Neuropathology of inflicted head injury in children. II. Microscopic brain injury in infants.
There are very few reports in the literature dealing with the neuropathology of infant head injury, and the question of whether diffuse traumatic brain damage [diffuse axonal injury (DAI)] occurs in such children has not yet been reliably established by detailed neuropathological studies. We report the findings in the brains of a series of 37 infants aged 9 months or less, all of whom died from inflicted head injuries, and 14 control infants who died of other causes. Axonal damage was identified using immunohistochemistry for beta-amyloid precursor protein. Full clinical details were available for each case, the most constant of which in the study cohort was an episode of significant apnoea at presentation, found to have been recorded in 75% of cases. Global hypoxic damage was the most common histological finding. Widespread axonal damage, interpreted as vascular, was present in 13 cases, but widespread traumatic axonal injury was found in only two children, both of whom had severe head injuries with multiple skull fractures. Epidural cervical haemorrhage and focal axonal damage to the brainstem and the spinal nerve roots, found in 11 cases but not in controls, indicate that the craniocervical junction is vulnerable in infant head injury, the neuropathology being that of stretch injury from cervical hyperextension/flexion. Damage to this region could account for the observed apnoea, which could in turn lead to hypoxic damage and brain swelling. The observation that the predominant histological abnormality in cases of inflicted head injury in the very young is diffuse hypoxic brain damage, not DAI, can be explained in one of two ways: either the unmyelinated axon of the immature cerebral hemispheres is relatively resistant to traumatic damage, or in shaking-type injuries the brain is not exposed to the forces necessary to produce DAI.
Geddes
J F
JF
Departments of Histopathology and Morbid Anatomy and Environmental and Preventative Medicine, Queen Mary, University of London, UK. j.f.geddes@mds.qmw.ac.uk
Vowles
G H
GH
Hackshaw
A K
AK
Nickols
C D
CD
Scott
I S
IS
Whitwell
H L
HL
D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D001929:Brain Edema / Q000453:epidemiology / Q000473:pathology; D001933:Brain Stem / Q000378:metabolism / Q000473:pathology; D002649:Child Abuse / Q000175:diagnosis*; D015331:Cohort Studies; D015897:Comorbidity; D006259:Craniocerebral Trauma / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology*; D020833:Diffuse Axonal Injury / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology; D005260:Female; D005554:Forensic Medicine; D006801:Humans; D002534:Hypoxia, Brain / Q000453:epidemiology / Q000473:pathology*; D007150:Immunohistochemistry; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D019838:Neck Injuries / Q000453:epidemiology / Q000473:pathology; D012887:Skull Fractures / Q000453:epidemiology / Q000473:pathology; D013126:Spinal Nerve Roots / Q000473:pathology; D006113:United Kingdom / Q000453:epidemiology
D016564:Amyloid beta-Protein Precursor