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Traumatic Brain Injury

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Contents

Description

Coup injuries occur at the site of impact, while contrecoup injuries develop as the brain hits the opposite side of the skull.
Coup injuries occur at the site of impact, while contrecoup injuries develop as the brain hits the opposite side of the skull.[1]

Traumatic brain injury (TBI) is “the negative effect on brain function resulting from external physical force.” It results from closed or open head injury and can cause both focal and diffuse damage. Focal brain damage can occur at the site of impact (coup) and opposite to it (contrecoup); coup and contrecoup injuries can occur independently or together. Diffuse damage is, like the term implies, widespread throughout the brain. Focal and diffuse damage occur simultaneously in 50% of TBI cases.

Injuries can also be classified as primary or secondary. Primary injuries are those that result from the impact of the brain on skull and forces from acceleration, deceleration, and rotation. Secondary injuries are caused by the brain’s response to trauma and can last for years. These injuries can lead to an altered state of consciousness, cognitive and physical impairment, and changes in behavior and emotion.


Incidence and Prevalence

The incidence of TBI is reported as ranging from 222 to 556 per 100,000 individuals or about 2 million TBIs per year. Each year, TBI leads to 500,000 hospitalizations and causes 175,000 deaths or significant disability. These rates are high, but fortunately, they are declining because of improved understanding of how to prevent secondary injury. It is estimated that there are currently 5 million individuals living with TBI in the United States. TBI is most prevalent in three age groups: early childhood, late adolescence and early adulthood, and older adulthood. As of January 2008, 5,500 Operation Enduring Freedom / Operation Iraqi Freedom soldiers had experienced a traumatic brain injury. Each year, traumatic brain injury leads to $56 billion in expenses in the United States.


Etiology and Risk Factors

Traumatic brain injury is caused most frequently by open or closed head injury, motor vehicle accidents, pedestrians being hit by cars, firearms, and explosions. Sixty percent of adults and 95% of children with severe head injuries were involved in a motor vehicle accident. Risk factors include the following:

  • Being male (Male: Female = 2:1)
  • Engaging in risky behaviors
  • Alcohol use (50% of people hospitalized for head trauma are intoxicated; brain injury is two to four times higher in alcoholics)
  • Lower socio-economic status
  • Living in a densely populated area


Pathophysiology

Primary Injury

The pathophysiology of primary brain injury depends on the type of injury. In open head injury, the meninges may be torn, leaving the brain exposed. If the injury is due to a penetrating missile, the person will have a focal lesion with limited brain damage. The extent of destruction is determined by the velocity of the missile; damage may be in the form of disruption or formation of aneurysms.

With closed head injury, there is no skull fracture or brain puncture. Damage is due to the impact of the brain on the skull, with or without the head contacting a surface. Decelerating forces may cause coup and contrecoup injuries, which result in contusions, lacerations, hematomas, and herniation. Head rotation causes diffuse axonal injury (DAI), rupture of veins, and damage to the brainstem.

Bruising and bleeding of the brain are common in both open and closed primary injury.


Secondary Injury

Secondary injuries occur as the brain responds to primary injury. Vascular changes are common and include:

  • Contusions
  • Gliding contusions, where shearing damages vessels at grey matter/white matter interfaces
  • Increased blood volume and increased intracranial pressure, leading to subdural hematomas, venous outflow blockage, and increased cerebral blood flow
  • Loss of homeostasis

Also associated with secondary injuries are parenchymal changes. As shear and tensile forces cause damage to axons in DAI, axons swell, the distal axon detaches and degenerates, and myelin pulls away from the axon. These parenchymal changes are seen diffusely throughout the brain. Compressive damage causes brain herniation, hypotension and hypoxia early in this stage of injury, and later intracranial hypertension. Brain herniation is the result of the brain shifting in the skull, compressing brain structures, and resulting in paralysis, death, or changes in the autonomic nervous system. Cell death and neurotransmitter changes may also occur in the secondary stage of injury.


Signs and Symptoms

Stages

At first, a person with traumatic brain injury may experience loss of consciousness or be in a coma; this stage lasts seconds to weeks in duration. In severe TBI, the person may be in a vegetative state, where he or she does not respond to commands or speak. After this first stage, the patient may have post-traumatic amnesia, where he or she experiences disorientation, memory disorders, and behavioral disturbance. This stage may last minutes to months in duration. Brain damage may ultimately result in chronic cognitive, behavioral, and sensorimotor disturbances.


