Lauren Burns; Therapy Service Co-ordinator; Life Rehabilitation; Life Eugene Marais Hospital

A traumatic brain injury is often the result of one moment of mischance, but it may have long lasting and far reaching repercussions. As is true of any neurological insult to the supremely powerful but paradoxically fragile organ that controls all our bodily functions and houses the intangible essence that makes each individual unique, a traumatic brain injury is a ruthless leveller of the playing field. It can reduce the most erudite university professor to the ignominy of groping desperately for his own name, or the world’s fastest sprinter to the level of a child learning to take its first steps once again. Some patients will walk away from a mild head injury with little concept of how much worse the outcome may have been. Others, more severely injured, may make what is termed a good recovery but be left with residual deficits that will leave a lasting imprint on their lives. Many sufferers will be left severely incapacitated and a lamentably large number will become part of the statistics on mortality following traumatic brain injury. This article discusses the etiology, mechanisms of injury and effects of traumatic brain injury. It also discusses some widely used tools for the assessment of patients with traumatic brain injuries, in preparation for a further article on the rehabilitation of such individuals.

Traumatic brain injury (TBI), defined as brain damage caused by externally inflicted trauma to the head, may result in significant impairment of an individual’s functioning – on physical, cognitive and psychosocial levels. Statistics on the incidence of TBI vary widely, but it is evident that the figures have increased steadily over recent years and that TBI is a leading cause of death and disability worldwide, particularly in young children and adults under the age of 40. Males are much more likely to incur traumatic brain injuries, with the highest risk age group between 15- and 30-year-olds.1,2 Although trauma is a leading cause of brain injury as well as spinal cord injury, brain injury as a result of trauma is much more likely to occur than spinal cord injury. The major causes of brain injury are motor vehicle accidents, violence (including gunshot wounds and assaults), falls, being hit by falling debris and pedestrian vehicle accidents.3 However, as the incidence of TBI has increased, so has the number of people surviving TBI, due to faster and more effective emergency care, quicker and safer transportation to specialised treatment facilities and advances in acute medical management. Because of the often irreversible and comprehensively debilitating loss of function often incurred as a result of severe brain injury, the increase in survival rates challenges the medical and rehabilitation teams to treat and rehabilitate patients to the fullest possible degree.

