ELSEVIER
EXTRADURAL EXTENSION OF GLIOBLASTOMA MULTIFORME INTO THE ORAL CAVITY: CASE
REPORT
Tetsuyoshi Horiuchi, M.D., Michihiko Osawa, M.D., Nobuo Itoh, M.D.,* Shigeaki Kobayashi, M.D., Junpei Nitta, M.D., and Kazuhiro Hongo, M.D. *Department of Neurosurgery and Pathology, Shinshu University School of Medicine, Matsumoto, Japan
Horiuchi T, Osawa Fxtradural extension cavity: case report.
M, ltoh N, Kobayashi S, Nitta .I, Hongo K. of glioblastoma multiforme into the oral Surg Neuroi 1996;46:42-6.
A rare case of glioblastoma multiforme with oral extension is presented in a 41-year-old female. She underwent two surgical treatments and both radiotherapy and chemotherapy for the right temporoparietal glioblastoma multiforme. A follow-up computed tomographic scan and magnetic resonance imaging demonstrated destruction of the temporal base and extradural extension of the tumor into the orbital, nasal, and oral cavities. This is the first report of the oral extension of glioblastoma multiforme. The mechanism for the extradural extension is discussed. KEY WORDS
Extradural extension, glioblastomamultifonne, oral cavity.
C
erebral gliomas rarely penetrate
the dura mater [ 1,3,12]. Some glioblastomas with extradural extension into the orbital or nasal cavity following surgical treatment and/or radiotherapy have been reported [2,4,6,8,9,11]. Glioblastoma multiforme invading the oral cavity has not previously been recorded in the literature.
CASEREPORT A 41-year-old female complained of mild occipital pain. She had no neurologic deficits. A computed tomographic (CT) scan showed a heterogeneously enhancing mass in the right temporal lobe. Magnetic resonance imaging (MRl) revealed another enhancing region around the trigone of the right lateral ventricle (Figure 1). These two lesions Address reprint requests to: Tetsuyoshi Horiuchi, M.D., Department of Neurosurgery, Shinshu University School of Medicine, 3-l-l Asahi, Matsumoto 390, Japan. Received February 27, 1995; accepted December 19, 1995. 00993019/96/515.00 PII S009@3019(96)00037-7
appeared to be the same tumor extending through the subependymal space of the lateral ventricular wall. At the first operation, which was performed on August 10, 1990, partial removal of the tumor was achieved. The tumor was not adherent to the dura mater of the middle cranial fossa. The gyri over the tumor were thick and discolored. The cut surface of the poorly circumscribed 4 X 4 cm tumor was fleshy gray with hemorrhagic and necrotic foci. Histologically, the neoplastic cells varied in size and shape. Necrosis with pseudopalisading and abnormal vascular proliferation were frequent. Immunoreactivity for glial fibril acidic protein (GFAP) was positive in some pleomorphic cells, as well as in many spindle cells that were arranged in a fascicular pattern. The cwl-antitrypsin (al-AT), cx smooth muscle actin (a SMA), and S-100 protein were negative. These features confirmed the diagnosis of glioblastoma multiforme. The postoperative course was uneventful. The patient received 55 Gy of whole brain radiotherapy and intraarterial chemotherapy with ACNU (total dose of 225 mg). Three months after the surgery, the patient noticed a left homonymous hemianopsia. MFU demonstrated an enlargement of the residual tumor around the right trigone. The tumor in the temporal lobe was of the same size and the temporal base was intact (Figure 2). The second operation was performed on December 13, 1990. The tumor was subtotally removed. The histologic features resembled the previous one. Six months after the second operation, MFU showed a recurrent tumor invading the right middle cranial fossa (Figure 3). Since the end of 1991, the patient had suffered frequent nasal bleeding and diplopia. Exophthalmos, chemosis, and swelling of 655 Avenue
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Surg Neurol 1996;46:42-6
Oral Extension of Gliohlastoma
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Coronal (left) and sagittal (right) T,-weighted enhanced MRI showing the mass located in the right temporal lobe and another mass around the trigone of the lateral ventricle.
