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Falx meningioma presenting as acute subdural hematoma: case report
Falx Meningioma Presenting As Acute Subdural Hematoma: Case Report Shuzo Okuno, M.D., Hajime Touho, M.D., Hideyuki Ohnishi, M.D., and Jun Karasawa, M.D. Department of Neurosurgery, Osaka Neurological Institute, Osaka, Japan
Okuno S, Touho H, Ohnishi H, Karasawa J. Falx meningioma presenting as acute subdural hematoma: case report. Surg Neurol 1999;52:180 – 4. BACKGROUND
Acute subdural hematomas caused by meningiomas have been rarely encountered. Pathophysiologic mechanisms and clinical considerations in these patients have not been sufficiently explored. We addressed the possible mechanism of spontaneous hemorrhage in our case and briefly discuss the optimal treatment. CASE DESCRIPTION
This case of falx meningioma presenting as an acute subdural hematoma in a 78-year-old woman is described. On initial computed tomography (CT), an enhancing tumor of the falx appeared to be the cause of hemorrhage. Only faint contrast staining in the periphery of the tumor was seen on right external carotid arteriograms, with no evidence of other vascular supply. Extravasation of contrast material during the procedure occurred suddenly and was successfully treated by endovascular embolization using a microcatheter. The hematoma was emergently evacuated with gross total removal of the tumor. Pathologic examination confirmed a transitional meningioma with abundant hyalinized structures. Disruption of a thinwalled vessel adjacent to the tumor capsule was assumed to be the site of hemorrhage.
pontaneous intracranial hemorrhages associated with brain tumors are well known events. In recent reviews, the incidence of spontaneous hemorrhage has been reported to range from 5%– 10% [12,16]. Malignant glioma, brain metastasis, and pituitary adenomas are recognized as the most frequent underlying pathologies. In contrast, hemorrhage due to meningiomas is thought to be a rare initial presentation [2,7]. In this report, we describe a case of meningioma presenting as acute subdural hematoma and propose a possible mechanism of spontaneous hemorrhage, based upon the pathologic examination. Early surgical intervention is thought to be the most effective treatment, although the prognosis is generally poor due to the devastating effect of the initial hemorrhage [2,6,7]. Careful immediate evaluation of the clinical features, neuroradiologic images, and underlying disease is mandatory in order to diagnose this rare event and to facilitate prompt treatment.
S
CONCLUSIONS
The longstanding ischemia of the tumor was considered to have produced the deposition of hyalin in the tissue, which changed the hemodynamics within the tumor, producing vascular stress leading to rupture. The prognosis of patients with meningiomas complicated by acute subdural hematoma is generally poor, with mortality reported in approximately one-half of such patients. Surgical exploration is the most effective treatment and should be conducted before irreversible brain damage has occurred. © 1999 by Elsevier Science Inc. KEY WORDS
Meningioma, acute subdural hemorrhage, extravasation, embolization.
Address reprint requests to: Shuzo Okuno, M.D., Department of Neurosurgery, Nara Medical University, 840, Shijo-cho, Kashihara, Nara, 634, Japan. Received June 12, 1996; accepted September 5, 1996. 0090-3019/99/$–see front matter PII S0090-3019(97)00028-1
Case Report This 78-year-old woman with no past history of trauma or bleeding abnormalities was admitted to our institute due to the sudden onset of vomiting and a loss of consciousness. On examination, she did not open her eyes to verbal or painful stimuli and exhibited only withdrawal responses in the left extremities. Her pupils were equal with a nearly intact reaction to light. Hemiparesis was observed in her right extremities with an ipsilateral Babinski sign. Laboratory data obtained on admission were essentially within normal limits and there was no evidence of an underlying predisposition to hemorrhage. Plain cranial roentgenograms yielded normal findings with no fracture lines or calcified lesions. © 1999 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
ASDH from Meningioma
Surg Neurol 181 1999;52:180 –4
(Left) Plain CT scans on admission revealing a massive left subdural hematoma extending from the anterior interhemispheric fissure; (center) a tumor attached to the falx on the left side, of relatively high density compared to the brain parenchyma. The lesion contains a small amount of high-density granular material suggestive of calcification; (right) a contrast CT scan demonstrating faint peripheral enhancement of the tumor.
