- Email: [email protected]
Metastatic prostate adenocarcinoma invading an atypical meningioma
1723
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1723–1725
Metastatic prostate adenocarcinoma invading an atypical meningioma R.A. Mitchell a,⇑, J. Dimou a,b, A. Tsui c, B. Kavar a a
Department of Neurosurgery, The Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia Department of Surgery, Royal Melbourne and Western Hospitals, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Parkville, Victoria, Australia c Department of Pathology, The Royal Melbourne Hospital, Parkville, Victoria, Australia b
a r t i c l e
i n f o
Article history: Received 7 March 2011 Accepted 15 March 2011
Keywords: Atypical meningioma Dural based metastasis Meningioma Prostate adenocarcinoma Tumour-to-tumour phenomenon
a b s t r a c t Although prostate adenocarcinoma is the most commonly diagnosed cancer in men, intracranial metastases are rare. We describe a 72-year-old patient with known metastatic prostate cancer, presenting with a dural-based parafalcine lesion on radiological imaging, following a seizure. Total macroscopic excision of the lesion was achieved at surgery, with histopathology confirming prostate adenocarcinoma embedded in an atypical (World Health Organization Grade II) meningioma, fulfilling all the criteria for true tumour-to-tumour metastasis. To our knowledge, this is the first report of prostate cancer metastasising to an atypical meningioma.
1. Case Report A 72-year-old man presented to hospital after an episode of conscious collapse, which was followed by a seizure. Post-ictally, he was noted to have a transient right hemiparesis, and deterioration in cognition with short-term memory loss and slight slowing of his speech. Past medical history was significant for prostate adenocarcinoma with known lung metastases, treated with radio- and hormone therapy. Physical examination revealed no focal neurological deficit. His CT scan showed a haemorrhagic enhancing lesion with fluid levels superior to the hypoplastic corpus callosal body extending to either side of the falx, and a further ring enhancing lesion to the left of this with associated vasogenic oedema (Fig. 1). MRI further characterised this complex cystic mass demonstrating lateral cystic components and a solid central portion with mild to moderate contrast enhancement (Fig. 2). The patient underwent a frontal craniotomy and excision of this falcine tumour, using an interhemispheric approach. The tumour was noted to be heterogeneous with solid, cystic, and haemorrhagic components. Although it did have a capsule, it was very adherent to the cortex. Total macroscopic excision was achieved (Fig. 4). Subsequently the patient underwent adjuvant localised radiation therapy with 36 Gy in 12 fractions and chemotherapy with docetaxel and zoledronic acid. 1.1. Neuropathological findings The tumour sections showed a malignant epithelioid tumour with invasion of the dura and areas of central necrosis, enlarged pleomorphic nuclei, prominent nucleoli, pale eosinophilic to foamy cytoplasm, and lympho–vascular invasion in the dura (Fig. 3). The tumour cells were positive for prostate specific antigen (PSA), alpha-methylacyl-CoA racemase (P504S), anticytokeratin CAM5.2, cytokeratin (CK)7 and epithelial membrane antigen (EMA), in keeping with a metastatic poorly differentiated adenocarcinoma from the prostate (Fig. 3). The Gleason score was 10. There was also a small amount of tumour which formed whorls, with enlarged nuclei and prominent nucleoli, and the cytoplasm was less foamy. Up to 16 mitoses per 10 high power fields were ⇑ Corresponding author. Tel.: +61 (0)3 9342 7000; fax: +61 (0)3 9342 8231. E-mail address: [email protected] (R.A. Mitchell).
Ó 2011 Elsevier Ltd. All rights reserved.
seen, but neither necrosis, nor brain invasion, were evident. These tumour cells were EMA positive but PR, PSA, P504S, CK7 and CAM5.2 negative (Fig. 3). The histological features were those of an atypical meningioma. The Ki-67 index was about 15%. The overall pathological diagnosis was of a metastatic poorly differentiated prostate adenocarcinoma invading into a World Health Organization Grade II atypical meningioma.