Mechanisms of Injury
A traumatic brain injury is usually caused by a dynamic loading or impact to the head from direct blows or from sudden movements produced by impacts to other body parts. This loading can result in any combination of compression, expansion, acceleration, deceleration and rotation of the brain inside the skull. Brain injuries may be diffuse, focal, or both. Motor vehicle accidents and falls involve acceleration and deceleration with rotation of the brain inside the skull. The brainstem is more stable than the cerebrum, which rotates around the brainstem during impact. The rotation places a stretch or shear force on the long axons that transmit information throughout the brain and brainstem. Such injuries are called diffuse axonal injuries (DIA) and may result in coma due to damage to the axons in the midbrain reticular activating system.The changes in the brain as a result of DIA are microscopic and may not visualise on computed tomography (CT scan) or magnetic resonance imaging (MRI) scans. Focal lesions involve contusions or lacerations of the brain, resulting in extra-axial (within the skull) or intra-axial (within the brain) haemorrhage.5 Although focal lesions can occur anywhere beneath the impact, they are usually seen at the anterior poles and inferior surfaces of the frontal and temporal lobes and are caused when the brain hits against the skull and scrapes over the irregular bony structures at these locations. The occipital and parietal lobes, which have smooth surfaces, are less likely to incur damage. Lesions of the brain and damage to the internal tissue and blood vessels can also be due to a mechanism called coup-countercoup. Damage directly related to trauma at the site of impact is called a coup lesion. As the brain is jolted away from the site of the original impact, it can hit the skull on the opposite side and cause internal damage referred to as a countercoup lesion. Cranial nerves can also be torn, stretched or contused as a result of TBI, resulting in particular clinical presentations. As the first line of defence, the skull is particularly vulnerable to injury. The skull may fracture from the force of the impact in the area of, or at a distance from the actual impact site. The type of fracture depends on the force of the blow.6
The injuries described above are termed primary injuries, as they are directly related to the trauma. However, secondary injuries may also occur, due to damage that results from neuronal death as a consequence of hypoxia, oedema and/or initiation of inflammatory cascades.7 Secondary injury is a significant cause of deterioration in TBI patients after the initial injury and contributes significantly to overall morbidity and mortality rates from TBI. The minimisation of these secondary effects is therefore vitally important in the medical and rehabilitative management of these patients.
Signs and Symptoms of TBI
Some symptoms of TBI are evident immediately, while others may not appear until days or even weeks after the injury. 
Symptoms of mild TBI include:
·        Brief loss of consciousness;
·        Headache;
·        Mental confusion;
·        Light headedness;
·        Dizziness;
·        Blurred or double vision;
·        Fatigue or lethargy;
·        Bad taste in the mouth;
·        A change in sleep patterns;
·        Behavioural or mood changes;
·        Trouble with memory, concentration or calculation.
With a moderate or severe TBI, the patient may demonstrate these same symptoms, but may also have:
  • Prolonged loss of consciousness;
  • Personality changes;
  • A severe, persistent or worsening headache;
  • Repeated vomiting or nausea;
  • Seizures;
  • Inability to waken;
  • Dilation of one or both pupils;
  • Slurred speech;
  • Weakness, numbness or paralysis of extremities;
  • Loss of co-ordination;
  • Increased confusion, restlessness or agitation.
Effects of Traumatic Brain Injury
Some brain injuries are mild, with symptoms disappearing over time. Others may result in a debilitating loss of function and permanent disability. Effects of traumatic brain injury may include8:
Insert Table I
Effects on Consciousness
A brain-injured person may exhibit any of a number of states of altered consciousness, depending on the severity of the injury. These states of arousal are best viewed on a continuum from complete consciousness to coma and brain death. 
Brain Death
Brain death is the lack of measurable brain function due to diffuse damage to the cerebral hemispheres and the brainstem, with loss of any integrated activity among distinct areas of the brain. It is irreversible and the removal of assistive devices will result in immediate cardiac arrest and cessation of breathing.
This term is used to refer to patients who are completely unconscious, have their eyes permanently closed, cannot be aroused by any sensory stimulation and who demonstrate an absence of any observable interaction with the environment. A coma results from the interruption of communication from the reticular activating system to the cerebral hemispheres.9
Stupor is a state in which the patient is unresponsive, but can be aroused briefly by a strong stimulus, such as a sharp pain.
Vegetative State
Patients in a vegetative state are unconscious and unaware of their surroundings, but continue to have a sleep-wake cycle and can have periods of wakefulness. At times, when they seem to be awake, their eyes open and sometimes wander. They can make a variety of spontaneous movements such as swallowing, grinding their teeth, crying, smiling and grasping another’s hand, but these motions are always reflexive and not the result of purposeful behaviour. It is possible for a person to function in a vegetative state but without consciousness; the deeper brainstem structures that regulate breathing, reflexes and heart rate are intact, but the cortex is completely impaired. After being in a vegetative state for more than a month after sustaining a brain injury, a patient is said to be in a persistent vegetative state (PVS) and the probability of recovery diminishes as more time passes. In 1994 the Multi-Society Task Force on PVS (a team of 11 researchers from various institutions) concluded that the chances of recovery are close to zero if the patient remains in a vegetative state one year after a traumatic brain injury or three months (later revised to six months) after brain damage from lack of oxygen or other causes. These patients were referred to as being in a “permanent vegetative state”.10  
Minimally ConsciousState
In the minimally conscious state a patient exhibits deliberate, or cognitively mediated, behaviour consistently enough to be distinguished from the entirely unconscious, reflexive responses that are seen in the persistent vegetative state. An important difference from the vegetative state is that patients who have remained in the minimally conscious state for years still have a chance of a recovery. Making the distinction between the vegetative and minimally conscious states can be difficult and requires repeated examinations by well-trained, experienced clinicians.11 Conscious awareness is a subjective experience that is inherently difficult to measure in another being. This difficulty highlights the importance of developing effective, objective ways to determine whether a patient is in a permanently vegetative state. It also raises a number of complex legal and ethical considerations regarding the long term management of such patients.