1
Computed tomography (CT) revealed a massive subdural hematoma, extending from the interhemispheric fissure to the left cerebral convexity (Figure 1 left), and an adjacent solid tumor attached to the left side of the falx (Figure 1 center). The tumor had a slightly higher density compared to the brain parenchyma and contained a granular high density area, possibly representing calcified material. Following the administration of contrast medium, homogeneous enhancement was seen in the periphery of the tumor (Figure 1 right). Digital subtraction angiography (DSA) demonstrated fanning of the anterior cerebral arteries with a shift to the right. The mass was fed exclusively by the right external carotid artery, mainly through falcial twigs of the middle meningeal artery (Figure 2, left). Following
lateral projections, an anteroposterior view was being taken, when extravasation of contrast material directed towards the anterior interhemispheric fissure suddenly occurred (Figure 2, right). Immediately, a Tracker-10 catheter (Target Therapeutics, San Jose, CA) was superselectively cannulated into the right middle meningeal artery, and the artery was completely embolized using 180 –300 mm polyvinyl alcohol particles (Ivalon). At this time, the patient’s neurologic condition remained unchanged, although CT demonstrated marked enhancement of an area caused by the contrast medium leak (Figure 3). She was promptly transferred to the operating room and underwent a left frontotemporal craniotomy across the midline. The dura was moderately tense but appeared to be intact.
(Left) A lateral view of the right external carotid artery angiogram showing faint staining in the periphery of the tumor (arrowheads) fed by the middle meningeal artery; (Right) anteroposterior view of the right external carotid artery demonstrating extravasation directed towards the anterior interhemispheric fissure (arrows). Superselective embolization using a microcatheter successfully obliterated the feeding artery, preventing further enlargement of the hematoma (not shown).
2
182 Surg Neurol 1999;52:180 –4
Okuno et al
(Left and right) CT scan obtained after angiography demonstrating leakage of the contrast medium superficially within the tumor and into the anterior interhemispheric fissure, showing markedly high density attenuation.
3
Upon opening the dura matter, a massive jelly-like subdural hematoma was encountered, which had no membranous tissue. After aspiration of the hematoma, no suggestion of head trauma (e.g., fractures, brain contusions) was found. Rather, an elastic firm tumor attached to the left side of the falx was seen adjacent to the interhemispheric fissure. Its capsule was torn in the superior portion near its dural attachment, from which the interhemispheric hematoma extended anteriorly. The bridging veins and cortical arteries had no direct contact with the tumor. Gross total removal of the tumor was performed, followed by electric coagulation of its dural attachment. The patient’s level of consciousness gradually improved enough to allow her to follow some verbal commands, but she remained abulic
with a mild right hemiparesis 2 months after the surgery. Pathologic analysis of the resected tumor demonstrated a transitional meningioma with abundant hyalinization. Hyalinized structure was preferentially found in the tissue and the vascular walls (Figure 4 left). Hemorrhage from a thin-walled vessel was seen in a part of the specimen close to the capsule (Figure 4 right). Hemosiderin deposition, necrosis, or findings suggestive of malignancy were not seen.
Discussion In most cases of meningioma, the early symptoms are seizures and neurologic signs associated with
(Left) A photomicrograph of the resected tumor revealing a transitional-type meningioma (hematoxylin and eosin, ⫻ 100) with abundant hyalinization within the tissue and vascular walls. (Right) Disruption of a thin-walled vessel (asterisk) with extravasation of red blood cells is disclosed at the superficial portion of the tumor (Elastica-van Gieson, ⫻ 240).
