Focal and Diffuse Traumatic Brain Injuries

• Focal TBIs are localized injuries often from direct mechanical forces, leading to contusions, lacerations, or hematomas
• Common causes for focal injuries include blunt trauma or penetrating injuries.

Mechanism of Injury:

• Focal injuries result from direct impact, leading to localized compression, deformation, and mechanical stress on neural tissue
• Contrecoup lesions or epidural/subdural hematomas may occur.

Pathophysiological Processes:

• Initial damage to blood vessels can cause hemorrhage, leading to local ischemia and cell death.

• Swelling and increased intracranial pressure can compress adjacent areas.

• Inflammation and excitotoxicity (excess glutamate release leading to calcium influx and neuronal damage) are secondary responses.

• Diffuse TBIs involve widespread damage to neurons and axons, typically from rotational or shearing forces, such as in motor vehicle accidents.

Diffuse Axonal Injury (DAI):

• DAI is the most common type of diffuse injury where axons tear or stretch due to rapid acceleration-deceleration forces
• Axonal shearing disrupts communication between neurons, often leading to loss of consciousness and long-term neurological impairments

Pathophysiological Mechanisms:

• Differences in brain tissue densities lead to varying acceleration rates, cause axonal damage via Shearing Forces
• Excitotoxicity occurs similarly to focal injuries, involving excess glutamate release leading to calcium-mediated damage to neurons
• Secondary injury includes:
  • Blood-brain barrier disruption
  • Neuroinflammation
  • Oxidative stress
  • Apoptotic pathways

Role of Microhemorrhages:

• Diffuse brain injuries may involve microhemorrhages (small areas of bleeding), often in the subarachnoid space due to vessel rupture

Long-Term Outcomes:

• Damage to axons can be either reversible with repair, or result in long-term deficits and disabilities

• Focal injuries are more localized & involve tissue deformation/hematomas

• Diffuse injuries involve shearing forces, leading to widespread axonal damage and functional impairments

General Symptoms Across TBIs:

• Physical symptoms: Headache, dizziness, fatigue, nausea, vomiting, and motor dysfunction
• Cognitive changes: Memory issues, confusion, difficulty concentrating, and altered mental status.
• Emotional/psychological disturbances include mood changes, irritability, and anxiety.

Mild TBI

• (GCS) 13-15
• Loss of consciousness: May or may not occur (<30 minutes)
• Symptoms: Headache, dizziness, and fatigue
• Amnesia: Possible anterograde amnesia (<24 hours)
• Other: Temporary motor or cognitive impairments that typically resolve with time

Moderate TBI

• (GCS) 9-12
• Loss of consciousness lasting between 30 minutes to 24 hours
• Long-duration post-trauma amnesia occurs
• Symptoms: Persistent headaches, dizziness, nausea
• Cognitive impairments: Difficulty focusing, memory problems
• Neurological deficits: Speech disturbances, motor weakness, and sensory changes

Severe TBI

• (GCS) 3-8
• Prolonged unconsciousness or coma lasts more than 24 hours
• Brainstem injury is often present
• Severe motor deficits include hemiplegia or loss of reflexes
• Persistent cognitive issues can lead to long-term disability
• Risk of seizures, hydrocephalus, and autonomic dysfunction

Focal Brain Injuries

• Involve contusions and intracranial hemorrhages (e.g., subdural, epidural hematomas)
• Depend on the brain region affected:
  • Frontal lobe: Personality changes, impaired judgment
  • Temporal lobe: Memory issues, auditory disturbances
  • Occipital lobe: Visual impairment
  • Brainstem: Breathing and heart rate irregularities

Diffuse Brain Injuries

• Caused by shear forces (e.g., diffuse axonal injury (DAI))
• Manifestations: Loss of consciousness or coma; cognitive deficits and memory loss; persistent motor impairments including coordination issues; long-term deficits in attention and executive function

Secondary Injuries

• Blood-brain barrier (BBB) disruption leads to neuroinflammation and cerebral edema
• Excitotoxicity: Excessive glutamate release causing neuronal damage
• Reactive oxygen species production causes oxidative stress that damages neurons
• Ischemia and metabolic dysfunction includes decreased blood flow leading to neuronal death and delayed recovery

Comparing mild, moderate, and severe TBIs

• Severity and Duration of Consciousness Loss: Mild TBIs typically involve little to no loss, while moderate/severe TBIs involve longer durations
• Cognitive and Motor Deficits: Mild cases often recover with minimal intervention; moderate cases risk permanent deficits; severe cases often result in major/lasting impairments
• Brain Imaging Findings: Mild TBIs often show no visible damage, while moderate/severe TBIs reveal more significant structural damage, including hemorrhage/axonal injury