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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
49 21%), thrombocytopenia (14%), and peripheral sensory neuropathy (12%).
50 treatment-related events included peripheral sensory neuropathy (14%), fatigue/asthenia (13%), myalgi
51                  Grade 3/4 treatment-related sensory neuropathy (21% v 0%), fatigue (9% v 3%), and ne
52 %), as well as a higher rate of grade 2 to 4 sensory neuropathy (26% vs. 18%); however, they had a lo
53 patients), rash (5 patients), and peripheral sensory neuropathy (3 patients).
54 patients), rash (2 patients), and peripheral sensory neuropathy (3 patients).
55 /vomiting (5%), myalgia/arthralgia (3%), and sensory neuropathy (3%).
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
59 usion-related reaction (45%), and peripheral sensory neuropathy (44%).
60 nd pyrexia (52% each), nausea and peripheral sensory neuropathy (48% each), and dyspnea (40%) were th
61 ia (2.7% v 3.6%), fatigue (7.9% v 3.4%), and sensory neuropathy (5.5% v 0%).
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
65          The most common AEs were peripheral sensory neuropathy (78%), fatigue (44%), and nausea (44%
66              Most common toxicities included sensory neuropathy (80%) and fatigue (64%), with only 27
67 ild to moderate, the most common being acute sensory neuropathy (85%).
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
72                                              Sensory neuropathy (all grade 1-3) was recorded in 17 (9
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
75 he field of axonal CMT and have relevance to sensory neuropathies and motor neuron disorders.
76 nful neuropathy and 28 without pain, 26 with sensory neuropathy and 24 with sensory and motor neuropa
77                Mutated CCT4/5 subunits cause sensory neuropathy and CCT5 expression is decreased in A
78                     A triad of hearing loss, sensory neuropathy and cognitive decline remains as the
79 of three patients experienced a DLT (grade 3 sensory neuropathy and febrile neutropenia).
80 xanes; such a neuropathy usually presents as sensory neuropathy and is more common with paclitaxel th
81                                              Sensory neuropathy and neutropenia were more common with
82                                              Sensory neuropathy and neutropenia were significantly mo
83 eutropenia was 2.3%, and the rate of grade 3 sensory neuropathy and of grade 3 motor neuropathy was 0
84 y adult-onset retinitis pigmentosa, anosmia, sensory neuropathy and phytanic acidaemia.
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
88 T was grade 3 pharyngolaryngeal dysesthesia, sensory neuropathy, and ataxia at 160 mg/m2.
89 de 3 events of neutropenia (14%), peripheral sensory neuropathy, and hyperkalemia (9% each).
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
95                                   Hereditary sensory neuropathies are a class of disorders marked by
96                           Late-onset painful sensory neuropathies are usually acquired conditions ass
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
99                                          The sensory neuropathies associated with HIV infection are a
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.
103                                      Chronic sensory neuropathy can be dose limiting and may have det
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%]),
110 of 45), anaemia (five [11%]), and peripheral sensory neuropathy (four [9%]).
111 atients experienced more frequent and severe sensory neuropathy (grade 1 to 4; 8% v 30%).
112 fect large nerve fibers; painful small fiber sensory neuropathy has not previously been described in
113                               HIV-associated sensory neuropathy (HIV-SN) is currently the most common
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
117 me 17p11.2 duplication (hereditary motor and sensory neuropathy-HMSN Ia).
118            The autosomal dominant peripheral sensory neuropathy HSAN1 results from mutations in the L
119 sities in 35 patients confirmed pretreatment sensory neuropathy in 20% and new or worsening neuropath
120 (day 21), consistent with the development of sensory neuropathy in SIV-infected macaques.
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
123                                  Small fiber sensory neuropathy is a common disorder in which progres
124 IGNIFICANCE STATEMENT Painful HIV-associated sensory neuropathy is a neurological complication of HIV
125                We hypothesized that diabetic sensory neuropathy is associated with activation of apop
126                                  The painful sensory neuropathy is associated with the use of dideoxy
127  any time, but early in the IBD course, pure sensory neuropathy is more common.
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 (&lt; 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
134           Resolution of grade 3/4 peripheral sensory neuropathy occurred after a median period of 5.4
135                                      Grade 3 sensory neuropathy occurred in 14% of patients, and 22.7
136 lecular genetics of the hereditary motor and sensory neuropathies of autosomal dominant and X-linked
137                The concept of a severe motor-sensory neuropathy of acute onset caused by an immune at
138 hy some individuals develop an acute painful sensory neuropathy on sustained cold exposure is not yet
139 ed to those of type III hereditary motor and sensory neuropathy or Dejerine-Sottas disease.
140 toplasmic dynein can either result in a pure sensory neuropathy or in a sensory neuropathy with motor
141                               HIV-associated sensory neuropathy remains the most common neurological
142              Our study indicates a prominent sensory neuropathy resulting from periaxin gene mutation
143 lkan Gypsies and termed hereditary motor and sensory neuropathy-Russe (HMSN-R).
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
146                                              Sensory neuropathy symptoms were more prominent than wer
147 spectively examined the relationship between sensory neuropathy symptoms, falls, and fall-related inj
148                                       Of the sensory neuropathy symptoms, numbness and tingling were
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
152                                   Hereditary sensory neuropathy type 1 (HSN1) is a dominantly inherit
153                                   Hereditary sensory neuropathy type 1 (HSN1, MIM 162400) genetically
154                                   Hereditary sensory neuropathy type 1 is an autosomal-dominant disor
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
157 tly inactivate SPT similar to the hereditary sensory neuropathy type 1-like mutations in Lcb1p.
158 at encodes for SPT subunits cause hereditary sensory neuropathy type 1.
159 palmitoyltransferase (SPT), cause hereditary sensory neuropathy type I .
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
162  for which is duplicated in hereditary motor sensory neuropathy type la, can also induce EAN.
163  has been designated as hereditary motor and sensory neuropathy type VI (HMSN VI).
164                The severity of the resultant sensory neuropathy was compared with behavioral, physiol
165 r in both arms, as was grade 3 rash, whereas sensory neuropathy was higher in the concurrent arm (15%
166                                              Sensory neuropathy was mild with grade 3 neurotoxicity r
167                                      Grade 3 sensory neuropathy was more common in the ABI-007 arm th
168                                 Grade 2 or 3 sensory neuropathy was present in 10 patients (53%) over
169 p had grade 3 sensory neuropathy; no grade 3 sensory neuropathy was seen in the 1.3 mg/m2 group.
170                                              Sensory neuropathy was seen more commonly than motor axo
171  Minimal hematologic toxicity and no grade 3 sensory neuropathy were noted.
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
174  result in a pure sensory neuropathy or in a sensory neuropathy with motor neuron involvement.
175 awling (Swl) mutation display an early-onset sensory neuropathy with muscle spindle deficiency.
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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