Cognitive and Behavioral Impairment

TBI presents similarly to post-traumatic stress disorder (PTSD), depression, and anxiety. Cognitive and behavioral symptoms depend on location of the brain lesion. Common impairments include:

  • Decreased attention
  • Loss of problem solving ability
  • Disorientation
  • Impaired concentration
  • Depression
  • Inability to adjust to environment
  • Impaired executive functioning
  • Confusion
  • Memory loss (retrograde amnesia, posttraumatic amnesia, or anterograde amnesia)


Physical Symptoms

A person with TBI may experience pain at and following the time of injury. He or she may have motor deficits among the following:

  • Monoplegia, hemiplegia, abnormal reflexes
  • Loss of motor control, balance, or sensory feedback
  • Tremors
  • Dystonia
  • Contractures

Heterotropic ossification, that is the spontaneous growth of extra bone outside the skeleton, may form four to twelve weeks after injury; it presents as decreased range of motion, local tenderness, swelling, and pain. Additionally, the patient may have cardiovascular or respiratory problems.


Medical Management

Diagnosis

CT scans are used to diagnose traumatic brain injury.  These scans show focal injuries (midline shifts and hematomas.)
CT scans are used to diagnose traumatic brain injury. These scans show focal injuries (midline shifts and hematomas.)

Traumatic brain injury is diagnosed by using several tests. Eye opening, motor responses, verbal responses, and reflex responses are used to generate a Glasgow Coma Scale (GCS) score. The severity of TBI is inversely proportional to the GCS score (13-15: mild TBI, 9-12: moderate TBI, <=8: severe TBI). Pupillary exams are used to establish baselines and for observing changes. Also, mental status exams and neuropsychological exams are performed to examine mental deficits. Diagnostic imaging should be performed in addition to the clinical exam. CT has a high sensitivity for focal injuries, while MRI can detect lesions like non-hemorrhagic contusions and edema. Recently, there has been interest in using MRI to detect diffuse axonal injury.


Treatment

As traumatic brain injury causes long lasting effects on physical, cognitive, and behavioral ability, it requires chronic care. At the early stages of injury, management is focused on stabilizing the patient and preventing secondary complications. To prevent secondary injury, surgery may be required to address hemorrhage, edema, and hematoma. Also, intracranial pressure, cerebral blood flow, and cerebral pressure are monitored and controlled.

For subacute management, the medical team tries to maintain brain homeostasis and pharmacologically manage spasticity, seizures, and behavior (aggression and depression). Rehabilitation plans are determined based on impairment and goals. There is a focus on mobility, self-care, employment, and recreational activities. Psychotherapy may be indicated for modification of debilitating behaviors.


Prognosis

Prognosis is largely dependent on the TBI severity. Patterns are more predictable in diffuse TBI than in focal injury. At six months post-injury, 15 to 29% of TBI patients have persistent problems. Poorer outcomes are expected for individuals with low GCS score; DAI; repeated brain injury; cognitive deficits affecting attention, motivation, learning, emotion, or memory; and history of substance abuse, low education, or psychiatric problems.

A large percentage of individuals are able to successfully reintegrate into society after their traumatic brain injury. Vocational, mobility, and social accommodations are necessary to assist the patient in this process.

To learn more about vocational accommodations, read the Employees with TBI wiki article.


References

  • Andriessen, T., Jacobs, B., & Vos, P. (2010). Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury. Journal of Cell and Molecular Medicine, In Press.
  • Goodman, C.C, Fuller, K.S. Pathology: Implications for the Physical Therapist. Saunders, 2009.
  • Belanger, H.G., Vanderploeg, R.D., Curtiss, G., Warden, D.L. (2007). Recent Neuroimaging Techniques in Mild Traumatic Brain Injury. Journal of Neuropsychiatry Clinical Neuroscience 19:1.
  • Kumar, R., Husain, M., Gupta, R.K., et. al. (2009). Serial Changes in the White Matter Diffusion Tensor Imaging Metrics in Moderate Traumatic Brain Injury and Correlation with Neuro-Cognitive Function. Journal of Neurotrauma 26:481-495.
  • Sayed, T.E., Mota, A., Fraternali, F., Ortiz, M. “Biomechanics of traumatic brain injury.” (2008). Computational Methods in Applied Mechanical Engineering. 197:4692-4701.
  • Cernak, I., Noble-Haeusslein, L.J., Traumatic brain injury: an overview of pathobiology with emphasis on military populations. (2010). Journal of Cerebral Blood Flow and Metabolism. 30:255-266.


External Links

Traumatic Brain Injury.com

CDC TBI page