Diffuse axonal injury in early infancy.

Vowles, G. H.; Scholtz, Carl L.; Cameron, J. M.

doi:10.1136/jcp.40.2.185

Cited by 76 publications

(27 citation statements)

References 10 publications

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“…This child was 4 years old at the time of injury, and the exact mechanism of injury remains unknown. Although autopsy studies of infants with inflicted TBI have documented cortical tears and shearing injuries, particularly in infants less than 5 months of age [7,27,37], MRI evaluation in our sample of children surviving assault, including 17 children less than 5 months of age, did not disclose shearing injury. Vowles et al [37] inferred that recurrent inflicted TBI in infants may result in diffuse axonal injury without tearing blood vessels.…”

Section: Discussionmentioning

confidence: 89%

“…Although autopsy studies of infants with inflicted TBI have documented cortical tears and shearing injuries, particularly in infants less than 5 months of age [7,27,37], MRI evaluation in our sample of children surviving assault, including 17 children less than 5 months of age, did not disclose shearing injury. Vowles et al [37] inferred that recurrent inflicted TBI in infants may result in diffuse axonal injury without tearing blood vessels. As the MRI protocol in this study relied on the presence of hemorrhage to identify shear injury, it may have underestimated the actual occurrence of shear injuries without obvious hemorrhage.…”

Section: Discussionmentioning

confidence: 89%

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Acute neuroradiologic findings in young children with inflicted or noninflicted traumatic brain injury

Ewing‐Cobbs¹,

Prasad²,

Kramer

et al. 2000

Child's Nervous System

147

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Acute CT/MRI findings were examined in a prospective, longitudinal study of 60 children 0-6 years of age hospitalized for moderate to severe traumatic brain injury (TBI). TBI was categorized as either inflicted (n = 31) or noninflicted (n = 29). Glasgow Coma Scale scores and perinatal history were comparable in both groups. Acute CT/MRI studies were visually inspected by a radiologist blind to group membership. Compared with the noninflicted TBI group, the inflicted TBI group had significantly elevated rates of subdural interhemispheric and convexity hemorrhages as well as signs of pre-existing brain abnormality, including cerebral atrophy, subdural hygroma, and ex vacuo ventriculomegaly. Intraparenchymal hemorrhage, shear injury, and skull fractures were more frequent after non-inflicted TBI. Subarachnoid hemorrhage and infarct/edema occurred with comparable frequency in both groups. Characteristic acute neuroimaging findings of inflicted TBI included multiple extraaxial hemorrhages in addition to the mild atrophy, subdural hygromas, and ventriculomegaly that suggest prior brain abnormality.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 89%

Acute neuroradiologic findings in young children with inflicted or noninflicted traumatic brain injury

Ewing‐Cobbs¹,

Prasad²,

Kramer

et al. 2000

Child's Nervous System

147

View full text Add to dashboard Cite

show abstract

“…16,17 DAI more commonly occurs with high-force deceleration or rotational injuries. 2,18,19 Motor vehicle accidents are believed to be the major cause of DAI, 20 and our patient population almost exclusively consisted Comparison of groups was performed using nonparametric Mann-Whitney u test (two-tailed). For 6-to 12-month outcome data, a Kendall's correlation coefficient is reported with p value (two-tailed).…”

Section: Susceptibility-weighted Imagingmentioning

confidence: 99%

Diffuse axonal injury in children: Clinical correlation with hemorrhagic lesions

Tong

Ashwal

Holshouser

et al. 2004

Annals of Neurology

307

210

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An inception cohort of 40 children and adolescents with traumatic brain injury and suspected diffuse axonal injury were studied using a new high-resolution magnetic resonance imaging susceptibility-weighted technique that is very sensitive for hemorrhage. A blinded comparison was performed between the extent of parenchymal hemorrhage and initial clinical variables as well as outcomes measured at 6 to 12 months after injury. Children with lower Glasgow Coma Scale scores (< or =8, n = 30) or prolonged coma (>4 days, n = 20) had a greater average number (p = 0.007) and volume (p = 0.008) of hemorrhagic lesions. Children with normal outcomes or mild disability (n = 30) at 6 to 12 months had, on average, fewer hemorrhagic lesions (p = 0.003) and lower volume (p = 0.003) of lesions than those who were moderately or severely disabled or in a vegetative state. Significant differences also were observed when comparing regional injury to clinical variables. Because susceptibility-weighted imaging is much more sensitive than conventional T2*-weighted gradient-echo sequences in detecting hemorrhagic diffuse axonal injury, more accurate and objective assessment of injury can be obtained early after insult, and may provide better prognostic information regarding duration of coma as well as long-term outcome.

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“…In shaken baby syndrome, edema, bleeding, infarcts, white matter contusional tears, and axonal injury have been reported (Zimmerman et al, 1979;Vowles et al, 1987;Jaspan et al, 1992;Duhaime et al, 1998). In other studies, contusional tears but no axonal injury in infants were described (Lindenberg and Freytag, 1969).…”

Section: Clinical and Neuropathological Fea-tures Of Tbi In Infants Amentioning

confidence: 90%

Neuropathological and biochemical features of traumatic injury in the developing brain

et al. 2003

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Trauma to the developing brain constitutes a poorly explored field. Some recent studies attempting to model and study pediatric head trauma, the leading cause of death and disability in the pediatric population, revealed interesting aspects and potential targets for future research. Trauma triggers both excitotoxic and apoptotic neurodegeneration in the developing rat brain. Excitotoxic neurodegeneration develops and subsides rapidly (within hours) whereas apoptotic cell death occurs in a delayed fashion over several days following the initial traumatic insult. Apoptotic neurodegeneration contributes in an age-dependent fashion to neuronal injury following head trauma, with the immature brain being exceedingly sensitive. In the most vulnerable ages the apoptosis contribution to the extent of traumatic brain damage far outweighs that of the excitotoxic component. Molecular and biochemical studies indicate that both extrinsic and intrinsic mechanisms are involved in pathogenesis of apoptotic cell death following trauma. Interestingly, in infant rats a pan-caspase inhibitor ameliorated apoptotic neurodegeneration with a therapeutic time window of up to 8 h after trauma. These results help explain unfavorable outcomes of very young pediatric head trauma patients and imply that regimens which target slow active forms of cell death may comprise a successful neuroprotective approach.

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Diffuse axonal injury in early infancy.

Cited by 76 publications

References 10 publications

Acute neuroradiologic findings in young children with inflicted or noninflicted traumatic brain injury

Acute neuroradiologic findings in young children with inflicted or noninflicted traumatic brain injury

Diffuse axonal injury in children: Clinical correlation with hemorrhagic lesions

Neuropathological and biochemical features of traumatic injury in the developing brain

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