University of California, Davis, California, USA.
Neurosurgery. 2011 Jul;69(1):173-83; discussion 183. doi: 10.1227/NEU.0b013e318212bc7b.
We define chronic traumatic encephalopathy (CTE) as a progressive neurodegenerative syndrome caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain.
We present emerging histomorphologic phenotypes of CTE that we identified in our cohort of CTE cases with apolipoprotein E genotyping and causes and manners of death.
Autopsy brain tissue of 14 professional athletes and 3 high school football players was examined after unexpected deaths. Histochemical and immunohistochemical tissue staining was performed with apolipoprotein E genotyping.
Ten of 14 professional athletes (71%) were positive for CTE: 7 of 8 football players, 2 of 4 wrestlers, and 1 boxer. One of 3 high school players manifested incipient CTE. The age range of those with CTE was 18 to 52 years; they were all male athletes. In all cases of CTE, Alzheimer-type cerebral cortical atrophy was absent; negligible to mild neocortical neuronal dropout was present. The fundamental neuropathologic feature of CTE was the topographic distribution of sparse, moderate, and frequent band-shaped, flame-shaped, small and large globose neurofibrillary tangles and neuritic threads in the cerebral cortex, subcortical nuclei/basal ganglia, hippocampus, and brainstem nuclei. Sparse to frequent diffuse amyloid plaques may accompany tauopathy and was seen in only 2 CTE cases. No α-synucleinopathy was present. All 7 CTE-positive professional athletes with known apolipoprotein E genotypes had at least 1 E3 allele comprising 5 E3/E3 (71%) and 2 E3/E4 (29%). Alcohol- and drug-related deaths, suicides, and accidental deaths were overrepresented in our CTE cohort.
The emerging histomorphologic features of our CTE cohort may specify histologic criteria for CTE diagnosis, may identify emerging histologic variants of CTE and may facilitate more objective surveillance and accurate identification of sentinel CTE cases.
我们将慢性创伤性脑病(CTE)定义为一种由头部单次、发作性或反复性钝力冲击以及加速度减速力向大脑传递引起的进行性神经退行性综合征。
我们介绍了 CTE 的新兴组织形态表型,这些表型是我们在具有载脂蛋白 E 基因分型的 CTE 病例队列以及死因和死亡方式中发现的。
对 14 名职业运动员和 3 名高中足球运动员的意外死亡尸检脑组织进行了检查。进行了载脂蛋白 E 基因分型的组织化学和免疫组织化学染色。
14 名职业运动员中有 10 名(71%)为 CTE 阳性:8 名足球运动员中有 7 名,4 名摔跤运动员中有 2 名,1 名拳击手。其中 1 名高中球员表现出初期 CTE。CTE 患者的年龄范围为 18 至 52 岁;他们均为男性运动员。在所有 CTE 病例中,均不存在阿尔茨海默病样大脑皮质萎缩;仅有轻微到中度的皮质神经元丢失。CTE 的基本神经病理学特征是稀疏、中度和频繁的带状、火焰状、小到大球形神经原纤维缠结和神经原纤维丝在大脑皮质、皮质下核/基底节、海马体和脑干核中的拓扑分布。稀疏到频繁的弥漫性淀粉样斑块可能伴有 tau 病,仅在 2 例 CTE 病例中可见。无α-突触核蛋白病。我们 CTE 队列中 7 名具有已知载脂蛋白 E 基因型的 CTE 阳性职业运动员至少有 1 个 E3 等位基因,包括 5 个 E3/E3(71%)和 2 个 E3/E4(29%)。我们的 CTE 队列中,酒精和药物相关死亡、自杀和意外死亡的比例过高。
我们的 CTE 队列的新兴组织形态学特征可能为 CTE 诊断指定组织学标准,可能确定 CTE 的新兴组织学变体,并有助于更客观的监测和准确识别哨兵 CTE 病例。