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1 neurons) that underlie the chronic phase of painful neuropathy.
2 get of several disorders, including a common painful neuropathy.
3 to paclitaxel-induced acute pain and chronic painful neuropathy.
4 and peripheral nerve axons, in patients with painful neuropathy.
5 levels can contribute to the development of painful neuropathies.
6 mutations are associated with two inherited painful neuropathies.
7 to innocuous light touching, is a symptom of painful neuropathies.
8 oximately 80% of these patients experiencing painful neuropathies.
9 hes for Parkinson's disease-linked and other painful neuropathies.
11 hannel function associated with an inherited painful neuropathy and suggest that these physiological
12 D in diabetic rodents exhibiting features of painful neuropathy and the translational potential of th
14 rial environment and the pathogenesis of the painful neuropathies associated with the macrophage-depe
15 changes during the progression of persistent painful neuropathy caused by paclitaxel (PTX) in male an
16 asis of erythermalgia, an autosomal dominant painful neuropathy characterized by redness of the skin
17 sticity during the progression of persistent painful neuropathy could be interpreted as a biological
18 ate that a variant of NaV1.7 associated with painful neuropathy depolarizes resting membrane potentia
21 on injury (CCI) to peripheral nerve causes a painful neuropathy in association with a process of axon
22 therapy drugs for treating many cancers, and painful neuropathy is a major dose-limiting adverse effe
23 V1.8 mRNA in the pathogenesis of SNE-induced painful neuropathy, NaV1.8 shRNA vector was delivered by
25 hort of patients with sodium channel-related painful neuropathy not responding to currently available
26 occurred in < or = 10% of patients; grade 2 painful neuropathy occurred in 7.5%; and grade 3 palmar-
27 Pathological sensations caused by peripheral painful neuropathy occurring in Type 2 diabetes mellitus
28 or sources of disability and often result in painful neuropathies or the impairment of muscle movemen
29 mol/l], and the mean was higher still in the painful neuropathy subgroup [92.2 (37.1) mmol/l] (P < 0.
33 al of modulating NK cell function to resolve painful neuropathy through the clearance of partially da
35 ility and familial episodic pain disorder or painful neuropathy, while mutations evoking larger membr
36 id substrate of this enzyme, leads to severe painful neuropathy with progressive renal, cardiovascula