ライフサイエンスコーパス: secondary hyperalgesia

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1 ivity in the skin surrounding tissue injury (secondary hyperalgesia).

2 sing in the spinal cord in capsaicin-induced secondary hyperalgesia.

3 ulation of normal skin and capsaicin-induced secondary hyperalgesia.

4 ely, development of primary hyperalgesia and secondary hyperalgesia.

5 ization of spinal neurons and development of secondary hyperalgesia.

6 to central sensitization and development of secondary hyperalgesia.

7 tside the injury area decreased post-injury (secondary hyperalgesia, allodynia), but primary (site of

8 ity or central sensitization that results in secondary hyperalgesia and allodynia.

9 re the first to show that the maintenance of secondary hyperalgesia and underlying central sensitizat

10 eptor, has been implicated in development of secondary hyperalgesia associated with somatic, neural,

11 ensitivity in neighbouring uninjured tissue (secondary hyperalgesia), because of increased neuronal e

12 ic, reducing primary hyperalgesia by 80% and secondary hyperalgesia by 40%.

13 In contrast, the maintenance of secondary hyperalgesia depended on central mechanisms.

14 s indicate that the induction of primary and secondary hyperalgesia depended on peripheral input from

15 Secondary hyperalgesia exhibited a tendency toward recov

16 orrelated to the levels of capsaicin-induced secondary hyperalgesia in mice with and without SOD-2 ma

17 primary hyperalgesia in the V2 territory and secondary hyperalgesia in territories innervated by the

18 itical for both induction and maintenance of secondary hyperalgesia induced by subcutaneous injection

19 eral input, whereas the maintenance phase of secondary hyperalgesia involved central sensitization in

20 The induction phase of secondary hyperalgesia involved central sensitization me

21 The centralization of the secondary hyperalgesia involved descending 5-HT drive fr

22 nt study hypothesizes that capsaicin-induced secondary hyperalgesia is a consequence of superoxide bu

23 ivity within the non-acid-exposed esophagus (secondary hyperalgesia) is mediated by PGE(2) activation

24 nged noxious stimulation could contribute to secondary hyperalgesia observed at the tail.

25 imary hyperalgesia at the site of injury and secondary hyperalgesia outside the injured zone.

26 These data suggest that secondary hyperalgesia produced by mustard oil is mediat

27 nding pain facilitatory systems in mediating secondary hyperalgesia produced by topical application o

28 Secondary hyperalgesia shares clinical characteristics w

29 baseline sensory thresholds but an enhanced secondary hyperalgesia to punctate stimuli on treatment

30 n, and NT-3 may suppress events that lead to secondary hyperalgesia triggered by insult to muscle aff

31 urotrophins to alter the development of this secondary hyperalgesia was assessed using transgenic mic

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