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Subarachnoid and intraventricular hemorrhage caused by hypernephroma metastasis, accompanied by innocent bilateral posterior communicating artery aneurysms
ELSEVIER
Vascular: Pediatric and Adult
SUBARACHNOID AND INTRAVENTRICULAR HEMORRHAGE CAUSED BY HYPERNEPHROMA METASTASIS, ACCOMPANIED BY INNOCENT BILATERAL POSTERIOR COMMUNICATING ARTERY ANEURYSMS Uwe Spetzger, M.D., Michael Mull, M.D., Ulrich Sure, M.D., and Joachim Gilsbach, M.D. Departments of Neurosurgery and Neuroradiology, Technical University (RWTH) Aachen, Germany and Department of Neuropathology, University of Zurich, Switzerland
Spetzger U, Mull M, Sure U, Gilsbach J. Subarachnoid and intraventricular hemorrhage caused by hypernephroma metastasis, accompanied by innocent bilateral posterior communicating artery aneurysms. Surg Neurol 1995;44:275-8.
We present a case of subarachnoid and intraventricular hemorrhage due to an infratentorial metastasisof a renal cell carcinoma. The lesion was not apparent on initial magnetic resonance imaging (MRI) or in a follow-up examination (MRl and angiography) 6 weeksafter the bleeding. The innocent bilateral posterior communicating artery aneurysms detected by cerebral angiography were treated surgically. The origin of the hemorrhage, however, remained unclear. Five months later, a surgically proven metastasis in the fourth ventricle subsequently gave the explanation for the bleeding. KEY
WORDS
Subarachnoid hemorrhage, nonaneurysmalSAH, intraventricular bleeding, cerebral metastases.
V
ascular malformations or occasionally cerebral tumors often are the origin of nontraumatic subarachnoid hemorrhage @AH) or intraventricular bleeding [7,10,12,13,18,19]. In the literature, the percentage of SAH without specific cause ranges from lo%-15% [l-4,6,9,16]. Whenever there is no demonstrable origin for the hemorrhage, we are affected with the general problem: whether this is a lack of diagnostic tools, or is the pathologic focus nonexistent. We present a patient with infratentorial SAH, intraventricular bleeding, and bilateral innocent posterior communicating artery aneuAddress reprint requests to: Uwe Spetzger M.D., Department of Neurosurgery, Technical University (RWTH) Aachen, PauwelsstralSe 30, D-52057 Aachen, Germany. Received November 17, 1994; accepted February 27, 1995. 0 1995 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
rysms. The explanation for this so-called “innocent hemorrhage” became evident 5 months later as an infratentorial metastasis of a renal cell carcinoma. This example of a very small and therefore inapparent lesion in C’T scan, angiography, and MRI confirms the presumption that micrometastases under the limit of demonstration can cause severe subarachnoid and intraventricular hemorrhages.
CASEREPORT A 60-year-old woman was admitted after a l-week history of progressive headache, nausea, vomiting, drowsiness, vertigo, and acute onset of diplopia. On first clinical examination she presented with anisocoria, slight meningism, positive unilateral Babinski’s sign, and moderately impaired coordination. It should be mentioned that the patient underwent nephrectomy because of hypernephroma 4 years earlier, but she was free of symptoms and regular follow-up examinations showed no metastatic disease. Initial computed tomography (CT) scan revealed an SAH and an intraventricular blood collection in the fourth ventricle with consecutive hydrocephalus (Figure 1 A). The following cerebral angiogram (Figure 1 B, C) showed bilateral posterior communicating artery aneurysms. At that time the left vertebral angiogram was normal (Figure 3 A). First a ventricular drain was inserted, resulting in an immediate improvement of the neurologic state. The following day both aneurysms were treated surgically. First a right pterional approach was used 0090-3019/95/$9.50 SSDI0090-3019(95)00170-9
276
Surg Nemo1 1995:44:275-S
Spetzger et al
CIR CM R
Initial neuroradiologic examinations on the day of first admission.(A) Unenhanced CT scan (slice thickness 4 mm) showed a hemorrhage in the fourth ventricle and left cerebellopontine cistern. (B) Right and (C) left common carotid angiogram (oblique view, arterial phase) revealed bilateral aneurysms of the posterior communicating arteries
II
(QfYOWS).
