Primary injury occurs at the moment of initial trauma, including
- skull fracture (breaking of the bony skull),
- contusions (bruise/bleed on the brain) that can lead to hematomas (blood clots in the meningeal layers or in the cortical/subcortical structures as a result of the trauma),
- concussions (low velocity injury resulting in functional deficits without pathological injury),
- lacerations (tears in brain tissue or blood vessels of the brain),
- diffuse axonal injury (traumatic shearing forces leading to tearing of nerve fibers in the white matter tracts).
Primary injuries can be caused by either a penetrating (open-head) injury or a nonpenetrating (closed-head) injury.
A penetrating (open-head) injury involves an open wound to the head from a foreign object (e.g., bullet). It is typically marked by focal damage that occurs along the route the object has traveled in the brain that includes fractured/perforated skull, torn meninges, and damage to the brain tissue (Hegde, 2006).
A nonpenetrating (closed-head) injury is marked by brain damage due to indirect impact without the entry of any foreign object into the brain. The skull may or may not be damaged, but there is no penetration of the meninges. Nonpenetrating injuries can be of two types:
- Acceleration injuries-caused by movement of the brain within the unrestrained head (e.g. whiplash injury). If the force impacting the head is strong enough, it can cause a contusion at the site of impact and the opposite side of the skull, causing an additional contusion (coup-contrecoup injury).
- Non-acceleration injuries-caused by injury to a restrained head and, therefore, no acceleration or deceleration of the brain occurs within the skull (e.g., blow to the head). These usually result in deformation (fracture) of the skull, causing focal localized damage to the meninges and brain.
Secondary injury occurs as an indirect result of the insult. It results from processes initiated by the initial trauma and typically evolves over time. These include
- ischemia (insufficient blood flow);
- hypoxia (insufficient oxygen in the brain);
- hypo/hypertension (low/high blood pressure);
- cerebral edema (swelling of the brain);
- raised intracranial pressure (increased pressure within the skull), which can lead to herniation (parts of the brain are displaced);
- hypercapnia (excessive carbon dioxide levels in the blood);
- meningitis (infection of the meningeal layers) and brain abscess;
- biochemical changes (changes in levels of neurotransmitters, sodium, potassium, etc.);
Hegde, M. N. (2006). A coursebook on aphasia and other neurogenic language disorders (3rd ed.). Clifton Park, NY: Delmar Cengage Learning.