Traumatic Brain Injury: Neuropathology

• Lecture 2 covers the neuropathology of traumatic brain injury (TBI), including biomechanics and pathophysiology.

Types of Traumatic Brain Injury

• Traumatic brain injury (TBI) is a type of acquired brain injury.
• Other types of acquired brain injuries include stroke, brain tumors, and encephalitis.
• Types of TBI include:
  • Closed Head Injury (CHI): Non-penetrating TBI where the head suffers a concussive or forceful blow.
  • Open Head Injury (OHI): Penetrating TBI where a foreign object enters or penetrates the skull.
• Closed head injuries are the most frequent cause of TBI

Biomechanics & Pathophysiology

• An area of study of TBI, covers both the biomechanics and pathophysiology of any such injury

Open Head Injury (OHI)

• Open Head Injury (OHI) results in penetration of the skull and meningeal layers of the brain
• Focal Damage is defined as the distruption in the neuronal networks along the path of a penetrating object
• Focal damage leads to cognitive and communicative deficits specific to the damaged brain region.
• A chart showes the brain lobes and functions, which are impacted with focal damage:
  • Frontal Lobe: Executive functions, motor control, language production, emotional regulation
  • Parietal Lobe: Sensory integration, spatial awareness, attention, mathematical processing
• Temporal Lobe: Auditory processing, memory, Language comprehension, emotion processing.
• Occipital Lobe: Visual processing, color recognition, motion perception, reading

Closed Head Injury (CHI)

• Primary damage from CHI is often the result of focal and diffuse lesions.
• Focal lesions result from linear acceleration-deceleration forces
  • Coup: Impact on site of contact.
  • Contrecoup: Impact on the opposite side of main contact.
• Frontal and temporal lobes are often compromised from acceleration-deceleration forces.
• Diffuse/Multifocal Lesions result often from rotational forces, causing diffuse axonal injury (DAI).
  • DAI is a key factor in disrupted neuronal communication.
  • Mild DAI can cause headaches.
  • Severe DAI can cause loss of consciousness or a vegetative state.

Secondary damage resulting from TBI includes:

• Hemorrhage
• Cerebral edema
• Intracranial pressure
• Hypoxia/Ischemia
• Seizures

Combat-related Blast Injury

• Combat-related blast injuries result from blast exposure that leads to the following:
  • Impact from blast wave
  • Impact from debris on skull
  • Body being thrown upon a surface by the blast
  • Inhalation of toxic substances from the blast

Chronic Traumatic Encephalopathy (CTE)

• Progressive neuropathology resulting from repetitive blows (concussions) to the head
• Neuronal degeneration results with sustained exposure to repetitive head impacts. CTE often causes:
  • Cognitive deficits: memory, executive functions.
  • Neurobehavioral dysregulation: Impulsivity, explosivity
  • CTE is diagnosed by examining brain tissue after death

Lecture on the neuropathology of traumatic brain injury (TBI). Covers biomechanics and pathophysiology. Discusses closed head injuries and open head injuries. Focal damage and neuronal network disruption are also examined.