Traumatic brain injury (TBI) is a frequent cause of death and disability affecting millions of people every year worldwide. It is initiated by mechanical forces that cause sudden head motion. Such motion produces deformation of the brain and surrounding tissues and thus may result in axonal injury, contusion, or hematoma. The trauma launches a cascade of biochemical reactions often leading to ischemia, hypoxia, brain swelling, and edema. TBI may also induce damages of the cranial vasculature, with alterations of the blood vessel that put the neural tissue at risk. TBI can either cause vessel rupture and hemorrhage (bleeding), or a pathophysiological change of the vessel structure which is secondary associated with some kind of dysfunction. Hemorrhage is easy to recognize, commonly categorized according to its location as epidural (between the skull and the dura mater – associated with disruption of the middle meningeal vessels), subdural (between the dura mater and arachnoid membrane – usually concerning the bridging veins), or subarachnoidal (between arachnoid membrane and the pia mater). Intracerebral bleeding may also occur when the membranes surrounding the brain are impaired. In case of contusion, vascular damage and mechanical cortical damage can occurr at the same time. Even if bleeding is not present, function and microstructure of the injured vessels might be impaired. Vessel disruption and hemorrhage alter the cerebral blood flow, increase the intracranial pressure, affect the maintenance of the blood-brain barrier (exchange of nutrients and waste that occurs at the capillary level), and disrupt the CNS homeostasis by exposing the neural tissue to disregulated blood flow.
Understanding cerebrovascular injuries and the mechanisms behind them is crucial for diagnostics and treatment strategies. Monson et al. (in press) describe the current state of knowledge on the mechanics of cerebral vessels during head trauma and how they respond to the applied loads. They provide a summary of the experimental research focused on the loading conditions during the TBI. Experiments with physical models for instance show that there is significant relative motion between the brain and skull during the trauma. In the sagittal plane, this motion tends to be largest at the vertex and smallest at the brain base. Constraints at the base can lead to brain rotation which pushes the parietal cortex into the cranial bones, possibly causing of contusion and subdural hematoma. In general, it appears that rotation is more damaging than translation. Computer models represent another approach of the TBI research and provide accurate predictions of brain deformation for many loading scenarios. These models enable to estimate exterior loading conditions according to the internal deformation of tissues that are directly involved in injury. However, validation of these models is needed, as well as specific models focusing on blood vessels. The authors also provide a summary of what is known about cerebral vessel response to extreme deformations, passive physical properties, structural failure, and subfailure damage and dysfunction. In another article, Saad et al. (in press) describe various kinds of intracranial hemorrhage in biomedical imaging. Both macroscopic hematomas and microhemorrhages are described according to the distinctions based on intracranial compartments, and traumatic vs nontraumatic cases.