Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Fukushima city, Fukushima, Japan.
Spine (Phila Pa 1976). 2009 Oct 15;34(22):2431-6. doi: 10.1097/BRS.0b013e3181b1fb76.
Cerebral activation by lumbar mechanical stimulus was investigated by functional magnetic resonance imaging in healthy subjects and patients with chronic low back pain (LBP).
To characterize the cerebral substrates of LBP, and to explore a possible pathologic pattern of cerebral activation in chronic LBP patients.
The cerebral substrates of LBP have been poorly defined in contrast to those of cutaneous somatic pain.
Eight healthy volunteers and 6 patients with idiopathic, chronic LBP were recruited. Each subject was placed in the prone position on a 3 Tesla MRI scanner, and stimulated by manual pressure with the tail of an air-filled, 20-mL syringe at 5 cm left of the fourth-fifth lumbar spinal interspace. Three blocks of 30-second painful stimulus, calibrated at either 3 or 5 on the 10-cm visual analog scale (VAS), were applied with intervening 30-second rest conditions during whole-brain echo-planar imaging. VAS of pain intensity and unpleasantness were evaluated after each session. Functional imaging was analyzed using a multisubject general linear model with Bonferroni multiple comparisons at P < 0.05.
Pain thresholds were smaller (P < 0.05) and VAS of unpleasantness was larger in LBP patients than in healthy subjects. Activation was observed at the prefrontal, insular, posterior cingulate cortices (PCC), supplementary motor, and premotor areas predominantly in the right hemisphere, but not at the somatosensory cortices. LBP patients showed augmented activation compared with healthy volunteers specifically at the right insula, supplementary motor, and PCC.
Chronic LBP patients showed increased tenderness at the lower back, higher aversive reaction to pain, and augmented LBP-related cerebral activation. The LBP-related activation is characterized by the absence of sensory-discriminative component and the involvement of PCC.
本研究采用功能磁共振成像技术,对健康受试者和慢性下腰痛(LBP)患者进行腰椎机械刺激后的大脑激活情况进行研究。
明确 LBP 的大脑中枢,并探讨慢性 LBP 患者大脑激活的可能病理模式。
与皮肤躯体痛相比,LBP 的大脑中枢尚未得到充分定义。
共招募 8 名健康志愿者和 6 名特发性慢性 LBP 患者。每位受试者均采用俯卧位,在 3T 磁共振扫描仪上,使用充满空气的 20ml 注射器的尾部,在第四和第五腰椎间隙的左侧 5cm 处进行手动压力刺激。以 10cm 视觉模拟量表(VAS)的 3 或 5 分对疼痛强度进行标定,施加 30 秒的疼痛刺激,每 30 秒休息一次,共进行 3 个块,在全脑回波平面成像过程中进行。每次刺激后,评估 VAS 疼痛强度和不愉快程度。采用多受试者一般线性模型进行功能成像分析,采用 Bonferroni 多重比较,P < 0.05。
LBP 患者的疼痛阈值较低(P < 0.05),不愉快 VAS 评分较高。在右侧大脑,主要在前额叶、岛叶、后扣带回皮质(PCC)、辅助运动和运动前区观察到激活,但在躯体感觉皮质区未观察到激活。与健康志愿者相比,LBP 患者在右侧岛叶、辅助运动和 PCC 区的 LBP 相关激活明显增强。
慢性 LBP 患者下腰痛更敏感,对疼痛的厌恶反应更高,与 LBP 相关的大脑激活增加。LBP 相关的激活特征为缺乏感觉辨别成分和涉及 PCC。