4
ASDH from Meningioma
increased intracranial pressure. Focal neurologic deficits, dependent on the tumor location, may accompany these symptoms with tumor growth. In contrast, a hemorrhagic presentation of a meningioma is an unusual event [4,7]. Cushing and Eisenhardt [3] reported that none of their 313 patients with meningiomas manifested hemorrhages. Furthermore, a series of 280 parasagittal meningiomas reported by Hoessly and Olivecrona did not include any cases involving hemorrhage from a tumor [5]. In 1991, Martinez-Lage et al. [7] reviewed 57 cases from the literature; they also reported their surgical experience in a series of 125 patients with meningiomas, revealing hemorrhage in only three cases (2.4%). This incidence is slightly higher than that reported by Wakai et al. in 1982 [16], who encountered four hemorrhagic cases in 310 meningiomas (1.3%). The commonly reported site of hemorrhage from meningiomas is the subarachnoid space including the intraventricular cavity. Intracerebral and intratumoral hemorrhages are the next most frequent types. Subdural hemorrhage from meningiomas is relatively rare, and 20 such cases were reviewed by Chaskis et al. [2] in 1992. Most of these hemorrhages were accompanied by other types of hemorrhage and rarely occurred alone. In addition, a considerable number of such cases have been presumed to be chronic subdural hematomas presenting with a more insidious onset, and having organized hematomas enclosed by a definite membrane [1,4,8,14,17]. Strictly speaking, only 11 cases of acute subdural hematoma associated with meningiomas have been reported previously in the English literature [2,6 –10,13,15,18]. They have had no predisposing factors such as preceding head trauma or anticoagulant therapy, and commonly developed the apoplectiform presentation directly associated with the hemorrhage. Only the histological subtype of the meningioma has been documented as playing an important role in the occurrence of hemorrhage [2,7,15]. Angioblastic and malignant meningiomas tend to bleed more frequently, although syncytial or meningotheliomatous subtypes account for the majority of cases. In angioblastic meningiomas, it has been assumed that the thin-walled vessels are too fragile, causing easy bleeding. This assumption also may be true of other subtypes of meningioma that demonstrate hypervascularity confined to portions of the specimen. In malignant meningiomas, like other anaplastic tumors, direct invasion or endothelial proliferation by the tumor may obstruct the vascular channel, producing congestion and necrosis within the tumor, resulting in hemorrhage. In these instances, the site of hemorrhage should exist
Surg Neurol 183 1999;52:180 –4
within the tumor, but may extend to the surroundings (i.e., the subarachnoid, intracerebral, and subdural spaces). The mechanical stretching and distortion of bridging veins by meningiomas may also be associated with hemorrhage. In the present case, vessels adjacent to the tumor were not involved, and histologic examination merely demonstrated a transitional pattern with no component of the angioblastic subtype, and a disruption of thin-walled vessels close to the tumor capsule. These findings are similar to those reported in the previous cases, but the great number of hyalinized structures seen in our case appears to be a relatively unusual finding in meningiomas. The definitive cause of the hemorrhage remains unclear, but vascular features may have contributed to the hemorrhage in our case. The tumor was fed by the contralateral extracarotid artery alone with only faint contrast staining, predominantly in the superficial portion. Although this may not be an exceptional finding in meningiomas, the regression of feeding arteries may be strongly associated with tumor degeneration resulting from the longstanding ischemia. Sato et al. [11] have reported a case of intraventricular ependymoma with prominent stromal degeneration in which the circulatory disturbance in the tumor seemed to cause the deposition of hyalin in the vessel and related histologic changes. Therefore, rich hyalinized structures may reflect insufficient nourishment by the associated feeding artery. Furthermore, disproportionate amounts of degenerated tissue caused by such ischemia might change the hemodynamics within the