title: Axonal injury and the neuropathology of shaken baby syndrome.
abstract: We examined an autopsy series of 14 children with shaken baby syndrome (SBS) who lacked skull fracture. Evidence of axonal injury was sought using immunohistochemical stains for neurofilament, 68-kDa neurofilament and beta-amyloid precursor protein (betaAPP). BetaAPP-positive axons were present in the cerebral white matter of all cases of SBS but were also present in 6 of 7 children dying of non-traumatic hypoxic ischemic encephalopathy (HIE). Swollen axons were present in 11 of 14 cases of SBS and in 6 of 7 cases of HIE. BetaAPP-positive axons were present in both groups in the midbrain and medulla. The cervical spinal cord in SBS contained betaAPP-positive axons in 7 of 11 cases; 5 of 7 contained swollen axons within the white matter tracts; in 2 immunoreactivity was localized to spinal nerve roots; in all 7 there was a predilection for staining at the glial head of the nerve root. Among cases of HIE, none showed abnormal axons or betaAPP-positive reactivity in the cervical cord white matter. We conclude that cerebral axonal injury is common in SBS, and may be due in part to hypoxic/ischemic injury. Cervical cord injury is also common, and cannot be attributed to HIE. These findings corroborate suggestions that flexion-extension injury about the cervical spinal column may be important in the pathogenesis of SBS.
authors.affiliation: Department of Pediatric Laboratory Medicine, Hospital For Sick Children and University of Toronto, Ontario, Canada.
authors.forename: P
authors.initials: P
authors.lastname: Shannon
authors.forename: C R
authors.initials: CR
authors.lastname: Smith
authors.forename: J
authors.initials: J
authors.lastname: Deck
authors.forename: L C
authors.initials: LC
authors.lastname: Ang
authors.forename: M
authors.initials: M
authors.lastname: Ho
authors.forename: L
authors.initials: L
authors.lastname: Becker
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000032:analysis*; D001369:Axons / Q000737:chemistry / Q000473:pathology*; D015415:Biomarkers; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001929:Brain Edema / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D001930:Brain Injuries / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology; D048429:Cell Size; D002543:Cerebral Hemorrhage / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D002649:Child Abuse; D002675:Child, Preschool; D006801:Humans; D002534:Hypoxia, Brain / Q000378:metabolism / Q000473:pathology; D007223:Infant; D007231:Infant, Newborn; D009419:Nerve Tissue Proteins / Q000032:analysis*; D016900:Neurofilament Proteins / Q000032:analysis; D012189:Retrospective Studies; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology; D013119:Spinal Cord Injuries / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D013126:Spinal Nerve Roots / Q000378:metabolism / Q000473:pathology; D013314:Stress, Mechanical; D013577:Syndrome; D014911:Whiplash Injuries / Q000150:complications / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology*
chemical_list: D016564:Amyloid beta-Protein Precursor; D015415:Biomarkers; D009419:Nerve Tissue Proteins; D016900:Neurofilament Proteins