並列タイトル等キモパパインを用いて誘発したカニクイザル椎間板性腰痛モデルにおける脳活動; 予備実験
タイトル（掲載誌）Spine surgery and related research
一般注記doctoral
医学系研究科
Background: There is currently a lack of translatable, preclinical models of low back pain (LBP). Chymopapain, a proteolytic enzyme used to treat lumbar intervertebral disc (IVD) herniation, could induce discogenic LBP. The current study developed a behavioral model of discogenic LBP in nonhuman primates. Significant brain activation is observed in clinical LBP. Thus, the current study also sought to define brain activation over time in a macaque with discogenic LBP.Methods: Responses to pressure applied to the back at L4/L5 were measured in eight adult male Macaca fasciculata using a pressure algometer. The nucleus pulpous of the IVD between L4 and L5 was aspirated and chymopapain (1mg/mL) was injected under fluoroscopic guidance (n=2). In two macaques, the nucleus pulpous was only aspirated. Brain activation in response to pressure applied to the lower back was assessed using a 3.0T magnetic resonance imaging scanner in four macaques before and 1,3,9, and 14 days after treatment.Results: The mean (±SD) response pressure before treatment was 1.4±0.1kg. One day after chymopapain treatment, the response pressure decreased to 0.6±0.05kg (P<0.01), suggestive of pressure hypersensitivity. Over time, the pressure thresholds following chymopapain treatment gradually returned to normal. Following aspiration only, the response pressure was 1.4±0.05kg, which was not significantly different from the uninjured controls. There was activation of the secondary somatosensory cortex and insular cortex one and three days after chymopapain treatment; there was no activation following aspiration only.Conclusions: Enzymatic treatment of the nucleus pulpous leads to acute LBP and pressure-evoked activation in pain-related brain areas. The current model of discogenic LBP parallels clinical LBP and could be used to further elaborate the mechanism of acute LBP.
DOIinfo:doi/10.22603/ssrr.2018-0110
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