Classification of Traumatic Brain Injury

Original Editor - Anna Ziemer

Top Contributors - Naomi O'Reilly and Kim Jackson  

Introduction

There are various classification determinants utilized to classify traumatic brain injury. The clinical presentation and prognosis depend on the individual nature of the injury with often coexisting types of TBI. The classification is important for acute management, treatment and prognosis as well as neurorehabilitation requirements. [1]
Traumatic Brain Injury Subtypes. There are several different variants of traumatic brain injury, which often coexist and have significant overlap. They can be broadly divided into focal and diffuse injuries, although it is worth noting that true focal injuries are rare and blast injuries lack a pure neuropathological correlate. The clinical presentation and prognosis of a traumatic brain injury varies depending on the individual nature of the injury. The inherent variability makes it challenging to establish the optimal treatment and there is recognition of the value of an individualised approach. [2]

Primary v Secondary Injuries

Depending on the timing and impact nature (Mechanical, Non-Mechanical) and accompanying pathophysiological processes.

Primary Injury

Occurs at the time of injury and is induced by mechanical forces. Two main mechanisms that cause primary injury are:

  • Contact (i.e.: an object striking the head or the brain striking the inside of the skull)
  • Acceleration - Deceleration.

Primary injury due to acceleration-deceleration results from unrestricted movement of the head and leads to shear, tensile, and compressive strains. These forces can cause intracranial hematoma, diffuse vascular injury, and injury to cranial nerves and the pituitary stalk. [3]

Secondary Injury

Is not mechanically induced; it may be delayed from the moment of impact, and it may superimpose injury on a brain already affected by a mechanical injury. [3] The secondary damage is caused by cascade of processes impacting “cerebral blood flow (hyper or hypoperfusion), impaired cerebrovascular autoregulation,  cerebral metabolic disfunction and impaired cerebral oxygenation.” [4] The ischemia and oedema are secondary injury types. [hyper link to pathophysiology to be added later]

The outcome form head injury is determined by above types with primary injury extend being only sensitive to preventative measures and secondary injury extend being susceptible to neuroprotective therapeutic interventions.
Cellular and Molecular Activities Resulting in Secondary Brain Injury. Following a traumatic insult to the brain, an extensive series of various cellular processes is initiated that leads to further neuronal dysfunction and death. This contributes to the complexity of traumatic brain injury but also provides a variety of therapeutic targets. [5]

Focal v Diffuse Injuries

Focal Injury

Usually due to contact and causing scalp injury, might present as skull fracture, contusions and/or intracranial haemorrhage. Those injuries are detectable by CT, MRI or PET scans. Contusions are the bleeding on the brain and include fracture contusion, coup contusion (at the site of the impact) and contrecoup contusion(directly opposite to the impact site). This mechanism is related to moving of intracranial content in the skull and impinging on internal surface of the skull. Commonly observed injury is coup-contrecoup injury presenting with contusion on opposite sides of the brain.

Diffuse Injury

Usually due to acceleration/deceleration injury and concussion resulting in diffuse axonal injury (DAI) and brain swelling. DAI is difficult to diagnose with commonly available CT or MRI scans, and is demonstrated by histological white matter injury of the cerebral hemispheres, the corpus callosum, the brain stem and, less commonly, the cerebellum. DAI might be accompanied by some focal lesions, but again only diagnosable microscopically. The tearing of the nerve tissue disrupts the brain’s regular communication metabolic processes. This disturbance in the brain can produce temporary or permanent widespread brain damage, coma, or death. The shaken baby syndrome is a type of diffuse axonal injury. These injuries are commonly found together.

Opened v Closed Injuries

Open / Penetrating Injury

Open/ Penetrating Injury occurs from the impact of a bullet, knife, or other sharp object that forces hair, skin, bone, and fragments from the object into the brain and dura mater is breached.  The area of damage is determined by the trajectory of the object and possible ricocheting when travelling through different density tissues (skulls, brain). A "through-and-through" injury occurs when an object enters the skull, goes through the brain, and exits the skull and has got complex impact on the brain tissue with penetration injuries, additional shearing, stretching, and rupture of brain tissue.

Closed / Non-Penetrating Injury

A closed injury is an injury to the brain caused by an outside force without any penetration of the skull. The most serious complication is the brain oedema within constrained space of the skull and resultant increase in the intracranial pressure and compression of brain structures and cranial nerves.

