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1 disabling neuropathic pain disorder due to a sensory neuropathy.
2 from physiological and structural indices of sensory neuropathy.
3 levant therapeutic target for HIV-associated sensory neuropathy.
4 increased insulin sensitivity, and previous sensory neuropathy.
5 ompounds that may prevent development of the sensory neuropathy.
6 d were fatigue, constipation, and peripheral sensory neuropathy.
7 ediabetic and develop insulin resistance and sensory neuropathy.
8 nausea or vomiting, headache, and transient sensory neuropathy.
9 ot genotype-specific in hereditary motor and sensory neuropathy.
10 Tooth disease, a severe hereditary motor and sensory neuropathy.
11 prague-Dawley rat strain with an early onset sensory neuropathy.
12 thy with associated radiculopathy and distal sensory neuropathy.
13 nic hyperglycemia results in a predominantly sensory neuropathy.
14 is, manifested clinically as a predominantly sensory neuropathy.
15 or days of therapy and a chronic, cumulative sensory neuropathy.
16 icantly mitigating oxaliplatin-induced acute sensory neuropathy.
17 y contribute to the pathogenesis of diabetic sensory neuropathy.
18 Total dose is limited by development of a sensory neuropathy.
19 s potentially efficacious for human diabetic sensory neuropathy.
20 g cells may contribute to the HIV-associated sensory neuropathy.
21 ratory chain and function and resulting in a sensory neuropathy.
22 the invariant presence of a prominent axonal sensory neuropathy.
23 in prediabetic mice while protecting against sensory neuropathy.
24 hereditary spastic paraplegia and hereditary sensory neuropathy.
25 th a dominantly inherited late-onset painful sensory neuropathy.
26 ), which has been associated with hereditary sensory neuropathy.
27 Eleven patients developed grade 3 sensory neuropathy.
28 ebrile seizures and recently (5) small fibre sensory neuropathy.
29 (CMT1C) is a dominantly inherited motor and sensory neuropathy.
30 of cisplatin chemotherapy causes substantial sensory neuropathy.
31 a musculorum (dt) mice results in hereditary sensory neuropathy.
32 trategy for attenuating cisplatin-associated sensory neuropathy.
33 te the importance of this model for study of sensory neuropathy.
34 e may be the initiating event in HIV-induced sensory neuropathy.
35 uninfected patients or HIV patients without sensory neuropathy.
36 ative sensory testing were consistent with a sensory neuropathy.
37 unrelated patients with hereditary motor and sensory neuropathy.
38 nt with a severe, early-onset proprioceptive sensory neuropathy.
39 intact animals, was absent after large-fiber sensory neuropathy.
40 nced grade 2, and none experienced grade 3/4 sensory neuropathy.
41 linated, but not myelinated nerve fibres, in sensory neuropathies.
42 le of disrupted ErbB signaling in peripheral sensory neuropathies.
43 fore an excellent model for human hereditary sensory neuropathies.
44 e beneficial in the treatment of large-fiber sensory neuropathies.
45 lications for pain sensitivity in peripheral sensory neuropathies.
46 es and in 1 patient because of a generalized sensory neuropathy; 1 patient refused to continue taking
47 vomiting (13%), nausea (11%), and peripheral sensory neuropathy (11%) in arm A, and diarrhea (33%), f
48 included grade 4 neutropenia (24%), grade 3 sensory neuropathy (11%), and grade 4 febrile neutropeni
50 treatment-related events included peripheral sensory neuropathy (14%), fatigue/asthenia (13%), myalgi
52 %), as well as a higher rate of grade 2 to 4 sensory neuropathy (26% vs. 18%); however, they had a lo
56 bocytopenia, 2% and 15%; anemia, 5% and 11%; sensory neuropathy, 3% and 0.8%; fatigue, 5% and 12%; pe
57 v 25.8%), febrile neutropenia (4.1% v 1.4%), sensory neuropathy (4.1% v 0%), and alopecia (grade 1 or
58 y common groups such as hereditary motor and sensory neuropathy (40/100,000) and mitochondrial disord
60 nd pyrexia (52% each), nausea and peripheral sensory neuropathy (48% each), and dyspnea (40%) were th
62 Common treatment-related toxicities included sensory neuropathy (53%), fatigue (50%), and neutropenia
63 ogic and hematologic, including grade 1 to 2 sensory neuropathy (55%), grade 3 to 4 neutropenia (35%)
64 es with HSAN I, 60 individuals with sporadic sensory neuropathy, 6 HSAN II families, 20 Charcot-Marie
68 he brentuximab vedotin group were peripheral sensory neuropathy (94 [56%] of 167 patients vs 25 [16%]
69 sly uncharacterized complex axonal motor and sensory neuropathy accompanied by severe nonprogressive
70 equired that patients have grade 1 or higher sensory neuropathy according to the NCI Common Terminolo
71 found between groups; only grade 2 or higher sensory neuropathy adverse events persisted at 24 months
73 ing, and potential therapeutic treatment, of sensory neuropathies and a number of neurological diseas
74 n and most frequent of a group of congenital sensory neuropathies and is characterized by widespread
76 nful neuropathy and 28 without pain, 26 with sensory neuropathy and 24 with sensory and motor neuropa
80 xanes; such a neuropathy usually presents as sensory neuropathy and is more common with paclitaxel th
83 eutropenia was 2.3%, and the rate of grade 3 sensory neuropathy and of grade 3 motor neuropathy was 0
85 (-/-) mice as an animal model of small fiber sensory neuropathy and provide new insight regarding the
86 ation of results from STZ models of diabetic sensory neuropathy and strongly argues that more refined
87 n important pathogenetic role in nociceptive sensory neuropathy and that C-peptide replacement may be
90 n adverse events were fatigue, constipation, sensory neuropathy, and infection; there was no treatmen
91 ade 3 hypothyroidism, and grade 3 peripheral sensory neuropathy, and one case of grade 4 pneumonitis.
