Ch. 2 Flashcards
TBI
traumatically induced physiological disruption of brain function and/or structure resulting from the application of a biomedical force to the head, rapid acceleration and deceleration, or blast related forces. (Kay, et, al, 1993)
Types of brain injuries
Focal Lesions
Multifocal lesions
Diffuse brain injury
Types of brain injuries: Focal Lesions
specific point in the brain
Effect is directly related to size, location, depth.
sudden onset is more severe than a tumor
Types of brain injuries: Multifocal Lesions
multiple areas of damage
Bilateral lesions are going to lead to more functional impairments compared to unilateral lesions.
Simultaneous lesions will be more severe than staged lesions.
Types of brain injuries: Diffuse Brain Injury
o Examples • Significant acceleration-deceleration forces • Hypoxic-ischemic injuries: lack of oxygen • Metabolic disorders • Infectious disorders • Inflammatory disorders o Effect of these injuries • Nature • Density of damage to brain structures
Mechanisms of Brain Injury
Focal Damage Acceleration-deceleration forces Cortical Contusions Coup Injuries Contre-coup Injuries Diffuse axonal injury
Mechanisms of Brain Injury: Focal Damage
skull fractures and focal damage to the underlying brain tissue occur when the head is struck by or the forceful contraction of a rigid surface
Mechanisms of Brain Injury: Acceleration-deceleration forces
occur when the head suddenly stops, but the brain continues to move in the original direction of motion and then rebounds in the opposite direction.
o These forces can tear some blood vessels of meninges and brain surface.
o The bleeding can result in bleeding into space surrounding the brain surface (extradural and subdural hematomas).
o The blood accumulations can cause damage or create pressure on the brain itself.
o Deep cerebral damage may occur due to torn arteries resulting in intracerebral hematomas or due to infarcts where tissues are deprived of blood perfusion for some time.
o Acceleration-deceleration forces may also cause stretching, deformation, and shearing effects on the neurons.
o Long fiber tracts coursing throughout the brain are vulnerable to acceleration-deceleration injuries.
Mechanisms of Brain Injury: Cortical Contusions
frequently accompanied by focal areas of bleeding and swelling and they are very common in motor vehicle accidents and falls. Rubbing of the tissues against each other, results in a lot of tissues damage.
Mechanisms of Brain Injury: Coup Injuries and Contre-Coup injuries
injuries in which the brain is thrust forward on impact and then rebound to opposite direction causing damage to opposite sides of the brain. Very common the MVA.
Mechanisms of Brain Injury: Diffuse axonal Injury
during rapid and powerful acceleration-deceleration forces, the axons of nerve cells may be damaged due to the widespread shearing and stretching action, and this is called DAI.
o A significant destruction or damage of neuron involves the entire neuron including the cell body.
o It is also possible that neighboring neurons, which receive inputs from the damaged neuron, may also die.
o Large portions of cerebral hemispheres and brainstem may be damaged depending on the amount and location of DAI.
o DAI follows a gradient, sequence in which injuries happen. Borders get the least injury. Least in the peripheral areas, most injury to the midbrain.
o In addition to axonal damage, DAI may also lead to destructive processes, such as problems with axonal transport, and axonal swelling which may further result in separation in proximal and distal ends of axons.
o The extent of DAI is directly related to the overall severity of TBI and the functional outcomes.
o Some commonly affected areas in DAI are
• Medial Frontal Lobe
• Corpus Callosum
• Superior Cerebellar Peduncles
Severity of Brain injury: Coma
period of unconsciousness or unawareness following a brain damage.
Tests to assess coma
o Glasgow Coma Scale (GCS) • Table 2.3 pg. 34 • Scores ranging 3-15 • 8 or less indicate severe injury o Galveston Orientation and Amnesia Test • Used to assess different levels of PTA
Post-Traumatic Amnesia definition
includes the period of coma and extends to the patients memory for ongoing events become reliable consistent and accurate.
Post-Traumatic Amnesia factors
• Duration of PTA correlates with residual physical and cognitive impairments
• Residual deficits are dependent on severity of TBI:
o Majority of individuals with mild TBI have relatively uncomplicated recovery and resume premorbid levels of functioning.
o Majority of individuals with moderate or severe TBI have more residual impairments that affect their levels of functioning.
Patterns of recovery: initial stage
o First 4 weeks
• Open eyes
• Sleep, wake cycles
• May not have purposeful behavioral responses or understanding of what is going on around them.
• If it continues for more than a year, it is called a vegetative state, 2% stay in this state. Can continue for weeks or years. Not alert or aware, but arousal.
o First signs of recovery
• Tracking of visual stimuli
• Orientation to auditory stimuli
• May also be seen in response to automatic or reflexive responses.
• Gradually they will come to have greater volitional control
o Other features
• Responses to commands
• Some agitation
• Restlessness
Patterns of recovery: Next phase
o Orientation and continuous memory may be restored.
o Deficits in memory and learning may persist.
o Length of this phase varies with severity of the injury.
o This stage involves emphasis on training and resumption/stabilization of self-care activities, and on ambulatory and other motor activities.
o Cognitive deficits may still persist and efforts are made to
1. Stabilize orientation.
2. Facilitate effective communication.
3. Improve attention.
4. Use compensatory strategies.
o Many individuals with TBI have no or limited awareness of the extent or implications of their deficits or functional impairments.
