Pathophysiology of TBI

• Traumatic brain injury or TBI is defined as an "alteration in brain function, or other evidence of brain pathology, caused by an external force."

  
• TBI occurs when an external force impacts the brain, and often is caused by a blow, bump, jolt, violent shaking or movement of the body, or penetrating wound to the head resulting in disruption of the normal function of the brain.

  
• The severity of TBI can range from mild or a concussion causing temporary change in mental status or consciousness to severe where the person is in an extended period of unconsciousness or amnesia after the injury.
• Not only can brain injury result in potentially lifelong physical and cognitive changes but the impact on a person's behavior can profoundly alter how they function day to day.

  
• The behavior challenges following damage to the brain can impede the person's recovery goals and may impact their ability to live independently.
• Profound changes in personality and behavior often represent the most significant barrier to successful reintegration back into the community, their families, work, and reactional/social behaviors.
• Traumatic brain injury is a global health issue associated with both acute and long-term disabilities that affects around 10 million people in the world yearly.
• In the United States, 2.8 million people sustain a traumatic brain injury annually.

  
• Over five million Americans currently have a long-term or lifelong need for help to perform activities of daily living as a result of TBI.
• TBIs affect the lives of people of all ages. People 75 years and older have the highest numbers and rates of TBI-related hospitalizations and deaths.
• TBI is more common in men, especially in the adolescent and young adult years ages 17–24 due to their activity level and high degree of risk-taking behaviors.
• Males are nearly two times more likely to be hospitalized and three times more likely to die from a TBI than females.
• American Indian and Alaska Native children and adults have higher rates of TBI-related hospitalizations and deaths than other racial or ethnic groups.
• More than 450,000 U.S. service members were diagnosed with a TBI between 2000 and 2021.
• Almost half of people in correctional or detention facilities such as prisons and jails have a history of TBI, but the exact number is not known.
• Compared to the general population, people who experience homelessness are 2 to 4 times more likely to have a history of any type of TBI and up to 10 times more likely to have a history of a moderate or severe TBI.
• The leading causes of TBI are falls, motor vehicle accidents, being hit by or colliding with an object, and assaults.
• Falls are the most common cause of TBI especially in young children and older adults.
• Types of traumatic brain injuries

  • Injuries from external forces hitting the head or the head hitting hard enough to cause brain movement
  • Injuries with skull fracture (open head injury)
  • Injuries without skull fracture (closed head injury)
  • Blast injuries
  • Penetrating injuries

  
• Open head injury


  • Penetrating objects
  • Skull is penetrated
  • Dura is open
  • Meninges are breached
  • Brain is exposed
  • Localized focal lesions
  • Skull Fracture
  • Direct cellular and vascular damage
  • Secondary damage due to injuries to the face and neck

  
• Closed head injury


  • No skull fracture or laceration of the brain itself
  • The dura and skull remain intact
  • The brain is forced into contact with the hard, bony, outer covering of the brain, the skull
  • Acceleration–deceleration Injury: there is a focal injury as the brain bumps into the skull as the body's momentum comes to a rapid stop (coup), and then a contre coup (opposite side) injury as it "bounces back" into the opposite side of the skull
  • Focal, multifocal, and diffuse lesions
  • Common areas of focal injury: anterior temporal poles, frontal poles, lateral and inferior temporal cortices, and orbital frontal cortices

  
• Traumatic brain injury causes diffuse axonal injury, which results from stretch injury to the membrane of an axon.
• In about 80 to 90 percent of the cases, traumatic brain injury is mild. Moderate to severe traumatic brain injuries occur in the rest of the cases.

  
• Moderate to severe TBI

  • The impact tends to damage the prefrontal region and the anterior and inferior temporal regions
  • People show poor judgment, decreased goal-directed behavior, memory deficits, slow information processing, attentional disorders, and poor divergent thinking
  • Inability to effectively use new information results in concrete thinking, an inability to appropriately apply rules, and trouble distinguishing relevant from irrelevant information
  • People are at significant risk for problems with substance abuse, aggression, and inappropriate sexual behaviors
  • Other problematic behaviors: agitation, emotional lability, lack of self-awareness, lack of empathy, lack of motivation, and inflexibility
• Unsteadiness consisting of impaired balance, agility, and incoordination may also be a persistent problem.
• Long-term neural degeneration, 1.5% loss of white and gray matter per year, continues after moderate to severe traumatic brain injury.

