| Vol. 3, Issue 1, Article 2 |
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Buadu, et al. |
Most intra-axial lesions in contrast to extra-axial lesions are nonhemorrhagic although hemorrhagic lesions can occur (fig 5). Nonhemorrhagic intra-axial lesions which are more difficult to identify early in their course and are responsible for most deaths from inflicted head injury [9]. Nonhemorrhagic intra-axial lesions may present as diffuse pathologic alterations like hyperemic cerebral swelling, diffuse cerebral edema or hypoxic ischemic injury. More focal manifestations include focal infarcts or axonal injury.
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| Intraparenchymal Hematoma Fig 5. 5-month-old female who presented with altered mental status and retinal hemorrhages on physical examination. Sagittal T1-weighted (fig 5a.) and gradient echo (fig 5b) images demonstrate an intra-parenchymal hematoma. |
Brain edema is the most profound pathologic alteration encountered with inflicted brain injury, yet the most poorly understood. Brain edema a consequence of increased brain water (cytotoxic and vasogenic) may occur as a response to direct focal injury such as cerebral contusion or diffuse primary injury such as diffuse axonal injury (DAI). Furthermore, vascular occlusion due to cerebral brain stem herniation as well as pressure necrosis may lead to cerebral edema. CT images obtained immediately after the traumatic event often show no evidence of swelling or edema. Swelling or edema may become manifest on CT within a few hours with extensive loss of gray-white differentiation and diffuse hypodensity. These findings carry a poor clinical outcome regardless of the clinical grade.
There is a tendency for profoundly injured infants to develop CT manifestations of brain edema that primarily involves the cerebral cortex and subcortical white matter but apparently spares the basal ganglia, thalami brainstem and cerebellum. This finding is often associated with subdural hematoma and can be unilateral or bilateral. Cohen and colleagues [10] coined the term reversal sign to describe this phenomenon (fig 6). The pathogenesis of the reversal sign is not entirely understood but experimental studies appear to indicate that cerebral cortical gray matter is particularly sensitive to hypoxic ischemic injury. Bird and associates suggest that the peripheral low density with relative central high density is related to the passive congestion and distension of deep medullary veins because of partial venous outflow form obstruction from the increased intracranial pressure [11].
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| Hypoxic Ischemic Injury Fig 6. 2-month-old female infant presenting with seizur es and apnea. Non-enhanced CT (NECT) shows the reversal sign with diffuse and extensive hypodensity of the cerebral cortices and relative sparing of the bas al ganglia and cerebellum. |
Shear injury of the white matter generally referred to as diffuse axonal injury results from angular acceleration during shaking or blunt impact trauma. Histologically the lesion is characterized by axonal swelling or the so called retraction balls. Lesions are commonly noted in the cerebral hemispheres at the gray-white matter junctions (fig 7), the corpus callosum, the dorsolateral aspect of the upper brainstem, the upper pons and the basal ganglia. Because of the superior conspicuity provided, T2* gradient echo and FLAIR imaging are the preferred MRI techniques for demonstrating DAI. However, DAI is particularly uncommon in infants.
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| Shear Injury Fig 7. 14-day-old male infant with new onset focal seizures, fever and swelling on the right forehead. Axial CT shows a focus of hemorrhage over the right temporal tip (arrow) (fig 7a). Axial T1 and T2-weighted images confirm the presence of hemorrhage at the right temporal tip (fig 7b & c). Diffusion weighted image shows two punctuate foci of restricted diffusion (arrows) in the left parietal lobe most consistent with axonal injury (fig 7d). ADC values (not shown) were diminished. |
Atrophy is often the result of primary and secondary traumatic brain injury. When serial imaging demonstrates an evolution from widespread cerebral edema to cerebral atrophy it is likely that hypoxic ischemia has played a major role in the cerebral injury. The time course for the development of cerebral atrophy is variable but the imaging findings may develop rapidly when the initial insult is severe (fig 8). These findings correspond with the development of cerebral spasticity and a vegetative state.
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| Atrophy Fig 8. 2-month-old female infant presenting with seizures and apnea (same patient as fig 7.) Initial midline sagittal T1WI shows relative preservation of parenchymal volume. Follow-up MR image 9 days later shows significant loss of volume and the relatively rapid progression of severe diffuse brain injury to atrophy. |
Despite the major advances made in recognizing indicators of NAHI, in some instances there may be no apparent morphological findings despite significant underlying brain injury. In these instances MR spectroscopy can be useful and is becoming an important part of the diagnostic armamentarium in helping to unmask biochemical alterations which may predate any morphological changes. Additionally MR spectroscopy has been shown to have prognostic implications in NAHI [12].
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