Berger Rachel Pardes, Heyes Melvyn P, Wisniewski Stephen R, Adelson P David, Thomas Neal, Kochanek Patrick M
Department of Pediatrics, Children's Hospital of Pittsburgh, 3705 Fifth Avenue, Pittsburgh, PA 15213, USA.
J Neurotrauma. 2004 Sep;21(9):1123-30. doi: 10.1089/neu.2004.21.1123.
This study measured quinolinic acid (QUIN), a macrophage-microglia derived neurotoxin, in the cerebrospinal fluid (CSF) of children after non-inflicted and inflicted traumatic brain injury (nTBI, iTBI), and correlated QUIN concentrations with age, mechanism of injury (nTBi vs. iTBI), Glasgow Coma Scale (GCS) score and 6-month Glasgow Outcome Score. One hundred fifty-two CSF samples were collected from 51 children with severe TBI (GCS < or = 8). CSF was collected at the time an intraventricular catheter was placed and daily thereafter. QUIN concentration was measured by gas chromatography-mass spectroscopy. Patients ranged in age from 2 months to 16 years. Eleven children (22%) had iTBI. Initial and peak CSF QUIN concentrations were higher in patients with iTBI versus nTBI after adjusting for time after injury and GCS. Despite the lack of a history of trauma in 82% of children with iTBI, 100% had a peak QUIN concentration of >100 nM. There was a significant increase in the CSF concentrations of QUIN following severe nTBI and iTBI in children. Higher initial and peak QUIN concentrations after iTBI may be due to severity of injury, young age, and/or delay in seeking medical care, which allows for increased secondary injury.
本研究测量了非创伤性和创伤性脑损伤(nTBI、iTBI)患儿脑脊液(CSF)中喹啉酸(QUIN,一种由巨噬细胞-小胶质细胞衍生的神经毒素),并将QUIN浓度与年龄、损伤机制(nTBi与iTBI)、格拉斯哥昏迷量表(GCS)评分及6个月后的格拉斯哥预后评分进行关联分析。从51例重度TBI(GCS≤8)患儿中收集了152份脑脊液样本。在放置脑室内导管时及之后每日采集脑脊液。通过气相色谱-质谱法测量QUIN浓度。患者年龄范围为2个月至16岁。11名儿童(22%)患有iTBI。在对损伤后时间和GCS进行校正后,iTBI患者脑脊液中QUIN的初始浓度和峰值浓度高于nTBI患者。尽管82%的iTBI患儿没有创伤史,但100%的患儿QUIN峰值浓度>100 nM。儿童严重nTBI和iTBI后脑脊液中QUIN浓度显著升高。iTBI后较高的初始和峰值QUIN浓度可能归因于损伤的严重程度、年龄较小和/或就医延迟,这会导致继发性损伤增加。