tumor, producing vascular stress in a thin-walled vessel, though this claim may be simply a speculation, and a rather rare mechanism in the occurrence of spontaneous hemorrhage from meningiomas. The prognosis of patients with meningioma with acute hemorrhage is generally poor, and approximately one-half of such patients die regardless of hemorrhage type. Factors responsible for the morbidity and mortality have not been precisely identified. However, the most frequently reported factor affecting prognosis is the clinical state of the patient at onset. The beneficial effect of surgical intervention was restricted to a small number of patients because even minor hemorrhages were associated with rapid increases in intracranial pressure to critical levels, particularly in patients with larger tumor volumes. Furthermore, direct critical injury to the surrounding brain may occur for which current treatment is ineffective. The propriety of prophylactic tumor removal in the presentation of future hemorrhage remains controversial as it is difficult to predict the possibility of hemorrhage, even using
184 Surg Neurol 1999;52:180 –4
modern neuroradiologic modalities [9,15]. Once a subdural hemorrhage has occurred in a patient with meningioma, one must promptly distinguish whether this situation resulted from the associated tumor or other causes such as head trauma, drugs, or a systemic bleeding tendency. Surgical exploration, whenever necessary, should be conducted before irreversible brain damage has occurred. Additionally, one may perform embolization of the arterial supply to the tumor to prevent extravasation during angiography, which may avoid enlargement of the hemorrhage and facilitate the surgical procedure. REFERENCES 1. Baskinis N, Grotenhuis A, Wandt H. Chronic subdural hematoma associated with an intracapsular meningioma. Case report and short review of the literature. J Neurosurg Sci 1984;28:17–23. 2. Chaskis C, Raftopoulos C, Noterman J, FlamentDurand J, Brotchi J. Meningioma associated with subdural haematoma: report of two cases and review of the literature. Clin Neurol Neurosurg 1992;94:269 –74. 3. Cushing H, Eisenhardt L. Meningiomas, their classification, regional behavior, life history, and surgical end result. Springfield, Ill: Charles C. Thomas 1938. 4. Cusick JF, Bailey OT. Association of ossified subdural hematomas and a meningioma. Case report. J Neurosurg 1972;37:731– 4. 5. Hoessly GF, Olivecrona H. Report on 280 cases of verified parasagittal meningiomas. J Neurosurg 1955; 12:614 –26. 6. Jones NR, Blumbergs PC. Intracranial haemorrhage from meningiomas: a report of five cases. Br J Neurosurg 1989;3:691– 8.
Okuno et al
7. Martı´nez-Lage JF, Martı´nez MPM, Esteban JA, Antu´nez MC, Sola J. Meningiomas with haemorrhagic onset. Acta Neurochir (Wien) 1991;110:129 –32. 8. Modesti LM, Binet EF, Collins GH. Meningiomas causing spontaneous intracranial hematomas. J Neurosurg 1976;45:437– 41. 9. Niikawa S, Kawaguchi M, Sugimoto S, Hattori T, Ohkuma A. Meningioma associated with subdural hematoma. Case report. Neurol Med Chir (Tokyo) 1990;30: 169 –72. 10. Renowden SA, Hourihan MD. Case report: acute subdural haematoma—an unusual presentation of a meningioma. Clin Radiol 1992;45:351–2. 11. Sato H, Ohmura K, Mizushima M, Ito J, Kuyama H. Myxopapillary ependymoma of the lateral ventricle. A study on the mechanism of its stromal myxoid change. Acta Pathol Jpn 1983;33:1017–25. 12. Scott M. Spontaneous intracerebral hematoma caused by cerebral neoplasms. Report of eight verified cases. J Neurosurg 1975;42:338 – 42. 13. Skultety FM. Meningioma simulating ruptured aneurysm. J Neurosurg 1968;28:380 –2. 14. Taptas JN. Intracranial meningioma in a four-monthold infant simulating subdural hematoma. J Neurosurg 1960;18:120 –1. 15. Ueno M, Nakai E, Naka Y, Kido T, Itakura T, Komai N. Acute subdural hematoma associated with vacuolated meningioma. Case report. Neurol Med Chir (Tokyo) 1993;33:36 –39. 16. Wakai S, Yamakawa K, Manaka S, Takakura K. Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance. Neurosurgery 1982;10:437– 44. 17. Walsh JW, Winston KR, Smith T. Meningioma with subdural hematoma. Surg Neurol 1977;8:293–5. 18. Wang A-M, Chinwuba CE, O’Reilly GV, Kleefield J. Subdural hematoma in patients with brain tumor: CT evaluation. J Comput Assist Tomogr 1985;9:511–3.
