ライフサイエンスコーパス: pain disorder

1 d a critical contribution of Nav1.7 to human pain disorders.

2 le stimuli and is implicated in a variety of pain disorders.

3 n approved for treatment of multiple chronic pain disorders.

4 pain pathway is believed to promote clinical pain disorders.

5 esent a class of agents for the treatment of pain disorders.

6 been linked to a spectrum of inherited human pain disorders.

7 ysiology of fibromyalgia and related chronic pain disorders.

8 cific hypotheses in a broad range of chronic pain disorders.

9 given to clinical studies related to chronic pain disorders.

10 al substance used to treat neuromuscular and pain disorders.

11 f negative context on symptoms in functional pain disorders.

12 ral sensitisation may contribute to visceral pain disorders.

13 es but rather associated with behavioral and pain disorders.

14 e included 1422 participants (median time of pain disorder 10 years [IQR 5-20]; median length of stro

15 mary erythromelalgia; (3) paroxysmal extreme pain disorder; (4) febrile seizures and recently (5) sma

16 Many chronic pain disorders alternate between bouts of pain and perio

17 These findings may integrate many pain disorders and provide an approach for developing an

18 nherited erythromelalgia, paroxysmal extreme pain disorder, and small-fibre neuropathy.

19 tified in three families with rare heritable pain disorders, and in patients with painful small-fibre

20 cated voltage-gated sodium channels in human pain disorders, and targeted and massively parallel geno

21 Numerous musculoskeletal pain disorders are based in dysfunction of peripheral pe

22 lood flow/oxygenation and a number of muscle pain disorders are based in problems of peripheral perfu

23 Although chronic neuropathic pain disorders are more prevalent in the senescent popul

24 cause erythromelalgia and paroxysmal extreme pain disorder as a result of hyperexcitability of sensor

25 the development of specialized treatment for pain disorders associated with I(NaR).

26 , 1.25; 95% CI, 1.10-1.42), and preoperative pain disorders (back pain: aOR, 1.57; 95% CI, 1.42-1.75;

27 Fibromyalgia is a common chronic pain disorder characterized by complex symptomatology an

28 ezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy.

29 The inherited pain disorder erythromelalgia (IEM) has been linked to N

30 ID) has been changed to functional abdominal pain disorders (FAPD) and we have derived a new term, "f

31 aine has traditionally been categorized as a pain disorder, focusing on headache as its central featu

32 ociation of genetic variants with idiopathic pain disorders has appeared in the literature, and here

33 terestingly, many of the heritable monogenic pain disorders have been mapped to mutations in genes en

34 ndromes, molecular substrates for hereditary pain disorders have been poorly understood.

35 Human hereditary gain- or loss-of-pain disorders have demonstrated an essential role of Na

36 Mendelian heritable pain disorders have provided insights into human pain me

37 syndrome (FMS) is a chronic musculoskeletal pain disorder in children and adolescents for which ther

38 Erythromelalgia is the first inherited pain disorder in which it is possible to link a mutation

39 erapies may be more appropriate for treating pain disorders in which hyperalgesia and not allodynia i

40 lth care services for symptoms of functional pain disorders, including irritable bowel syndrome, than

41 sory hyperinnervation, a hallmark of several pain disorders, including vulvodynia.

42 ral Nav isoform) associated with two genetic pain disorders, inherited erythromelalgia (IEM) and paro

43 This study expands the spectrum of heritable pain disorders linked to gain-of-function mutations in N

44 Understanding rare heritable pain disorders not only improves diagnosis and treatment

45 ivity associated with inherited and acquired pain disorders occurs through increased excitability of

46 ause hyperexcitability and familial episodic pain disorder or painful neuropathy, while mutations evo

47 Paroxysmal extreme pain disorder (PEPD) and inherited erythromelalgia (IEM)

48 We demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral ne

49 nonoverlapping syndrome, paroxysmal extreme pain disorder (PEPD), characterized by rectal, periocula

50 erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD), enhance Nav1.7 function via distin

51 Paroxysmal extreme pain disorder (PEPD), previously known as familial recta

52 erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD).

53 erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD).

54 nful inherited neuropathy paroxysmal extreme pain disorder (PEPD).

55 Inherited "paroxysmal extreme pain disorder" (PEPD) differs in its clinical picture an

56 uld contribute to the development of certain pain disorders, possibly including those modulated by es

57 tage-gated Na(+) channel NaV1.9 cause severe pain disorders ranging from neuropathic pain to congenit

58 mal models, the role of glial cells in human pain disorders remains unknown.

59 In chronic pain disorders, rumination can impede treatment efficacy

60 contribute to etiology of functional pelvic pain disorders such as interstitial cystitis/bladder pai

61 sodium channel (NaV) mutations cause genetic pain disorders that range from severe paroxysmal pain to