The interface between inhibition of descending noradrenergic pain control pathways and negative affects in post-traumatic pain patients

  • Yulong Cui
  • Junmei Xu
  • Ruping Dai
  • Liang He

Abstract

Background. Animal studies have shown that surgical trauma activates the descending noradrenergic pathway. However, perioperative patients have decreased concentrations of noradrenaline (NA) in the cerebrospinal fluid (CSF). We proposed that the descending monoaminergic pathway is altered in post-traumatic pain patients and that CSF monoamine neurotransmitters may be more closely related to affective symptoms. We investigated the levels of monoamine neurotransmitters and assessed pain in these patients.

Methods. Patients were divided into a post-traumatic pain group, a pain-free group, a painful labor group, and a pain-free labor group. CSF was collected from all patients, and concentrations of NA, 3-methoxy-4-hydroxyphenylglycol (MHPG), dopamine, homovanillic acid, and 5-hydroxyindoleacetic acid (5-HIAA) were measured by high-performance liquid chromatography.

Results. In the post-traumatic pain group, lumbar CSF concentrations of NA and MHPG were significantly decreased (P < 0.01) compared to the control group. The post-traumatic pain group displayed a significant negative correlation between NA and the respective total value of the short form of the McGill pain questionnaire (SF-MPQ), SF-MPQ (affective), and visual analog scale (r = –0.388, r = –0.433, and r = –0.367; P < 0.05).

Conclusions. Post-traumatic pain patients demonstrated decreased concentrations of NAin CSF, indicating that descending noradrenergic pain control pathways may be inhibited. NA is more closely related to negative affects in post-traumatic pain patients.

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Published
2012-02-03
How to Cite
Cui Y., Xu J., Dai R., & He L. (2012). The interface between inhibition of descending noradrenergic pain control pathways and negative affects in post-traumatic pain patients. Upsala Journal of Medical Sciences, 117(3). https://doi.org/10.3109/03009734.2011.653606
Section
Original Articles