Okuno S, Touho H, Ohnishi H, Karasawa J. Falx meningioma presenting as acute subdural hematoma: case report. Surg Neurol 1999;52:180 – 4. BACKGROUND
Acute subdural hematomas caused by meningiomas have been rarely encountered. Pathophysiologic mechanisms and clinical considerations in these patients have not been sufficiently explored. We addressed the possible mechanism of spontaneous hemorrhage in our case and briefly discuss the optimal treatment. CASE DESCRIPTION
This case of falx meningioma presenting as an acute subdural hematoma in a 78-year-old woman is described. On initial computed tomography (CT), an enhancing tumor of the falx appeared to be the cause of hemorrhage. Only faint contrast staining in the periphery of the tumor was seen on right external carotid arteriograms, with no evidence of other vascular supply. Extravasation of contrast material during the procedure occurred suddenly and was successfully treated by endovascular embolization using a microcatheter. The hematoma was emergently evacuated with gross total removal of the tumor. Pathologic examination confirmed a transitional meningioma with abundant hyalinized structures. Disruption of a thinwalled vessel adjacent to the tumor capsule was assumed to be the site of hemorrhage.
pontaneous intracranial hemorrhages associated with brain tumors are well known events. In recent reviews, the incidence of spontaneous hemorrhage has been reported to range from 5%– 10% [12,16]. Malignant glioma, brain metastasis, and pituitary adenomas are recognized as the most frequent underlying pathologies. In contrast, hemorrhage due to meningiomas is thought to be a rare initial presentation [2,7]. In this report, we describe a case of meningioma presenting as acute subdural hematoma and propose a possible mechanism of spontaneous hemorrhage, based upon the pathologic examination. Early surgical intervention is thought to be the most effective treatment, although the prognosis is generally poor due to the devastating effect of the initial hemorrhage [2,6,7]. Careful immediate evaluation of the clinical features, neuroradiologic images, and underlying disease is mandatory in order to diagnose this rare event and to facilitate prompt treatment.
S
CONCLUSIONS
The longstanding ischemia of the tumor was considered to have produced the deposition of hyalin in the tissue, which changed the hemodynamics within the tumor, producing vascular stress leading to rupture. The prognosis of patients with meningiomas complicated by acute subdural hematoma is generally poor, with mortality reported in approximately one-half of such patients. Surgical exploration is the most effective treatment and should be conducted before irreversible brain damage has occurred. © 1999 by Elsevier Science Inc. KEY WORDS
Meningioma, acute subdural hemorrhage, extravasation, embolization.
Address reprint requests to: Shuzo Okuno, M.D., Department of Neurosurgery, Nara Medical University, 840, Shijo-cho, Kashihara, Nara, 634, Japan. Received June 12, 1996; accepted September 5, 1996. 0090-3019/99/$–see front matter PII S0090-3019(97)00028-1
Case Report This 78-year-old woman with no past history of trauma or bleeding abnormalities was admitted to our institute due to the sudden onset of vomiting and a loss of consciousness. On examination, she did not open her eyes to verbal or painful stimuli and exhibited only withdrawal responses in the left extremities. Her pupils were equal with a nearly intact reaction to light. Hemiparesis was observed in her right extremities with an ipsilateral Babinski sign. Laboratory data obtained on admission were essentially within normal limits and there was no evidence of an underlying predisposition to hemorrhage. Plain cranial roentgenograms yielded normal findings with no fracture lines or calcified lesions. © 1999 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
ASDH from Meningioma
Surg Neurol 181 1999;52:180 –4
(Left) Plain CT scans on admission revealing a massive left subdural hematoma extending from the anterior interhemispheric fissure; (center) a tumor attached to the falx on the left side, of relatively high density compared to the brain parenchyma. The lesion contains a small amount of high-density granular material suggestive of calcification; (right) a contrast CT scan demonstrating faint peripheral enhancement of the tumor.
