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1 (five [11%] patients had grade 3 peripheral neuropathy).
2 oped to prevent cisplatin induced peripheral neuropathy.
3 cluding those affected by glaucomatous optic neuropathy.
4 ncidence and severity of the later-occurring neuropathy.
5 get in the treatment of chemotherapy-induced neuropathy.
6 e most frequent recessive form of hereditary neuropathy.
7 tion (pONT) is an established model of optic neuropathy.
8 rticipants with type 2 diabetes mellitus and neuropathy.
9 orneal innervation of patients with diabetic neuropathy.
10 familial dysautonomia (FD) causes peripheral neuropathy.
11 e (CKD), peripheral artery disease (PAD) and neuropathy.
12 ient died of treatment-related cranial nerve neuropathy.
13 rebalance that significantly ameliorated the neuropathy.
14 , missense alleles cause dominant peripheral neuropathy.
15 ain in a subset of patients with small fibre neuropathy.
16 g coronary heart disease (CHD), CKD, PAD and neuropathy.
17 %) showed retinitis or uveitis without optic neuropathy.
18 educed QoL in patients with painful diabetic neuropathy.
19 sted in a mouse model of oxaliplatin-induced neuropathy.
20 ropathy than in those with painless diabetic neuropathy.
21 ed in the development of vincristine-induced neuropathy.
22 neuropathies such as Leber Hereditary Optic Neuropathy.
23 ha) against diabetic keratopathy and corneal neuropathy.
24 layer, that resembles the phenotype of optic neuropathy.
25 preserved ejection fraction, and peripheral neuropathy.
26 of visual acuity in Leber's hereditary optic neuropathy.
27 ngiectasia type 2, as well as for peripheral neuropathy.
28 t associate with high risk of retinopathy or neuropathy.
29 sease (CMT) is a length-dependent peripheral neuropathy.
30 ad polymicrogyria, and four had a peripheral neuropathy.
31 he toxic gain-of-function that underlies the neuropathy.
32 tment for pain in Nav1.7-related small fibre neuropathy.
33 CMT2A), a dominant axonal form of peripheral neuropathy.
34 all patients with an acquired demyelinating neuropathy.
35 lion cell (RGC) death, the endpoint of optic neuropathy.
36 miting neurotoxicity resulting in peripheral neuropathy.
37 cancer, but frequently result in peripheral neuropathy.
38 There was no grade 3 to 4 peripheral neuropathy.
39 line arrays) consistent with a mitochondrial neuropathy.
40 ol pathway previously implicated in diabetic neuropathy.
41 erapeutic agent, produces painful peripheral neuropathy.
42 h for the management of chemotherapy-induced neuropathy.
43 auses multiple forms of inherited peripheral neuropathy.
44 L81R and p.R212W mutations can lead to optic neuropathy.
45 amentous and tendon injuries, and entrapment neuropathies.
46 ffect mitochondrial function result in optic neuropathies.
47 ogression of Obesity and Diabetes associated-neuropathies.
48 can contribute to the development of painful neuropathies.
49 neuroinflammation pain associated with mixed neuropathies.
50 abnormalities account for ~80% of hereditary neuropathies.
51 sent a general treatment for hypomyelinating neuropathies.
52 uring Wallerian degeneration associated with neuropathies.
53 hes to prevent or relieve obesity-associated neuropathies.
54 ying the pathobiology of mitochondrial optic neuropathies.
55 euritis, and compressive and inherited optic neuropathies.
56 dural pain (2.2% [seven of 320]), peripheral neuropathy (0.9% [three of 320]), and temporary paresthe
57 7 patients in the placebo group), peripheral neuropathy (25 [6%] vs 12 [3%]), decreased neutrophil co
59 , diarrhoea (23 [5%] vs 16 [3%]), peripheral neuropathy (44 [8%] vs four [<1%]), dyspnoea (nine [2%]
60 lateral sclerosis or distal hereditary motor neuropathy (56%), multinevritis with cranial nerve invol
62 ommon adverse events were peripheral sensory neuropathy (79%), neutropenia (76%), fatigue (74%), and
63 uptake of NCPs and the absence of peripheral neuropathy allow for repeated dosing to afford 100% tumo
64 NT Axonal degeneration is a major feature of neuropathies and nerve injuries and occurs via a cell au
66 ations, tumor progression, the onset of some neuropathies and other disorders have been linked to mis
68 llodynia in a rat model of cisplatin-induced neuropathy and attenuates the associated inflammatory pr
69 clinical diagnosis of cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (
72 gs identify novel contributors to peripheral neuropathy and emphasize the fundamental dependence of n
73 h a novel and potentially treatable cause of neuropathy and may contribute to a better understanding
76 loped a novel strategy to predict peripheral neuropathy and subsequently adjust the vincristine dose
77 an interval between onset of radiation optic neuropathy and the last patient visit was 34 months (24-
79 er MMN represents an axonal or demyelinating neuropathy and whether the underlying pathophysiology is
80 r and chemotherapy as a major contributor to neuropathy and will have significant and immediate impac
82 populations in histological samples of optic neuropathies, and early work in this field suggested tha
83 hemotherapy-induced, diabetic, and inherited neuropathies, and ocular disorders, such as glaucoma.