92 icities included myelosuppression, vomiting, sensory neuropathy, and ototoxicity and were worse with
93 l mechanism for dideoxynucleoside-associated sensory neuropathy, and questions arise about enhanced r
94 s and were characterized by cough, asthenia, sensory neuropathy, anorexia, serum sickness, and hypert
97 as diabetic and human immunodeficiency virus sensory neuropathies) are characterized by distal axonal
98 ognitive disorders, vacuolar myelopathy, and sensory neuropathies associated with HIV are the most co
100 he SLC12A6 gene, causes hereditary motor and sensory neuropathy associated with agenesis of the corpu
101 ogical disease (brainstem encephalopathy and sensory neuropathy being common extracerebellar manifest
102 1 (GDAP1) cause severe peripheral motor and sensory neuropathies called Charcot-Marie-Tooth disease.
104 is an uncommon form of hereditary motor and sensory neuropathy caused by mutations in the P(0) myeli
105 T4B) is a demyelinating hereditary motor and sensory neuropathy characterized by abnormal folding of
106 athogenic mutations for hereditary motor and sensory neuropathy, distal hereditary motor neuropathy,
107 nosis gene TPP1 and the hereditary motor and sensory neuropathy DNMT1 gene, highlighting the genetic
108 autosomal-dominant disorder that leads to a sensory neuropathy due to mutations in the serine palmit
109 ients), hypokalaemia (six [33%]), peripheral sensory neuropathy (five [28%]), diarrhoea (five [28%]),
112 fect large nerve fibers; painful small fiber sensory neuropathy has not previously been described in
114 uman immunodeficiency virus (HIV)-associated sensory neuropathy (HIV-SN) is difficult but needed for
115 uman immunodeficiency virus (HIV)-associated sensory neuropathy (HIV-SN) is the most common neurologi
116 t in human immunodeficiency virus-associated sensory neuropathy (HIV-SN), damaged mtDNA accumulates i
119 sities in 35 patients confirmed pretreatment sensory neuropathy in 20% and new or worsening neuropath
121 cy of neurotrophic or regenerative drugs for sensory neuropathies including those caused by HIV, diab
122 compasses axonal and demyelinating motor and sensory neuropathies, including four young patients pres
124 IGNIFICANCE STATEMENT Painful HIV-associated sensory neuropathy is a neurological complication of HIV
128 jority of patients, the cause of small fiber sensory neuropathy is unknown, and treatment options are
129 they ensheath cause the hereditary motor and sensory neuropathies known as Charcot-Marie-Tooth (CMT)
130 febrile neutropenia (9%, 3%, 3%; P < .001), sensory neuropathy (< 1%, 7%, 6%; P < .001), and diarrhe
131 nduced by streptozotocin (STZ) resulted in a sensory neuropathy manifest by a decrease in the foot se
132 tment-related adverse events were peripheral sensory neuropathy, nausea, fatigue, neutropenia, and di
133 e patient in the 1.5 mg/m2 group had grade 3 sensory neuropathy; no grade 3 sensory neuropathy was se
136 lecular genetics of the hereditary motor and sensory neuropathies of autosomal dominant and X-linked
138 hy some individuals develop an acute painful sensory neuropathy on sustained cold exposure is not yet
140 toplasmic dynein can either result in a pure sensory neuropathy or in a sensory neuropathy with motor
144 e for the important complication of diabetic sensory neuropathy, since hyperglycemia for longer than
145 uman immunodeficiency virus (HIV)-associated sensory neuropathy (SN) is the most common neurological
147 spectively examined the relationship between sensory neuropathy symptoms, falls, and fall-related inj
149 ng side effect of paclitaxel is a peripheral sensory neuropathy that can last days to a lifetime.
150 type, SIMPLE develop a late-onset motor and sensory neuropathy that recapitulates key clinical featu
151 fatigue, depressed consciousness, dizziness, sensory neuropathy, tremor, constipation, dyspnea, hypox
155 ng hereditary spastic paraplegia, hereditary sensory neuropathy type 1, and non-5q spinal muscular at
156 mapped to this region, including hereditary sensory neuropathy type 1, self-healing squamous epithel
160 esidues that are mutated to cause hereditary sensory neuropathy type I reside in a highly conserved r
161 lar atrophy (SPSMA) and hereditary motor and sensory neuropathy type IIC (HMSN IIC, also known as HMS
165 r in both arms, as was grade 3 rash, whereas sensory neuropathy was higher in the concurrent arm (15%
169 p had grade 3 sensory neuropathy; no grade 3 sensory neuropathy was seen in the 1.3 mg/m2 group.
172 nausea, fatigue, arthralgias, and peripheral sensory neuropathy, were mild to moderate and matched th
173 In 4 infants with a new lethal autonomic sensory neuropathy with clinical features similar to fam
176 tive diseases including hereditary motor and sensory neuropathy with proximal dominant involvement (H
177 We produced a dose-dependent large-fiber sensory neuropathy, without detrimental effects on gener
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