Abstract | STUDY DESIGN: Animal experimental study with intervention. OBJECTIVE: SUMMARY OF BACKGROUND DATA: The abnormal sympathetic-somatosensory interaction may underlie some forms of neuropathic pain. There are several reports that sympathectomy and pharmacological sympathetic blockades are often effective to treat neuropathic pain. However, its pathophysiological mechanisms remain obscure. METHODS: RESULTS: CONCLUSION: We considered that pain behaviors of neuropathic pain are due, at least in part, to enhanced sympathetic noradrenergic transmission within the DRG. Suppression of sympathetic activity by reducing adrenergic release, α2-adrenoceptor stimulation, and/or α2-adrenoceptor upregulation in the DRG may relieve neuropathic pain. LEVEL OF EVIDENCE: 3.
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Authors | Izaya Ogon, Tsuneo Takebayashi, Takehito Iwase, Makoto Emori, Katsumasa Tanimoto, Tsuyoshi Miyakawa, Yoshinori Terashima, Takeshi Kobayashi, Noritsugu Tohse, Toshihiko Yamashita |
Journal | Spine
(Spine (Phila Pa 1976))
Vol. 40
Issue 24
Pg. E1269-75
(Dec 2015)
ISSN: 1528-1159 [Electronic] United States |
PMID | 26165214
(Publication Type: Journal Article)
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Chemical References |
- Receptors, Adrenergic, alpha-2
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Topics |
- Animals
- Behavior, Animal
- Disease Models, Animal
- Ganglia, Spinal
(physiopathology, surgery)
- Hyperalgesia
- Male
- Pain
(physiopathology)
- Radiculopathy
(surgery)
- Rats
- Rats, Sprague-Dawley
- Receptors, Adrenergic, alpha-2
(metabolism)
- Sympathectomy
(methods)
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