Categorization Brain Injury

Brain can be injured in several ways. One of the most important distinctions is between a traumatic brain injury (TBI) and acquired brain injury as a traumatic injury will be usually acute and require immediate or a very prompt treatment.

Traumatic brain injury (TBI) usually follows head injury, but can also be a result of other physical trauma, for example oxygen deprivation. Acquired brain injury is a term used for brain injuries which occur as a result of a perinatal trauma, disease or congenital condition which impairs development or leads to a damage to brain cells and neural connections.

The most common causes of brain injury (both traumatic and acquired) include direct trauma to the head, strokes, neurological diseases and respiratory failure. These happen most commonly as a result of falls, car accidents, striking objects or being struck by objects and assaults.

Another common distinction is made between diffuse brain injuries and focal ones. Diffuse injuries are caused by (relatively small) damage to many areas of the brain. This type of brain injury is often difficult to diagnose as the damage (shearing of the nerve cells) is microscopic. Focal injuries are localized and limited to a specific area of the brain. Diffuse injuries tend to result in general lowering of mental functioning (for example distractibility, memory impairment), while focal injuries can produce symptoms related to the damaged area (specific aphasia, loss of sense of smell, emotional disturbance).

Other distinctions include primary and secondary injury as well as open (penetrating) versus blunt injury. Primary brain injury may be caused by a direct impact or by inertial forces. Secondary injury may be caused by edema, ischemia, increases in inter-cranial pressure.

Classification of brain injuries based on pathological and neurophysiological features

(1) Laceration: a type of primary, open head injury caused by an object (often a sharp object, and commonly a bullet). Lacerations can lead to damage to large blood vessels and consequent bleeding into the skull, including the brain and sub-arachnoid space. Edema and hematomas can follow as well as direct destruction of neural matter.

(2) Contusion: direct damage to the brain, resulting in a visible bruising and bleeding. This may lead to swelling and destruction of brain tissue.

(3) Concussion: brain injury that results from a blunt impact or inertial forces including a movement and momentum change. This can lead to stretching of blood vessels and damage to the nerves.

(4) Coup-countrecoup: a specific sub-type of primary injury (usually contusion), where injury at a site of an impact is followed by one on the opposite side where the brain impacts the skull.

(5) Diffuse axonal injury: primary injury which features extensive and generalized damage to the nerve cells’ axons (white matter); tearing of axons results from shaking or other sudden movement.

(6) Hypoxic-ischemic injury: primary, diffuse injury caused by restriction of blood flow to the brain tissue, leading to insufficient oxygen and nutrients reaching the brain cells.

(7) Hematoma and hemorrhage: a localized bleeding, resulting from a rupture of blood vessels. Inter-cranial hematomas are classified into subdural hematomas (SDH), epidural hematomas (EDH), subarachnoid hemorrhages (SAH). These can lead to increase of pressure and damage to the neural tissue in the brain.

(8) Infraction (stroke): can be associated with or caused by TBI, mostly when an artery to the brain is compressed by the surrounding tissues as a result of edema or increased ICP.

Secondary brain injury is often caused as a result of neurochemical changes that follow from the primary injury. Excitatory amino acids (EAAs), such as glutamate and aspartate, which can cause swelling and cell damage, increase significantly after TBI. Another factor that leads to secondary damage is increased inter-cranial pressure (often caused by edema) can lead to further and more permanent damage to the nerve tissue and connections within the brain.

All types of brain injury may result in similar symptoms and functional deficiencies as they can all lead to tearing and compression of neuronal and vascular tissues. There are differences in symptomatology, but the main difference regarding prognosis and treatment options relates to the level of brain injury that the patient suffered from.

Classification of brain injuries based on severity level

Brain injury can be classified according to the duration of the loss of consciousness. Injuries with loss of consciousness lasting less than 30 minutes are classified as mild, those with 30 minutes to 6 hours as moderate, and when consciousness is lost for more than for hours, severe.

The most common classification uses Glasgow Coma Scale, a 15 point scoring scale which assesses eye opening, motor response and verbal responses of the patient. The minimum score (with no response on any of the three dimensions) is 3, and any score between 3 and 8 signifies severe TBI (coma). Moderate brain injury corresponds to scores between 9 and 12, and mild TBI is characterized by scores between 13 and 15.

Appendix: Glasgow Coma Scale

Eye opening scores

Spontaneous = 4

To sound/speech = 3

To pain = 2

No response = 1

Motor response

Obeys commands = 6

Localizes pain = 5

Withdraws from pain = 4

Flexure (abnormal) from pain = 3

Extension (abnormal) from pain = 2

No response = 1

Verbal response

Oriented and communicates = 5

Communicates but disoriented = 4

Inappropriate words = 3

Incomprehensible sounds = 2

No response = 1

Sources and further reading:

Dhiraj Raja. Neuropsychiatric Aspects of Traumatic Brain Injury. PowerPoint presentation retrieved on 16 Jan 2011 from

Moppett, I.K. Traumatic brain injury: assessment, resuscitation and early management. Br. J. Anaesth. (2007) 99 (1): 18-31 retrieved on 16 Jan 2011 from

Types of Brain Injury. Retrieved on 16 Jan 2011 from

Brain Injury: Severity Levels and the Recovery Process. Retrieved on 16 Jan 2011 from

Dawodu, Segun T. Traumatic Brain Injury (TBI) – Definition, Epidemiology, Pathophysiology Retrieved on 16 Jan 2011 from