- Email: [email protected]
Melanoma of the sellar region
154
Case Reports / Journal of Clinical Neuroscience 18 (2011) 154–156
or atherosclerosis at the aneurysm neck, or an efferent artery originating from the aneurysmal dome, precluding obliteration by clipping or coiling. They can be treated by proximal parent artery ligation or trapping, with or without cerebral revascularization, depending on collateral circulation. Steinberg et al.6 reported complete thrombosis in 87% of patients with giant vertebral artery aneurysms after ipsilateral parent vessel occlusion. Complete thrombosis is usually observed within months after surgery,6 with gradual thrombus retraction causing involution of the GA by progressive fibrosis and reduction of mass effect.7 However, growing mass effect of GA in the posterior circulation, even after complete thrombosis and parent vessel occlusion, has been reported.2 We present this same phenomenon in the anterior circulation. 4. Conclusion Exclusion from flow by Hunterian ligation and thrombosis, with or without high-flow bypass, is generally the recommended approach to management of unclippable GA; however secondary clinical deterioration may occur following aneurysmal thrombosis. Aneurysmal decompression may achieve normal neurological function. We suggest a need for meticulous characterization of these unique aneurysms as a distinct entity, to determine optimum timing for decompression to prevent irreversible neurological damage.
Acknowledgement The authors wish to thank Mrs Shifra Fraifeld for her editorial assistance in the preparation of this manuscript. References 1. Shi ZS, Ziegler J, Duckwiler GR, et al. Management of giant middle cerebral artery aneurysms with incorporated branches: partial endovascular coiling or combined extracranial–intracranial bypass – a team approach. Neurosurgery 2009;65(6 Suppl.):121–31. 2. O’Shaughnessy BA, Getch CC, Bendok BR, et al. Progressive growth of a giant dolichoectatic vertebrobasilar artery aneurysm after complete Hunterian occlusion of the posterior circulation: case report. Neurosurgery 2004;55:1223. 3. de Oliveira JG, Borba LA, Rassi-Neto A, et al. Intracranial aneurysms presenting with mass effect over the anterior optic pathways: neurosurgical management and outcomes. Neurosurg Focus 2009;26:E3. 4. Barrow DL, Cawley CM. Clinical manifestations of giant intracranial aneurysms. In: Awad IA, Barrow DL, editors. Giant intracranial aneurysms. Park Ridge, IL, USA: American Association of Neurological Surgeons; 1995. 5. Whittle IR, Dorsch NW, Besser M. Spontaneous thrombosis in giant intracranial aneurysms. J Neurol Neurosurg Psychiatry 1982;45:1040–7. 6. Steinberg GK, Drake CG, Peerless SJ. Deliberate basilar or vertebral artery occlusion in the treatment of intracranial aneurysms. Immediate results and long-term outcome in 201 patients. J Neurosurg 1993;79:161–73. 7. Strother CM, Eldevik P, Kikuchi Y, et al. Thrombus formation and structure and the evolution of mass effect in intracranial aneurysms treated by balloon embolization: emphasis on MR findings. AJNR Am J Neuroradiol 1989;10:787–96.
doi:10.1016/j.jocn.2010.06.017
Melanoma of the sellar region Y.Y. Wang a,⇑, Andrea Norris b, D. du Plessis c, K.K. Gnanalingham a a
Department of Neurosurgery, Greater Manchester Neurosciences Centre, Salford Royal Foundation Trust (SRFT), Stott Lane, Salford M6 8HD, UK Department of Endocrinology, North Manchester General Hospital, Manchester, UK c Department of Neuropathology, Greater Manchester Neurosciences Centre, Salford Royal Foundation Trust (SRFT), Salford, UK b
a r t i c l e
i n f o
Article history: Received 31 May 2010 Accepted 4 July 2010
Keywords: Metastatic melanoma Pituitary Sellar Trans-sphenoidal
a b s t r a c t Metastatic melanoma has a propensity for multiple intra cranial deposits. Rarely, metastatic melanoma to the pituitary gland has been reported, usually in conjunction with widespread systemic metastases. We describe a patient with metastatic melanoma to the pituitary gland as the first clinical presentation of widespread metastatic disease and review the relevant literature. Ó 2010 Elsevier Ltd. All rights reserved.
