Axonal injury and the neuropathology of shaken baby syndrome

Shannon, Patricia J.; Smith, Charles R.; Deck, John H. N.; Ang, Lee Cyn; Ho, Margaret T.; Le, Becker

doi:10.1007/s004010050849

Cited by 144 publications

(71 citation statements)

References 16 publications

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“…12 A number of other small case series have documented upper cervical spinal cord injuries in fatal cases of AHT. 15,20,26 In the largest study to date, Brennan and colleagues documented cervicomedullary and/or upper spinal cord injuries in 29 (71%) of 41 fatal cases of AHT. 4 The senior author has also observed spinal cord injury on MRI in survivors of AHT (unpublished observations).…”

Section: Contribution Of Neuroimaging To Timing Of Ahtmentioning

confidence: 99%

Serial neuroimaging in infants with abusive head trauma: timing abusive injuries

Bradford¹,

Choudhary²,

Dias

2013

PED

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Object The appearance and evolution of neuroimaging abnormalities following abusive head trauma (AHT) is important for establishing the time frame over which these injuries might have occurred. From a legal perspective this frames the timing of the abuse and therefore identifies and excludes potential perpetrators. A previous pilot study involving 33 infants with AHT helped to refine the timing of these injuries but was limited by its small sample size. In the present study, the authors analyzed a larger group of 210 cases involving infants with AHT to chronicle the first appearance and evolution of radiological (CT, MRI) abnormalities. Methods All children younger than 24 months admitted to the Penn State Hershey Medical Center with AHT over a 10-year period were identified from a medical record review; the time of injury was determined through an evaluation of the clinical records. All imaging studies were analyzed, and the appearance and evolution of abnormalities were chronicled on serial neuroimaging studies obtained in the days and weeks after injury. Results One hundred five infants with specific injury dates and available imaging studies were identified; a subset of 43 children additionally had documented times of injury. In infants with homogeneously hyperdense subdural hematomas (SDHs) on initial CT scans, the first hypodense component appeared within the SDH between 0.3 and 16 days after injury, and the last hyperdense subdural component disappeared between 2 and 40 days after injury. In infants with mixed-density SDHs on initial scans, the last hyperdense component disappeared between 1 and 181 days. Parenchymal hypodensities appeared on CT scans performed as early as 1.2 hours, and all were visible within 27 hours after the injury. Rebleeding into SDHs was documented in 17 cases (16%) and was always asymptomatic. Magnetic resonance imaging of the brain was performed in 49 infants. Among those with SDH, 5 patterns were observed. Patterns I and II reflected homogeneous SDH; Pattern I (T1 hyperintensity and T2/FLAIR hypointensity, “early subacute”) more commonly appeared on scans performed earlier after injury compared with Pattern II (T1 hyperintensity and T2/FLAIR hyperintensity, “late subacute”), although there was considerable overlap. Patterns III and IV reflected heterogeneous SDH; Pattern III contained relatively equal mixtures having different intensities, whereas Pattern IV had fluid that was predominantly T1 hypointense and T2/FLAIR hyperintense. Again, Pattern III more commonly appeared on scans performed earlier after injury compared with Pattern IV, although there was significant overlap. Conclusions These data extend the preliminary data reported by Dias and colleagues and provide a framework upon which injuries in AHT can be timed as well as the limitations on such timing estimates.

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Section: Contribution Of Neuroimaging To Timing Of Ahtmentioning

confidence: 99%

Serial neuroimaging in infants with abusive head trauma: timing abusive injuries

Bradford¹,

Choudhary²,

Dias

2013

PED

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show abstract

“…Although on the basis of the distribution of the energy/ forces evoking TAI, it is reasonable to assume the potential occurrence of spinal cord (SC) damage, to date only limited information has been collected on this issue, with limited descriptions of axonal injury in the cervical segments in controlled cortical impact (CCI) (Lighthall, 1988) and rotational acceleration injury (Hamberger et al, 2003). In humans, only anecdotal data are available regarding the occurrence of DAI in the cervical spinal cord, primarily in shaken baby syndrome (SBS) (Shannon et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Traumatic Axonal Injury in the Spinal Cord Evoked by Traumatic Brain Injury

