Skull Metastasis from Hepatocellular Carcinoma
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1 Acta Radiologica ISSN: (Print) (Online) Journal homepage: Skull Metastasis from Hepatocellular Carcinoma Ryuji Murakami, Y. Korogi, Y. Sakamoto, M. Takahashi, T. Okuda, T. Yasunaga, R. Nishimura & S. Yoshimatsu To cite this article: Ryuji Murakami, Y. Korogi, Y. Sakamoto, M. Takahashi, T. Okuda, T. Yasunaga, R. Nishimura & S. Yoshimatsu (1995) Skull Metastasis from Hepatocellular Carcinoma, Acta Radiologica, 36:6, To link to this article: Published online: 07 Jan Submit your article to this journal Article views: 72 Full Terms & Conditions of access and use can be found at
2 ACTA RA D I0 LOG I CA ISSN o2n4-1~~1 SKULL METASTASIS FROM HEPATOCELLULAR CARCINOMA CT, MR and angiographic findings R. MURAKAMI', Y. KOROGI', Y. SAKAMOTO', M. TAKAHASHI', T. OKUDA', T. YASUNAGA', R. NISHIMURA3 and s. YOSHIMATSU4 'Department of Radiology, Kumamoto University School of Medicine, 'Department of Radiology, Kumamoto City Hospital, 'Department of Radiology, National Saishunso Hospital; and 4Department of Radiology, Kumamoto Regional Medical Center, Kumamoto, Japan. I Abstract I C.T. MR and angiographic findings of 6 patients with 9 skull metastases from hepatocellular carcinoma (HCC) were reviewed. In 3 of 6 patients, local pain or neurologic deficit was the initial main manifestation of the disease, although all had been treated for chronic liver disease. In the remaining 3 patients, skull metastases were detected following treatment of HCC. The metastatic lesions appeared as expansile osteolytic masses on CT ahd as hypervascular masses on angiography. All lesions were demonstrated on MR imaging. Compared with the brain parenchyma, the lesions were iso- or hypointense on T1-weighted and TZweighted MR images. The lesions were moderately to markedly enhanced by Gd-DTPA. Flow voids were shown in the tumors in 5 lesions. HCC should be included in the differential diagndsis of an osteolytic hypervascular lesion of the skull, especially in Oriental patients. The relatively hypointense tumor on T2-weighted MR images associated with flow void, different from primary skull tumors or directly invasive tumors, may support the diagnosis of HCC metal stasis. Key words: Hepatocellular carcinoma, skull metastasis; osseous metastasis; MR imaging; angiography; CT. Correspondence: Ryuji Murakami, Radiology, Kumamoto University School of Medicine, Honjo. Kumamoto 860, Japan. FAX * Aecepted.for publication 20 December The most frequent primary sites of skull metastases are breast and lung tumors. Hepatocellular carcinoma (HCC) metastasis to the skull is relatively rare. Recently, the clinical importance of skull metastasis from HCC has increased, with improvement of prognosis in patients with HCC. CT and angiographic findings in HCC metastases to the skull have been reported (3, 7, 9), while MR imaging has been documented in only a few cases (4, 8). The purpose of the present study was to evaluate the radiologic and clinical findings of 6 patients with skull metastasis from HCC, with special attention to the MR findings. Material and Methods Nine skull metastases from HCC in 6 patients were retrospectively reviewed (Table). CT and MR im- aging were performed in all patients and in 3 patients, angiography was also performed. In 3 of 6 patients (cases 1, 3 and 4), local pain or neurologic deficit was the first main manifestation of the disease, although all had been treated for chronic liver disease. In the remaining 3 patients, a skull metastasis was detected following treatment for a liver tumor of HCC. The skull lesions were treated with radiation therapy in 4 patients and transcatheter arterial embolization therapy (TAE) in 1 patient. Another patient was treated with preoperative TAE followed by surgical removal of the tumor. MR was performed on either a 1.5 T (Magnetom, Siemens) or a 0.5 T (Gyroscan T5, Philips) unit. The pulse sequences used were the spin-echo technique with TRiTE of 600/15 at 1.5 T and at 0.5 T for T1-weighted images. T2-weighted images were performed with TR/TE of at 597
