Pediatric Radiology

, Volume 33, Issue 8, pp 574–577

Diffusion-weighted MRI in shaken baby syndrome

Authors

    • Department of Diagnostic Radiology and Organ ImagingPrince of Wales Hospital
  • Winnie C. W. Chu
    • Department of Diagnostic Radiology and Organ ImagingPrince of Wales Hospital
  • Gary W. K. Wong
    • Department of PaediatricsPrince of Wales Hospital
  • David K. W. Yeung
    • Department of Clinical OncologyPrince of Wales Hospital
Case Report

DOI: 10.1007/s00247-003-0949-y

Cite this article as:
Chan, Y., Chu, W.C.W., Wong, G.W.K. et al. Pediatr Radiol (2003) 33: 574. doi:10.1007/s00247-003-0949-y

Abstract

We present the characteristic CT and MRI findings of a 2-month-old girl with shaken baby syndrome. Diffusion-weighted MR imaging performed 8 days after the insult established the presence of injury to the white matter in the corpus callosum and subcortical white matter in the temporo-occipito-parietal region. Diffusion-weighted MR imaging is valuable in the diagnostic work-up of suspected shaken baby syndrome, as injury to the white matter can be demonstrated days after the injury.

Keywords

HeadBrainTraumaShaken baby syndromeChild abuseMRIMR (diffusion)

Introduction

Shaken baby syndrome (SBS) is a serious form of child abuse elicited by violent shaking or shaking with impact. The most common clinical presentation is that of an irritable or abnormally subdued child with difficulty with respiration or cyanotic attacks, frequently accompanied by seizure [1, 2]. Brain imaging is important in the diagnostic work-up of the condition with intracranial lesions characterized by cerebral contusion, subdural and subarachnoid haemorrhage and diffuse cerebral oedema.

Case report

A 2-month-old girl presented with cyanosis after feeding. At the Accident and Emergency Department, she was drowsy, lethargic and hypotonic with asymmetrical pupil size. There was no evidence of external injury and physical examination of the cardiovascular, respiratory and gastrointestinal systems was normal. The baby, born at term with normal weight by elective Caesarean section because of previous Caesarean section, was well after birth before the presentation. Initial laboratory results showed slightly low haemoglobin (8.1 g/dl) whilst renal and liver function tests, plasma ammonia and lactate were unremarkable. After admission, a fall of haemoglobin to 6.4 g/dl necessitated a blood transfusion. She also developed several episodes of tonic-clonic convulsion, which were controlled with phenobarbitone. Non-contrast CT of the brain showed right frontal and temporo-parietal subdural haematomas and interhemispheric subdural haematoma (SDH) (Fig. 1). An intracranial pressure catheter was inserted subsequently to monitor the SDH. Ophthalmological examination revealed bilateral retinal haemorrhages. Because of apnoea she was intubated and received intermittent positive pressure ventilation.
Fig. 1.

Non-contrast CT on the day of admission shows acute right temporo-parieto-occipital SDH (arrows)

On the second CT performed on day 6 after admission, the right cerebral hemisphere appeared hypodense with effacement of cerebral sulci. MRI performed on day 8 after admission, when her condition had stabilized, confirmed the right parieto-occipital and frontal SDHs, but also detected smaller SDHs in the left occipital region and the posterior aspect of the posterior fossa bilaterally (Fig. 2a). No significant mass effect was associated with these SDHs. A slight increase in signal intensity in the white matter of the right parietal occipital lobe was shown on T2-weighted (T2-W) images (Fig. 2b). Fluid-attenuated and inversion recovery (FLAIR) images showed the SDH and effacement of cerebral sulci, but did not show the white matter signal change (Fig. 2c). On diffusion-weighted imaging (DWI), the high signal change in the white matter of the right parietal and occipital lobes was more conspicuous than on the T2-W images. Hyperintensity was clearly evident in the corpus callosum (Fig. 3). The apparent diffusion coefficient map showed decrease of signal intensity in the corresponding areas (Fig. 4). The diagnosis of white-matter injury of the corpus callosum and subcortical regions of the right temporal, occipital and parietal regions was made, in addition to the SDHs.
Fig. 2a–c.