84 48 were observed only after radiation optic neuropathy, and 45 were treated with intravitreal therap
85 tified in a patient with a severe peripheral neuropathy, and a mouse model precisely recreating the m
86 urodevelopmental delay, seizures, peripheral neuropathy, and ataxia, with de novo heterozygous and bi
87 ons of low serine availability(8,9)-to drive neuropathy, and deoxysphinganine has previously been inv
89 (the most common being cytopenia, peripheral neuropathy, and heart failure) were more common in the B
90 sociated mutations exhibited mild peripheral neuropathy, and homozygous expression resulted in embryo
92 revalent microvascular disease (retinopathy, neuropathy, and nephropathy) and peripheral artery disea
99 ing the Sarm1 gene do not develop peripheral neuropathy as evaluated by both behavioral or pathologic
100 ide a basis for the evaluation of peripheral neuropathy as part of the clinical development of Notch
101 nisms resulting in the loss of RGCs in optic neuropathies, as well as the development of targeted the
103 ict a patient's susceptibility to peripheral neuropathy at different time points during the treatment
105 ed with severe bortezomib-induced peripheral neuropathy (BiPN) in patients with multiple myeloma (MM)
106 el of blast-induced indirect traumatic optic neuropathy (bITON) showed that PPS and PLGA MP-mediated
107 of the ER (ER-phagy) is implicated in human neuropathy but is poorly understood beyond a few autopha
108 antibodies have been associated with sensory neuropathy, but many questions remain regarding their us
109 ne mutations cause human Charcot-Marie-Tooth neuropathy, but the mature myelin sheath assembly mechan
110 uggest that MUFAs reverse the progression of neuropathy by protecting mitochondrial function and tran
112 cement therapy after the onset of peripheral neuropathy can provide a therapeutic benefit in the Gjb1
114 cohort study uses the most common entrapment neuropathy (carpal tunnel syndrome) as a human model sys
117 e gene expression and phenocopy a peripheral neuropathy caused by the HNPP-associated deletion encomp
118 type 1 (HSN1) is a rare, slowly progressive neuropathy causing profound sensory deficits and often s
119 Here, we show that in vivo expression of a neuropathy-causing TRPV4 mutant (TRPV4(R269C)) causes do
120 , unstable myelin, resulting in a peripheral neuropathy characterized by hypomyelination and progress
121 y, the periaxin-deficient mouse model of the neuropathy Charcot-Marie-Tooth 4F displays a highly path
122 nrelated families with the hereditary axonal neuropathy Charcot-Marie-Tooth disease type 2 (CMT2).
123 several subtypes of the inherited peripheral neuropathy Charcot-Marie-Tooth disease; however, the mec
126 CE STATEMENT Chemotherapy-induced peripheral neuropathy (CIPN) is a major side effect in cancer patie
131 a chronic progressive immune-mediated motor neuropathy clinically characterised by progressive asymm
132 athies (HMNs) and axonal Charcot-Marie-Tooth neuropathy (CMT2) are clinically and genetically heterog
134 sent the first evidence that chronic sensory neuropathy depends on nonlinear interactions between can
135 ls ameliorated, rather than worsened, S63del neuropathy despite reduced levels of phosphorylated eIF2
136 n contrast, nSIRT1OE prevented a HFD-induced neuropathy despite the animals remaining hyperglycaemic.
137 um kinase (PERK) also ameliorated the S63del neuropathy, despite reduced levels of eIF2alpha phosphor
138 n clinical activity score, 6.2) but no optic neuropathy, diabetes, recent steroid treatment, previous
139 the nerve was positively correlated with the neuropathy disability score (r = 0.23; 95% CI: 0.03, 0.3
140 nerve lesions correlated positively with the neuropathy disability score (r = 0.37; 95% confidence in
142 ed developmental mRNA-abundance profiles and neuropathy disease genes illustrates the utility of this
144 e optic disc had the largest impact on optic neuropathy, dose to 20% of cornea had the largest impact
145 d the risk of developing diabetic peripheral neuropathy (DPN) and cardiovascular autonomic neuropathy
152 iting (seven [5%] vs seven [5%]), peripheral neuropathy (eight [6%] vs five [4%]), and pain (six [4%]
153 hase 2 dose, 19 (27%) had grade 1 peripheral neuropathy, eight (11%) grade 2, and two (3%) grade 3.
