Neuropathology of inflicted head injury in children II. Microscopic brain injury in infants

Citation
Jf. Geddes et al., Neuropathology of inflicted head injury in children II. Microscopic brain injury in infants, BRAIN, 124, 2001, pp. 1299-1306
Citations number
31
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
BRAIN
ISSN journal
00068950 → ACNP
Volume
124
Year of publication
2001
Part
7
Pages
1299 - 1306
Database
ISI
SICI code
0006-8950(200107)124:<1299:NOIHII>2.0.ZU;2-D
Abstract
There are very few reports in the literature dealing with the neuropatholog y of infant head injury, and the question of whether diffuse traumatic brai n 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 immunohistochemist ry for beta -amyloid precursor protein. Full clinical details were availabl e for each case, the most constant of which in the study cohort was an epis ode of significant apnoea at presentation, found to have been recorded in 7 5% of cases. Global hypoxic damage was the most common histological finding . Widespread axonal damage, interpreted as vascular, was present in 13 case s, but widespread traumatic axonal injury was found in only two children, b oth of whom had severe head injuries with multiple skull fractures. Epidura l cervical haemorrhage and focal axonal damage to the brainstem and the spi nal nerve roots, found in 11 cases but not in controls, indicate that the c raniocervical junction is vulnerable in infant head injury, the neuropathol ogy being that of stretch injury from cervical hyperextension/flexion. Dama ge to this region could account for the observed apnoea, which could in tur n lead to hypoxic damage and brain swelling, The observation that the predo minant histological abnormality in cases of inflicted head injury in the ve ry young is diffuse hypoxic brain damage, not DAI, can be explained in one of two ways: either the unmyelinated axon of the immature cerebral hemisphe res is relatively resistant to traumatic damage, or in shaking-type injurie s the brain is not exposed to the forces necessary to produce DAI.