1
Computed tomography (CT) revealed a massive subdural hematoma, extending from the interhemispheric fissure to the left cerebral convexity (Figure 1 left), and an adjacent solid tumor attached to the left side of the falx (Figure 1 center). The tumor had a slightly higher density compared to the brain parenchyma and contained a granular high density area, possibly representing calcified material. Following the administration of contrast medium, homogeneous enhancement was seen in the periphery of the tumor (Figure 1 right). Digital subtraction angiography (DSA) demonstrated fanning of the anterior cerebral arteries with a shift to the right. The mass was fed exclusively by the right external carotid artery, mainly through falcial twigs of the middle meningeal artery (Figure 2, left). Following
lateral projections, an anteroposterior view was being taken, when extravasation of contrast material directed towards the anterior interhemispheric fissure suddenly occurred (Figure 2, right). Immediately, a Tracker-10 catheter (Target Therapeutics, San Jose, CA) was superselectively cannulated into the right middle meningeal artery, and the artery was completely embolized using 180 –300 mm polyvinyl alcohol particles (Ivalon). At this time, the patient’s neurologic condition remained unchanged, although CT demonstrated marked enhancement of an area caused by the contrast medium leak (Figure 3). She was promptly transferred to the operating room and underwent a left frontotemporal craniotomy across the midline. The dura was moderately tense but appeared to be intact.
(Left) A lateral view of the right external carotid artery angiogram showing faint staining in the periphery of the tumor (arrowheads) fed by the middle meningeal artery; (Right) anteroposterior view of the right external carotid artery demonstrating extravasation directed towards the anterior interhemispheric fissure (arrows). Superselective embolization using a microcatheter successfully obliterated the feeding artery, preventing further enlargement of the hematoma (not shown).
2
182 Surg Neurol 1999;52:180 –4
Okuno et al
(Left and right) CT scan obtained after angiography demonstrating leakage of the contrast medium superficially within the tumor and into the anterior interhemispheric fissure, showing markedly high density attenuation.
3
Upon opening the dura matter, a massive jelly-like subdural hematoma was encountered, which had no membranous tissue. After aspiration of the hematoma, no suggestion of head trauma (e.g., fractures, brain contusions) was found. Rather, an elastic firm tumor attached to the left side of the falx was seen adjacent to the interhemispheric fissure. Its capsule was torn in the superior portion near its dural attachment, from which the interhemispheric hematoma extended anteriorly. The bridging veins and cortical arteries had no direct contact with the tumor. Gross total removal of the tumor was performed, followed by electric coagulation of its dural attachment. The patient’s level of consciousness gradually improved enough to allow her to follow some verbal commands, but she remained abulic
with a mild right hemiparesis 2 months after the surgery. Pathologic analysis of the resected tumor demonstrated a transitional meningioma with abundant hyalinization. Hyalinized structure was preferentially found in the tissue and the vascular walls (Figure 4 left). Hemorrhage from a thin-walled vessel was seen in a part of the specimen close to the capsule (Figure 4 right). Hemosiderin deposition, necrosis, or findings suggestive of malignancy were not seen.
Discussion In most cases of meningioma, the early symptoms are seizures and neurologic signs associated with
(Left) A photomicrograph of the resected tumor revealing a transitional-type meningioma (hematoxylin and eosin, ⫻ 100) with abundant hyalinization within the tissue and vascular walls. (Right) Disruption of a thin-walled vessel (asterisk) with extravasation of red blood cells is disclosed at the superficial portion of the tumor (Elastica-van Gieson, ⫻ 240).