1. Introduction Metastatic deposits to the pituitary gland occur in 1% to 3.6% of patients with cancer.1,2 Breast and lung metastases demonstrate the highest affinity for the pituitary gland; however, prostatic, renal, colorectal and thyroid deposits have all been described. Melanoma of the sellar region has been reported rarely and is usually discovered as an autopsy finding or as part of multiple secondary deposits in terminal patients.3–7 We report a patient with a sellar
⇑ Corresponding author. Tel.: +44 0161 206 4340; fax: +44 0161 206 4606. E-mail address: [email protected] (Y.Y. Wang).
melanoma as the first clinical manifestation of a rapidly progressing systemic disease load.
2. Case report A 78-year-old man presented with a 3 month history of postural hypotension, blackouts and weight loss. There was no known oncological history and in particular no history of cutaneous melanoma. He was found to have pituitary (cortisol, thyroid and testosterone) deficiency, with a mild bitemporal hemianopia. There was no evidence of diabetes insipidus (DI). A brain MRI and subsequent specific pituitary scans revealed a sellar and suprasellar lesion, with compression of the optic chiasm. The lesion
Case Reports / Journal of Clinical Neuroscience 18 (2011) 154–156
155
Fig. 1. Pre-operative MRI of a 78-year-old man showing (A–C) coronal and (D) axial views of a dumb-bell shaped sellar and suprasellar lesion with (A) a high signal on T1-weighted and (B) a low signal on T2-weighted images with (C) minimal contrast enhancement. (D) An immediate pre-operative image guidance scan with contrast 8 weeks later also revealed a further lesion in the left frontal lobe.
Fig. 2. A tumour sample showing an infiltrate of heavily pigmented malignant tumour cells with focal necrosis (haematoxylin and eosin stain, original magnification 400). This figure is available in colour at www.sciencedirect.com.
cerebral lesion evident. Trans sphenoidal resection of the lesion was planned. Interestingly, the immediate pre-operative MRI undertaken 8 weeks later for image guidance purposes demonstrated a new lesion within the left frontal lobe (Fig. 1D). At surgery, direct visualisation with the endoscope revealed a heavily pigmented dark-brown lesion within the pituitary gland extending up along the pituitary stalk. A subtotal resection was performed with a small residuum left on the under surface of the optic chiasm. Formal histopathology confirmed the diagnosis of a malignant melanoma with heavy melanin pigmentation and significant cytological atypia (Fig. 2). The patient’s immediate post-operative course was uneventful with discharge home on day 3. A full dermatological screen including formal fundoscopy prior to discharge did not reveal a primary melanoma. A screening CT scan of the chest and abdomen revealed possible liver and splenic lesions and an oncology referral was made for adjuvant treatment. Unfortunately the patient represented 1 week post-discharge with meningitis, a cerebrospinal fluid leak and aspiration pneumonia. Despite intensive medical treatment he failed to improve and was palliated.
3. Discussion demonstrated a high signal on T1-weighted MRI, a low signal on T2-weighted MRI and minimal enhancement, suggestive of haemorrhagic or proteinaceous content (Fig. 1A–C). There was no other
Melanoma metastases to the pituitary gland are rare. To our knowledge there have been only 30 patients reported previ-
156
Case Reports / Journal of Clinical Neuroscience 18 (2011) 154–156
ously.4–11 The majority of these were autopsy findings in the context of disseminated spread; however, there are seven patients where clinical symptoms associated with the pituitary metastasis are described.3,4,6,8 There have also been occasional reports of melanomas originating unequivocally from the leptomeninges of the sellar region.9–12 In the present patient we were unable to identify a primary site of origin of the melanoma despite detailed dermatological and radiological review. We acknowledge that there are reports of primary melanoma of the gastrointestinal system that might not be identified on CT scanning of the abdomen,13 as well as documented regression of cutaneous malignant melanoma.14,15 Further investigations (that is with positron emission tomographs scans and gastrointestinal tract endoscopy) were not possible due to the patient’s clinical deterioration. Metastatic disease to the pituitary gland can be entirely asymptomatic (an autopsy finding) or cause a variety of symptoms including visual disturbance, hypopituitarism and DI.2,11 The higher incidence of DI in patients with pituitary metastases is thought to be related to the preferential