scholarly journals Brain-Derived Neurotrophic Factor and Immune Cells in Osteoarthritis, Chronic Low Back Pain, and Chronic Widespread Pain Patients: Association with Anxiety and Depression

Medicina ◽  
2021 ◽  
Vol 57 (4) ◽  
pp. 327
Author(s):  
Dominique Josephine Dimmek ◽  
Christoph Korallus ◽  
Sabine Buyny ◽  
Gutenbrunner Christoph ◽  
Ralf Lichtinghagen ◽  
...  

Background and Objectives: Musculoskeletal dysfunction can induce several types of chronic pain syndromes. It is of particular interest to elucidate the pathomechanism of different forms of chronic pain. It is possible that patients who have developed chronic widespread pain (CWP) may endure different pathomechanisms as compared to those who suffer from local pain (osteoarthritis, OA) and regional pain (chronic low back pain, cLBP), especially with regard to pain regulation and its related biomediators. The aim of this study was to determine the differences in pathomechanisms among these patients by measuring pain-related biomediators, particularly brain-derived neurotrophic factor (BDNF). Additionally, subpopulations of immune cells were determined in parallel. Materials and Methods: Patients and healthy subjects (HSs) were recruited (age and gender-matched). BDNF was measured from serum samples of patients and HSs and the data of body composition parameters were recorded. Additionally, both patients and HSs were asked to fill in questionnaires related to pain intensity, anxiety, and depression. Results: Our results highlight that the levels of both free and total BDNF are significantly lower in pain patients compared to HSs, with p values of 0.041 and 0.024, respectively. The number of CD3− CD56bright natural killer (NK) cells shows significant differences between the groups. Comparing all chronic pain patients with HSs reveals a significantly lower number of CD4+ CD8+ T cells (p = 0.031), CD3− CD56bright NK cells (p = 0.049) and CD20+ CD3− cells (p = 0.007). Conclusions: To conclude, it seems that a general conformity between the pathomechanisms of different chronic pain diseases exists, although there are unique findings only in specific chronic pain patients.

Spine ◽  
2015 ◽  
Vol 40 (15) ◽  
pp. E890-E899 ◽  
Author(s):  
Annika Viniol ◽  
Nikita Jegan ◽  
Markus Brugger ◽  
Corinna Leonhardt ◽  
Jürgen Barth ◽  
...  

Pain ◽  
1986 ◽  
Vol 24 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Randal D. France ◽  
Ranga K. Rama Krishnan ◽  
Mary Trainor

Pain ◽  
1977 ◽  
Vol 4 (Supp C) ◽  
pp. 283-292 ◽  
Author(s):  
Richard I. Newman ◽  
Joel L. Seres ◽  
Leonard P. Yospe ◽  
Bonnie Garlington

Pain ◽  
1985 ◽  
Vol 22 (3) ◽  
pp. 289-294 ◽  
Author(s):  
Ranga Rama K. Krishnan ◽  
Randal D. France ◽  
Susan Pelton ◽  
Una D. McCann ◽  
Jonathan Davidson ◽  
...  

2020 ◽  
Vol 117 (18) ◽  
pp. 10015-10023 ◽  
Author(s):  
Meena M. Makary ◽  
Pablo Polosecki ◽  
Guillermo A. Cecchi ◽  
Ivan E. DeAraujo ◽  
Daniel S. Barron ◽  
...  

Chronic pain is a highly prevalent disease with poorly understood pathophysiology. In particular, the brain mechanisms mediating the transition from acute to chronic pain remain largely unknown. Here, we identify a subcortical signature of back pain. Specifically, subacute back pain patients who are at risk for developing chronic pain exhibit a smaller nucleus accumbens volume, which persists in the chronic phase, compared to healthy controls. The smaller accumbens volume was also observed in a separate cohort of chronic low-back pain patients and was associated with dynamic changes in functional connectivity. At baseline, subacute back pain patients showed altered local nucleus accumbens connectivity between putative shell and core, irrespective of the risk of transition to chronic pain. At follow-up, connectivity changes were observed between nucleus accumbens and rostral anterior cingulate cortex in the patients with persistent pain. Analysis of the power spectral density of nucleus accumbens resting-state activity in the subacute and chronic back pain patients revealed loss of power in the slow-5 frequency band (0.01 to 0.027 Hz) which developed only in the chronic phase of pain. This loss of power was reproducible across two cohorts of chronic low-back pain patients obtained from different sites and accurately classified chronic low-back pain patients in two additional independent datasets. Our results provide evidence that lower nucleus accumbens volume confers risk for developing chronic pain and altered nucleus accumbens activity is a signature of the state of chronic pain.


Pain ◽  
1985 ◽  
Vol 22 (3) ◽  
pp. 279-287 ◽  
Author(s):  
Ranga Rama K. Krishnan ◽  
Randal D. France ◽  
Susan Pelton ◽  
Una D. McCann ◽  
Jonathan Davidson ◽  
...  

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