3 R. MURAKAMI ET AL. Table Putients wirh skull rnrtnstasis from HCC Case/ Age/ Sex Symptoms and signs MR imaging Flow Location CT Angio TI T2 Enh. void Treatment Outcome 1/57/M 2/58/M* 3/59/M Headache, d ysphagia Visual disturbance Headache, double vision L petrous bone Osteolytic Hypervasc Hypo Hypo + - L sphenoid bone Osteolytic** NP Is0 Iso*** + + R temporal calvaria Osteolytic NP Is0 Is0 + - L parietal calvaria Osteolytic NP Is0 Is0 + - R petrous bone Osteolytic NP ISO Hypo + - RT RT None None RT 21 months alive 4 months alive 11 months 4/59/M Painful mass R sphenoid bone Osteolytic** Hypervasc Is0 Hypo*** + + TAE+surg 12 months 5/59/F* Painful mass L mandible Osteolytic** Hypervasc Is0 Iso*** + + TAE 2 months 6173/M* Headache Clivus Osteolytic NP Hypo NP NP RT 4 months L frontal calvaria Osteolytic NP Is0 NP NP + RT L - left, R - right. NP - not performed. Hypo - hypointense to brain parenchyma. Is0 - isointense to brain parenchyma. RT - radiation therapy. TAE - transcatheter embolization therapy. * previously treated for liver tumor of HCC. ** together with large soft tissue density mass. *** together with hyperintense foci. 1.5 T and 2 100/100 at 0.5 T. Contrastenhanced MR images were obtained with routine T1-weighted images after i.v. injection of 0.1 mmol/kg b.w. Gd-DTPA (Magnevist, Schering). In 3 patients (cases 1, 2 and 5), dynamic MR images were also obtained using the spin-echo technique with TR/TE of 200/15 at 1.5 T (16). Results The clinical and radiologic findings of the 6 patients are summarized in the Table. Four patients had solitary skull lesions; the remaining 2 patients (cases 2 and 6) had multiple skull lesions. Lesions of the skull base were seen in 5 patients. On CT, all lesions were osteolytic, expansile and well-enhanced masses extending from the skull. Three lesions in 3 patients (cases 2, 4 and 5) were accompanied by large soft tissue masses. Angiograms showed hypervascular tumors fed by branches of the external carotid artery. All lesions were clearly demonstrated by MR imaging. Compared with brain parenchyma, the lesions were isoor hypointense on T1-weighted MR images and relatively hypointense on T2-weighted images (Figs 1, 2). In 3 lesions with large soft tissue masses, there were scattered hyperintense foci within the tumors on T2-weighted images (Figs 1, 2). Flow voids in tumors, indicating tumor vessels, were observed in 5 lesions (Figs 1-3). Gd-DTPA-enhanced images were moderately to markedly enhanced in the corresponding areas. Three lesions evaluated by dynamic MR imaging showed rapid contrast enhancement after administration of Gd-DTPA (Fig. 1 e). The patients were treated with various techniques, including radiation therapy, TAE and surgical removal of the tumors. These treatments were effective for the relief of symptoms, but 4 patients died from liver failure 2, 4, 11 and 12 months after diagnosis. Discussion HCC is a common disease in the Orient. Invasion of the hepatic, portal, and vertebral venous plexuses may account for the distribution of hematogeneous metastases (13). The most common sites of hepatic metastases are the lung and regional lymph nodes, but rarely the osseous system. The incidence of metastasis to the osseous system from HCC ranges from 2 to 16% (6, 13, 18). The most frequent sites of osseous metastases are the vertebrae and the ribs. Skull metastases from HCC are relatively rare and have been reported to range from 0.5 to 1.6% (3, 6). Most cases with skull metastases from HCC are men in their 6th and 7th decades (3, 4, 7, 8). The common symptoms include a painful mass, headache and neurologic deficits. In some cases, these symptoms have appeared as the first overt clinical manifestations of HCC, as in 3 of our 6 patients (cases 1, 3 and 4). Reports of MR findings of skull metastases from HCC are limited (4, 8). In our series, the metastatic lesions were relatively hypointense to the brain parenchyma on T2-weighted MR images. CARRIER 598
