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1 such as chronic pain diseases like inherited erythromelalgia.
2 ructural small fiber studies when evaluating erythromelalgia.
3 of early satiety, night sweats, pruritus, or erythromelalgia.
4 d redness of the extremities consistent with erythromelalgia.
5 haracterised cohort of patients with CIP and erythromelalgia.
6 mily with carbamazepine-responsive inherited erythromelalgia.
7 een linked to the painful disorder inherited erythromelalgia.
8 sodium channel mutation, S211P, which causes erythromelalgia.
9 n this kindred with CBZ-responsive inherited erythromelalgia.
10 solely based on their clinical diagnosis of erythromelalgia.
11 the painful inherited neuropathy, hereditary erythromelalgia.
12 al proliferation, which is usually seen with erythromelalgia.
13 function Na(V)1.7 mutation causing inherited erythromelalgia.
14 tal insensitivity to pain (CIP); (2) primary erythromelalgia; (3) paroxysmal extreme pain disorder; (
16 ly well-studied cases including 6 CIP and 13 erythromelalgia (9 with family history, 10 with small-fi
18 C-SNs) to answer this question for inherited erythromelalgia, a pain disorder caused by gain-of-funct
21 gested between the age of onset of inherited erythromelalgia and the extent of hyperpolarizing shifts
22 romes (hepatotoxic, accelerated nephrotoxic, erythromelalgia); and three delayed syndromes (delayed n
27 a severe inherited pain syndrome (inherited erythromelalgia) causes a substantial hyperpolarizing sh
28 eptor hyperexcitability underlying inherited erythromelalgia, characterized in most kindreds by early
29 (Tricholoma equestre, Russula subnigricans), erythromelalgia (Clitocybe amoenolens, Clitocybe acromel
30 ervate the epidermis, one hypothesis is that erythromelalgia could similarly be associated with a los
31 ivotal role of activation shift in inherited erythromelalgia development, slow inactivation may regul
35 e linked to inherited pain syndromes such as erythromelalgia (IEM) and paroxysmal extreme pain disord
36 sing and have been associated with inherited erythromelalgia (IEM) and paroxysmal extreme pain disord
37 d with two genetic pain disorders, inherited erythromelalgia (IEM) and paroxysmal extreme pain disord
38 l extreme pain disorder (PEPD) and inherited erythromelalgia (IEM) are inherited pain syndromes arisi
42 or chronic pain, including pain in inherited erythromelalgia (IEM) in which gain-of-function mutation
43 several pain syndromes, including inherited erythromelalgia (IEM), a disorder in which gain-of-funct
44 ions (GOF) of Nav1.7 identified in inherited erythromelalgia (IEM), a human genetic model of neuropat
45 nction Nav1.7 mutation that causes inherited erythromelalgia (IEM), a human genetic model of neuropat
49 ns that enhance activation produce inherited erythromelalgia (IEM), characterized by burning pain in
54 e describe a novel mutation in a family with erythromelalgia in SCN9A, the gene that encodes the Na(v
56 t studies, however, have shown that familial erythromelalgia is a channelopathy caused by mutations i
62 erve fibers that cause acral pain syndromes, erythromelalgia is not characterized by loss of ENFD.
63 erve fibers that cause acral pain syndromes, erythromelalgia is not characterized by loss of ENFD.
67 rs, involve altered sodium channel function, erythromelalgia may emerge as a model disease that holds
68 but, if associated with OS, the features of erythromelalgia may expand the phenotypic spectrum of th
70 ity with those produced by another inherited erythromelalgia mutation (L858F) that does not enhance s
71 differences in Nav1.7 caused by a hereditary erythromelalgia mutation (N395K) that lies within the lo
72 ctivation and inactivation of this inherited erythromelalgia mutation in Na(v)1.7 but does not affect
74 erminant of the hyperexcitability induced by erythromelalgia mutations in sensory neurons, but that c
75 , a smaller shift than seen with early-onset erythromelalgia mutations, but similar to that of I136V,
76 -SNs associated with two different inherited erythromelalgia mutations, NaV1.7-S241T and NaV1.7-I848T
79 ce distinct pain syndromes such as inherited erythromelalgia, paroxysmal extreme pain disorder, and s
80 characterization of a well-defined inherited erythromelalgia population indicates the importance of c
82 ty of pain both between and within inherited erythromelalgia subjects, even those within a family who
83 nt (P610>T) previously considered causal for erythromelalgia, supporting recently raised doubt on its
85 the response of individuals with hereditary erythromelalgia to lidocaine treatment may be determined
88 s produce pain syndromes including inherited erythromelalgia, which is usually resistant to pharmacot
89 been linked to early age of onset inherited erythromelalgia, while mutations causing small activatio
90 ective study of 52 consecutive patients with erythromelalgia who were seen between September 1, 2010,
91 ective study of 52 consecutive patients with erythromelalgia who were seen between September 1, 2010,
93 esting of 13 subjects with primary inherited erythromelalgia with mutations of SCN9A, the gene encodi
94 Measures: The hypothesis that patients with erythromelalgia would have decreased ENFD was formulated