  
• Mild TBI (Concussion)


  • Loss of consciousness: ≤ 30 minutes
  • Alteration of Consciousness: brief to 24 hours
  • Post-Traumatic Amnesia: < 0 to 1 day
  • Glasgow Coma Scale: 13 to 15
  • Neuroimaging: normal
  • Post-Concussion Syndrome: poor cognitive function, difficulty with concentration, and irritability
  • Chronic Traumatic Encephalopathy: due to repeated mild TBIs, especially during the recovery period after previous injury
  • Results in long-term white matter pathology and neuronal loss that correlates with the level of behavioral problems

  
• Moderate TBI


  • Loss of Consciousness: > 30 minutes < 24 hours
  • Alteration of Consciousness: > 24 hours
  • Post-Traumatic Amnesia: > 1 to < 7 days
  • Glasgow Coma Scale: 9 to 12
  • Neuroimaging: normal or abnormal
• Severe TBI


  • Loss of Consciousness: > 24 hours
  • Alteration of Consciousness: > 24 hours
  • Post-Traumatic Amnesia: > 7 days
  • Glasgow Coma Scale: < 9
  • Neuroimaging: normal or abnormal
• Brain tissue damage is classified as either a primary injury due to direct trauma to the parenchyma or secondary injury resulting from a cascade of biochemical, cellular, and molecular events that evolve over time due to the initial injury and injury-related hypoxia, edema, and elevated intracranial pressure.

  
• Primary injury


  • Acceleration, deceleration, rotational forces, and penetrating objects cause tissue laceration, compression, tension, shearing, or a combination, resulting in primary injury to the central nervous system structures
  • Immediate neurologic damage produced by trauma is usually not alterable
  • Contusions, lacerations, hematomas, hemorrhages, diffuse axonal injuries, and excitotoxicity and oxidative stress cause direct injury to central nervous system structures
• Contusions


  • Bruising of the brain surface; local area of edema and small capillary hemorrhages
  • Object hits head, neck, face or head hits an object
  • Damage to any area of the brain
  • Occipital blows more likely vs frontal or lateral
  • Common injured areas: irregular surfaces on cranial vault such as anterior poles, temporal and frontal lobe inferior aspects
  • Can injure cranial nerves: optic, vestibulocochlear, oculomotor, abducens, and facial nerves

  
• Lacerations


  • Tearing of the pia or arachnoid matter or brain tissue
  • Dural or arachnoid space lacerations: CSF to discharge from the nose which increases with neck flexion, coughing or straining
  • Common injured areas: irregular surfaces on cranial vault such as anterior poles, temporal and frontal lobe undersurfaces
  • Can injure cranial nerves: optic, vestibulocochlear, oculomotor, abducens, and facial nerves
• Intracranial Hematomas or Hemorrhages

  • Bleeding into the subdural, epidural, or subarachnoid spaces or within the brain tissue (intraparenchymal) due to traumatic rupture of blood vessels
  • Intraventricular hemorrhage
  • Subdural hematomas: occur with acceleration-deceleration injuries when bridging veins to the superior sagittal sinus are torn
  • Epidural hematomas: tearing of meningeal vessels results in blood collecting between the skull and dura; skull fracture present in most cases
  • Subarachnoid hemorrhage
• Diffuse Axonal Injury


  • Rapid rotational and linear acceleration and deceleration of the brain causing shear, tensile, and compression forces within the brain injuring axons (stretching, tearing) disrupting nerve communication
  • Common areas: parasagittal projections in lateral hemispheres, corpus callosum, pontine-mesencephalic junction adjacent to superior cerebellar peduncles (brainstem)
  • Focal, multifocal, or diffuse
  • Disruption of neurofilaments → Wallerian-type axonal degeneration
  • Severing of the axons may be severe enough to result in coma
  • Mild DAI: deficits such as memory loss, concentration difficulties, decreased attention span, headaches, sleep disturbances, and seizures
  • Common in high-speed motor vehicle accidents and some sports-related TBIs
• Excitotoxicity and Oxidative Stress

  • Excessive release of glutamate, dopamine, and norepinephrine
  • Excessive glutamate leads to: Influx of Na+ and Ca++ into the cell with subsequent cellular edema and contraction of the extracellular space, Stimulates reactive oxygen species production which are detrimental to neurons attacking the cell membrane and degrading other key cellular components leading to cell death
• Secondary cell death results from a cascade of biochemical, cellular, and molecular events evolving over time due to tissue damage.
• Secondary processes develop over hours and days, and include glutamate neurotoxicity, influx of calcium and other ions, free radical release, cytokines, and inflammatory responses that can lead to cell death.
• Hypoxic-ischemic injury results from a lack of oxygenated blood flow to the brain tissue. It can be caused by systemic hypotension, anoxia, or damage to specific vascular territories of the brain.
• Because the rigid skull surrounds the brain, swelling, abnormal brain fluid dynamics, or hematoma can result in elevated ICP. Severely increased ICP typically results in herniation of the brain.