A 2-year-old Omani boy presented with a one week history of headache and vomiting. On examination he had a right third cranial nerve palsy but normal fundi. His haemoglobin showed evidence of sickle cell trait. A lumbar puncture was carried out and showed a normal CSF. The patient was then transferred to our hospital for a computed tomography (CT) scan. Scans pre and post-contrast (Figs 1 & 2) revealed a well marginated, lobulated hyperdense mass that enhanced with contrast. It involved the left temporal and parietal lobes, extended into the deep frontal lobe and the thalamic-basal ganglia regions. No cystic change or calcification was seen. There was vasogenic oedema of the white mat ter posterolaterat to the mass and marked compression of the ipsilateral ventricle with midline shift to the contralateral side. No bone destruction was seen. The clinical diagnosis at this stage was a sarcoma or a glioma with unusual ly high attenuation. A craniotomy was performed. I n spite of the enhancement noted on CT, the mass was surprisingly hypovascular, greyish-white in colour with soft consistency and was attached to the dura. It did not extend through the dura and was not related to any muscle. The mass was resected as far as possible. Microscopic examination showed tumour tissue rich in undifferentiated cells with round to oval nuclei, vesicular nuclei, nucleoli and mitotic activity. Some cells had ample eosinophylic cytoplasm, and the turnout was initially thought to be a rhabdomyosarcoma. Fur ther examination with special stains showed focal keratin positivity, diffuse vimentin positivity but no synaptophysin positivity (Fig. 3), and this suggested that it was a malignant rhabdoid tumour. Ultrasound of the abdomen was then carried out to find a primary site. The kidneys were found to be normal. Radiation therapy was given two weeks after surgery, but the boy died two mon ths after presentation. Post-mortem examination was not carried out. examination it has the appearance of a rhabdomyosarcoma, but further light microscopic, immunohistochemical and ultrastructural data provides evidence that malignant rhabdoid tumour should be classed as a separate neoplasm. The histogenesis remains a source of speculation and it is now considered unrelated to Wilms tumour or rhabdomyosarcoma [3]. The tumour found in our patient had a morphology and immunohistochemical profile matching that described in malignant rhabdoid tumour. It was vimentin positive and keratin positive for groups of cells and negative for desmin and myoglobin [3], unlike the rhabdomyosarcoma which should show reactions with antibodies against glial fibrillary acid protein, neurofilament or synaptophysin. A hyperdense lesion on CT as in this case could be a childhood meningioma (sarcoma) especially with its dural base. The CT appearance then is a uniform intrinsic increased density lesion, accompanied by flecks of calcification. The tumour is generally well circumscribed, rounded, ovoid or lobulated and enhances with contrast uniformly. Metastases are usually multiple.