4
ASDH from Meningioma
increased intracranial pressure. Focal neurologic deficits, dependent on the tumor location, may accompany these symptoms with tumor growth. In contrast, a hemorrhagic presentation of a meningioma is an unusual event [4,7]. Cushing and Eisenhardt [3] reported that none of their 313 patients with meningiomas manifested hemorrhages. Furthermore, a series of 280 parasagittal meningiomas reported by Hoessly and Olivecrona did not include any cases involving hemorrhage from a tumor [5]. In 1991, Martinez-Lage et al. [7] reviewed 57 cases from the literature; they also reported their surgical experience in a series of 125 patients with meningiomas, revealing hemorrhage in only three cases (2.4%). This incidence is slightly higher than that reported by Wakai et al. in 1982 [16], who encountered four hemorrhagic cases in 310 meningiomas (1.3%). The commonly reported site of hemorrhage from meningiomas is the subarachnoid space including the intraventricular cavity. Intracerebral and intratumoral hemorrhages are the next most frequent types. Subdural hemorrhage from meningiomas is relatively rare, and 20 such cases were reviewed by Chaskis et al. [2] in 1992. Most of these hemorrhages were accompanied by other types of hemorrhage and rarely occurred alone. In addition, a considerable number of such cases have been presumed to be chronic subdural hematomas presenting with a more insidious onset, and having organized hematomas enclosed by a definite membrane [1,4,8,14,17]. Strictly speaking, only 11 cases of acute subdural hematoma associated with meningiomas have been reported previously in the English literature [2,6 –10,13,15,18]. They have had no predisposing factors such as preceding head trauma or anticoagulant therapy, and commonly developed the apoplectiform presentation directly associated with the hemorrhage. Only the histological subtype of the meningioma has been documented as playing an important role in the occurrence of hemorrhage [2,7,15]. Angioblastic and malignant meningiomas tend to bleed more frequently, although syncytial or meningotheliomatous subtypes account for the majority of cases. In angioblastic meningiomas, it has been assumed that the thin-walled vessels are too fragile, causing easy bleeding. This assumption also may be true of other subtypes of meningioma that demonstrate hypervascularity confined to portions of the specimen. In malignant meningiomas, like other anaplastic tumors, direct invasion or endothelial proliferation by the tumor may obstruct the vascular channel, producing congestion and necrosis within the tumor, resulting in hemorrhage. In these instances, the site of hemorrhage should exist
Surg Neurol 183 1999;52:180 –4
within the tumor, but may extend to the surroundings (i.e., the subarachnoid, intracerebral, and subdural spaces). The mechanical stretching and distortion of bridging veins by meningiomas may also be associated with hemorrhage. In the present case, vessels adjacent to the tumor were not involved, and histologic examination merely demonstrated a transitional pattern with no component of the angioblastic subtype, and a disruption of thin-walled vessels close to the tumor capsule. These findings are similar to those reported in the previous cases, but the great number of hyalinized structures seen in our case appears to be a relatively unusual finding in meningiomas. The definitive cause of the hemorrhage remains unclear, but vascular features may have contributed to the hemorrhage in our case. The tumor was fed by the contralateral extracarotid artery alone with only faint contrast staining, predominantly in the superficial portion. Although this may not be an exceptional finding in meningiomas, the regression of feeding arteries may be strongly associated with tumor degeneration resulting from the longstanding ischemia. Sato et al. [11] have reported a case of intraventricular ependymoma with prominent stromal degeneration in which the circulatory disturbance in the tumor seemed to cause the deposition of hyalin in the vessel and related histologic changes. Therefore, rich hyalinized structures may reflect insufficient nourishment by the associated feeding artery. Furthermore, disproportionate amounts of degenerated tissue caused by such ischemia might change the hemodynamics within the