Traumatic Brain Injury (TBI)

Determining the severity level of a traumatic brain injury is difficult.  The following tools are routinely utilized to determine the severity of the initial injury

·  Glasgow Coma Scale (GCS) – the length of coma, and

·  the length of Post Traumatic Amnesia (PTA).

This information is routinely found in the “History and Physical Discharge Report” completed by the treating physician during the acute hospitalization.

The GCS is a scale utilized by physicians at the time of injury and shortly after to determine the severity of injury and to note improvement or deterioration.  The GCS consists of three subtests: best eye, best verbal and best motor response.  Scores on the GCS have a range of three (no response) to fifteen (alert and oriented).  The following is the severity level of a TBI as rated by the GCS:

• Mild  GCS  13 – 15

• Moderate  GCS  9 – 12

• Severe  GCS  3 –  8

The length of coma is also utilized to help identify the severity level of a traumatic brain injury.  Research has found that six hours or more of coma indicates a severe traumatic brain injury (Christensen, 2001).  The International Classification of Diseases classifies severity of traumatic brain injury as follows:

• Mild  less than one hour of coma

• Moderate  1 – 24 hours of coma

• Severe  24 or more hours of coma

The length of the period of post traumatic amnesia (PTA) is the third major predictor of severity of a traumatic brain injury.  Post traumatic amnesia is the period of time following the initial injury characterized by confusion and disorientation and the inability to remember ongoing events.  Many rehabilitation professionals feel that the length of PTA is the most useful indicator of the severity of the TBI.

• Mild    <1 hour

• Moderate     1 – 24 hours

• Severe     1 –  7 days

• Very severe    >7 days

The following definition of Mild Traumatic Brain Injury (mTBI, also known as "concussion") was developed by the Mild Traumatic Brain Injury Committee of the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine.  It was formally published in the Journal of Head Trauma Rehabilitation 1993:8(3): 86-87.  

The definition is:

A patient with mild traumatic brain injury is a person who has had a traumatically induced physiological disruption of brain function, as manifested by a least one of the following:

1.  any period of loss of consciousness;

2.  any loss of memory for events immediately before or after the accident;

3.  any alteration in mental state at the time of the accident (e.g., feeling dazed, disoriented, or confused); and 

4.  focal neurological deficit(s) that may or may not be transient; but where the severity of the injury does not exceed the following:

•  post traumatic amnesia (PTA) not greater than 24 hours.
•  after thirty (30) minutes, an initial Glasgow Coma Scale (GCS) of 13-15; and
• loss of consciousness of approximately 30 minutes or less.

Symptoms of a Mild Traumatic Brain Injury

a.  cognitive deficits – a reduction in attention, concentration, perception, memory, speech/language or executive functioning skills that cannot be completely accounted for by emotional state or other causes;

b.  behavioral changes and emotional changes – irritability, quickness to anger, disinhibition and/or emotional lability that cannot be accounted for by a psychological reaction to physical or emotional stress or other causes; and

c.  physical symptoms – including nausea, vomiting, dizziness, headache, blurred vision, sleep disturbance, fatigue or other sensory loss that cannot be accounted for by peripheral injury or other causes.

1.)  Diffuse Axonal Injury (DAI) – breaking/shearing/stretching of myelinated axons

·  Due to acceleration/deceleration and rotational injuries (with subsequent LOC)

·  Occurs over time – compression/stretching, swelling, evolving changes (e.g., changes in glucose transport, blood flow, toxins, etc.)

2.)  Focal or Subcortical Contusion (FCC) – local abrasions (tearing  hemorrhage; swelling ® edematous)

1)  Due to coup/contrecoup, depressed skull fracture, inertial/rotational force, skull features (e.g., orbital frontal, inferior anterior temporal), hematomas, subcortical bleeds (CVA effects)

3.)  Hypoxic-Ischemic Injury (HII) – infarction in distribution of one artery

·  Due to lack of oxygen, often secondary to physical injuries/chest injuries/airway obstructions

·  Get increased intracranial pressure (ICP)  and decreased arterial pressure; results in severe and pervasive memory d/o (because hippocampus requires much oxygen)

·  Edema increases ICP, which increases edema, which increases ICP, and so on.

·  Other secondary insults: from multiple/systemic injuries may get hypoxia/anoxia and fat emboli (fracture of femur)

·  Delayed Effects: white matter degeneration (ventricular enlargement), disturbed CSF flow (hydrocephalus)

1.  Primary (immediate on impact)

·  Macroscopic Lesions (contusions at site of impact – coup; contrecoup; laceration)

·  Microscopic Lesions (shearing/stretching of nerve fibers)

2.  Secondary mechanisms of brain injury

·  Intracranial hemorrhage

·  Edema in white matter – adjacent to lesion

·  Hyperemia (diffuse swelling)

·  Ischemic brain damage

·  Raised ICP

·  Brain shift/herniation

3.  Secondary insult from extracerebral events

·  Effects of multiple systemic injury – e.g., hypoxia, fat emboli

4.  Delayed Effects

·  White matter degeneration

·  Disturbed flow of CSF

1.  Anterograde degeneration (aka orthograde or Wallerian) – degeneration of severed axon

2.  Astrocyte activity – invade to remove debris; may seal or scar the area

3.  Calcification – large deposits where neural degeneration takes place

4.  Chromatolyses – color dissolution (cell Nissel substance breaks down); therefore, no stain uptake and are colorless for microscope

5.  Gliosis – replacement of cell bodies by glial cells

6.  Necrosis – localized death of individual or groups of cells

7.  Phagocytosis – removal of dead cells by mitochondria and astrocytes

8.  Retrograde Degeneration – death of remaining axon, cell body, and dendrites after being severed

9.  Terminal Degeneration – shrinkage/degeneration of terminals after axon severed

10.  Transneuronal Degeneration – death of neurons that innervate or are innervated by damaged or destroyed neuron

1.  Diaschesis: a sudden change of function in a portion of the brain connected to a distant, but damaged, brain area

2.  Shock (e.g., spinal) – cells everywhere show temporary depression when input removed

3.  Edema : swelling from injury or inflammation

4.  Blood Flow – decreased CO2, decreased flow, decreased metabolic activity; therefore, decreased overall brain activity

5.  Neurotransmitter Releases - levels change

6.  Glucose Uptake – decreased metabolic activity (not just due to edema)

7.  Changes in electrical activity – can be an index of posttraumatic function

8.  Autoneurotoxicity – delayed tissue death due to increased release of glutamate (due to oxygen deprivation; overexcites cells)