2. Discussion We report a patient with a cystic prostate adenocarcinoma metastasis into an atypical meningioma. Intracranial metastases from prostate cancer are rare and represent 1% to 2% of patients with metastatic prostate carcinoma.1,2 Most intracranial prostate metastases are durally based (67%).1,3 The prognosis of intracranial prostate metastases is very poor, with a 1-year survival rate of 18%, and an average survival of 7.6 months.1 A recent retrospective review of 122 patients with intracranial metastases to the dura showed that prostate adenocarcinoma is the second most common primary (17%) after breast carcinoma (34%).4 It is thought that prostate metastases usually occur in a cascade fashion, beginning with bone or lung involvement, leading to secondary seeding of other sites, including the brain. However, where only brain metastases are found, direct haematogenous spread is most likely.5 The tendency of prostate carcinoma to metastasise to the dura has been attributed to venous dissemination through the Batson vertebral plexuses. This is supported by reports of neoplastic emboli in the dural cranial veins.6 However, arterial spread has also been postulated, supported by the association with secondary cutaneous lesions in the territory of the ipsilateral external carotid artery.6 Intracranial dural metastases, including those from the prostate, can be mistaken for meningioma. This is in part because they often present as an isolated meningeal mass.6,7 Distinguishing between these two lesions is important particularly given the poor prognosis of intracranial metastatic prostate disease, and differentiating them radiologically can be particularly difficult in patients with a single lesion, as up to 44% of such prostate metastases have a dural tail.4 A review of the literature showed that of metastases to the dura that simulate meningioma, prostate is the most common primary cancer (17 out of 29 cases).6
1724
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1723–1725
Fig. 1. Sagittal pre-operative brain CT scan showing a haemorrhagic enhancing lesion with fluid levels superior to the hypoplastic corpus callosal body extending to either side of the falx, and a further ring enhancing lesion to the left of this with associated vasogenic oedema.
Fig. 2. Pre-operative brain MRI (a) axial fluid attenuated inversion recovery (FLAIR) and (b) coronal showing a complex cystic mass demonstrating lateral cystic components and a solid central portion with mild to moderate contrast enhancement.
Fig. 3. Haematoxylin and eosin stained sections showing: (a) (top right) prostatic adenocarcinoma and (bottom left) atypical meningioma (40); (b) a prostatic adenocarcinoma forming solid areas (200); and (c) atypical meningioma with focal whirling (200). (d) Immunohistopathology showing: (left) positive P504 staining in the prostatic carcinoma and (right) no staining in the meningioma (100) (The figure is available in colour ar www.sciencedirect.com).
1725
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1725–1728
We could not find a previous report in the literature of a prostate carcinoma metastasising to an atypical meningioma, as occurred in this patient. Given the propensity of prostate metastases to be durally based, at times with a dural tail on neuroimaging, the investigative challenges of the presented patient are considerable, requiring a definitive tissue diagnosis. Moreover, prostate metastases to meningioma have been rarely described,8,9 adding to the diagnostic difficulty. References
Fig. 4. Post-operative axial fluid attenuated inversion recovery (FLAIR) brain MRI showing that total macroscopic excision had been achieved.
1. Benjamin R. Neurologic complications of prostate cancer. Am Fam Physician 2002;65:1834–40. 2. Tremont-Lukats IW, Bobustuc G, Lagos GK, et al. Brain metastasis from prostate carcinoma. Cancer 2003;98:363–8. 3. Tsai V, Kim S, Clatterbuck RE, et al. Cystic prostate metastases to the brain parenchyma: report of two cases and review of the literature. J Neurooncol 2001;51:167–73. 4. Nayak L, Abrey LE, Iwamoto FM. Intracranial dural metastases. Cancer 2009;115:1947–53. 5. Behrens B, Husain MM, Schmidley JW. Cystic solitary intracerebral metastasis from prostate adenocarcinoma. Neuroradiology 2001;43:162–4. 6. Tagle P, Villanueva P, Torreabla G, et al. Intracranial metastasis or meningioma? An uncommon clinical diagnostic dilemma. Surg Neurol 2002;58:241–5. 7. Lath CO, Khanna PC, Gadewar S, et al. Intracranial metastasis from prostatic adenocarcinoma simulating a meningioma. Australas Radiol 2005;49:497–500. 8. Doering L. Metastasis of carcinoma of prostate to meningioma. Virchows Archiv – A Pathol Anat Histol 1975;366:87–91. 9. Bernstein RA, Grumet KA, Wetzel N. Metastasis of prostatic carcinoma to intracranial meningioma. J Neurosurg 1983;53:774–7.