and the ipsilateral aneurysm was eliminated. Intraoperatively the contralateral posterior communiwas verified, but a safe cating artery aneurysm
placement of the clip was impossible via the right sided trepanation. Subsequently the aneurysm was clipped by performing a left pterional craniotomy. The intraoperative aspect confirmed that both aneurysms were innocent and could not be accepted as the origin of the SAH. The postoperative course was uneventful, the ventricular drain was removed after the second postoperative day, and 2 weeks later the patient was discharged without any neurologic deficit. Since the source of the bleeding still remained unclear, neuroradiologic examinations were repeated 6 weeks after the acute event. On MRI (T,-weighted
MRl scans (gd-DTPA enhanced, SE 600115, slice thickness 5 mm) obtained 5 months after first admission. (A) Axial and (J3)sagittal images showed a dense and sharply delineated paramagnetic enhancement in the fourth ventricle, causing obstructive hydrocephalus.
sagittal, proton and T,-weighted axial images), only a low signal area could be detected in the fourth ventricle, corresponding to the residual intraventricular blood. Repeated angiography was normal. Five months after the initial course, the patient again was admitted after a short episode of disorientation, ataxia, progressive headache, and visual disturbance. On MRI a well-defined oval mass lesion in the fourth ventricle with dense paramagnetic enhancement was detected (Figure 2 A, B). Repeated left vertebral angiography showed a ringlike network of fine neoplastic vessels with sharply delineated tumor stain (Figure 3 B).
Suboccipital
craniotomy
was performed
and the
grayish, soft and intensely vascularized tumor was
removed
microsurgically
using a medial
infracer-
Subarachnoid and lntraventricular
Hemorrhage
Surg Neurol 1995;44:275-8
Left vertebral
277
angiogram
(lateral view, late arterial phase). (A) Initial angiogram
showed no evidence of pathologic tumor vascularisation. Q!) Follow-up angiogram 5 months later revealed a lesion with a prominent tumor blush, mainly supplied by cerebellar >s . superior . .,. erior inrerior cer-
ebellar approach with elevation of the inferior vermis. The lesion (4 X 3 X 3 cm) originated from the floor of the fourth ventricle without a well-defined border to the underlying brain stem. Histologic examination showed a tumor specimen of soft consistency with a white to grayish cut surface and few brown dots. After processing and staining for microscopic investigation, the tumor cells had small round to oval nuclei with a dense and stippled chromatine (Figure 4 A). The cytoplasm appeared clear after processing for embedding in paraffin wax due to the content of lipids and glycogen. All cells exhibited a strong reaction of the cytoplasmatic membrane, with immunostain for pancytokeratine (polyclonal antibody Lu-5) which is characteristic for metastases (Figure 4 B). A local rebleeding on the second postoperative day with consecutive hydrocephalus required the insertion of an external ventricular drainage; the bleeding was not removed surgically. One week later the patient developed staphylococcal meningitis that delayed recovery. On discharge 8 weeks
later, the patient had no focal neurologic deficit, only presenting moderate psychomotor impairment. Eighteen months later a follow-up MRl demonstrated the reoccurrence of the metastasis at the same location.
DISCUSSION The origin of an SAH (e.g., vascular malformations, tumors, cerebral metastases) mostly can be proven by CT, MRl, and cerebral angiography [5-7, lo-13,18,19]. However, in lo%-15% a causal focus could not be found [l-4,6,9,16]. The coexistence of brain tumors and cerebral aneurysms is well known, especially associated with pituitary adenomas, meningeomas, and gliomas [14,15]. lncidental cerebral aneurysms are found in approximately 0.5% of patients with brain tumors [ 7,8,15]. Nevertheless, SAH or intraventricular bleeding caused by cerebral tumors is generally
1 Microphotographs of the cerebellar tumor specimen (metastasis of a renal cell carcinoma). (A) Clear cells with qintense stain for pancytokeratine (Lu-5) with apparently empty cytoplasm (H&E stain, x100). (B) lmmunohistochemical reaction of the cytoplasmatic membrane and occasionally of the cytoplasm (hematoxylin counterstain, X 200).
