Nonaccidental Head Injury in Children: New Clues from Neuropathology
Abstracts & Commentary
Sources: Geddes JF, et al. Brain. 2001;124:1290-1298, 1299-1306; Shannon P, Becker L. Lancet. 2001;358:686-687; Graham DI. Brain. 2001;124(Pt 7):1261-1262.
Nonaccidental trauma (largely related to child abuse) is an important cause of brain injury in young infants. Head injury is the most common neurological cause of death and disability in young children. Some studies (Duhaime AC, et al. Pediatrics. 1992;90: 179-185) have suggested that approximately 25% of cases of head injury in children younger than age 2 are due to nonaccidental trauma. Due to sensitive medico-legal implications, reliable history is rarely available to help determine precisely what happened.
A prominent feature of nonaccidental head trauma, especially in younger children, is the presence of subdural hematoma, subarachnoid hemorrhage, and retinal hemorrhage in the face of minimal external evidence of trauma in many patients. This led to the concept of the "shaken-baby syndrome," brain injury related to repetitive whiplash motions at the relatively hyperextensible neck of the young child. More recent data (Duhaime AC, et al. N Engl J Med. 1998;338:1822-1829) suggest that some sort of impact was likely necessary to account for the spectrum of brain injury seen in these cases (so called "shaken impact syndrome").
Relatively little is known about the mechanisms of injury in these children. Two sequential papers by Geddes and colleagues make important new contributions to our understanding. Geddes et al performed detailed neuropathological studies on 53 infants with nonaccidental head trauma on whom complete autopsies were also performed. These patients were subdivided into 2 groups: 37 infants, age ranging from 20 days to 9 months, and 16 children ranging from 13 months to 8 years. Patterns of brain injury seemed to differ between the 2 groups. Whereas 75% of children had evidence of extracranial injury, only 41% of infants had such evidence. More than 50% of infants had no evidence of skull fracture and approximately a quarter had no evidence of subscalp bruising. In contrast, children always had evidence of subscalp bleeding. Microscopic neuropathology showed that diffuse axonal injury is rare in both infants and children (seen in about 5% of cases), but focal traumatic axonal injury was much more common, seen in about 40% of cases. Strikingly, traumatic axonal injury was present at the craniocervical junction in the majority of infants in which focal traumatic axonal injury was seen (11/16 cases), whereas no children had such injury but rather had injury to deep white matter.
In a second paper, Geddes et al used immunohistochemical methods to study the mechanisms underlying the axonal injury they observed. In this study, only the infants considered in the prior paper (37 cases) were examined. Using beta-amyloid precursor protein (beta-APP) immunohistochemistry to detect axonal damage, they could document evidence of diffuse axonal injury in only 2 of 37 cases. This suggests that the "diffuse axonal shearing" seen in severe traumatic injury (ie, motor vehicle accidents) is not an important mechanism of nonaccidental traumatic injury in infants. Global hypoxic-ischemic injury was by far the most common finding, and evidence of vascular axonal injury in 12 of 37 cases. Global hypoxic-ischemic injury was a necessary concomitant to focal axonal injury in almost all cases (11/12) where focal axonal injury was seen.
Commentary
The 2 sequential papers by Geddes et al appear to be a major landmark in the relatively sparse neurological literature on nonaccidental trauma in infants and children. These papers revise our current concept of "shaken-baby syndrome" in that it clearly demonstrates that the shaking does not produce sufficient force to produce diffuse axonal injury in the majority of cases. In infants, shaking of the highly hyperextensible neck may lead to, in many cases, focal axonal injury at the craniocervical junction, which then leads to apnea and global hypoxic-ischemic injury. We eagerly await a paper from this group regarding further studies on the 16 children who appear to have important differences from the 37 infants studied. Obviously, as an autopsy study, these papers shed the most light on the most severe cases, but one would presume similar mechanisms operative in survivors of such trauma.
One aspect of the nonaccidental trauma problem which the Geddes et al papers cannot yet address is causality. In the infants subjected to such trauma, which came first: the apnea or the shaking (which leads to brainstem injury and apnea)? In my experience, many parents will indicate that they shook their infants vigorously because they believed them to have stopped breathing, hardly a criminal act. Clearly these issues have major medicolegal implications. —Rosario Trifiletti
Dr. Trifiletti, Assistant Professor, Neurology and Pediatrics, New York Presbyterian Hospital-Cornell Campus, is Assistant Editor of Neurology Alert.
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