Can cortisol levels predict the severity of acute whiplash-associated disorders?
Cortisol
Neck injury
Stress
Whiplash
Journal
European journal of trauma and emergency surgery : official publication of the European Trauma Society
ISSN: 1863-9941
Titre abrégé: Eur J Trauma Emerg Surg
Pays: Germany
ID NLM: 101313350
Informations de publication
Date de publication:
Apr 2020
Apr 2020
Historique:
received:
16
04
2018
accepted:
08
10
2018
pubmed:
14
10
2018
medline:
4
2
2021
entrez:
14
10
2018
Statut:
ppublish
Résumé
The exact underlying mechanism of whiplash-associated disorders still remains obscure. Central sensitization of the brain to painful stimulus and disturbances in the hypothalamic-pituitary-adrenal axis has been suggested to contribute to the development of whiplash-associated disorders. Although cortisol is a well-known factor in the acute stress response and its effects on chronic pain sensation were studied, information is lacking regarding the relation between acute phase cortisol concentrations and the intensity of whiplash-associated disorders. The aim of this prospective observational study was to investigate the relationship between acute serum cortisol concentrations and the severity of whiplash-associated disorders. 55 patients enrolled in the study and they answered a pertinent questionnaire. A blood sample was drawn to determine serum cortisol concentration. The mean cortisol concentration of the whiplash-associated disorder score 2-3 patients was significantly lower compared to the whiplash-associated disorder score 1 patients, 9.5 ± 6.9 vs. 13.22 ± 8.3 µg% (p = 0.02). The mean cortisol concentrations increased significantly from mild through moderate to serious grade of severity of accident as perceived by the patient, 9.64 ± 4.82, 11.59 ± 6.85, 17.39 ± 12.1 µg% (p = 0.02). The study supports the possibility that cortisol plays a role in the development of whiplash-associated disorders. Low or relatively low cortisol concentrations might be associated with more severe forms of the disorder.
Sections du résumé
BACKGROUND
BACKGROUND
The exact underlying mechanism of whiplash-associated disorders still remains obscure. Central sensitization of the brain to painful stimulus and disturbances in the hypothalamic-pituitary-adrenal axis has been suggested to contribute to the development of whiplash-associated disorders. Although cortisol is a well-known factor in the acute stress response and its effects on chronic pain sensation were studied, information is lacking regarding the relation between acute phase cortisol concentrations and the intensity of whiplash-associated disorders. The aim of this prospective observational study was to investigate the relationship between acute serum cortisol concentrations and the severity of whiplash-associated disorders.
METHODS
METHODS
55 patients enrolled in the study and they answered a pertinent questionnaire. A blood sample was drawn to determine serum cortisol concentration.
RESULTS
RESULTS
The mean cortisol concentration of the whiplash-associated disorder score 2-3 patients was significantly lower compared to the whiplash-associated disorder score 1 patients, 9.5 ± 6.9 vs. 13.22 ± 8.3 µg% (p = 0.02). The mean cortisol concentrations increased significantly from mild through moderate to serious grade of severity of accident as perceived by the patient, 9.64 ± 4.82, 11.59 ± 6.85, 17.39 ± 12.1 µg% (p = 0.02).
CONCLUSIONS
CONCLUSIONS
The study supports the possibility that cortisol plays a role in the development of whiplash-associated disorders. Low or relatively low cortisol concentrations might be associated with more severe forms of the disorder.
Identifiants
pubmed: 30315329
doi: 10.1007/s00068-018-1028-2
pii: 10.1007/s00068-018-1028-2
doi:
Substances chimiques
Hydrocortisone
WI4X0X7BPJ
Types de publication
Journal Article
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
357-362Références
Man Ther. 2010 Jun;15(3):e1; author reply e2
pubmed: 20097114
Accid Anal Prev. 2004 Jan;36(1):21-7
pubmed: 14572823
Clin Biomech (Bristol, Avon). 2000 Jul;15(6):426-35
pubmed: 10771121
Psychosom Med. 2005 Sep-Oct;67(5):783-90
pubmed: 16204439
Psychoneuroendocrinology. 2011 Nov;36(10):1540-52
pubmed: 21601366
Pain. 2003 Aug;104(3):509-17
pubmed: 12927623
Clin J Pain. 2001 Dec;17(4):306-15
pubmed: 11783810
Dan Med J. 2012 Dec;59(12):B4560
pubmed: 23290295
Br Med Bull. 1991 Jul;47(3):534-48
pubmed: 1724403
Pain. 2005 Dec 15;119(1-3):219-24
pubmed: 16298068
Phys Ther. 2014 May;94(5):730-8
pubmed: 24481595
Arthritis Res Ther. 2015 Dec 10;17:355
pubmed: 26654189
J Neurol Neurosurg Psychiatry. 2001 Jun;70(6):722-6
pubmed: 11385003
Spine (Phila Pa 1976). 1998 May 1;23(9):1023-8
pubmed: 9589541
Clin Biomech (Bristol, Avon). 1998 Jun;13(4-5):239-249
pubmed: 11415793
Spine (Phila Pa 1976). 2011 Dec 1;36(25 Suppl):S226-32
pubmed: 22020617
Accid Anal Prev. 2002 Mar;34(2):247-55
pubmed: 11829295
J Rheumatol. 2006 May;33(5):968-74
pubmed: 16541476
Spine (Phila Pa 1976). 1995 Apr 15;20(8 Suppl):1S-73S
pubmed: 7604354
Pain. 2007 May;129(1-2):28-34
pubmed: 17218057
Spine (Phila Pa 1976). 2007 Apr 1;32(7):776-81
pubmed: 17414913
J Orthop Sports Phys Ther. 2017 Jul;47(7):462-471
pubmed: 28622487
Pain. 2010 Apr;149(1):143-51
pubmed: 20167428