278
Surg Neurol 1995;44:275-8
rare and has been described only in several individual cases [5,7,10,12,13]. In our presented case, the neuroradiologic and the intraoperative findings with bilateral innocent posterior communicating artery aneurysms did not offer a sufficient explanation for the hemorrhage. Therefore, further examinations were carried out after reabsorbtion of the blood. Six weeks later in spite of better conditions, again no origin of the bleeding was found in the MRI and angiography. Five months later clinical signs reoccurred and the neuroradiologic examinations revealed the explanation for the initial bleeding in form of a huge metastatic lesion in the fourth ventricle. The diagnosis of renal cell carcinoma metastasis was confirmed histologically by immunostain reaction. With respect to occasionally similar histologic features and cerebellar localisation, the major histologic and neuroradiologic differential diagnosis was hemangioblastoma. The positive reaction, however, to pancytokeratine ruled out a hemangioblastoma and confirmed the diagnosis of a metastasis. The location of this pathology is uncommon [ 5,111, because in an overview of 3187 cases of intracranial metastases only 12 (0.4%) were found in the fourth ventricle [ 171.
CONCLUSION As summary in this case, we ascertain that a micrometastasis of a hypernephroma, invisible in early angiography, CT scan, and MRI, is able to cause a severe subarachnoid and intraventricular hemorrhage. Therefore, we should intensify our efforts to detect the origin of so-called unclear bleeding.
Spetzger et al
4.
5. 6. 7.
8. 9. 10. 11. 12. 13. 14.
15. 16. 17.
REFERENCES 1. Alexander M, Dias P, Uttley D. Spontaneous SAH and negative cerebral panangiography. J Neurosurg 1986; 641537-42. 2. Andrioli GC, Salar G, Rigobello L. Subarachnoid hemorrhage of unknown etiology. Acta Neurochir (Wien) 1979;48:217-21. 3. Eskesen 0, Sorensen EB, Rosenorn J, Schmidt K. The
18. 19.
prognosis in subarachnoid hemorrhage of unknown etiology. J Neurosurg 1984;61:1029-31. Ferbert A, Hubo I, Bieniek R. Non-traumatic subarachnoid hemorrhage with normal angiogram. Long-term follow-up and CT predictors of complications. J Neurol Sciences 1992;107:14-8. Gildersleeve W, Koo AH, MC Donald J. Metastatic tumor presenting as intracerebral hemorrhage. Radiology 1977;124:109-12. Giombini S, Bruzzone MG, Pluchino F. SAH of unknown cause. Neurosurgery 1988;22:313-6. Glass B, Abbott KH. Subarachnoid hemorrhage consequent to intracranial tumors. Review of literature and report of seven cases. Arch Neurol Psychiatry 1955;73:369-79. Handa J, Matsuda I, Handa H. Association of brain tumor and intracranial aneurysms. Surg Neurol 1976; 6:25-g. Juul R, Torbjorn A, Frederiksen TA, Ringkjob R. Prognosis in subarachnoid hemorrhage of unknown etiology. J Neurosurg 1986;64:359-62. Latchaw JP Jr, Dohn DF, Hahn JF, von der Luft E. Subarachnoid hemorrhage from an intracranial meningioma. Neurosurgery 1981;9:433-5. Macdonald DR, Walker R, Posner JB. Brain metastasis from renal carcinoma. Neurology 1983;33 suppl.2:139 abstr. Mandybur TI. Intracranial hemorrhage caused by metastatic tumors. Neurology 1977;27:650-5. Niizuma H, Nakasoto N, Yonemitsu T, Ito S, Suzuki J. lntracerebral hemorrhage for a metastatic brain tumor. Surg Neurol 1988;29:231-6. Okamura T, Watanabe Y, Kameda H. Coexistence of brain tumors and cerebral aneurysms-Clinical considerations from 8 cases. Neurol Med Chir (Tokyo) 1981;21:601-8. Pia HW, Obrador S, Martin J. Association of brain tumors and arterial intracranial aneurysms. Acta Neurochir (Wien) 1972;27:189-204. Renowden SA, Molyneux AJ, Anslow P, Byrne JV. The value of MRI in angiogram-negative intracranial hemorrhage. Neuroradiology 1994;36:422-5. Sano K. Intracranial metastatic tumors: An overview. In: Paoletti P et al, eds. Neurooncology. Kluwer Academic Publishers, 1991:309-19. Scott M. Spontaneous intracranial hematoma caused by cerebral neoplasms. J Neurosurg 1975;43:338-42. Wakai S, Yamakowa K, Manaka S, Takakura K. Spontaneous intracerebral hemorrhage caused by brain tumor. Its incidence and clinical significance. Neurosurgery 1982;10:437-44.
