop

174 al nerve fibers can be selectively linked to neuropathy, highlighting the possibility that it is the

175 unodeficiency virus (HIV)-associated sensory neuropathy (HIV-SN) is difficult but needed for diagnosi

176 tions due to side effects such as peripheral neuropathy, hypotension, and hypersensitivity.

177 present (amyloid burden), fiber subtype, and Neuropathy Impairment Score in the Lower Limbs (NIS-LL)

178 mutations in common distal hereditary motor neuropathy-implicated genes had been excluded.

179 egnant women, causing microcephaly and other neuropathies in developing fetuses.

180 We demonstrated an age-related optic neuropathy in AD by OCT, with a significant reduction of

181 tides (ASOs) to reduce PMP22 and ameliorated neuropathy in both mouse and rat models of CMT1A.

182 ar complications including uveitis and optic neuropathy in EVD survivors, level of VA impairment in E

183 elin protein whose mutation causes inherited neuropathy in humans, is O-GlcNAcylated.

184 IIalpha as a cellular mechanism for pain and neuropathy in multiple sclerosis and IL-17 may act upstr

185 eview, we discuss the approach to peripheral neuropathy in patients with cancer and address the clini

186 Objective quantification of small fiber neuropathy in patients with human immunodeficiency virus

187 tes, suggesting the existence of small fibre neuropathy in symptomatic sites.

188 pRS) gene (WARS) that co-segregates with the neuropathy in the family.

189 The treatment of mitochondrial optic neuropathy in the US is only supportive.

190 n autosomal dominant distal hereditary motor neuropathy in which mutations in common distal hereditar

191 The diagnostic tests to identify small fibre neuropathy include skin biopsy, quantitative sensory, an

192 Peripheral neuropathies included axonal and demyelinating polyradic

193 each increase in age of 1 year, the odds of neuropathy increased 4% (P = .006).

194 irenzepine and MT7 also prevented peripheral neuropathy induced by the chemotherapeutic agents dichlo

195 ssion among neuronal cells, and probably the neuropathy induced by VZV infection.IMPORTANCE The neuro

196 d providing a new target for intervention of neuropathy induced by VZV.

197 s well as in the progression of PD and other neuropathies involving oxidative stress.

198 Peripheral neuropathy is a common finding in patients with complex

199 A major cause of peripheral neuropathy is a copy number variant involving the Periph

200 Anti-MAG (myelin-associated glycoprotein) neuropathy is a disabling autoimmune peripheral neuropat

201 Distal hereditary motor neuropathy is a heterogeneous group of inherited neuropa

202 NCE STATEMENT Painful HIV-associated sensory neuropathy is a neurological complication of HIV infecti

203 Auditory neuropathy is a significant and understudied cause of hu

204 Our findings indicate autonomic neuropathy is an early and prominent deficit in the db/d

205 The impact of this regulation in leprosy neuropathy is discussed.

206 This auditory neuropathy is not associated with synaptic loss, but rat

207 erve fibres in human patients when autonomic neuropathy is suspected.

208 typical clinical presentation of small fibre neuropathy is that of a symmetrical, length-dependent po

209 ndness worldwide and, along with other optic neuropathies, is characterized by loss of retinal gangli

210 angle glaucoma (POAG), the most common optic neuropathy, is a heritable disease.

211 CMT1X, an X-linked inherited neuropathy, is caused by mutations in GJB1, which codes

212 hereditary autosomal dominant demyelinating neuropathy known as Charcot-Marie-Tooth disease type 1A

213 uropathies, such as Leber's hereditary optic neuropathy (LHON) and Autosomal dominant optic atrophy (

214 D4v2 in patients with Leber hereditary optic neuropathy (LHON).

215 natural history of Leber's hereditary optic neuropathy (LHON).

216 eases, such as amyloid diseases, cancer, and neuropathies, making TRiC a potential therapeutic target

217 ndrial abnormalities in mutant Hsp27-induced neuropathies may be a primary cause of pathology, leadin

218 Optic neuropathies may range from non-syndromic genetic entiti

219 us avoiding the floor effect seen with other neuropathy measures.