doi:10.1016/j.jocn.2011.03.019
Reversible cerebral vasoconstriction following carotid endarterectomy Teddy Y. Wu a, Richard W. Frith b, P. Alan Barber c,⇑ a b c
Department of Neurology, Christchurch Hospital, Christchurch, New Zealand Department of Neurology, Auckland City Hospital, Auckland, New Zealand Department of Medicine, Faculty of Medicine and Health Sciences, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
a r t i c l e
i n f o
Article history: Received 17 February 2011 Accepted 25 March 2011
a b s t r a c t Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by the triad of severe ‘‘thunderclap’’ headaches, neurological symptoms and transient segmental cerebral arterial vasoconstriction. We report a patient with RCVS following carotid endarterectomy and review the literature on RCVS following carotid revascularisation.
Keywords: Carotid endarterectomy Headache Reversible vasoconstriction syndrome Stroke Vasospasm
1. Introduction Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by the triad of severe ‘‘thunderclap’’ headaches, neurological symptoms and transient segmental cerebral arterial vasoconstriction.1 RCVS has been described in patients of all ages but most commonly occurs in the fifth decade of life and has a female preponderance.1,2 The pathophysiology of RCVS remains unknown but is thought likely to be due to a transient disturbance of
Ó 2011 Elsevier Ltd. All rights reserved.
cerebral vascular autoregulation leading to segmental and multifocal arterial constriction and dilatation.2 Primary RCVS can occur without any clear precipitant but may also be secondary; due to recent use of a vasoactive substance, pheochromocytoma, or occuring in the postpartum period.1,2 We report a patient with RCVS following carotid endarterectomy (CEA) and review the literature on RCVS following carotid revascularisation.
2. Case report ⇑ Corresponding author. Tel.: +64 9 307 4949; fax: +64 9 375 4309. E-mail addresses: [email protected], [email protected] (P.A. Barber).
A 58-year-old woman underwent an elective right CEA for asymptomatic 95% internal carotid artery (ICA) stenosis. She was
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1723–1725
Metastatic prostate adenocarcinoma invading an atypical meningioma R.A. Mitchell a,⇑, J. Dimou a,b, A. Tsui c, B. Kavar a a
Department of Neurosurgery, The Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia Department of Surgery, Royal Melbourne and Western Hospitals, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Parkville, Victoria, Australia c Department of Pathology, The Royal Melbourne Hospital, Parkville, Victoria, Australia b
a r t i c l e
i n f o
Article history: Received 7 March 2011 Accepted 15 March 2011
Keywords: Atypical meningioma Dural based metastasis Meningioma Prostate adenocarcinoma Tumour-to-tumour phenomenon
a b s t r a c t Although prostate adenocarcinoma is the most commonly diagnosed cancer in men, intracranial metastases are rare. We describe a 72-year-old patient with known metastatic prostate cancer, presenting with a dural-based parafalcine lesion on radiological imaging, following a seizure. Total macroscopic excision of the lesion was achieved at surgery, with histopathology confirming prostate adenocarcinoma embedded in an atypical (World Health Organization Grade II) meningioma, fulfilling all the criteria for true tumour-to-tumour metastasis. To our knowledge, this is the first report of prostate cancer metastasising to an atypical meningioma.
