There have been relatively wide variations in the results of studies examining the outcomes of severe brain injury in children. Among the reasons for these variations in outcome, prehospital care can be considered as one of the factors. In Korea, major hospitals use an aggressive and sophisticated management policy very similar to that practiced in the West. However, effective prehospital management, such as emergency care at the scene of injury and during transport by paramedics, have not yet been established. In order to evaluate the influence of prehospital care on the outcome in severely brain-injured children, we report the outcome recorded in 73 pediatric patients treated in our hospital following severe brain injury and compare these results with those reported from centers in the western community, where well-trained paramedic care and an excellent transfer system are in operation. The overall mortality rate in our patients was 23%; 41% had a good recovery, 22% moderate disability, and 12% severe disability, and 1% remained in a vegetative state. In conclusion, we would like to suggest that prehospital care does not remarkably influence mortality rates in severely brain-injured children.
This 40-year-old woman presented to our hospital with severe headache, nausea, and vomiting. Computerized tomography and magnetic resonance (MR) images revealed an approximately 4 ϫ 4.5 ϫ 7-cm rounded lobulated mass with a large amount of calcification in the right temporoparietal convexity area. Except for the calcific area, the mass was well enhanced on MR imaging after addition of gadolinium-diethylenetriamine pentaacetic acid (Fig. 1). The patient underwent right-sided temporoparietal craniotomy. At surgery, the dura was easily peeled away from the tumor mass. The tumor was well demarcated and had a rubbery consistency, and two small cortical arteries were attached to the mass on the medial side. Histological examination revealed that the tumor was densely composed of spindle cells with cigar-shaped nuclei and a moderate amount of eosinophilic cytoplasm (Fig. 2 upper). There was no mitosis or pleomorphism. On immunohistochemical examination, the tumor displayed positive staining for vimentin and smooth-muscle actin. Electron microscopy disclosed myofilaments with dense bodies characteristic of smooth-muscle cells (Fig. 2 lower). Leiomyoma is a benign tumor originating from smooth-muscle cells. It tends to be relatively common in the genitourinary and gastrointestinal tracts. However, the occurrence of leiomyoma in the intracranial cavity is extremely rare. To our knowledge, this is the fourth case of benign intracranial leiomyoma and the first documented by MR imaging. Because in the cranial cavity smooth-muscle cells are located only in blood vessels, Kroe and colleagues 1 and Thierauf and Weiland 3 thought that their cases originated from hypophyseal vessels. The tumor reported by Lach and associates 2 was grossly similar to an arteriovenous malformation, and they believed it had developed on the basis of a preexisting vascular malformation. We also found two small cortical arteries attached to the brain mass and regarded those arteries as the origin of the leiomyoma. It is sometimes difficult to differentiate leiomyoma from fibroma by using light microscopy alone. Therefore, immunohistochemical staining for vimentin and smooth-muscle actin and electron microscopy must be used to confirm this rare brain tumor.
Purpose: To describe the imaging findings of traumatic intracranial aneurysms (TICA) in children. Materials and Methods: Five boys aged 3 15 (mean, 7) years with surgically confirmed TICA were included in this study. All had a history of nonpenetrating head trauma, and they underwent precontrast CT imaging immediately after the injury and follow-up CT or MRI. In all cases, angiography revealed the presence of aneurysms, which at surgery were shown to be pseudoaneurysms with severe adhesions. Results: Angiography demonstrated that all aneurysms were located in the anterior cerebral artery (ACA) or its branches. The precise locations were the A2 segment of the ACA, the site of origin of the callosomarginal artery or its first branch, or of the anterior internal frontal artery, or between the first and second branch of the pericallosal artery. In all patients, precontrast CT performed immediately after trauma depicted subarachnoid hemorrhage (SAH) in the anterior interhemispheric fissure (AIHF). Follow-up precontrast CT showed nodular high density around the anterior falx in three, recurrent SAH in the AIHF in two, and intracerebral hemorrhage (ICH) with intraventricular hemorrhage in two. In two patients with a nodular high-density lesion, nodular enhancement was demonstrated at postcontrast CT, and in one, follow-up MRI revealed a nodular signal void around the anterior falx; nodular enhancement was seen at postcontrast imaging, and MR angiogram depicted a saccular aneurysm. In one patient, MRI demonstrated infarction in the caudate nucleus and ACA territory. Conclusion: If, after head injury, an area of nodular high density is revealed by CT, or a signal void by MRI, or if SAH or ICH is present around the anterior falx, the possibility of TICA should be considered.
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