From the Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging (M.B., B.R.R., L.L.W., B.L.E.), and Center for Neurotechnology and Neurorecovery, Department of Neurology (B.L.E.), Massachusetts General Hospital and Harvard Medical School; Division of Sleep Medicine (M.B.), Harvard University; and Department of Neurology (S.I.), Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Neurology. 2021 Jul 13;97(2):e113-e123. doi: 10.1212/WNL.0000000000012192. Epub 2021 May 28.
In patients with severe traumatic brain injury (TBI), coma is associated with impaired subcortical arousal mechanisms. However, it is unknown which nuclei involved in arousal (arousal nuclei) are implicated in coma pathogenesis and are compatible with coma recovery.
We mapped an atlas of arousal nuclei in the brainstem, thalamus, hypothalamus, and basal forebrain onto 3 tesla susceptibility-weighted images (SWI) in 12 patients with acute severe TBI who presented in coma and recovered consciousness within 6 months. We assessed the spatial distribution and volume of SWI microbleeds and evaluated the association of microbleed volume with the duration of unresponsiveness and functional recovery at 6 months.
There was no single arousal nucleus affected by microbleeds in all patients. Rather, multiple combinations of microbleeds in brainstem, thalamic, and hypothalamic arousal nuclei were associated with coma and were compatible with recovery of consciousness. Microbleeds were frequently detected in the midbrain (100%), thalamus (83%), and pons (75%). Within the brainstem, the microbleed incidence was largest within the mesopontine tegmentum (e.g., pedunculotegmental nucleus, mesencephalic reticular formation) and ventral midbrain (e.g., substantia nigra, ventral tegmental area). Brainstem arousal nuclei were partially affected by microbleeds, with microbleed volume not exceeding 35% of brainstem nucleus volume on average. Compared to microbleed volume within nonarousal brainstem regions, the microbleed volume within arousal brainstem nuclei accounted for a larger proportion of variance in the duration of unresponsiveness and 6-month Glasgow Outcome Scale-Extended scores.
These results suggest resilience of arousal mechanisms in the human brain after severe TBI.
在严重创伤性脑损伤(TBI)患者中,昏迷与皮质下唤醒机制受损有关。然而,目前尚不清楚哪些参与唤醒的核团(唤醒核团)与昏迷发病机制有关,并且与昏迷恢复兼容。
我们将脑桥、丘脑、下丘脑和基底前脑的唤醒核团图谱映射到 12 例急性严重 TBI 患者的 3 特斯拉磁化率加权图像(SWI)上,这些患者在昏迷中出现并在 6 个月内恢复意识。我们评估了 SWI 微出血的空间分布和体积,并评估了微出血体积与无反应时间和 6 个月时功能恢复的相关性。
在所有患者中,没有一个单一的唤醒核团受到微出血的影响。相反,脑桥、丘脑和下丘脑唤醒核团的多个微出血组合与昏迷有关,并且与意识恢复兼容。微出血在中脑(100%)、丘脑(83%)和脑桥(75%)中经常被检测到。在脑桥内,微出血发生率最大的是中脑桥被盖(例如,脚脑桥核、中脑网状结构)和腹侧中脑(例如,黑质、腹侧被盖区)。脑桥唤醒核团部分受到微出血的影响,微出血体积平均不超过脑桥核体积的 35%。与非唤醒脑桥区域内的微出血体积相比,唤醒脑桥核内的微出血体积占无反应时间和 6 个月格拉斯哥结局量表扩展评分方差的比例更大。
这些结果表明,严重 TBI 后人类大脑的唤醒机制具有弹性。