Trauma is a common cause of death in neonatal New Zealand sea lion pups, and subadult male sea lions have been observed picking up and violently shaking some pups. In humans, axonal injury is a common result of
traumatic brain injury, and can be due to direct
trauma to axons or to ischaemic damage secondary to
trauma. '
Shaken baby syndrome', which has been described in human infants, is characterised by
retinal and intracranial subdural haemorrhages, and has been associated with axonal injury to the brain, spinal cord and optic nerve. This study identifies mechanisms of
traumatic brain injury in New Zealand sea lion pups, including impact
injuries and shaking-type
injuries, and identifies gross lesions of
head trauma in 22/36 sea lion pups found dead at a breeding site in the Auckland Islands. Despite the high frequency of such gross lesions, only three of the pups had died of
traumatic brain injury. Observational studies confirmed that shaking of pups occurred, but none were shown to die as a direct result of these shaking events. Axonal injury was evaluated in all 36 pup brains using β-
amyloid precursor
protein immunohistochemistry. Immunoreactive axons were present in the brains of all pups examined including seven with vascular axonal injury and two with
diffuse axonal injury, but the severity and pattern of injury was not reliably associated with death due to
traumatic brain injury. No dead pups had the typical combination of gross lesions and immunohistochemical findings that would conform to descriptions of '
shaken baby syndrome'. Axonal injury was present in the optic nerves of most pups, irrespective of cause of death, but was associated with ischaemia rather than
trauma.