Neuropathology of inflicted head injury in children

Geddeset al. have raised several interesting questions about the pathogenesis of non‐accidental head injury. It has been suspected previously that hypoxia secondary to apnoea rather than direct impact is responsible for the diffuse brain damage seen in non‐accidental injury (Johnsonet al., 1995). The authors’ neuro‐pathological findings support this theory and also demonstrate injuries at the cranio‐cervical junction that account for the apnoea and hypoxia in infants with non‐accidental injury (Geddeset al., 2001a, b). Although we accept that it may not be necessary to shake an infant very violently to produce a stretch injury to its neuraxis, we disagree with the authors’ proposal that repetitive acceleration‐deceleration injury need not occur in the shaken baby syndrome. This hypothesis does not explain the characteristic presence of retinal haemorrhages in these infants (Kivlin, 2000), including those examined by the authors. Of the theories that have been proposed for the mechanism of retinal haemorrhages in non‐accidental shaking injury, traction between the vitreous gel and the retina is the likeliest mechanism. The infant eye has strong adhesions between the vitreous gel and retina, especially around the optic disc and in the retinal periphery. The differential movement at the interface between the vitreous and retina due to acceleration–deceleration forces (Duhaime, 1987; Massicotte, 1991; Green 1996) is believed to result in shearing of retinal vessels, which may be dilated as a result of increased intracranial or intrathoracic pressure (Gilkes and Mann, 1967). Anterior tracking of sub‐arachnoid haemorrhage was proposed as a possible mechanism (Jacobi, 1986), but this theory has been disproved by clinico‐pathological studies (Giangiacomo, 1988; Riffenburgh, 1991). It is evident that some factor or factors unique to the trauma suffered by these infants are needed to produce haemorrhages of the distribution and severity consistently seen in non‐accidental injury. Retinal haemorrhages are very rarely seen after witnessed or independently verifiable single impact accidental trauma in infants and children, including whiplash injury and even in fatal injury (Buys, 1992; Duhaime, 1992; Johnson and Braun, 1993). Similarly, vigorous cardio‐pulmonary resuscitation or epileptic fits rarely produce retinal haemorrhages. From consideration of the likely mechanism of retinal haemorrhages in non‐accidental shaking injury and the rare description of the trauma by perpetrators, it is evident that sufficient acceleration‐deceleration forces must be generated by repetitive to and fro shaking. An infant may not need to be shaken for long, but the shaking is necessarily violent. Apnoea induced by cranio‐cervical injury might be primarily responsible for the diffuse brain changes seen in non‐accidental injury. However, we conclude from the authors' own data that severe acceleration‐deceleration must occur in shaken baby syndrome. The ocular changes cannot be ignored, and require a sufficiently severe angular velocity change that could not be generated by anything short of violent shaking. The authors’ conclusions are open to misinterpretation, and may have serious implications, both scientific and legal, on the mechanism of non‐accidental shaking injuries.