Traumatic injury to the brain resulting from high-speed acceleration of the brain within the skull cavity in the direction of inertial force.
During acceleration injury, movement of the head is unrestricted. One of the most common scenarios resulting in acceleration injury is a high-speed motor vehicle accident. Primary brain injury results from brain tissue and brain structures compressing against one another in the force of inertia. This may result in bruising, hemorrhage, and shearing of the underlying tensile strength of white matter connections deep within the brain. Secondary injury may occur hours or even days after the inciting traumatic event. Secondary effects of injury can include decreased cerebral blood flow, edema, hemorrhage, increased intracranial pressure, and biochemical changes that may cause excitotoxicity and more extensive damage to the surrounding brain structures and their associated connections.
Theoretical models of linear acceleration injury now address the heterogeneity of effects that can result from such biomechanical injuries. Although diffuse brain damage may result from this type of injury, a key factor that predicts the extent of damage following acceleration injury is the area of initial impact. Given that the structure and projection pathways of the brain have varying densities and tensile strengths within different regions of the brain, the point of impact is most likely the key in determining the extent of damage that takes place and the likelihood and course of recovery that is possible following injury.
Patients sustaining acceleration injury may experience headache, photophobia, phonophobia, nausea, and dizziness immediately following injury onset. On neuropsychological evaluation, patients with acceleration injuries are more likely to demonstrate a diffuse, rather than focal, profile of cognitive impairment when cognitive impairment is present. The lateralization of cognitive impairment that is typically observed in focal brain injury is relatively uncommon following acceleration injury. A diffuse profile of cognitive impairment in acceleration injury is due to the disruption of white matter tracts that are responsible for efficiency and coordination of communication between functional brain injuries. As such, a patient with acceleration injury may demonstrate cognitive slowing, executive dysfunction, and problems with simple and complex attention as a consequence of his/her brain injury.