156 of 48 in the RVd-elotuzumab group), sensory neuropathy (four [8%] of 52 in the RVd group, six [13%]
158 eg, hypoxic encephalopathy and critical care neuropathy) from those caused directly or indirectly by
160 for the probability of glaucomatous optical neuropathy (GON), and estimates of cup-to-disc (C/D) rat
162 field abnormality but not glaucomatous optic neuropathy had a higher tendency to be missed by deep le
165 ects, dopaminergic neuronal loss, peripheral neuropathy, impaired respiratory chain complex III activ
166 ncluded measures of polyneuropathy (modified Neuropathy Impairment Score +7 [mNIS+7]), quality of lif
168 (2) electrophysiological evidence of axonal neuropathy in at least two nerves without any evidence o
170 t causes Charcot-Marie-Tooth type 1B (CMT1B) neuropathy in humans and a similar demyelinating neuropa
172 also underlies paclitaxel-induced peripheral neuropathy in mammals, indicating that epidermal mitocho
175 female S63del mice showed a worsening of the neuropathy in the absence of eIF2alpha phosphorylation.
176 ment of severe retinopathy, nephropathy, and neuropathy in those treated intensively compared with co
177 opathy in humans and a similar demyelinating neuropathy in transgenic mice, is instead retained the E
178 are no established predictors of peripheral neuropathy incidence during the early stage of chemother
181 ould benefit patients affected by peripheral neuropathies, including Charcot-Marie-Tooth disease.
182 insert documents and other resources for 224 neuropathy-inducing drugs discovered that many drugs (e.
185 ing for patients with acquired demyelinating neuropathy is a cost-effective strategy allowing for ear
190 atinum-based chemotherapy-induced peripheral neuropathy is one of the most common causes of dose redu
192 available to attenuate chemotherapy-induced neuropathy is to limit or discontinue this treatment.
193 ing or slowing the progression of peripheral neuropathy is to maintain close glycemic control, while
197 ifferent acquired or genetic causes of motor neuropathies, it is a diagnosis not to be missed since h
198 tic kidney disease, diabetic retinopathy and neuropathy) lead to increased mortality, blindness, kidn
199 d, such as multiple sclerosis and peripheral neuropathies, lead to severe pathologies, illustrating m
200 cal acquired demyelinating sensory and motor neuropathy (Lewis-Sumner syndrome) and 'distal acquired
204 e Complex I disease Leber's hereditary optic neuropathy (LHON), but has been less successful in clini
205 associated with Charcot-Marie-Tooth type 2B neuropathy, markedly decreases axonal protein synthesis,
206 tients who are not susceptible to peripheral neuropathy may receive sub-therapeutic treatment due to
207 ers known as chemotherapy-induced peripheral neuropathy, mechanistic understanding and treatment rema
208 ntroversies associated with multifocal motor neuropathy (MMN) including disease pathophysiology, diag
209 lateral sclerosis (ALS) and multifocal motor neuropathy (MMN) relies on clinical examination and elec
213 iagnostic options in patients with suspected neuropathies, nerve conduction studies, and magnetic res
214 -mediated myopathies, myasthenia, peripheral neuropathies, neuromyelitis and other CNS disorders.