Vascular: Pediatric and Adult
SUBARACHNOID AND INTRAVENTRICULAR HEMORRHAGE CAUSED BY HYPERNEPHROMA METASTASIS, ACCOMPANIED BY INNOCENT BILATERAL POSTERIOR COMMUNICATING ARTERY ANEURYSMS Uwe Spetzger, M.D., Michael Mull, M.D., Ulrich Sure, M.D., and Joachim Gilsbach, M.D. Departments of Neurosurgery and Neuroradiology, Technical University (RWTH) Aachen, Germany and Department of Neuropathology, University of Zurich, Switzerland
Spetzger U, Mull M, Sure U, Gilsbach J. Subarachnoid and intraventricular hemorrhage caused by hypernephroma metastasis, accompanied by innocent bilateral posterior communicating artery aneurysms. Surg Neurol 1995;44:275-8.
We present a case of subarachnoid and intraventricular hemorrhage due to an infratentorial metastasisof a renal cell carcinoma. The lesion was not apparent on initial magnetic resonance imaging (MRI) or in a follow-up examination (MRl and angiography) 6 weeksafter the bleeding. The innocent bilateral posterior communicating artery aneurysms detected by cerebral angiography were treated surgically. The origin of the hemorrhage, however, remained unclear. Five months later, a surgically proven metastasis in the fourth ventricle subsequently gave the explanation for the bleeding. KEY
WORDS
Subarachnoid hemorrhage, nonaneurysmalSAH, intraventricular bleeding, cerebral metastases.
V
ascular malformations or occasionally cerebral tumors often are the origin of nontraumatic subarachnoid hemorrhage @AH) or intraventricular bleeding [7,10,12,13,18,19]. In the literature, the percentage of SAH without specific cause ranges from lo%-15% [l-4,6,9,16]. Whenever there is no demonstrable origin for the hemorrhage, we are affected with the general problem: whether this is a lack of diagnostic tools, or is the pathologic focus nonexistent. We present a patient with infratentorial SAH, intraventricular bleeding, and bilateral innocent posterior communicating artery aneuAddress reprint requests to: Uwe Spetzger M.D., Department of Neurosurgery, Technical University (RWTH) Aachen, PauwelsstralSe 30, D-52057 Aachen, Germany. Received November 17, 1994; accepted February 27, 1995. 0 1995 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010
rysms. The explanation for this so-called “innocent hemorrhage” became evident 5 months later as an infratentorial metastasis of a renal cell carcinoma. This example of a very small and therefore inapparent lesion in C’T scan, angiography, and MRI confirms the presumption that micrometastases under the limit of demonstration can cause severe subarachnoid and intraventricular hemorrhages.
CASEREPORT A 60-year-old woman was admitted after a l-week history of progressive headache, nausea, vomiting, drowsiness, vertigo, and acute onset of diplopia. On first clinical examination she presented with anisocoria, slight meningism, positive unilateral Babinski’s sign, and moderately impaired coordination. It should be mentioned that the patient underwent nephrectomy because of hypernephroma 4 years earlier, but she was free of symptoms and regular follow-up examinations showed no metastatic disease. Initial computed tomography (CT) scan revealed an SAH and an intraventricular blood collection in the fourth ventricle with consecutive hydrocephalus (Figure 1 A). The following cerebral angiogram (Figure 1 B, C) showed bilateral posterior communicating artery aneurysms. At that time the left vertebral angiogram was normal (Figure 3 A). First a ventricular drain was inserted, resulting in an immediate improvement of the neurologic state. The following day both aneurysms were treated surgically. First a right pterional approach was used 0090-3019/95/$9.50 SSDI0090-3019(95)00170-9
276
Surg Nemo1 1995:44:275-S
Spetzger et al
CIR CM R
Initial neuroradiologic examinations on the day of first admission.(A) Unenhanced CT scan (slice thickness 4 mm) showed a hemorrhage in the fourth ventricle and left cerebellopontine cistern. (B) Right and (C) left common carotid angiogram (oblique view, arterial phase) revealed bilateral aneurysms of the posterior communicating arteries
II
(QfYOWS).