tumor, producing vascular stress in a thin-walled vessel, though this claim may be simply a speculation, and a rather rare mechanism in the occurrence of spontaneous hemorrhage from meningiomas. The prognosis of patients with meningioma with acute hemorrhage is generally poor, and approximately one-half of such patients die regardless of hemorrhage type. Factors responsible for the morbidity and mortality have not been precisely identified. However, the most frequently reported factor affecting prognosis is the clinical state of the patient at onset. The beneficial effect of surgical intervention was restricted to a small number of patients because even minor hemorrhages were associated with rapid increases in intracranial pressure to critical levels, particularly in patients with larger tumor volumes. Furthermore, direct critical injury to the surrounding brain may occur for which current treatment is ineffective. The propriety of prophylactic tumor removal in the presentation of future hemorrhage remains controversial as it is difficult to predict the possibility of hemorrhage, even using
184 Surg Neurol 1999;52:180 –4
modern neuroradiologic modalities [9,15]. Once a subdural hemorrhage has occurred in a patient with meningioma, one must promptly distinguish whether this situation resulted from the associated tumor or other causes such as head trauma, drugs, or a systemic bleeding tendency. Surgical exploration, whenever necessary, should be conducted before irreversible brain damage has occurred. Additionally, one may perform embolization of the arterial supply to the tumor to prevent extravasation during angiography, which may avoid enlargement of the hemorrhage and facilitate the surgical procedure. REFERENCES 1. Baskinis N, Grotenhuis A, Wandt H. Chronic subdural hematoma associated with an intracapsular meningioma. Case report and short review of the literature. J Neurosurg Sci 1984;28:17–23. 2. Chaskis C, Raftopoulos C, Noterman J, FlamentDurand J, Brotchi J. Meningioma associated with subdural haematoma: report of two cases and review of the literature. Clin Neurol Neurosurg 1992;94:269 –74. 3. Cushing H, Eisenhardt L. Meningiomas, their classification, regional behavior, life history, and surgical end result. Springfield, Ill: Charles C. Thomas 1938. 4. Cusick JF, Bailey OT. Association of ossified subdural hematomas and a meningioma. Case report. J Neurosurg 1972;37:731– 4. 5. Hoessly GF, Olivecrona H. Report on 280 cases of verified parasagittal meningiomas. J Neurosurg 1955; 12:614 –26. 6. Jones NR, Blumbergs PC. Intracranial haemorrhage from meningiomas: a report of five cases. Br J Neurosurg 1989;3:691– 8.
Okuno et al
7. Martı´nez-Lage JF, Martı´nez MPM, Esteban JA, Antu´nez MC, Sola J. Meningiomas with haemorrhagic onset. Acta Neurochir (Wien) 1991;110:129 –32. 8. Modesti LM, Binet EF, Collins GH. Meningiomas causing spontaneous intracranial hematomas. J Neurosurg 1976;45:437– 41. 9. Niikawa S, Kawaguchi M, Sugimoto S, Hattori T, Ohkuma A. Meningioma associated with subdural hematoma. Case report. Neurol Med Chir (Tokyo) 1990;30: 169 –72. 10. Renowden SA, Hourihan MD. Case report: acute subdural haematoma—an unusual presentation of a meningioma. Clin Radiol 1992;45:351–2. 11. Sato H, Ohmura K, Mizushima M, Ito J, Kuyama H. Myxopapillary ependymoma of the lateral ventricle. A study on the mechanism of its stromal myxoid change. Acta Pathol Jpn 1983;33:1017–25. 12. Scott M. Spontaneous intracerebral hematoma caused by cerebral neoplasms. Report of eight verified cases. J Neurosurg 1975;42:338 – 42. 13. Skultety FM. Meningioma simulating ruptured aneurysm. J Neurosurg 1968;28:380 –2. 14. Taptas JN. Intracranial meningioma in a four-monthold infant simulating subdural hematoma. J Neurosurg 1960;18:120 –1. 15. Ueno M, Nakai E, Naka Y, Kido T, Itakura T, Komai N. Acute subdural hematoma associated with vacuolated meningioma. Case report. Neurol Med Chir (Tokyo) 1993;33:36 –39. 16. Wakai S, Yamakawa K, Manaka S, Takakura K. Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance. Neurosurgery 1982;10:437– 44. 17. Walsh JW, Winston KR, Smith T. Meningioma with subdural hematoma. Surg Neurol 1977;8:293–5. 18. Wang A-M, Chinwuba CE, O’Reilly GV, Kleefield J. Subdural hematoma in patients with brain tumor: CT evaluation. J Comput Assist Tomogr 1985;9:511–3.