220 ivity in demyelinating disease or peripheral neuropathies must be approached with caution.

221 diculoneuropathies (n = 2), length-dependent neuropathies (n = 1), and asymmetric vasculitic neuropat

222 plications included myopathy (n = 2), varied neuropathies (n = 4), cerebellar ataxia (n = 1), autoimm

223 3), and nonarteritic anterior ischemic optic neuropathy (n = 1) in the repositioning group, and IOP i

224 ropathies (n = 1), and asymmetric vasculitic neuropathy (n = 1).

225 (OIS), non-arteritic anterior ischemic optic neuropathy (NA-AION) and amaurosis fugax (AF).

226 h acute nonarteritic anterior ischemic optic neuropathy (NAION) and normal age-related cataract contr

227 osis of nonarteritic anterior ischemic optic neuropathy (NAION) seen in the Wilmer Eye Network system

228 risk of nonarteritic anterior ischemic optic neuropathy (NAION) than nondiabetic patients.

229 ateral non-arteritic anterior ischemic optic neuropathy (NAION) will eventually develop the same cond

230 ronic non-arteritic anterior ischaemic optic neuropathy (NAION).

231 Grade 1 to 2 neuropathy occurred in 10 patients but resolved in 5.

232 Peripheral neuropathy occurred in 11 (11%) of 104 patients receivin

233 n autosomal dominant distal hereditary motor neuropathy of a dominant-negative frameshift mutation at

234 pectrum of motor, sensory, and cranial nerve neuropathy, often with ataxia, optic atrophy and respira

235 e sclerosis with chronic demyelinating optic neuropathy on stable immunomodulatory therapy.

236 individuals develop an acute painful sensory neuropathy on sustained cold exposure is not yet known,

237 es of disability and often result in painful neuropathies or the impairment of muscle movement and/or

238 9% were LGI1-IgG seropositive (7% had solely neuropathy or pain).

239 95% CI, 1.11-4.50; P = .02), and peripheral neuropathy (OR, 2.52; 95% CI, 1.43-4.43; P = .001), but

240 on mechanism is responsible for ARS-mediated neuropathy, or if a combination of these mechanisms oper

241 Ndufs4 KO mouse model of mitochondrial optic neuropathy, papaverine and zolpidem provided significant

242 and incidence of post-cataract surgery optic neuropathy (PCSON) in the modern era.

243 in another Taiwanese distal hereditary motor neuropathy pedigree with different ancestries and one ad

244 uria were more frequent with C25; peripheral neuropathy, peripheral edema, alopecia, and nail disorde

245 CI = 1.21-1.60), and potential treatment of neuropathy (PR = 1.39; 95% CI = 1.28-1.51).

246 nological surrogate mouse model for anti-MAG neuropathy producing high levels of anti-MAG IgM was dev

247 freedom from radiation retinopathy and optic neuropathy rates were higher in the apex LD than HD grou

248 ul conditions of the distal extremities (ie, neuropathy related to human immunodeficiency virus, diab

249 genetic mutations, the cause of small fibre neuropathy remains unknown in up to 50% of cases.

250 which demonstrated a high rate of peripheral neuropathy resolution, and durable remissions in a subse

251 tients with ALS from those with inflammatory neuropathy, respectively.

252 Schwann cells causes loss of myelination and neuropathies, results attributed to loss of laminin-rece

253 From all patients, the CMT neuropathy score and secondary outcome measures were obt

254 per deficiency (<0.78 mug/mL) and peripheral neuropathy seen at the Mayo Clinic from 1985 to 2005 wer

255 based therapies for glaucoma and other optic neuropathies.SIGNIFICANCE STATEMENT Glaucoma is the most

256 arrhoea (18 [4%] vs 39 [9%]), and peripheral neuropathy (six [1%] vs 28 [6%]).

257 ilable on the natural history of small fiber neuropathy (SNF).