4 SKULL METASTASIS FROM HCC Fig. 1. Case 2. a, b) Axial TI-weighted MR images (1.5 T) show isointense masses in the right temporal calvarium (+) in (a) and the left sphenoid bone accompanied by flow void (+) in (b). Symmetrically increased intensity in the basal ganglia is seen (b) in (a), representing acquired hepatocerebra1 degeneration. (c) Axial T2-weighted image shows an isointense mass. Hyperintense foci within the tumor are also demonstrated (b). (d) Gd- DTPA-enhanced MR image shows marked enhancement. (e) Dynamic MR images show marked rapid enhancement (+). 599
5 R. MURAKAMI ET AL. Fig. 2. Case 4. a) Contrast-enhanced CT shows an osteolytic lesion accompanied by a well-enhanced mass of soft tissue density extending from the right sphenoid bone (+). b) Right external carotid arteriography shows marked tumor vessels and tumor stain in the corresponding region. c) Axial T2-weighted MR image (0.5 T) shows a mass hypointense to the brain parenchyma. The lesion has hyperintense foci (b) and flow voids (+). d) Coronal contrast-enhanced MR image shows enhancement with Gd-DTPA. Flow void within the tumor is also demonstrated (+). 600
6 SKULL METASTASIS FROM HCC Fig. 3.'Case 6. Axial T1-weighted MR image (1.5.T) shows a hypointense mass with flow voids (+) in the clivus. et al. (2) reported the presence of a hypointense intraaxial mass on T2-weighted MR images to strongly suggest the possibility of metastatic a- denocarcinoma. They believed that these findings most likely reflected the relaxation parameters of the tissue from which the metastasis arose. Their suggestions might also apply to skull metastases. Relatively large lesions were accompanied by scattered hyperintense foci on T2-weighted MR images, which probably represented histologic changes such as hemorrhage and/or degeneration. In primary HCC, however, KADOYA et a]. (5) have demonstrated correlations between dilatation of intratumoral sinusoids and localized hyperintense foci on T2-weighted MR images, especially in tumors exceeding 2.0 cm in diameter. The same histologic changes would occur in metastatic lesions and would influence the MR findings. The skull metastases were enhanced by Gd-DTPA, and dynamic MR studies showed rapid strong enhancement. These hypervascular findings are similar to those of primary HCC (12). MR imaging is superior to CT for showing tumor extension and the relation to adjacent structures, although osseous destruction is more easily detected by CT (15). It is possible to differentiate HCC metastases from primary skull tumors, such as chordoma and chondrosarcoma, and from direct extensions of sinonasal tumors, based on the presence of a relatively hypointense mass on T2- weighted MR images (14, 17) and the presence of flow voids within the tumors (Figs 1-3). Some hypervascular metastases such as renal cell carcinomas and thyroid carcinomas may show similar appearances. The presence of symmetrically increased intensity in the basal ganglia on T1- weighted images, which is sometimes observed in patients with chronic liver disease - so-called acquired hepatocerebral degeneration ( 1) - would support the diagnosis of skull metastases from HCC (Fig. 1 a). Their angiographic differentiation from meningiomas may