and the ipsilateral aneurysm was eliminated. Intraoperatively the contralateral posterior communiwas verified, but a safe cating artery aneurysm
placement of the clip was impossible via the right sided trepanation. Subsequently the aneurysm was clipped by performing a left pterional craniotomy. The intraoperative aspect confirmed that both aneurysms were innocent and could not be accepted as the origin of the SAH. The postoperative course was uneventful, the ventricular drain was removed after the second postoperative day, and 2 weeks later the patient was discharged without any neurologic deficit. Since the source of the bleeding still remained unclear, neuroradiologic examinations were repeated 6 weeks after the acute event. On MRI (T,-weighted
MRl scans (gd-DTPA enhanced, SE 600115, slice thickness 5 mm) obtained 5 months after first admission. (A) Axial and (J3)sagittal images showed a dense and sharply delineated paramagnetic enhancement in the fourth ventricle, causing obstructive hydrocephalus.
sagittal, proton and T,-weighted axial images), only a low signal area could be detected in the fourth ventricle, corresponding to the residual intraventricular blood. Repeated angiography was normal. Five months after the initial course, the patient again was admitted after a short episode of disorientation, ataxia, progressive headache, and visual disturbance. On MRI a well-defined oval mass lesion in the fourth ventricle with dense paramagnetic enhancement was detected (Figure 2 A, B). Repeated left vertebral angiography showed a ringlike network of fine neoplastic vessels with sharply delineated tumor stain (Figure 3 B).
Suboccipital
craniotomy
was performed
and the
grayish, soft and intensely vascularized tumor was
removed
microsurgically
using a medial
infracer-
Subarachnoid and lntraventricular
Hemorrhage
Surg Neurol 1995;44:275-8
Left vertebral
277
angiogram
(lateral view, late arterial phase). (A) Initial angiogram
showed no evidence of pathologic tumor vascularisation. Q!) Follow-up angiogram 5 months later revealed a lesion with a prominent tumor blush, mainly supplied by cerebellar >s . superior . .,. erior inrerior cer-
ebellar approach with elevation of the inferior vermis. The lesion (4 X 3 X 3 cm) originated from the floor of the fourth ventricle without a well-defined border to the underlying brain stem. Histologic examination showed a tumor specimen of soft consistency with a white to grayish cut surface and few brown dots. After processing and staining for microscopic investigation, the tumor cells had small round to oval nuclei with a dense and stippled chromatine (Figure 4 A). The cytoplasm appeared clear after processing for embedding in paraffin wax due to the content of lipids and glycogen. All cells exhibited a strong reaction of the cytoplasmatic membrane, with immunostain for pancytokeratine (polyclonal antibody Lu-5) which is characteristic for metastases (Figure 4 B). A local rebleeding on the second postoperative day with consecutive hydrocephalus required the insertion of an external ventricular drainage; the bleeding was not removed surgically. One week later the patient developed staphylococcal meningitis that delayed recovery. On discharge 8 weeks
later, the patient had no focal neurologic deficit, only presenting moderate psychomotor impairment. Eighteen months later a follow-up MRl demonstrated the reoccurrence of the metastasis at the same location.
DISCUSSION The origin of an SAH (e.g., vascular malformations, tumors, cerebral metastases) mostly can be proven by CT, MRl, and cerebral angiography [5-7, lo-13,18,19]. However, in lo%-15% a causal focus could not be found [l-4,6,9,16]. The coexistence of brain tumors and cerebral aneurysms is well known, especially associated with pituitary adenomas, meningeomas, and gliomas [14,15]. lncidental cerebral aneurysms are found in approximately 0.5% of patients with brain tumors [ 7,8,15]. Nevertheless, SAH or intraventricular bleeding caused by cerebral tumors is generally
1 Microphotographs of the cerebellar tumor specimen (metastasis of a renal cell carcinoma). (A) Clear cells with qintense stain for pancytokeratine (Lu-5) with apparently empty cytoplasm (H&E stain, x100). (B) lmmunohistochemical reaction of the cytoplasmatic membrane and occasionally of the cytoplasm (hematoxylin counterstain, X 200).
