Chang Wei-Ju, Jenkins Luke C, Humburg Peter, Schabrun Siobhan M
Centre for Pain IMPACT, Neuroscience Research Australia (NeuRA), Randwick, New South Wales, Australia.
School of Health Sciences, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, New South Wales, Australia.
Eur J Pain. 2023 Apr;27(4):530-545. doi: 10.1002/ejp.2078. Epub 2023 Jan 11.
Early evidence suggests human assumed central sensitization (HACS) is present in some people with acute low back pain (LBP). Factors influencing individual variation in HACS during acute LBP have not been fully explored. We aimed to examine the evidence for HACS in acute LBP and the contribution of brain-derived neurotrophic factor (BDNF), clinical, psychological and demographic factors to HACS.
Participants with acute LBP (<6 weeks after pain onset, N = 118) and pain-free controls (N = 57) from a longitudinal trial were included. Quantitative sensory testing including pressure and heat pain thresholds and conditioned pain modulation, BDNF serum concentration and genotype and questionnaires were assessed.
There were no signs of HACS during acute LBP at group level when compared with controls. Sensory measures did not differ when compared between controls and LBP participants with different BDNF genotypes. Two LBP subgroups with distinct sensory profiles were identified. Although one subgroup (N = 60) demonstrated features of HACS including pressure/heat pain hypersensitivity at a remote site and deficient conditioned pain modulation, pain severity and disability did not differ between the two subgroups. Variation in sensory measures (~33%) was partially explained by BDNF genotype, sex, age and psychological factors.
This study confirms that HACS is present in some people with acute LBP, but this was not associated with pain or disability. Further, no relationship was observed between BDNF and HACS in acute LBP. More research is needed to understand factors contributing to individual variation in sensory measures in LBP.
Human assumed central sensitization (HACS) is present in acute low back pain (LBP) but factors contributing to individual variation are not fully explored. This study investigated the relationship between factors such as brain derived neurotrophic factor (BDNF) and HACS in acute LBP. Our findings indicate that HACS was present in specific LBP subgroups but BDNF was unrelated to HACS. Combinations of BDNF genotype, demographic and psychological factors explained a small proportion of the variation in sensory measures during acute LBP.
早期证据表明,人类假定的中枢敏化(HACS)存在于一些急性下腰痛(LBP)患者中。急性LBP期间影响HACS个体差异的因素尚未得到充分研究。我们旨在研究急性LBP中HACS的证据,以及脑源性神经营养因子(BDNF)、临床、心理和人口统计学因素对HACS的影响。
纳入一项纵向试验中的急性LBP患者(疼痛发作后<6周,N = 118)和无疼痛对照组(N = 57)。评估包括压力和热痛阈值以及条件性疼痛调制在内的定量感觉测试、BDNF血清浓度和基因型以及问卷。
与对照组相比,急性LBP期间在组水平上没有HACS的迹象。在对照组和具有不同BDNF基因型的LBP参与者之间比较时,感觉测量没有差异。识别出两个具有不同感觉特征的LBP亚组。虽然一个亚组(N = 60)表现出HACS的特征,包括远处部位的压力/热痛超敏反应和条件性疼痛调制不足,但两个亚组之间的疼痛严重程度和残疾情况没有差异。感觉测量的变异(约33%)部分由BDNF基因型、性别、年龄和心理因素解释。
本研究证实,一些急性LBP患者存在HACS,但这与疼痛或残疾无关。此外,在急性LBP中未观察到BDNF与HACS之间的关系。需要更多研究来了解导致LBP感觉测量个体差异的因素。
人类假定的中枢敏化(HACS)存在于急性下腰痛(LBP)中,但导致个体差异的因素尚未得到充分研究。本研究调查了急性LBP中脑源性神经营养因子(BDNF)等因素与HACS之间的关系。我们的研究结果表明,特定的LBP亚组中存在HACS,但BDNF与HACS无关。BDNF基因型、人口统计学和心理因素的组合解释了急性LBP期间感觉测量变异的一小部分。