deposition to the posterior pituitary, which receives a direct arterial supply rather than the anterior pituitary receiving blood via the portal-hypophyseal system.16 There was no evidence of DI in our patient, although DI has also been apparent in some of the previously reported patients with melanoma of the sellar region. Melanomas are recognised to have a tendency for microhaemorrhages that may have been the cause of the apoplexy-like presenting symptoms in our patient. On MRI, melanin is said to demonstrate high signal on T1weighted and low signal on T2-weighted images relative to the cerebral cortex.17 In reality a varying amount of heterogeneity may be present with melanoma deposits, due to the differential amounts of microhaemorrhages and melanin content within each lesion. Most lesions demonstrated enhancement, although some heterogeneity may again be expected.17,18 Thus, as in the present patient, unless metastatic disease from a known primary elsewhere is suspected, the diagnosis is often made on histological grounds. The prognosis from metastatic melanoma to the sellar region remains generally poor by the time patients present with symptoms attributable to pituitary spread. Average survival from the published clinical cases following diagnosis and treatment is approximately 4 months.3,4,6,8 Trans sphenoidal surgery for establishing the histological diagnosis and tumour debulking is performed in most instances, with post-operative adjuvant radio - and/or chemotherapy. Surgery can also disseminate the disease if the arachnoid layer is breached during the trans sphenoidal approach. In an eldoi:10.1016/j.jocn.2010.07.111
derly patient with widespread metastatic disease and a previous history of metastatic melanoma, consideration could be given to supportive treatment. Metastatic melanoma is becoming increasingly prevalent among Caucasian people.19 With its propensity for systemic spread, it is inevitable that more patients with sellar deposits will be reported. This report emphasises the need to consider metastatic melanoma to the pituitary gland in the differential diagnosis. References 1. Abrams H, Spiro R, Goldstein N. Metastases in carcinoma: analysis of 1000 autopsied cases. Cancer 1950;3:74–85. 2. Fassett DR, Couldwell WT. Metastases to the pituitary gland. Neurosurg Focus 2004;16:E8. 3. Guzel A, Maciaczyk J, Dohmen-Scheufler H, et al. Multiple intracranial melanoma metastases: case report and review of the literature. J Neurooncol 2009;93:413–20. 4. Leung GKK, Chow WS, Tan KCB, et al. Metastatic melanoma of the pituitary gland. Case report. J Neurosurg 2003;99:913–5. 5. Max M, Deck M, Rottenberg D. Pituitary metastasis: incidence in cancer patients and clinical differentiation from pituitary adenoma. Neurology 1981;31:998–1002. 6. McCutcheon IE, Waguespack SG, Fuller GN, et al. Metastatic melanoma to the pituitary gland. Can J Neurol Sci 2007;34:322–7. 7. Kovacs K. Metastatic cancer of the pituitary gland. Oncology 1973;27:533–42. 8. Jung SM, Hsu YY, Chuang CC, et al. A man in his mid-70s with a sellar mass. Brain Pathol 2007;17:115–6. 21. 9. Neilson JM, Moffat AD. Hypopituitarism caused by a melanoma of the pituitary gland. J Clin Pathol 1963;16:144–9. 10. Scholtz CL, Siu K. Melanoma of the pituitary. Case report. J Neurosurg 1976;45:101–3. 11. Rousseau A, Bernier M, Kujas M, et al. Primary intracranial melanocytic tumor simulating pituitary macroadenoma: case report and review of the literature. Neurosurgery 2005;57:E369. 12. Tuttenberg J, Fink W, Back W, et al. A rare primary sellar melanoma. Case report. J Neurosurg 2004;100:931–4. 13. Cox H, Sloan L. Melanoma. Report of a case apparently primary in the jejunum, the presenting symptoms resulting from metastasis in the hypophysis cerebri. J Am Med Assoc 1924;82:2021–5. 14. Avril MF, Charpentier P, Margulis A, et al. Regression of primary melanoma with metastases. Cancer 1992;69:1377–81. 15. Baldo M, Schiavon M, Cicogna PA, et al. Spontaneous regression of subcutaneous metastasis of cutaneous melanoma. Plast Reconstr Surg 1992;90:1073–6. 16. Teears RJ, Silverman EM. Clinicopathologic review of 88 cases of carcinoma metastatic to the pituitary gland. Cancer 1975;36:216–20. 17. Gaviani P, Mullins M, Braga T, et al. Improved detection of metastatic melanome by T2*-weighted imaging. Am J Neuroradiol 2006;27:605–8. 18. Isiklar I, Leeds NE, Fuller GN, et al. Intracranial metastatic melanoma: correlation between MR imaging characteristics and melanin content. AJR Am J Roentgenol 1995;165:1503–12. 19. Daryanani D, Plukker JT, de Jong MA, et al. Increased incidence of brain metastases in cutaneous head and neck melanoma. Melanoma Res 2005;15:119–24.