278
Surg Neurol 1995;44:275-8
rare and has been described only in several individual cases [5,7,10,12,13]. In our presented case, the neuroradiologic and the intraoperative findings with bilateral innocent posterior communicating artery aneurysms did not offer a sufficient explanation for the hemorrhage. Therefore, further examinations were carried out after reabsorbtion of the blood. Six weeks later in spite of better conditions, again no origin of the bleeding was found in the MRI and angiography. Five months later clinical signs reoccurred and the neuroradiologic examinations revealed the explanation for the initial bleeding in form of a huge metastatic lesion in the fourth ventricle. The diagnosis of renal cell carcinoma metastasis was confirmed histologically by immunostain reaction. With respect to occasionally similar histologic features and cerebellar localisation, the major histologic and neuroradiologic differential diagnosis was hemangioblastoma. The positive reaction, however, to pancytokeratine ruled out a hemangioblastoma and confirmed the diagnosis of a metastasis. The location of this pathology is uncommon [ 5,111, because in an overview of 3187 cases of intracranial metastases only 12 (0.4%) were found in the fourth ventricle [ 171.
CONCLUSION As summary in this case, we ascertain that a micrometastasis of a hypernephroma, invisible in early angiography, CT scan, and MRI, is able to cause a severe subarachnoid and intraventricular hemorrhage. Therefore, we should intensify our efforts to detect the origin of so-called unclear bleeding.
Spetzger et al
4.
5. 6. 7.
8. 9. 10. 11. 12. 13. 14.
15. 16. 17.
REFERENCES 1. Alexander M, Dias P, Uttley D. Spontaneous SAH and negative cerebral panangiography. J Neurosurg 1986; 641537-42. 2. Andrioli GC, Salar G, Rigobello L. Subarachnoid hemorrhage of unknown etiology. Acta Neurochir (Wien) 1979;48:217-21. 3. Eskesen 0, Sorensen EB, Rosenorn J, Schmidt K. The
18. 19.
prognosis in subarachnoid hemorrhage of unknown etiology. J Neurosurg 1984;61:1029-31. Ferbert A, Hubo I, Bieniek R. Non-traumatic subarachnoid hemorrhage with normal angiogram. Long-term follow-up and CT predictors of complications. J Neurol Sciences 1992;107:14-8. Gildersleeve W, Koo AH, MC Donald J. Metastatic tumor presenting as intracerebral hemorrhage. Radiology 1977;124:109-12. Giombini S, Bruzzone MG, Pluchino F. SAH of unknown cause. Neurosurgery 1988;22:313-6. Glass B, Abbott KH. Subarachnoid hemorrhage consequent to intracranial tumors. Review of literature and report of seven cases. Arch Neurol Psychiatry 1955;73:369-79. Handa J, Matsuda I, Handa H. Association of brain tumor and intracranial aneurysms. Surg Neurol 1976; 6:25-g. Juul R, Torbjorn A, Frederiksen TA, Ringkjob R. Prognosis in subarachnoid hemorrhage of unknown etiology. J Neurosurg 1986;64:359-62. Latchaw JP Jr, Dohn DF, Hahn JF, von der Luft E. Subarachnoid hemorrhage from an intracranial meningioma. Neurosurgery 1981;9:433-5. Macdonald DR, Walker R, Posner JB. Brain metastasis from renal carcinoma. Neurology 1983;33 suppl.2:139 abstr. Mandybur TI. Intracranial hemorrhage caused by metastatic tumors. Neurology 1977;27:650-5. Niizuma H, Nakasoto N, Yonemitsu T, Ito S, Suzuki J. lntracerebral hemorrhage for a metastatic brain tumor. Surg Neurol 1988;29:231-6. Okamura T, Watanabe Y, Kameda H. Coexistence of brain tumors and cerebral aneurysms-Clinical considerations from 8 cases. Neurol Med Chir (Tokyo) 1981;21:601-8. Pia HW, Obrador S, Martin J. Association of brain tumors and arterial intracranial aneurysms. Acta Neurochir (Wien) 1972;27:189-204. Renowden SA, Molyneux AJ, Anslow P, Byrne JV. The value of MRI in angiogram-negative intracranial hemorrhage. Neuroradiology 1994;36:422-5. Sano K. Intracranial metastatic tumors: An overview. In: Paoletti P et al, eds. Neurooncology. Kluwer Academic Publishers, 1991:309-19. Scott M. Spontaneous intracranial hematoma caused by cerebral neoplasms. J Neurosurg 1975;43:338-42. Wakai S, Yamakowa K, Manaka S, Takakura K. Spontaneous intracerebral hemorrhage caused by brain tumor. Its incidence and clinical significance. Neurosurgery 1982;10:437-44.