1. Case Report A 72-year-old man presented to hospital after an episode of conscious collapse, which was followed by a seizure. Post-ictally, he was noted to have a transient right hemiparesis, and deterioration in cognition with short-term memory loss and slight slowing of his speech. Past medical history was significant for prostate adenocarcinoma with known lung metastases, treated with radio- and hormone therapy. Physical examination revealed no focal neurological deficit. His CT scan showed a haemorrhagic enhancing lesion with fluid levels superior to the hypoplastic corpus callosal body extending to either side of the falx, and a further ring enhancing lesion to the left of this with associated vasogenic oedema (Fig. 1). MRI further characterised this complex cystic mass demonstrating lateral cystic components and a solid central portion with mild to moderate contrast enhancement (Fig. 2). The patient underwent a frontal craniotomy and excision of this falcine tumour, using an interhemispheric approach. The tumour was noted to be heterogeneous with solid, cystic, and haemorrhagic components. Although it did have a capsule, it was very adherent to the cortex. Total macroscopic excision was achieved (Fig. 4). Subsequently the patient underwent adjuvant localised radiation therapy with 36 Gy in 12 fractions and chemotherapy with docetaxel and zoledronic acid. 1.1. Neuropathological findings The tumour sections showed a malignant epithelioid tumour with invasion of the dura and areas of central necrosis, enlarged pleomorphic nuclei, prominent nucleoli, pale eosinophilic to foamy cytoplasm, and lympho–vascular invasion in the dura (Fig. 3). The tumour cells were positive for prostate specific antigen (PSA), alpha-methylacyl-CoA racemase (P504S), anticytokeratin CAM5.2, cytokeratin (CK)7 and epithelial membrane antigen (EMA), in keeping with a metastatic poorly differentiated adenocarcinoma from the prostate (Fig. 3). The Gleason score was 10. There was also a small amount of tumour which formed whorls, with enlarged nuclei and prominent nucleoli, and the cytoplasm was less foamy. Up to 16 mitoses per 10 high power fields were ⇑ Corresponding author. Tel.: +61 (0)3 9342 7000; fax: +61 (0)3 9342 8231. E-mail address: [email protected] (R.A. Mitchell).
Ó 2011 Elsevier Ltd. All rights reserved.
seen, but neither necrosis, nor brain invasion, were evident. These tumour cells were EMA positive but PR, PSA, P504S, CK7 and CAM5.2 negative (Fig. 3). The histological features were those of an atypical meningioma. The Ki-67 index was about 15%. The overall pathological diagnosis was of a metastatic poorly differentiated prostate adenocarcinoma invading into a World Health Organization Grade II atypical meningioma.
2. Discussion We report a patient with a cystic prostate adenocarcinoma metastasis into an atypical meningioma. Intracranial metastases from prostate cancer are rare and represent 1% to 2% of patients with metastatic prostate carcinoma.1,2 Most intracranial prostate metastases are durally based (67%).1,3 The prognosis of intracranial prostate metastases is very poor, with a 1-year survival rate of 18%, and an average survival of 7.6 months.1 A recent retrospective review of 122 patients with intracranial metastases to the dura showed that prostate adenocarcinoma is the second most common primary (17%) after breast carcinoma (34%).4 It is thought that prostate metastases usually occur in a cascade fashion, beginning with bone or lung involvement, leading to secondary seeding of other sites, including the brain. However, where only brain metastases are found, direct haematogenous spread is most likely.5 The tendency of prostate carcinoma to metastasise to the dura has been attributed to venous dissemination through the Batson vertebral plexuses. This is supported by reports of neoplastic emboli in the dural cranial veins.6 However, arterial spread has also been postulated, supported by the association with secondary cutaneous lesions in the territory of the ipsilateral external carotid artery.6 Intracranial dural metastases, including those from the prostate, can be mistaken for meningioma. This is in part because they often present as an isolated meningeal mass.6,7 Distinguishing between these two lesions is important particularly given the poor prognosis of intracranial metastatic prostate disease, and differentiating them radiologically can be particularly difficult in patients with a single lesion, as up to 44% of such prostate metastases have a dural tail.4 A review of the literature showed that of metastases to the dura that simulate meningioma, prostate is the most common primary cancer (17 out of 29 cases).6
1724
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1723–1725
Fig. 1. Sagittal pre-operative brain CT scan showing a haemorrhagic enhancing lesion with fluid levels superior to the hypoplastic corpus callosal body extending to either side of the falx, and a further ring enhancing lesion to the left of this with associated vasogenic oedema.
Fig. 2. Pre-operative brain MRI (a) axial fluid attenuated inversion recovery (FLAIR) and (b) coronal showing a complex cystic mass demonstrating lateral cystic components and a solid central portion with mild to moderate contrast enhancement.
Fig. 3. Haematoxylin and eosin stained sections showing: (a) (top right) prostatic adenocarcinoma and (bottom left) atypical meningioma (40); (b) a prostatic adenocarcinoma forming solid areas (200); and (c) atypical meningioma with focal whirling (200). (d) Immunohistopathology showing: (left) positive P504 staining in the prostatic carcinoma and (right) no staining in the meningioma (100) (The figure is available in colour ar www.sciencedirect.com).