MRI, 8 days after admission. a T1-W image confirms the hyperintense right temporo-parieto-occipital SDH (arrows) and also shows SDHs in the left posterior occipital region (thick arrow) and along the posterior interhemispheric fissure (open arrow). b T2-W image shows hyperintensity in the right temporo-occipital white matter (open arrows). c FLAIR coronal image shows the SDH (black arrows). Effacement of sulci in the temporal lobe and parietal lobe near the vertex is shown (white arrows), but the white matter lesions are not evident

Fig. 3a, b.

DWI. a Hyperintensity in the right temporo-occipital white matter (arrow) and in the genu of the corpus callosum (thin arrow). b At a more cranial level there are hyperintense lesions in the right temporo-occipital white matter (arrow) and in the splenium of the corpus callosum (thin arrow)

Fig. 4.

Apparent diffusion coefficient map shows hypointense change owing to restricted diffusion in the right temporo-occipital white matter (arrow) and in the splenium of the corpus callosum (thin arrow)

The diagnosis of SBS was established by a special investigatory committee. Psychiatric interview of the baby's mother revealed postpartum depression, which was linked to the recent unemployment of the baby's father and tension between the parents. The child was stable in her subsequent course.

Discussion

SDH is the most common intracranial manifestation of child abuse [3]. SDH signal was mostly low on T1-weighted (T1-W) images and high on T2-W images, suggesting chronic SDH. A focal high signal on T1-W images suggested that re-bleeding had occurred [3, 4, 5]. SDHs were better demonstrated on MRI than CT [3, 5]. Haemorrhages at the vertex, in the subfrontal region, along the tentorium and in the middle and posterior cranial fossae were demonstrated to particular advantage on MRI [3]. The delineation of subdural haemorrhages in the posterior fossa bilaterally on MRI but not on CT in our patient also illustrated this fact.

In child abuse involving vigorous shaking in young babies, white-matter injury similar to diffuse axonal injury observed in accidental trauma, may occur; it is characteristically located at the grey-white junction, centrum semiovale and corpus callosum. MRI detection of diffuse axonal injuries has been shown to be superior to CT [5], which is also demonstrated by the superior detection of white-matter injury in the right cerebral hemispheric white matter on T2-W MRI in our patient.

DWI has been shown to be of value in diffuse axonal injury in adult patients and is shown as increased signal on isotropic DWI with a corresponding reduction in the apparent diffusion coefficient [6]. DWI in our patient showed greater extent of injury to the cerebral white matter compared to conventional T2-W images. The finding was consistent with the observation by Biousse et al. [7], who showed that these lesions were larger on DWI than on conventional T2-W MRI in 18 patients aged 6 weeks to 24 months with confirmed SBS. In the present case, lesions in the genu and splenium of the corpus callosum were seen on DWI but not on conventional T2-W images. The hemispheric white-matter lesion was more distinct on DWI.

The biomechanical origin of injury to the white matter in SBS is not fully understood. The high signal on DWI has suggested that cerebral ischaemia plays a major role [7]. In an autopsy series of 14 children with SBS, evidence of axonal injury from immunohistochemical stains for beta-amyloid precursor protein was seen in the cerebral white matter of all cases while swollen axons were present in 11 cases. These changes, however, were also seen in six of seven children dying of non-traumatic hypoxic ischemic encephalopathy. The results suggest that hypoxic/ischaemic injury may partly explain the cerebral axonal injury in SBS [8].

However, the restricted diffusion on DWI in our patient at least 8 days after injury does not seem to support ischaemia as the only mechanism because ischaemia-induced cytotoxic oedema and reduced apparent diffusion coefficient typically returns to normal about 10 days after infarction. It has been reported that decreased ADC can be seen in adult traumatic shearing axonal injury 18 days after the initial event, which is well beyond that described for cytotoxic oedema in ischaemia [6]. Such a prolonged change may be related to a propagated injury from oxidants or free radicals to which differentiating oligodendrocytes in cerebral white matter seem to be very vulnerable [9]. Delayed neuronal and oligodendroglial cell death from apoptosis in hypoxic ischaemic encephalopathy has been shown in newborn rat models [10].

In conclusion, the current case illustrates the value of DWI in the detection of white-matter injury in the work-up of suspected SBS. It should, therefore, be incorporated into the MRI examination of all such cases, whether in the acute or subacute stage.

Copyright information

© Springer-Verlag 2003