258 ents with audiological hallmarks of auditory neuropathy spectrum disorder, whereas all other PJVK all

259 -Marie-Tooth type-2, distal hereditary motor neuropathies, spinal muscular atrophy with parkinsonism

260 oral and histologic indicators of peripheral neuropathy, stimulated tissue NAD recovery, improved gen

261 tations in the DNAJB2 gene lead to inherited neuropathies such as Charcot-Marie-Tooth type-2, distal

262 ght in susceptible individuals lead to optic neuropathies such as normal tension glaucoma.

263 Inherited mitochondrial optic neuropathies, such as Leber's hereditary optic neuropath

264 prevented or reversed indices of peripheral neuropathy, such as depletion of sensory nerve terminals

265 Peripheral neuropathy symptoms after systemic chemotherapy for brea

266 rate category of complex inherited relapsing neuropathy syndromes, some of which may mimic Guillain-B

267 g), GG genotypes had 6.9-fold higher odds of neuropathy than CC genotypes (OR: 6.9; 95% CI: 1.31, 36.

268 ally do not elicit pain, produce pain during neuropathy that is reversed by gabapentin.

269 heterogeneous, inherited and severe optical neuropathy that originates from maldevelopment of the an

270 e been implicated in distal hereditary motor neuropathy, the genetic causes remain elusive in many fa

271 plantation in a mouse model of human enteric neuropathy, the neuronal nitric oxide synthase (nNOS(-/-

272 onditions following nerve injury or diabetic neuropathy, the slightest touch can produce pain, and he

273 hology of acquired, inflammatory, peripheral neuropathies.The identification of new target antigens i

274 r understanding of the pathobiology of these neuropathies, there continues to be a gap in the transla

275 that vitamin B12 deficiency causes an optic neuropathy through unknown mechanisms and that it is a p

276 Traumatic optic neuropathy (TON) is a devastating cause of permanent vis

277 Traumatic optic neuropathy (TON) is an acute injury of the optic nerve s

278 estionnaires and the Clinical HIV-Associated Neuropathy Tool.

279 (2) TTR mutation carriers without peripheral neuropathy (TTR-noPN; n = 10), (3) healthy controls (n =

280 Hereditary sensory and autonomic neuropathy type III, or familial dysautonomia [FD; Onlin

281 Peripheral neuropathy typically follows a length-dependent pattern,

282 clinical and electrophysiological pattern of neuropathy was a sensory predominant length-dependent pe

283 Peripheral neuropathy was seen in 44 (67%) of 66 patients in the br

284 nset severe sensory, motor and cranial nerve neuropathy we confirmed the strong genetic link between

285 onal causal gene for distal hereditary motor neuropathy, we performed exome sequencing for two affect

286 Conversely, 11.9% of the glaucomatous neuropathies were misdiagnosed as neurophthalmological d

287 In our study, isquemic and compressive optic neuropathies were the ones that most often did so.

288 red one cases of amyloidosis with peripheral neuropathy were identified, 60 primary and 41 transthyre

289 cm and without grade 2 or greater peripheral neuropathy were included in the study.

290 ly were found to have sensorimotor autonomic neuropathy, whereas 2 others had subclinical autonomic d

291 a, vomiting, nausea, fatigue, and peripheral neuropathy, whereas edema was more frequent after DC.

292 A have also been shown to cause distal motor neuropathy, whereas polymorphisms in ATP7B are associate

293 d familial episodic pain disorder or painful neuropathy, while mutations evoking larger membrane depo

294 ents with spinally mediated painful diabetic neuropathy who may respond optimally to therapies such a

295 ith acute predominantly motor, demyelinating neuropathy with conduction block, and secondary axonal d

296 ent with a sensory predominant, inflammatory neuropathy with mixed axonal and demyelinating electroph

297 Using this approach, we associated neuropathy with one of three major syndromic categories:

298 eases including hereditary motor and sensory neuropathy with proximal dominant involvement (HMSN-P).

299 MFN2 mutations cause axonal neuropathy, with associated lipodystrophy only occasiona

300 The other 4 mutations exhibit neuropathy without clinical or subclinical CNS abnormali