ライフサイエンスコーパス: central pain

1 tDCS with 2 mA for the treatment of chronic central pain.

2 not sufficient factor in the pathogenesis of central pain.

3 from CNS disorders could lead to undesirable central pain.

4 motor cortex stimulation in the treatment of central pain.

5 dorsal horn neurons, and behavioral signs of central pain.

6 thic pain as well as in a reserpine model of central pain.

7 Patients with central pain after stroke were the least likely to repor

8 e toward visceral stimuli may play a role in central pain amplification and irritable bowel syndrome

9 These results support the view that central pain and temperature pathways contain anatomical

10 Our poor understanding of the etiology of central pain and the relative lack of effective treatmen

11 ble overlap between effective treatments for central pain and those for peripheral neuropathic pain.

12 nisms linking trkB.T1 to SCI-induced chronic central pain are unknown.

13 Central pain augmentation resulting from enhanced excita

14 role in the pathophysiology of FM and other central pain augmentation syndromes.

15 ion of the CNS, such as a stroke [poststroke central pain (CPSP)].

16 nociceptive and affective components during central pain development.

17 PL) nucleus, establishing a basis for tiered central pain generators or amplifiers.

18 Central pain is neuropathic pain resulting from a lesion

19 nd its resistance to conventional treatment, central pain is one of the most formidable challenges pa

20 Central pain is reduced by reorganization of cortical bo

21 Stable activation of the central pain matrix was observed over 12 months, and act

22 ked enhanced activity within components of a central pain matrix, including dorsal anterior cingulate

23 n distributed in two well-known areas of the central pain matrix: the insula and the somatosensory co

24 o interpersonal context and extranociceptive central pain mechanisms and suggest that nociceptive pai

25 volves a complex interplay of peripheral and central pain mechanisms, pelvic floor muscle and autonom

26 erience benefit from new therapies targeting central pain mechanisms.

27 lgia, secondary post-inflammatory damage and central pain mechanisms.

28 s an important target for future research of central pain mechanisms.

29 modulators of pacemaker activity in newborn central pain networks.

30 nate receptors are also expressed throughout central pain neuraxis, where their functional contributi

31 c candidate gives pain relief, by modulating central pain neurobiology, we propose a 'pre-proof-of-co

32 in the responsiveness (ie, sensitization) of central pain neurons that process information arising fr

33 ptor antagonists in the treatment of chronic central pain, particularly where input from low threshol

34 at points to hyperexcitability of a specific central pain pathway that subserves intracranial sensati

35 er pacemaker-like neurons are present within central pain pathways in the neonate.

36 ct the framework of cold allodynia-activated central pain pathways.

37 tion (PENFS) in the external ear to modulate central pain pathways.

38 Visceral hyperalgesia or heightened central pain perception may contribute to pain in chroni

39 in infancy can have a lasting influence upon central pain processing and adult pain sensitivity.

40 tol (LPI), in nociception, yet their role in central pain processing has not been explored.

41 There is strong evidence for abnormal central pain processing in FMS.

42 consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP

43 ity of this approach in the study of altered central pain processing in reserpine induced myalgia.

44 atments, but nonvisceral pain due to altered central pain processing may respond to agents such as pr

45 imal experiments suggest that alterations in central pain processing occur so that tactile stimuli co

46 that NMUR2 plays a more significant role in central pain processing than other brain functions inclu

47 pheral nociceptive input as well as abnormal central pain processing.

48 mpaired cognition," "confusion-ataxia," and "central pain," respectively.

49 ome, this finding supports the proposal that central pain results from loss of the normal inhibition

50 Central pain sensitisation can also occur, and psychosoc

51 a state with MOR inverse agonists reinstated central pain sensitization and precipitated hallmarks of

52 Among other mechanisms, central pain sensitization processes seem to be involved

53 was the most sensitive cut-off for detecting central pain sensitization when prioritizing diagnostic

54 trophysiological model for the triggering of central pain sensitization.

55 ing treatments to CeA-SST neurons to prevent central pain sensitization.

56 ptive afferents become capable of activating central pain signalling neurons.

57 te receptors (which are often upregulated in central pain states) were shown to benefit fibromyalgia

58 t not only injuries commonly associated with central pain, such as strokes and spinal cord lesions, b

59 w that conditioning with the activation of a central pain-suppressing circuit is sufficient to engine

60 Central pain syndrome (CPS) is defined as pain associate

61 ory and pain integration may account for the central pain syndrome that can occur after stroke damage

62 ons at this site can produce the post-stroke central pain syndrome, this finding supports the proposa

63 n a devastating loss of function and chronic central pain syndromes frequently develop in the majorit

64 role in the pathophysiology of FM and other central pain syndromes.

65 In particular, the central pain system comprising ascending and descending

66 an decrease pain in patients with refractory central pain, we hypothesized that tDCS treatment would

67 only in motor impairment but also in chronic central pain, which can be refractory to conventional tr

68 ogy, clinical presentation, and treatment of central pain, with special emphasis being placed on stud