1725
Case Reports / Journal of Clinical Neuroscience 18 (2011) 1725–1728
We could not find a previous report in the literature of a prostate carcinoma metastasising to an atypical meningioma, as occurred in this patient. Given the propensity of prostate metastases to be durally based, at times with a dural tail on neuroimaging, the investigative challenges of the presented patient are considerable, requiring a definitive tissue diagnosis. Moreover, prostate metastases to meningioma have been rarely described,8,9 adding to the diagnostic difficulty. References
Fig. 4. Post-operative axial fluid attenuated inversion recovery (FLAIR) brain MRI showing that total macroscopic excision had been achieved.
1. Benjamin R. Neurologic complications of prostate cancer. Am Fam Physician 2002;65:1834–40. 2. Tremont-Lukats IW, Bobustuc G, Lagos GK, et al. Brain metastasis from prostate carcinoma. Cancer 2003;98:363–8. 3. Tsai V, Kim S, Clatterbuck RE, et al. Cystic prostate metastases to the brain parenchyma: report of two cases and review of the literature. J Neurooncol 2001;51:167–73. 4. Nayak L, Abrey LE, Iwamoto FM. Intracranial dural metastases. Cancer 2009;115:1947–53. 5. Behrens B, Husain MM, Schmidley JW. Cystic solitary intracerebral metastasis from prostate adenocarcinoma. Neuroradiology 2001;43:162–4. 6. Tagle P, Villanueva P, Torreabla G, et al. Intracranial metastasis or meningioma? An uncommon clinical diagnostic dilemma. Surg Neurol 2002;58:241–5. 7. Lath CO, Khanna PC, Gadewar S, et al. Intracranial metastasis from prostatic adenocarcinoma simulating a meningioma. Australas Radiol 2005;49:497–500. 8. Doering L. Metastasis of carcinoma of prostate to meningioma. Virchows Archiv – A Pathol Anat Histol 1975;366:87–91. 9. Bernstein RA, Grumet KA, Wetzel N. Metastasis of prostatic carcinoma to intracranial meningioma. J Neurosurg 1983;53:774–7.
doi:10.1016/j.jocn.2011.03.019
Reversible cerebral vasoconstriction following carotid endarterectomy Teddy Y. Wu a, Richard W. Frith b, P. Alan Barber c,⇑ a b c
Department of Neurology, Christchurch Hospital, Christchurch, New Zealand Department of Neurology, Auckland City Hospital, Auckland, New Zealand Department of Medicine, Faculty of Medicine and Health Sciences, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
a r t i c l e
i n f o
Article history: Received 17 February 2011 Accepted 25 March 2011
a b s t r a c t Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by the triad of severe ‘‘thunderclap’’ headaches, neurological symptoms and transient segmental cerebral arterial vasoconstriction. We report a patient with RCVS following carotid endarterectomy and review the literature on RCVS following carotid revascularisation.
Keywords: Carotid endarterectomy Headache Reversible vasoconstriction syndrome Stroke Vasospasm
1. Introduction Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by the triad of severe ‘‘thunderclap’’ headaches, neurological symptoms and transient segmental cerebral arterial vasoconstriction.1 RCVS has been described in patients of all ages but most commonly occurs in the fifth decade of life and has a female preponderance.1,2 The pathophysiology of RCVS remains unknown but is thought likely to be due to a transient disturbance of
Ó 2011 Elsevier Ltd. All rights reserved.
cerebral vascular autoregulation leading to segmental and multifocal arterial constriction and dilatation.2 Primary RCVS can occur without any clear precipitant but may also be secondary; due to recent use of a vasoactive substance, pheochromocytoma, or occuring in the postpartum period.1,2 We report a patient with RCVS following carotid endarterectomy (CEA) and review the literature on RCVS following carotid revascularisation.
2. Case report ⇑ Corresponding author. Tel.: +64 9 307 4949; fax: +64 9 375 4309. E-mail addresses: [email protected], [email protected] (P.A. Barber).
A 58-year-old woman underwent an elective right CEA for asymptomatic 95% internal carotid artery (ICA) stenosis. She was