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创伤性脑损伤(traumatic brain injury,TBI)是由外伤引起的脑组织损害。美国脑损伤协会(the Brain Injury Association of America,BIAA)将其定义为由外力导致的大脑功能的改变或其他脑病理性变化。TBI已成为日益严重的全球性公共卫生问题,据美国疾病控制与预防中心调查,在美国每年约有170万新发病例,约占所有创伤导致死亡的1/3,其中文献报道的TBI约75%为轻微脑损伤(mild traumatic brain injury,mTBI)[1]。TBI患者的健康状况不断下降已经引起关注,抑郁症、焦虑、自杀、药物及酒精滥用、人格障碍及其他一些精神症状在TBI患者中的发生率逐渐升高[2-5]。
临床常规应用CT和MRI来诊断颅内出血、脑损伤和颅骨骨折。然而,mTBI患者脑部解剖结构变化不明显,MRI或CT检查难以发现,而且部分患者颅内存在金属碎片并不适合进行MRI检查。很多mTBI患者在受伤后会出现头痛、头晕、乏力、抑郁、焦虑、睡眠障碍、畏光、健忘及不能集中注意力等症状,这些症状均不能通过CT或MRI评价[6]。PET显像是一种定量测定脑血流灌注及代谢的显像技术,可以在纳克水平显示体内小分子变化情况,与毫克或微克水平的MRI或CT相比,灵敏度更高。
创伤性脑损伤PET显像研究进展
Progress in PET imaging evaluating of traumatic brain injury
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摘要: 创伤性脑损伤(TBI)是由外伤引起的脑组织损害,有着较高的发生率及病死率。传统医学影像学技术难以做出诊断。PET作为一种定量测定脑糖代谢及脑血流量变化的显像技术,可以比较精确地显示TBI所致的脑功能变化。目前,18F-FDG PET显像通过评价脑内葡萄糖代谢及脑血流量变化对TBI做出诊断。笔者对TBI 18F-FDG PET显像及脑血流灌注显像进行综述。
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关键词:
- 脑损伤 /
- 正电子发射断层显像术 /
- 氟脱氧葡萄糖F18 /
- 脑血流量
Abstract: Traumatic brain injury(TBI)is the damage of brain tissue caused by external injuries and it has a higher incidence of incidence rate and death rate. It is difficult to diagnose TBI with classic medical imaging technology. PET is an imaging technology that can measure the cerebral glycometabolism and cerebral blood flow quantitatively. It can display the brain functional change caused by TBI. Currently, 18F-FDG PET imaging can diagnose TBI by evaluating the cerebral glycometabolism and cerebral blood flow variation. This paper has comprehensively discussed the current conditions of 18F-FDG PET imaging and cerebral blood flow perfusion PET imaging. -
[1] Huang MX, Nichols S, Baker DG, et al. Single-subject-based whole-brain MEG slow-wave imaging approach for detecting abnormality in patients with mild traumatic brain injury[J]. Neuroimage Clin, 2014, 5:109-119. doi: 10.1016/j.nicl.2014.06.004 [2] Jeyaraj JA, Clendenning A, Bellemare-Lapierre V, et al. Clinicians' perceptions of factors contributing to complexity and intensity of care of outpatients with traumatic brain injury[J]. Brain Inj, 2013, 27(12):1338-1347. doi: 10.3109/02699052.2013.823650 [3] Vasterling JJ, Brailey K, Proctor SP, et al. Neuropsychological outcomes of mild traumatic brain injury, post-traumatic stress disorder and depression in Iraq-deployed US Army soldiers[J]. Br J Psychiatry, 2012, 201(3):186-192. doi: 10.1192/bjp.bp.111.096461 [4] Ilie G, Boak A, Adlaf EM, et al. Prevalence and correlates of traumatic brain injuries among adolescents[J]. JAMA, 2013, 309(24):2550-2552. doi: 10.1001/jama.2013.6750 [5] Rockhill CM, Jaffe K, Zhou C, et al. Health care costs associated with traumatic brain injury and psychiatric illness in adults[J]. J Neurotrauma, 2012, 29(6):1038-1046. doi: 10.1089/neu.2010.1562 [6] Taylor HG, Dietrich A, Nuss K, et al. Post-concussive symptoms inchildren with mild traumatic brain injury[J]. Neuropsychology, 2010, 24(2):148-159. [7] Bigler ED. Neuroimaging biomarkers in mild traumatic brain injury(mTBI)[J]. Neuropsychol Rev, 2013, 23(3):169-209. [8] Bombardier CH, Fann JR, Temkin NR, et al. Rates of major depressive disorder and clinical outcomes following traumatic brain injury[J]. JAMA, 2010, 303(19):1938-1945. doi: 10.1001/jama.2010.599 [9] Hart T, Hoffman JM, Pretz C, et al. A longitudinal study of major and minor depression following traumatic brain injury[J]. Arch Phys Med Rehabil, 2012, 93(8):1343-1349. doi: 10.1016/j.apmr.2012.03.036 [10] McMahon P, Hricik A, Yue JK, et al. Symptomatology and functional outcome in mild traumatic brain injury:results from the prospective TRACK-TBI study[J]. J Neurotrauma, 2014, 31(1):26-33. doi: 10.1089/neu.2013.2984 [11] Umile EM, Sandel ME, Alavi A, et al. Dynamic imaging in mild traumatic brain injury:support for the theory of medial temporal vulnerability[J]. Arch Phys Med Rehabil, 2002, 83(11):1506-1513. doi: 10.1053/apmr.2002.35092 [12] Peskind