Neurosurgical Center Amsterdam, VU University Medical Center, Amsterdam, The Netherlands.
J Nucl Med. 2011 Aug;52(8):1235-9. doi: 10.2967/jnumed.110.084061. Epub 2011 Jul 15.
Our objective was to measure (R)-(11)C-PK11195 binding as an indirect marker of neuronal damage after traumatic brain injury (TBI).
Dynamic (R)-(11)C-PK11195 PET scans were acquired for 8 patients 6 mo after TBI and for 7 age-matched healthy controls. (R)-(11)C-PK11195 binding was assessed using the simplified reference tissue model. Because of widespread traumatic changes in TBI, an anatomic reference region could not be defined. Therefore, supervised cluster analysis was used to generate an appropriate reference tissue input.
Increased whole-brain binding of (R)-(11)C-PK11195 was observed in TBI patients. Regional analysis indicated that increased (R)-(11)C-PK11195 binding was widespread over the brain.
Six months after TBI, there was a prolonged and widespread increase in (R)-(11)C-PK11195 binding, which is indicative of diffuse neuronal damage.
测量创伤性脑损伤(TBI)后神经元损伤的间接标志物(R)-(11)C-PK11195 结合情况。
对 8 例 TBI 后 6 个月的患者和 7 例年龄匹配的健康对照者进行动态(R)-(11)C-PK11195 PET 扫描。使用简化参考组织模型评估(R)-(11)C-PK11195 结合情况。由于 TBI 广泛的创伤性改变,无法定义解剖参考区域。因此,采用监督聚类分析生成适当的参考组织输入。
TBI 患者全脑(R)-(11)C-PK11195 结合增加。区域分析表明,(R)-(11)C-PK11195 结合在大脑中广泛增加。
TBI 后 6 个月,(R)-(11)C-PK11195 结合持续广泛增加,提示弥漫性神经元损伤。