Beitchman Joshua A, Lifshitz Jonathan, Harris Neil G, Thomas Theresa Currier, Lafrenaye Audrey D, Hånell Anders, Dixon C Edward, Povlishock John T, Rowe Rachel K
BARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona, USA.
Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona, USA.
Neurotrauma Rep. 2021 Feb 8;2(1):59-75. doi: 10.1089/neur.2020.0046. eCollection 2021.
Diffuse brain injury is better described as multi-focal, where pathology can be found adjacent to seemingly uninjured neural tissue. In experimental diffuse brain injury, pathology and pathophysiology have been reported far more lateral than predicted by the impact site. We hypothesized that local thickening of the rodent skull at the temporal ridges serves to focus the intracranial mechanical forces experienced during brain injury and generate predictable pathology. We demonstrated local thickening of the skull at the temporal ridges using contour analysis on magnetic resonance imaging. After diffuse brain injury induced by midline fluid percussion injury (mFPI), pathological foci along the anterior-posterior length of cortex under the temporal ridges were evident acutely (1, 2, and 7 days) and chronically (28 days) post-injury by deposition of argyophilic reaction product. Area CA3 of the hippocampus and lateral nuclei of the thalamus showed pathological change, suggesting that mechanical forces to or from the temporal ridges shear subcortical regions. A proposed model of mFPI biomechanics suggests that injury force vectors reflect off the skull base and radiate toward the temporal ridge, thereby injuring ventral thalamus, dorsolateral hippocampus, and sensorimotor cortex. Surgically thinning the temporal ridge before injury reduced injury-induced inflammation in the sensorimotor cortex. These data build evidence for temporal ridges of the rodent skull to contribute to the observed pathology, whether by focusing extracranial forces to enter the cranium or intracranial forces to escape the cranium. Pre-clinical investigations can take advantage of the predicted pathology to explore injury mechanisms and treatment efficacy.
弥漫性脑损伤更确切地说是多灶性的,其病理改变可在看似未受损伤的神经组织附近发现。在实验性弥漫性脑损伤中,已报道病理改变和病理生理改变远比撞击部位所预测的更靠外侧。我们推测,啮齿动物颞嵴处颅骨局部增厚有助于在脑损伤时集中颅内机械力,并产生可预测的病理改变。我们通过磁共振成像的轮廓分析证实了颞嵴处颅骨的局部增厚。在中线流体冲击伤(mFPI)诱导的弥漫性脑损伤后,颞嵴下方皮质前后长度上的病理病灶在伤后急性期(1、2和7天)和慢性期(28天)通过嗜银反应产物的沉积而明显可见。海马体的CA3区和丘脑外侧核出现了病理变化,这表明进出颞嵴的机械力会剪切皮质下区域。一个提出的mFPI生物力学模型表明,损伤力向量从颅底反射并向颞嵴辐射,从而损伤腹侧丘脑、背外侧海马体和感觉运动皮层。在损伤前手术削薄颞嵴可减轻感觉运动皮层的损伤诱导炎症。这些数据为啮齿动物颅骨的颞嵴导致观察到的病理改变提供了证据,无论是通过集中颅外力量进入颅骨还是颅内力量逃离颅骨。临床前研究可以利用预测的病理改变来探索损伤机制和治疗效果。