Skip Navigation LinksHome > March 2008 - Volume 28 - Issue 1 > Homonymous Hemianopia Caused by Solitary Skull Metastasis of...
Journal of Neuro-Ophthalmology:
doi: 10.1097/WNO.0b013e3181675438
Photo Essay

Homonymous Hemianopia Caused by Solitary Skull Metastasis of Hepatocellular Carcinoma

Hsu, Sheng-Yao MD; Chang, Fang-Ling MD; Sheu, Min-Muh MD; Tsai, Rong-Kung MD

Free Access
Article Outline
Collapse Box

Author Information

Department of Ophthalmology (S-YH, F-LC, M-MS, R-KT), Buddhist Tzu Chi General Hospital, Hualien, Taiwan; Institute of Medical Sciences and Medicine (S-YH), College of Medicine, Tzu Chi University, Hualien, Taiwan; and Institute of Medicine (M-MS, R-KT), College of Medicine, Tzu Chi University, Hualien, Taiwan.

S.-Y.H. and F.-L.C. contributed equally to this work.

Address correspondence to Rong-Kung Tsai, MD, Department of Ophthalmology, Buddhist Tzu Chi General Hospital, 707, Section 3, Chungyang Road, Hualien, Taiwan; E-mail: wps59@yahoo.com.tw

Collapse Box

Abstract

We report a patient who developed a complete left homonymous hemianopia from mass effect of a solitary skull metastasis of hepatocellular carcinoma (HCC). After chemoembolization and resection, the visual field defect improved markedly. This is the first reported case demonstrating this phenomenon in HCC. It supports aggressive treatment of a solitary skull metastasis in this setting.

A 53-year-old man complained of blurred vision in his right visual field for the past 2 months. He had noted a protruding bump over his left parieto-occipital area for 4 months.

The patient had a long history of type 2 diabetes mellitus, alcoholism with cirrhosis, and hepatitis B virus infection. Tea-colored urine with occasional tarry stools had been noted for more than 1 year. Seven months earlier, hepatocellular carcinoma (HCC) had been diagnosed, and he had received transarterial chemoembolization. Abdominal sonography had disclosed the tumor and cirrhosis, splenomegaly, and gallstones.

Best-corrected visual acuities were 20/20, and results of all other aspects of our examination were normal except for Humphrey automatic perimetry, which showed complete right homonymous hemianopia (Fig. 1).

Fig. 1
Fig. 1
Image Tools

Brain MRI showed a mass in the left parieto-occipital calvarium with osteolytic change and compression of the left posterior ventricular horn and left cerebral sulci with midline shift to the right. The cerebral parenchyma showed normal signal intensity without brain metastasis (Fig. 1). Chest and abdominal CT, including visualization of vertebrae, showed no abnormalities. We concluded that the patient had developed a solitary metastasis of HCC to the skull.

Cerebral angiography showed a large hypervascular tumor stain and venous aneurysms in the left parieto-occipital bone supplied by the left occipital and posterior branches of the left superficial temporal artery, findings compatible with a solitary skull metastasis (Fig. 1).

Selective transarterial embolization of the feeding arteries was performed via coaxial microcatheter systems with 300-500 μm microspheres and four metallic microcoils. After the chemoembolization, angiography revealed 80% reduction in vascularity. On the following day, left parietooccipital craniectomy revealed a large epidural and subgaleal mass with skull bone erosion and intact dura. The pathologic study showed HCC (Fig. 2).

Fig. 2
Fig. 2
Image Tools

One month postoperatively, head CT showed less compression of the left posterior ventricular horn and less effacement of the left cerebral sulci with residual cranial osteolytic change and epidural effusion (Fig. 3). The dura remained intact and free of metastasis. Repeat perimetry showed visual field improvement (Fig. 3). Results of the ophthalmologic examination remained normal.

Fig. 3
Fig. 3
Image Tools

The patient later received 28 fractions of 180 cGy for a total of 5,040 cGy of whole brain x-irradiation. During a follow-up of 9 months, he remained free of known recurrence of HCC or any complications of treatment.

The highest annual incidence rates of HCC, approaching 150 per 100,000, are found in Taiwan, Korea, Mozambique, and Southeast China and are strongly linked to the prevalence of hepatitis B infection (1). In Taiwan, HCC is the leading cause of death by malignant neoplasm in men. In China, the lifetime risk of developing HCC in patients with chronic hepatitis B approaches 40% (2).

We believe that our description of a solitary skull metastasis of HCC in a Taiwanese man represents the first report of this phenomenon. Although HCC is a relatively more common malignant tumor in Taiwan than in non-Asian areas, HCC skull metastasis is still a relatively rare condition, even in Taiwan.

The incidence of HCC is increasing, not only in Asia but also in the United States, perhaps because of an increase in the rate of detection of viral hepatitis (3). HCC is four times more common in men than in women and usually arises in a cirrhotic liver (4). It commonly metastasizes to the lung, regional lymph nodes, peritoneum, adrenal glands, and bone (5-7), the most common bony site being the vertebra (8,9). Skull metastasis occurs presumably via Batson's venous plexus (10,11).

Because the visual field defect improved markedly after surgical intervention, we postulate that it was caused entirely by mass effect from the skull metastasis. Whether removal of this solitary metastasis also prolongs survival is uncertain.

Back to Top | Article Outline

Acknowledgment

The authors thank Professor Jung-Chung Lin and Barry Lee Reynolds for assistance with the manuscript.

Back to Top | Article Outline

REFERENCES

1. Cotran RS, Kumar V, Tucker C. Robbins Pathologic Basis of Disease. 6th ed. Philadelphia: WB Saunders; 1999:888-91.

2. Isselbacher KJ, Dienstag JL. Tumors of the liver and biliary tract. In: Fauci AS, Braunwald E, Isselbacher KJ, eds. Harrison's Principles of Internal Medicine. 14th ed. New York: McGraw Hill; 1998;578-80.

3. Lotze MT, Fleckinger JC, Carr BI. Hepato-biliary neoplasms. In: DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology. 4th ed. Philadelphia: Lippincott; 1993:883-914.

4. Chang L, Chen YL, Kao MC. Intracranial metastasis of hepatocellular carcinoma: review of 45 cases. Surg Neurol 2004;62:172-7.

5. Inagaki Y, Unoura M, Urabe T, et al. Distant metastasis of hepatocellular carcinoma after successful treatment of the primary lesion. Hepatogastroenterology 1993;40:316-9.

6. Okazaki N, Yoshino M, Yoshida T, et al. Bone metastasis in hepatocellular carcinoma. Cancer 1985;55:1991-4.

7. Kay RM, Eckardt JJ, Goldstein LI, et al. Metastatic hepatocellular carcinoma to bone in a liver transplant patient: a case report. Clin Orthop Relat Res 1994;303:237-41.

8. Nam SW, Han JY, Kim JI, et al. Spontaneous regression of a large hepatocellular carcinoma with skull metastasis. J Gastroenterol Hepatol 2005;20:488-92.

9. Yanase Y, Sano K, Hama H. Case report of a primary hepatoma with metastasis to the femur and statistical review. J Kansai Denryoku Hosp 1972;4:94-9.

10. Chan CH, Trost N, McKelvie P, et al. Unusual case of skull metastasis from hepatocellular carcinoma. Aust NZ J Surg 2004;74:710-3.

11. Hayashi K, Matsuo T, Kurihara M, et al. Skull metastasis of hepatocellular carcinoma associated with acute epidural hematoma: a case report. Surg Neurol 2000;53:379-82.

© 2008 Lippincott Williams & Wilkins, Inc.

Login