Crider Tiffany, Eng Derrick, Sarkar Pooja R, Cordero Janet, Krusz John Claude, Sarkar Subhendra N
HackensackUMC Palisades, North Bergen, NJ, United States.
Orange Regional Medical Center, Middletown, NY, United States.
Clin Neurol Neurosurg. 2018 Jul;170:159-164. doi: 10.1016/j.clineuro.2018.05.019. Epub 2018 May 18.
MRI and CT scans are usually normal in mild traumatic brain injury (mTBI) although 15-20% of such patients suffer for months from fatigue, headache, anxiety, sleep and other disorders. mTBI is suspected to be a cerebrovascular injury, similar to moderate and severe TBI. Brain SPECT is more sensitive and shows perfusion abnormalities immediately after mTBI. This work explores the perfusion abnormalities for young patients suffering from fatigue several months after mTBI.
Twelve mTBI patients (age:8-36 yr, 4 male) with no history of fatigue prior to trauma were prospectively studied following onset of fatigue 6-12 months after mTBI utilizing 99 m-Tc ECD brain SPECT with early and delayed radiotracer imaging.
The perfusion pattern in the mTBI + fatigue group included left hemispheric deficits in frontal lobes (early phase: 15.2 ± 4.2%, delayed phase: 9.9 ± 2.2%) and medial temporal lobes (early phase 11.2 ± 3.7%, delayed phase: 9.0 ± 2.3%). Seven patients additionally showed excess tracer accumulation in the parenchyma surrounding internal jugular bulb inferior to temporal lobe. This was modeled as due to increased cellular permeability from TBI induced oxidative stress affecting endothelial tight junctions and consequent tracer leakage across jugular bulbs. Prolonged posture changes from erect to supine position during imaging increase jugular cross-sectional area and venous wall pressure as has been observed in other disease processes and seem to be responsible for tracer leakage from jugular bulbs in our study.
This work supports an oxidative stress and BBB disruption model for mTBI. The frontal and temporal lobe perfusion deficits are attributed to anatomical vulnerabilities of these lobes. During a mild TBI both of these lobes are susceptible to grazing impacts with underlying bony ridges. We propose a relation between mTBI and fatigue arising from oxidative stress in mTBI affecting ATP generation and altering endothelial homeostasis for both micro-and-large vasculatures. The tracer leakage observed around jugular veins is due to posture induced changes in venous cross-sections and wall pressure as well as from compromised endothelium post TBI induced oxidative stress.
在轻度创伤性脑损伤(mTBI)中,MRI和CT扫描通常显示正常,尽管15%-20%的此类患者会持续数月遭受疲劳、头痛、焦虑、睡眠及其他障碍的困扰。mTBI被怀疑是一种脑血管损伤,类似于中度和重度TBI。脑SPECT更为敏感,在mTBI后即刻就能显示灌注异常。本研究探讨mTBI数月后出现疲劳的年轻患者的灌注异常情况。
前瞻性研究了12例mTBI患者(年龄8-36岁,4例男性),这些患者在创伤前无疲劳病史,于mTBI后6-12个月出现疲劳时,采用99m-Tc ECD脑SPECT进行早期和延迟放射性示踪剂成像。
mTBI+疲劳组的灌注模式包括额叶左半球缺损(早期:15.2±4.2%,延迟期:9.9±2.2%)和颞叶内侧缺损(早期:11.2±3.7%,延迟期:9.0±2.3%)。另外7例患者显示颞叶下方颈静脉球周围实质内示踪剂积聚过多。这被认为是由于TBI诱导的氧化应激导致细胞通透性增加,影响内皮紧密连接,进而导致示踪剂通过颈静脉球泄漏。成像过程中从直立位到仰卧位的长时间姿势改变会增加颈静脉横截面积和静脉壁压力,正如在其他疾病过程中所观察到的,这似乎是我们研究中示踪剂从颈静脉球泄漏的原因。
本研究支持mTBI的氧化应激和血脑屏障破坏模型。额叶和颞叶灌注缺损归因于这些脑叶的解剖易损性。在轻度TBI期间,这两个脑叶都容易受到下方骨嵴的擦过性撞击。我们提出mTBI与mTBI中氧化应激导致的疲劳之间存在关联,氧化应激会影响ATP生成,并改变微血管和大血管的内皮稳态。在颈静脉周围观察到的示踪剂泄漏是由于姿势引起的静脉横截面积和壁压力变化,以及TBI诱导的氧化应激后内皮受损所致。