216 ogic diagnosis (amblyopia, strabismus, optic neuropathy, nystagmus, or retinopathy of prematurity) by
218 pected linezolid toxic effects of peripheral neuropathy (occurring in 81% of patients) and myelosuppr
219 ur findings may have direct implications for neuropathies of unknown etiology characterized by reduce
225 and emphasize the fundamental dependence of neuropathy on the systemic interaction between chemother
226 f 48 in the RVd-elotuzumab group), and motor neuropathy (one [2%] of 52 in the RVd group, four [8%] o
228 e related to chemotherapy-induced peripheral neuropathies or CNS diseases in which axonal degeneratio
232 be considered in all cases of sensory ataxic neuropathy, particularly, but not only, if cerebellar dy
233 e worldwide and is accompanied by peripheral neuropathy (PN) and an associated poorer quality of life
234 Growing evidence indicates that peripheral neuropathy (PN) is common even in the absence of diabete
235 and 'distal acquired demyelinating symmetric neuropathy', possibly having different immunopathogenesi
236 with neuro-ophthalmic manifestations, optic neuropathy presented with optic disc edema, often associ
238 G and 54 with NGON, including ischemic optic neuropathy, previous optic neuritis, and compressive and
239 ing cardiomyopathy, lipodystrophy, myopathy, neuropathy, progeria, bone/skin disorders, and overlap s
241 -19 secondary to postinfectious inflammatory neuropathy, prone positioning-related stretch and/or com
242 l models of antiglycolipid antibody-mediated neuropathies proved that some of these antibodies are di
244 o type 2 diabetic db/db mice with peripheral neuropathy remarkably ameliorated DPN by improving sciat
247 uropathy Score, the pediatric-modified Total Neuropathy Score and the Total Neuropathy Score-pediatri
248 icity in children, two variants of the Total Neuropathy Score, the pediatric-modified Total Neuropath
249 We identified two variants of the Total Neuropathy Score, two grading scales, two semi-objective
250 odified Total Neuropathy Score and the Total Neuropathy Score-pediatric vincristine, are promising bu
253 ablished a novel mouse model for small fiber neuropathy (SFN) in which grin1, the gene that encodes t
254 A variants in patients with pure small fibre neuropathy (SFN), analyse their clinical features and pr
255 d provide effective neuroprotection in optic neuropathies.SIGNIFICANCE STATEMENT Here, we present an
256 iral infections promote pain and can lead to neuropathies.SIGNIFICANCE STATEMENT It is increasingly u
257 ipheral pain and the subsequent long-lasting neuropathy.SIGNIFICANCE STATEMENT The first-line cytosta
258 nic epilepsy myopathy sensory ataxia; ataxia neuropathy spectrum; autosomal recessive progressive ext
260 s or their myelin sheaths lead to peripheral neuropathies such as Charcot-Marie-Tooth disease in huma
263 or currently untreatable mitochondrial optic neuropathies such as Leber Hereditary Optic Neuropathy.
264 tion, CCM, neuropathic symptoms (small fibre neuropathy symptom inventory questionnaire, neuropathic
265 7; 95% CI: 0.20, 0.52, respectively) and the neuropathy symptom score (r = 0.41; 95% CI: 0.25, 0.55;
266 % vs. 18% at 5 years), whereas that of optic neuropathy tended to be higher with the 15-mm plaque (2%
267 ocal deletion of this gene causes a separate neuropathy termed hereditary neuropathy with liability t
268 re greater in patients with painful diabetic neuropathy than in those with painless diabetic neuropat
270 Glaucoma is a group of progressive optic neuropathies that share common biological and clinical c
271 and phenotypes of participants with diabetic neuropathy that can be used in the design of new interve
272 a promising gene therapy strategy for optic neuropathies, the most common form of eye diseases that
273 response rates with low rates of peripheral neuropathy, the main dose-limiting toxicity of bortezomi
275 eIF2alpha phosphorylation in P0S63del-CMT1B neuropathy through the generation of mice in which eIF2a
276 ry feedback from the limbs due to peripheral neuropathy to result in motor impairments in individuals
277 chemotherapy-induced and diabetic peripheral neuropathies, traumatic brain injury, and amyotrophic la
280 iduals with hereditary sensory and autonomic neuropathy type III (HSAN III), also known as Riley-Day
281 s, are mostly detected in acute motor axonal neuropathy type of GBS and in FS, and less frequently in
282 1 (RFC1) as the cause of cerebellar ataxia, neuropathy, vestibular areflexia syndrome (CANVAS) and a
287 ectrophysiologic abnormalities suggestive of neuropathy were frequently observed but were not the pre
288 Patients with Nav1.7-related small fibre neuropathy were randomized to start with lacosamide foll
289 (SIDD) had increased risk of retinopathy and neuropathy, whereas the severe insulin-resistant diabete
290 tment-related adverse event of any grade was neuropathy, which was reported in 36 (97%) of 37 patient
291 ly without imaging abnormalities; peripheral neuropathy with distal sensory symptoms, such as numbnes
292 uses a separate neuropathy termed hereditary neuropathy with liability to pressure palsies (HNPP).
294 e autosomal recessive early-onset peripheral neuropathy with or without intellectual disability.
295 is a rare syndrome characterized by chronic neuropathy with sensory ataxia, ocular, and/or bulbar mo
296 Testing patients with acquired demyelinating neuropathy with serum vascular endothelial growth factor
297 ated sodium channel mutations in small fibre neuropathy (with mutations in SCN9A, encoding for Nav1.7
298 teen of 17 patients (82%) demonstrated optic neuropathy, with 12 of these patients also showing retin
300 ing for patients with acquired demyelinating neuropathy would lead to annual cost-savings of pound 10