Department of Descriptive and Clinical Anatomy (R.R., M.S., B.C.), Medical University of Warsaw, Poland.
First Department of Anesthesiology and Intensive Care (R.R.), Medical University of Warsaw, Poland.
Stroke. 2022 Nov;53(11):3474-3480. doi: 10.1161/STROKEAHA.122.040143. Epub 2022 Sep 8.
Despite advances in understanding various risk and prognostic factors, spontaneous intracerebral hemorrhage is connected to very high morbidity and mortality, while the therapy is mainly supportive. Understanding of the pathophysiology of initial hematoma expansion is limited due to insufficient clinical data and lack of a suitable animal model.
We injected 40 anatomic specimens of the basal ganglia with contrast medium, scanned them with a micro-computed tomography scanner and analyzed the results of radiological studies, direct and histological examinations.
In 9 cases, micro-computed tomography and histological examinations revealed contrast medium extravasations mimicking intracerebral hematomas. The artificial hematomas spread both proximally and distally along the ruptured perforator and its branches in the perivascular spaces and detached the branches from the adjacent neural tissue leading to destruction of the tissue and secondary extravasations. Moreover, some contrast extravasations skipped to the perivascular spaces of unruptured perforators, created further extravasation sites and aggravated the expansion of the artificial hematoma. There was no subarachnoid extension of any artificial hematoma.
We postulate that a forming basal ganglia intracerebral hematoma spreads initially in the perivascular space, detaches the branches from the neural tissue and causes secondary bleeding. It can also skip to the perivascular space of a nearby perforator. The proposed mechanism of hematoma initiation and formation explains extent of damage to the neural tissue, variability of growth in time and space, creation of secondary bleeding sites, and limited usefulness of surgical interventions. The model is reproducible, the extent of the artificial hematoma can be easily controlled, the rupture sites of the perforating arteries can be determined, and preparation of the model does not require specialized, expensive equipment apart from the micro-computed tomography scanner.
尽管对各种风险和预后因素的认识有所提高，但自发性脑出血仍然导致极高的发病率和死亡率，而治疗主要是支持性的。由于临床数据不足和缺乏合适的动物模型，对初始血肿扩大的病理生理学的理解有限。
我们将造影剂注入 40 个基底节的解剖标本中，用微计算机断层扫描扫描仪进行扫描，并分析放射学研究、直接和组织学检查的结果。
在 9 例中，微计算机断层扫描和组织学检查显示造影剂外渗模拟脑出血。人工血肿沿着破裂的穿支血管及其分支在血管周围空间向远近两端扩散，并使分支与邻近的神经组织分离，导致组织破坏和继发性出血。此外，一些造影剂外渗跳过未破裂的穿支血管的血管周围空间，创建了进一步的外渗部位，并加剧了人工血肿的扩大。没有任何人工血肿延伸到蛛网膜下腔。
我们假设正在形成的基底节脑出血最初在血管周围空间中扩散，使分支与神经组织分离并导致继发性出血。它也可以跳到附近穿支血管的血管周围空间。提出的血肿形成机制解释了对神经组织的损伤程度、时间和空间上的变化、继发性出血部位的形成以及手术干预的局限性。该模型具有可重复性，人工血肿的程度可以很容易地控制，穿支动脉的破裂部位可以确定，除了微计算机断层扫描扫描仪外，模型制备不需要专门的昂贵设备。
