Background: 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.
Methods: 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.
Results: 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.
Conclusions: 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.