Degree of Severity

Mild, Moderate, or Severe Traumatic Brain Injury depending on degrees of severity. Mild traumatic brain injury may affect the brain cells temporarily, but more serious injuries can result in long-term complications or death.

Measures of Severity

The main measures of severity used to classify the injury include:

  • Glasgow Coma Scale (GCS): is a point scale used to assess a patient's level of consciousness and neurological functioning after brain injury. The scoring is based on best eye-opening response (1-4 points), best motor response (1-6points) and best verbal response (1-5 points) with cut off point for coma at 8 points. For more in depth information see GCS student’s guide

Duration of Loss of Consciousness

Describing alteration in consciousness duration:

  • Mild (mental status change or loss of consciousness [LOC] < 30 min),
  • Moderate (mental status change or LOC 30 min to 6 hr),
  • Severe (mental status change or LOC > 6 hr)

Posttraumatic Amnesia (PTA)

Posttraumatic Amnesia is described by the time elapsed from injury to the moment when patient presents with continuous memory of what is happening around them.

Overview of Classification Criteria for TBI Severity based on Glasgow Coma Scale, Loss of Consciousness, Posttraumatic Amnesia and structural imaging:

Severity GCS LOC Structural Imaging
Mild 13 - 15 < 20 min to 1 Hour Definition Dependant
Moderate 9 - 12 1 hour to 24 Hours Normal or Abnormal
Severe 3 - 8 > 24 Hours Normal or Abnormal

Symptoms

Traumatic brain injury can have wide-ranging physical, cognitive, psychological and physiological effects occurring immediately or elapsed. The symptoms might differ depending on the severity of TBI, but some are not specific to the type of injury.

Mild TBI

Physical Symptoms Sensory Symptoms Cognitive Symptoms
With or without loss of consciousness. If loss of consciousness: a few seconds to a few minutes Blurred Vision State of being dazed, confused or disoriented
Headache Ringing in the Ears Memory or concentration deficits
Nausea or Vomiting Bad taste in the mouth or changes in the ability to smell Mood changes or mood swings
Fatigue or Drowsiness Sensitivity to light or sound Irritability
Problems with speech Feeling depressed or anxious
Difficulty sleeping or sleeping more than usually Fatiguability
Dizziness or loss of balance

Moderate to Severe TBI

Physical Symptoms Sensory Symptoms Cognitive Symptoms
Loss of consciousness from several minutes to hours or days Blurred vision Coma and other disorders of consciousness
Persistent headache or headache that worsens Double vision Profound confusion
Repeated vomiting or nausea Ringing in the ears Irritability
Convulsions or seizures Bad taste in the mouth or changes in the ability to smell Agitation, combativeness or other unusual behaviour
Dilation of one or both pupils of the eyes Sensitivity to light or sound Sad or depressed mood
Clear fluid or blood draining from the nose or ears Fatiguability
Sudden swelling or bruises behind the ears or around eyes
Inability to awaken from sleep
Weakness or numbness
Loss of coordination or balance
Irregular breathing
Difficulty speaking

Resources

References

  1. Hill CS, Coleman MP, Menon DK. Traumatic Axonal Injury: Mechanisms and Translational Opportunities. Trends in Neuroscience. 2016;39,5:311-324. doi.org/10.1016/j.tins.2016.03.002
  2. Hill CS, Coleman MP, Menon DK. Traumatic Axonal Injury: Mechanisms and Translational Opportunities. Trends in Neuroscience. 2016;39,5:311-324. doi.org/10.1016/j.tins.2016.03.002
  3. 3.0 3.1 Silver JM, McAllister TW, Yodofsky SC, eds. Textbook of Traumatic Brain Injury. Arlington, Va: American Psychiatric Publishing; 2005. Arlington, VA: 27-39.
  4. Werner C, Engelhard K. Pathophysiology of traumatic brain injury. British Journal of Anaesthesia. 2007;99(1):4-9. DOI: 10.1093/bja/aem131
  5. Hill CS, Coleman MP, Menon DK. Traumatic Axonal Injury: Mechanisms and Translational Opportunities. Trends in Neuroscience. 2016;39,5:311-324. doi.org/10.1016/j.tins.2016.03.002