also be difficult, but osseous destruction and tumor extension are helpful for making the diagnosis. A single calvarial metastasis can be treated surgically (7). Radiation therapy and TAE are effective means of palliation for symptomatic osseous metastases (1 1, 18). However, nearly all patients with skull metastases from HCC have died of liver failure within 1 year after diagnosis (3, 7). With the development of effective local treatment for the primary liver-tumors of HCC, the prognosis of HCC has improved markedly (lo), and skull metastasis from HCC has been seen more frequently. HCC should be included in the differential diagnosis of skull lesions, especially in Oriental patients. Osteolytic extensions on CT and relatively hypointense signals on T2-weighted MR images associated with flow voids in the tumors are findings helpful for making the diagnosis. REFERENCES 1. BRUNBERG J. A., KANAL E., HIRSCH W. & VAN THIEL D. H.: Chronic acquired hepatic failure. MR imaging of the brain at 1.5 T. AJNR 12 (1991), CARRIER D. A., MAWAD M. E., KIRKPATRICK J. B. & SCHMID M. E: Metastatic adenocarcinoma to the brain. MR with pathologic correlation. AJNR 15 (1994) CHANG J. W. & HOWNG S. L.: Skull metastasis of primary hepatoma. Case report. Kaohsiung J. Med. Sci. 7 (1991), ITO H., KAMIRYO T., KAJIWARA K., YOKOYAMA T., NA- GAMITU T. & KASHIWAGI S.: Skull metastases of malignant tumor (In Japanese). Tumor & Infection 3 (1990), KADOYA M., MATSUI O., TAKASHIMA T. & NONOMURA A.: Hepatocellular carcinoma. Correlation of MR imaging and histopathologic findings. Radiology 183 (1992), KUHLMAN J. E., FISHMAN E. K., LEICHNER I? K., MAGID D., ORDER S. E. & SIECELMAN S. S.: Skeletal metastases from hepatoma. Frequency, distribution, and radiographic features. Radiology 160 (1986) KURATSU J., MURAKAMI M., UEMURA S. & USHIO Y.: Brain and skull metastases of hepatic or pancreatic cancer. Report of six cases. Neurol. Med. Chir. 30 (1990),
7 R. MURAKAMI ET AL. 8. KUROKAWA Y., UEDE T., OHTA K., HONMOU 0. & YOSH- IDA Y.: Magnetic resonance imaging of skull metastasis of hepatoma (In Japanese). Progress in CT 12 (1990), MIURA T., HIRABUKI N. & KOZUKA T.: Case report. Cranial metastasis from hepatocellular carcinoma. Clin. Radiol. 42 (1990), MURAKAMI R., YOSHIMATSU S., YAMASHITA Y., SAGARA K., ARAKAWA. & TAKAHASHI M.: Transcatheter hepatic subsegmental arterial chemoembolization therapy using iodized oil for small hepatocellular carcinomas. Correlation between Lipiodol accumulation pattern and local recurrence. Acta Radiol. 35 (1994), NAGATA Y., NAKANO Y., ABE M., TAKAHASHI M. & KOHNO S.: Osseous metastases from hepatocellular carcinoma. Embolization for pain control. Cardiovasc. Intervent. Radiol. 12 (1989), OHTOMO K., ITAI Y., YOSHIKAWA K. et al.: Hepatic tumors. Dynamic MR imaging. Radiology 163 (1987), OKAZAKI N., YOSHINO M., YOSHIDA T., HIROHASHI S., KISHI K. & SHIMOSATO Y.: Bone metastasis in hepatocellular carcinoma. Cancer 55 (1985), OOT R. E, MELVILLE G. E., NEW I? E J. et al.: The role of MR and CT in evaluating clival chordomas and chondrosarcomas. AJNR 9 (1988), PALING M. R., BLACK W. C., LEVINE I? A. & CANTRELL R. W.: Tumor invasion of the anterior skull base. A comparison of MR and CT studies. J. Comput. Assist. Tomogr. 11 (1987), SAKAMOTO Y., TAKAHASHI M., KOROGI Y. BUSSAKA H. & USHIO Y.: Normal and abnormal pituitary glands. Gadopentetate dimeglumine-enhanced MR imaging. Radiology 178 (1991), SOM F! M., SHAPIRO M. D., BILLER H. E, SASAKI C. & LAWSON W.: Sinonasal tumors and inflammatory tissues. Differentiation with MR imaging. Radiology 167 (1988), TAKI Y., YAMAOKA Y., TAKAYASU T. et al.: Bone metastases of hepatocellular carcinoma after liver resection. J. Surg. Oncol. 50 (1992),
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