ER, Petrie EC, Cross DJ, et al. Cerebrocerebellar hypometabolism associated with repetitive blas texposure mild traumatic brain injury in 12 Iraq war Veterans with persistent post-concussive symptoms[J]. Neuroimage, 2011, 54 Suppl1:S76-82. [13] Byrnes KR, Wilson CM, Brabazon F, et al. FDG-PET imaging in mild traumatic brain injury:a critical review[J]. Front Neuroenergetics, 2014, 5:13. [14] Mendez MF, Owens EM, Reza Berenji G, et al. Mild traumatic brain injury from primary blast vs. blunt forces:post-concussion consequences and functional neuroimaging[J]. Neuro Rehabilitation, 2013, 32(2):397-407. [15] Petrie EC, Cross DJ, Yarnykh VL, et al. Neuroimaging, behavioral, and psychological sequelae of repetitive combined blast/impact mild traumatic brain injury in Iraq and Afghanistan war veterans[J]. J Neurotrauma, 2014, 31(5):425-436. doi: 10.1089/neu.2013.2952 [16] Selwyn R, Hockenbury N, Jaiswal S, et al. Mild traumatic brain injury results in depressed cerebral glucose uptake:an FDG PET study[J]. J Neurotrauma, 2013, 30(23):1943-1953. doi: 10.1089/neu.2013.2928 [17] Diaz-Arrastia R, Kochanek PM, Bergold P, et al. Pharmacotherapy of traumatic brain injury:state of the science and the road forward report of the department of defense neurotrauma pharmacology workgroup[J]. J Neurotrauma, 2014, 31(2):135-158. doi: 10.1089/neu.2013.3019 [18] Bergsneider M, Hovda DA, McArthur DL, et al. Metabolic recovery following human traumatic brain injury based on FDG-PET:time course and relationship to neurological disability[J]. J Head Trauma Rehabil, 2001, 16(2):135-148. doi: 10.1097/00001199-200104000-00004 [19] Provenzano FA, Jordan B, Tikofsky RS, et al. F-18 FDG PET imaging of chronic traumatic brain injury in boxers:a statistical parametric analysis[J]. Nucl Med Commun, 2010, 31(11):952-957. doi: 10.1097/MNM.0b013e32833e37c4 [20] Garcia-Panach J, Lull N, Lull JJ, et al. A voxel-based analysis of FDG-PET in traumatic brain injury:regional metabolism and relationship between the thalamus and cortical areas[J]. J Neurotrauma, 2011, 28(9):1707-1717. doi: 10.1089/neu.2011.1851 [21] Wu HM, Huang SC, Hattori N, et al. Selective metabolic reduction in gray matter acutely following human traumatic brain injury[J]. J Neurotrauma, 2004, 21(2):149-161. doi: 10.1089/089771504322778613 [22] Xu Y, McArthur DL, Alger JR, et al. Early nonischemic oxidative metabolic dysfunction leads to chronic brain atrophy in traumatic brain injury[J]. J Cereb Blood Flow Metab, 2010, 30(4):883-894. doi: 10.1038/jcbfm.2009.263 [23] Wu HM, Huang SC, Vespa P, et al. Redefining the pericontusional penumbra following traumatic brain injury:evidence of deteriorating metabolic derangements based on positron emission tomography[J]. J Neurotrauma, 2013, 30(5):352-360. doi: 10.1089/neu.2012.2610 [24] Cunningham AS, Salvador R, Coles JP, et al. Physiological thresholds for irreversible tissue damage in contusional regions following traumatic brain injury[J]. Brain, 2005, 128(Pt 8):1931-1942. [25] Kawai N, Nakamura T, Tamiya T, et al. Metabolic disturbance without brain ischemia in traumatic brain injury:a positron emission tomography study[J]. Acta Neurochir Suppl, 2008, 102:241-245. [26] Hattori N, Huang SC, Wu HM, et al. PET investigation of post-traumatic cerebral blood volume and blood flow[J]. Acta Neurochir Suppl, 2003, 86:49-52. [27] Rostami E, Engquist H, Enblad P. Imaging of cerebral blood flow in patients with severe traumatic brain injury in the neurointensive care[J]. Front Neurol, 2014, 5:114. [28] Hamilton JP, Chen MC, Gotlib IH. Neural systems approaches to understanding major depressive disorder:an intrinsic functional organization perspective[J]. Neurobiol Dis, 2013, 52(1):4-11. [29] Nielsen TH, Bindslev TT, Pedersen SM, et al. Cerebral energy metabolism during induced mitochondrial dysfunction[J]. Acta Anaesthesiol Scand, 2013, 57(2):229-235. doi: 10.1111/j.1399-6576.2012.02783.x
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