Locked-in Syndrome
This is a rare condition in which a patient is conscious and aware, but is unable to move due to complete paralysis of the body’s voluntary muscles. Generally, vertical eye movement and blinking are preserved, this ability usually being the only means of communication with the surrounding world. If this condition is not adequately understood and diagnosed, the patient could be thought to be in lower level of consciousness than he/she actually is.
After brain injury that leads to coma, a patient’s progress may follow one of several paths. If the patient does not die or quickly recover, he or she will most likely transition to the vegetative state. The patient may then evolve to the minimally conscious state and often to further recovery of consciousness or remain in the vegetative state permanently.12 
Insert Illustration 1
Assessment Tools
As survival rates after traumatic brain injury increase, so the objective measurement of functional impairment becomes more and more vital, both in predicting outcome as well as in justifying and evaluating growing rehabilitation services post injury. The following are three widely used instruments for the assessment of patients with brain injury.
Glasgow Coma Scale
The Glasgow Coma Scale (GCS) was created as a standardised clinical scale to facilitate the reliable interobserver neurological assessments of head-injured patients in a coma. It is now used as a simple neurological scale in order to record the conscious state of a person. The value of the scale lies largely in using serial GCS scores as a predictor of outcome. A low GCS score that remains low, or a high GCS score that decreases, predicts poorer outcomes than high GCS scores that remain high, or a low GCS score that progressively improves.13
The GCS provides a score in the range of 3-15; patients with scores of 3-8 are usually said to be in a coma. The total score is the sum of the scores in three categories, as depicted below:
Insert Table II
Rancho Los Amigos Scale
This scale was designed as an easy, useful tool to classify the cognitive functioning of patients with traumatic brain injury. It is widely used in the acute phase and is also currently used as an outcome measure following discharge. The Rancho Los Amigos Scale has eight levels to which a patient can be assigned as follows14:
Insert Table III
The Functional Independence and Functional Assessment Measures
The Functional Independence Measure (FIM) was developed as a tool to evaluate the functional status of neurologically impaired patients. The FIM is composed of 18 items with a seven-point rating scale (a score of 1 indicates complete dependence; a score of 7 indicates complete independence). The FIM evaluates self-care, sphincter control, mobility, communication, psychosocial adjustment and cognitive function. However, the FIM mainly measures motor and self-care tasks which are common in everyday activities, while cognitive and social deficits are underrepresented. This results in a ceiling effect, which undermines the effectiveness of the FIM scale. As a result, the Functional Assessment Measure (FAM) was developed, which contributes an additional 12 new items to the original FIM scale. The new items evaluate more complex cognitive, behavioural, emotional, communicative and psychosocial aspects of neurological impairment.15 
Insert Table IV
It is evident that a traumatic brain injury can result in a myriad of physical, functional, cognitive and psychosocial deficits in a previously normally functioning individual. Significant morbidity and mortality rates are associated with moderate and severe injuries. Mild injuries, although producing far less morbidity, are still a serious problem because of their extremely high prevalence. While many patients will demonstrate some form of recovery following even severe brain injury, the nature and extent of the recovery depends on a multitude of intrinsic and extrinsic factors. Predicting the outcome following a traumatic brain injury is challenging and as survival rates increase steadily, it is becoming increasingly important to evaluate the effectiveness of treatment as well as to justify the cost of further rehabilitative services. As the long term effects of traumatic brain injury are evaluated and the significant economic and social consequences are understood (particularly considering the high incidence of TBI in child- and young adult-hood), the efficacious rehabilitation of patients post TBI is of vital importance. In a following article, this rehabilitative process will be explored in greater detail.   
  1. Scott AD, Dow PW. Traumatic Brain Injury. Archives of Physical Medicine Rehabilitation 2003; 84: 705.
  2. Traumatic Brain Injury. [O]. Retrieved December 28, 2007, from
  3. Scott AD, Dow PW. Traumatic Brain Injury. Archives of Physical Medicine Rehabilitation 2003; 84: 705.
  4. Scott AD, Dow PW. Traumatic Brain Injury. Archives of Physical Medicine Rehabilitation 2003; 84: 706.
  5. Traumatic Brain Injury. [O]. Retrieved December 28, 2007, from
  6. Scott AD, Dow PW. Traumatic Brain Injury. Archives of Physical Medicine Rehabilitation 2003; 84: 706.
  7. Jagoda A, Bruns J. 2006. Prehospital Management of Traumatic Brain Injury. In León-Carrión J, von Wild KRH, Zitnay GA (Ed). 2006. Brain Injury Treatment: Theories and Practices. East Sussex: Taylor & Francis.
  8. Traumatic Brain Injury. [O]. Retrieved December 26, 2007, from
  9. Scott AD, Dow PW. Traumatic Brain Injury. Archives of Physical Medicine Rehabilitation 2003; 84: 709.
  10. Laureys S. Eyes Open, Brain Shut. Scientific American 2007; 296(5): 66-68.
  11. Laureys S. Eyes Open, Brain Shut. Scientific American 2007; 296(5): 68.
  12. Laureys S. Eyes Open, Brain Shut. Scientific American 2007; 296(5): 68-69.
  13. Jagoda A, Bruns J. 2006. Prehospital management of traumatic brain injury. In León-Carrión J, von Wild KRH, Zitnay GA (Ed). 2006. Brain Injury Treatment: Theories and Practices. East Sussex: Taylor & Francis.
  14. León-Carrión J. 2006. Methods and tools for the assessment of outcome after brain injury rehabilitation. In León-Carrión J, von Wild KRH, Zitnay GA (Ed). 2006. Brain Injury Treatment: Theories and Practices. East Sussex: Taylor & Francis.
  15. León-Carrión J. 2006. Methods and tools for the assessment of outcome after brain injury rehabilitation. In León-Carrión J, von Wild KRH, Zitnay GA (Ed). 2006. Brain Injury Treatment: Theories and Practices. East Sussex: Taylor & Francis.

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This document contains tables intended to accompany the article entitled 'TRAUMATIC BRAIN INJURY' by Lauren Burns.



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