Case Reports / Journal of Clinical Neuroscience 18 (2011) 154–156
or atherosclerosis at the aneurysm neck, or an efferent artery originating from the aneurysmal dome, precluding obliteration by clipping or coiling. They can be treated by proximal parent artery ligation or trapping, with or without cerebral revascularization, depending on collateral circulation. Steinberg et al.6 reported complete thrombosis in 87% of patients with giant vertebral artery aneurysms after ipsilateral parent vessel occlusion. Complete thrombosis is usually observed within months after surgery,6 with gradual thrombus retraction causing involution of the GA by progressive fibrosis and reduction of mass effect.7 However, growing mass effect of GA in the posterior circulation, even after complete thrombosis and parent vessel occlusion, has been reported.2 We present this same phenomenon in the anterior circulation. 4. Conclusion Exclusion from flow by Hunterian ligation and thrombosis, with or without high-flow bypass, is generally the recommended approach to management of unclippable GA; however secondary clinical deterioration may occur following aneurysmal thrombosis. Aneurysmal decompression may achieve normal neurological function. We suggest a need for meticulous characterization of these unique aneurysms as a distinct entity, to determine optimum timing for decompression to prevent irreversible neurological damage.
Acknowledgement The authors wish to thank Mrs Shifra Fraifeld for her editorial assistance in the preparation of this manuscript. References 1. Shi ZS, Ziegler J, Duckwiler GR, et al. Management of giant middle cerebral artery aneurysms with incorporated branches: partial endovascular coiling or combined extracranial–intracranial bypass – a team approach. Neurosurgery 2009;65(6 Suppl.):121–31. 2. O’Shaughnessy BA, Getch CC, Bendok BR, et al. Progressive growth of a giant dolichoectatic vertebrobasilar artery aneurysm after complete Hunterian occlusion of the posterior circulation: case report. Neurosurgery 2004;55:1223. 3. de Oliveira JG, Borba LA, Rassi-Neto A, et al. Intracranial aneurysms presenting with mass effect over the anterior optic pathways: neurosurgical management and outcomes. Neurosurg Focus 2009;26:E3. 4. Barrow DL, Cawley CM. Clinical manifestations of giant intracranial aneurysms. In: Awad IA, Barrow DL, editors. Giant intracranial aneurysms. Park Ridge, IL, USA: American Association of Neurological Surgeons; 1995. 5. Whittle IR, Dorsch NW, Besser M. Spontaneous thrombosis in giant intracranial aneurysms. J Neurol Neurosurg Psychiatry 1982;45:1040–7. 6. Steinberg GK, Drake CG, Peerless SJ. Deliberate basilar or vertebral artery occlusion in the treatment of intracranial aneurysms. Immediate results and long-term outcome in 201 patients. J Neurosurg 1993;79:161–73. 7. Strother CM, Eldevik P, Kikuchi Y, et al. Thrombus formation and structure and the evolution of mass effect in intracranial aneurysms treated by balloon embolization: emphasis on MR findings. AJNR Am J Neuroradiol 1989;10:787–96.
doi:10.1016/j.jocn.2010.06.017
Melanoma of the sellar region Y.Y. Wang a,⇑, Andrea Norris b, D. du Plessis c, K.K. Gnanalingham a a
Department of Neurosurgery, Greater Manchester Neurosciences Centre, Salford Royal Foundation Trust (SRFT), Stott Lane, Salford M6 8HD, UK Department of Endocrinology, North Manchester General Hospital, Manchester, UK c Department of Neuropathology, Greater Manchester Neurosciences Centre, Salford Royal Foundation Trust (SRFT), Salford, UK b
a r t i c l e
i n f o
Article history: Received 31 May 2010 Accepted 4 July 2010
Keywords: Metastatic melanoma Pituitary Sellar Trans-sphenoidal
a b s t r a c t Metastatic melanoma has a propensity for multiple intra cranial deposits. Rarely, metastatic melanoma to the pituitary gland has been reported, usually in conjunction with widespread systemic metastases. We describe a patient with metastatic melanoma to the pituitary gland as the first clinical presentation of widespread metastatic disease and review the relevant literature. Ó 2010 Elsevier Ltd. All rights reserved.
