Coup-Contrecoup Brain Injury: Mechanism, Patterns, and Clinical Significance

Coup-contrecoup injury describes dual brain contusions: at the site of impact (coup) and the opposite side (contrecoup), caused by brain movement within the skull.

Mechanism

1. Coup: Direct impact → skull deformation → brain compression/contusion at impact site (e.g., frontal lobe in frontal crash).
2. Contrecoup: Brain continues moving (inertia) after skull decelerates → strikes opposite inner skull → contusion (e.g., occipital lobe in frontal crash).

Acceleration-deceleration forces (MVA, falls, assaults) cause shearing/stretching of axons (diffuse axonal injury) plus focal contusions.

Common Patterns

• Frontal-temporal coup → occipital contrecoup.
• Temporal coup → contralateral temporal/frontal contrecoup.
• Occipital coup → frontal contrecoup.

Clinical Significance

• Contrecoup lesions often larger/more severe than coup.
• Frontal/temporal contusions → executive dysfunction, personality change, memory deficits, seizures.
• Brainstem involvement (from rotation) → coma, cranial nerve palsies, respiratory compromise.
• Associated: subdural/epidural hematoma, SAH, skull fracture.

Management

• ABCs, ICP monitoring, neurosurgical evacuation if mass effect.
• Seizure prophylaxis, DVT prophylaxis, early rehab.
• Outcome depends on GCS, lesion volume, age, secondary insults (hypoxia, hypotension).

Coup-contrecoup signifies severe TBI; even "mild" initial presentation can deteriorate. Urgent neuroimaging and neurosurgical consultation are mandatory.