Etiology

The most common causes of TBI in patients attending the emergency department are:[17]

  • Falls (48%)

  • Non-intentionally struck by or against an object (17%)

  • Motor vehicle-related injury (13%).

Falls are the most common cause of TBI, primarily occurring in very young children and older adults.[17]​ Falls are the second leading cause of TBI-related mortality.​[2]​ Older age is the strongest predictor of poor outcome in any type of TBI in high-income countries, and is more predictive than the specific cause of the injury.[38]

Being non-intentionally struck by or against an object is the second leading cause of TBI, and associated mortality is the lowest of the common causes of TBI.​​​​[2][17]​ These injuries encompass being non-intentionally struck (hit) by or crushed by a human, animal, or inanimate object or force other than a vehicle, and therefore include injuries due to contact sports or high-risk recreational activities.

Suicide is associated with the highest rate of TBI-related death.​[2]​ Suicide accounts for 35.5% of all TBI-related deaths in the US; the average annual age-adjusted rate is highest among older adults ≥75 years (12.2 per 100,000 population).​[2]

Concussion

Involves an impact leading to microscopic injury at the level of the neuronal membrane that initiates a cascade of neurohormonal and neuroexcitatory processes demonstrated clinically as cognitive, somatic and/or affective symptoms. These microscopic injuries are not evident on standard computed tomography (CT), therefore: the diagnosis of concussion is symptom-based; patients with concussion are often excluded from neurologic follow-up.

Concussion is likely present in a majority of patients after any TBI, but older patients may have intracranial injury without the typical initial concussive symptoms.[39]​ Patients with concussion commonly report headaches, dizziness, difficulty concentrating, and confusion.[40] 

The five major subtypes of concussion include headache, cognitive, vestibular, mood and ocular-motor. One meta-analysis demonstrated that headache and cognitive symptoms are the most common subtypes in both adults and children.[22] 

Hemorrhage

Subarachnoid hemorrhage (SAH) is caused by the tearing of pial vessels and, if severe, hemorrhage can extend into the ventricles, causing intraventricular hemorrhage. SAH is associated with a poorer outcome in patients with moderate or severe TBI, but it is unclear whether the SAH is simply a marker of severity of injury or if the hemorrhage itself causes poorer outcomes due to vasospasm.[41]

Subdural hematoma (SDH) most often occurs as a result of tearing of the bridging veins coursing to the dural venous sinuses. SDH most commonly occurs after a motor vehicle-related injury (younger adults) or fall (older adults).[7][30][31]​​ People with pre-existing cerebral atrophy or coagulopathies have an increased risk of SDH.

Epidural hematoma is a collection of blood between the skull and the dura, typically caused by a direct force to the skull from a motor vehicle injury, fall, or assault. Classically, a blow to the side of the head causes a temporal bone fracture with associated middle meningeal artery disruption and subsequent hematoma formation.

Intracerebral hematomas are thought to be caused by a tear of a parenchymal vessel or the coalescence of cerebral contusions.

Cerebral contusions

Contusions are caused by direct trauma, or due to acceleration-deceleration injury causing the brain to impact the frontal or temporal regions of the skull, resulting in multiple scattered punctate hemorrhages and edema. Although appearing minor on initial CT, contusions are clinically important because they are more likely to progressively worsen compared with other intracranial injuries. Depending on the severity of the TBI, studies have demonstrated that more than half of cerebral contusions progress with associated edema or transform into cerebral hemorrhage, leading to significant morbidity and mortality.[42][43]​​

Diffuse axonal injury

Diffuse axonal injury (DAI) occurs due to a rapid rotational or deceleration force that causes stretching and tearing of neurons, followed by focal areas of hemorrhage and edema.

In mild axonal injury, damage is typically microscopic. In more severe injury, the CT scan may be normal or may show small petechial hemorrhages and edema located at the gray-white matter junction (Grade 1) as well as in the corpus callosum (Grade 2) and in the brainstem (Grade 3); the grades correspond well with severity of injury and ultimate outcomes.

Magnetic resonance imaging is indicated when CT does not explain the clinical findings. Severe DAI can result in almost instantaneous loss of consciousness and lead to a persistent vegetative state.[34]

Skull fractures

Skull fractures are caused by direct impact and may be linear or comminuted. Fractures may be located on the cranial vault or in the basilar skull, and may have a varying degree of depression. Fractures can be closed or open, communicating externally via wounds, facial sinuses, the auditory canal, or the oropharynx. The location of skull fractures has implications for adjacent anatomical structures as follows:

  • Fractures of the temporal bone that cross the meningeal artery are associated with epidural hematomas; those that cross a dural sinus can cause significant subdural hemorrhage and hematoma formation. Fractures that cross a dural sinus can also lead to cerebral venous sinus thrombosis.

  • The bones of the base of the skull are relatively thick; therefore, any basilar skull fracture implies a serious mechanism of injury with a high risk of intracerebral injury.

  • Because the dura is tightly adhered to the base of the skull, basilar skull fractures are frequently associated with dural tears and cerebrospinal fluid leaks.

  • Fractures that involve the carotid canal can cause carotid artery dissection.

  • Basilar skull fractures that extend to the petrous part of the temporal bone can damage cranial nerves VII and VIII.

Penetrating injuries

Penetrating injuries are either high- or low-velocity. High-velocity missiles such as bullets can cause skull fractures, parenchymal lacerations, contusions, axonal shear, and hematoma formation. Low-velocity wounds such as a knife wound can penetrate the thinner bones of the skull, including the orbital wall and parts of the temporal bone.

Damage to the parenchyma tends to be limited to the wound tract in low-velocity injuries, but high-velocity missiles can cause concomitant blast injury to surrounding structures.

Blast injuries

Blast injuries cause a variety of complex damage patterns. The initial blast wave is thought to cause a concussive shearing force that leads to axonal injury, SAH, and contusions. The secondary blast effects of flying debris can cause penetrating injuries, and the tertiary effects are the acceleration-deceleration impact injuries seen after the blast wave passes.

TBI due to blast is most commonly manifest as diffuse axonal injury, contusion, and subdural hemorrhage.[44] Patients with moderate to severe TBI due to blasts or explosions tend to be self-evident due to the associated decreased Glasgow Coma Scale (GCS) score. Mild TBI may be under-diagnosed when obscured by other injuries in patients with normal, or near normal, GCS.

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