Czeiter

Pál

Kövesdi

et al. 2008

Journal of Neurotrauma

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Although it is well known that traumatic brain injury (TBI) evokes traumatic axonal injury (TAI) within the brain, TBI-induced axonal damage in the spinal cord (SC) has been less extensively investigated. Detection of such axonal injury in the spinal cord would further the complexity of TBI while also challenging some functional neurobehavioral endpoints frequently used to assess recovery in various models of TBI. To assess TAI in the spinal cord associated with TBI, we analyzed the craniocervical junction (CCJ), cervico-thoracic (CT), and thoraco-lumber (ThL) spinal cord in a rodent model of impact acceleration of TBI of varying severities. Rats were transcardially fixed with aldehydes at 2, 6, and 24 h post-injury (n ‫؍‬ 36); each group included on sham-injured rodent. Semi-serial vibratome sections were reacted with antibodies targeting TAI via alteration in cytoskeletal integrity or impaired axonal transport. Consistent with previous observations in this model, the CCJ contained numerous injured axons. Immunoreactive, damaged axonal profiles were also detected as caudal, as the ThL spinal cord displayed morphological characteristics entirely consistent with those described in the brainstem and the CCJ. Quantitative analyses demonstrated that the occurrence and extent of TAI is positively associated with the impact/energy of injury and negatively with the distance from the brainstem. These observations show that TBI can evoke TAI in regions remote from the injury site, including the spinal cord itself. This finding is relevant to shaken baby syndrome as well as during the analysis of data in functional recovery in various models of TBI.

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“…34,35 Following experimental brain trauma, this protein can persist in small amounts for up to 1 year following experimental trauma. 36 We were surprised not to see more extensive staining in our sections, although a lack of sustained damage may have terminated elaboration or retention of this protein after the initial insult.…”

Section: Discussionmentioning

confidence: 99%

Effects of methylprednisolone and MK-801 on functional recovery after experimental chronic spinal cord injury

et al. 2000

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Study design: An experimental study was conducted to evaluate the eects of methylprednisolone and MK-801 after the compressive injury of spinal cord in rats. Objectives: To investigate the eect of methylprednisolone and non-competitive NMDA antagonist MK-801 in long-term functional outcome after spinal cord injury (SCI). Methods: A randomized group A of Sprague-Dawley rats were treated with MK-801 (1.0 mg/kg, n=10; Group A) after a compression injury. A group of methylprednisolone (MP)-treated (30 mg/kg, n=10; Group B) and non-treated animals (n=9; Group C) were included for comparison. The functional motor outcome such as inclined plane (IP), toe spreading re¯ex (TSR), and modi®ed Tarlov scale (TS) were measured in each animal at regular time points up to 8 weeks post-treatment. Histologically the injury site was scored in four groups and immunohistochemically Wallerian Degeneration (WD), astrocytosis and expression of b-amyloid protein was identi®ed. Results: In examining the IP data, no signi®cant dierence was recognized between the group means (P-value40.5). For the TSR, there were no dierences in the group responses. For the TS, the dierences were not statistically signi®cant. Only group B showed signi®cance in cavitation scores compared to group A (P40.0094), WD was signi®cantly dierent than group C (P40.03), astrocytosis was signi®cantly higher than group A (P40.001) and modest presence of b-amyloid protein.

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Axonal injury and the neuropathology of shaken baby syndrome

Cited by 144 publications

References 16 publications

Serial neuroimaging in infants with abusive head trauma: timing abusive injuries

Serial neuroimaging in infants with abusive head trauma: timing abusive injuries

Traumatic Axonal Injury in the Spinal Cord Evoked by Traumatic Brain Injury

Effects of methylprednisolone and MK-801 on functional recovery after experimental chronic spinal cord injury

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