the face on the right side progressively developed and a hard mass occupying her oral cavity was noticed (Figure 4). MRl and a CT scan revealed orbital, nasal, and oral masses extending inferiorly from the recurrent tumor in the right temporal lobe through the anterior and middle cranial fossa base (Figure 5). A total body CT scan showed no systemic metastases. The tumor in the oral cavity and the swelling of the patient’s face increased rapidly. Finally, she
deteriorated neurologically in parallel with the growth of the intracranial tumor and died on February 19, 1992. A necropsy examination of the tumor in the oral cavity showed same histologic features as those at the previous two operations (Figure 6, left>. There was no evidence of a sarcomatous component, since the tumor that stained positive for CFAP (Figure 6, right) was negative with the al-AT, cx SMA and S-100 protein reactions. Autopsy was not performed.
(lefi) and sagittal qmentCoronal MRI with enhancebefore the second opera(right)
tion demonstrating an enlarge ment of the residual tumor around the trigone of the right lateral ventricle. Coronal image, however, showed that the middle cranial fossa was not destroyed.
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Horiuchi et al
MRI revealing qtumor Follow-up that a recurrent enhancing invades the right middle cranial fossa.
DISCUSSION Occasionally neuroectodermal tumors have been reported to involve the inner layer of the dura mater. Intracranial gliomas with extradural extension are rare [ 1,3,12]. The dura mater is the most important barrier to extracranial extension [ 1, lo]. Only surgical intervention and radiationinduced damage of the dura mater can possibly cause the extradural extension of glioma [4,6,8-
1 Frontal view of the mouth LI showing the mass occupying oral cavity.
111. Spontaneous extradural extension is rarely reported [ 1,3,5,7,12]. Kawano et al. [3] proposed three routes of the extradural extension of gliomas: (1) along the perivas cular or dural slit, (2) through the cranial or spinal nerves, and (3) direct destruction. The orbital and nasal extension of glioma through both anterior and middle cranial bases had been reported previously [1,2,6,8,9,11]. Pompili et al. [9] speculated that cere bra1 gliomas would perforate the base of the skull and
Oral Extension of Glioblastoma
Surg Neurol 1996;46:42-6
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Bone window computed tomographic scans of coronal section (Top) revealing the destruction of anterior and middle cranial fossa. MRf of coronal section with enhance ment (bottom) showing the tumor extending to the orbital, nasal, and oral cavities.
destroy the bone when the tumor had direct contact with the basal dura under increased intracranial pressure. Frequent modes of extradural invasion through the anterior cranial fossa are by direct destruction or through the olfactory nerve [1,2&Q, 111. The extradural passage of temporal gliomas through the middle cranial fossa is considered to be probably through the perivascular slit as many meningeal vessels exist at the temporal base [5]. On histologic analysis, the ability of gliomas with a sarcomatous component to invade the extradural
space was much greater than that of other tumors [ 2,131. Murphy et al. [6] presented a case of gliosarcoma extending to the orbital and nasal cavities with bony destruction. In the case described, the tumor was located in the temporal base and might have intruded into the perivascular slit secondary to chronic increased intracranial pressure. Furthermore, intraarterially infused ACNU might have damaged both the dura mater and the meningeal artery. Irradiation might have had an additional
affect. The tumor
into the oral cavity with muscular
extended
invasion
of the
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Horiuchi et al
Photomicrograph of the necropsy specimen. Lek The tumor cells below the squamous epithelia vary greatly in qpalisading. * size and configuration and show necrosis surrounded by a distinctive collar of the cells referred to as pseudoMitotic figures are often seen. (hematoxylin and eosin stain, original magnification X33). Right Neoplastic cells with GFAP-positive cytoplasm were noted. (GFAP stain, original magnification X132). pterygoid fossa and destruction of maxilla. There has been no description of oral extension of gliomas before.
7. 8.
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