1. Introduction Metastatic deposits to the pituitary gland occur in 1% to 3.6% of patients with cancer.1,2 Breast and lung metastases demonstrate the highest affinity for the pituitary gland; however, prostatic, renal, colorectal and thyroid deposits have all been described. Melanoma of the sellar region has been reported rarely and is usually discovered as an autopsy finding or as part of multiple secondary deposits in terminal patients.3–7 We report a patient with a sellar
⇑ Corresponding author. Tel.: +44 0161 206 4340; fax: +44 0161 206 4606. E-mail address: [email protected] (Y.Y. Wang).
melanoma as the first clinical manifestation of a rapidly progressing systemic disease load.
2. Case report A 78-year-old man presented with a 3 month history of postural hypotension, blackouts and weight loss. There was no known oncological history and in particular no history of cutaneous melanoma. He was found to have pituitary (cortisol, thyroid and testosterone) deficiency, with a mild bitemporal hemianopia. There was no evidence of diabetes insipidus (DI). A brain MRI and subsequent specific pituitary scans revealed a sellar and suprasellar lesion, with compression of the optic chiasm. The lesion
Case Reports / Journal of Clinical Neuroscience 18 (2011) 154–156
155
Fig. 1. Pre-operative MRI of a 78-year-old man showing (A–C) coronal and (D) axial views of a dumb-bell shaped sellar and suprasellar lesion with (A) a high signal on T1-weighted and (B) a low signal on T2-weighted images with (C) minimal contrast enhancement. (D) An immediate pre-operative image guidance scan with contrast 8 weeks later also revealed a further lesion in the left frontal lobe.
Fig. 2. A tumour sample showing an infiltrate of heavily pigmented malignant tumour cells with focal necrosis (haematoxylin and eosin stain, original magnification 400). This figure is available in colour at www.sciencedirect.com.
cerebral lesion evident. Trans sphenoidal resection of the lesion was planned. Interestingly, the immediate pre-operative MRI undertaken 8 weeks later for image guidance purposes demonstrated a new lesion within the left frontal lobe (Fig. 1D). At surgery, direct visualisation with the endoscope revealed a heavily pigmented dark-brown lesion within the pituitary gland extending up along the pituitary stalk. A subtotal resection was performed with a small residuum left on the under surface of the optic chiasm. Formal histopathology confirmed the diagnosis of a malignant melanoma with heavy melanin pigmentation and significant cytological atypia (Fig. 2). The patient’s immediate post-operative course was uneventful with discharge home on day 3. A full dermatological screen including formal fundoscopy prior to discharge did not reveal a primary melanoma. A screening CT scan of the chest and abdomen revealed possible liver and splenic lesions and an oncology referral was made for adjuvant treatment. Unfortunately the patient represented 1 week post-discharge with meningitis, a cerebrospinal fluid leak and aspiration pneumonia. Despite intensive medical treatment he failed to improve and was palliated.
3. Discussion demonstrated a high signal on T1-weighted MRI, a low signal on T2-weighted MRI and minimal enhancement, suggestive of haemorrhagic or proteinaceous content (Fig. 1A–C). There was no other
Melanoma metastases to the pituitary gland are rare. To our knowledge there have been only 30 patients reported previ-
156
Case Reports / Journal of Clinical Neuroscience 18 (2011) 154–156
ously.4–11 The majority of these were autopsy findings in the context of disseminated spread; however, there are seven patients where clinical symptoms associated with the pituitary metastasis are described.3,4,6,8 There have also been occasional reports of melanomas originating unequivocally from the leptomeninges of the sellar region.9–12 In the present patient we were unable to identify a primary site of origin of the melanoma despite detailed dermatological and radiological review. We acknowledge that there are reports of primary melanoma of the gastrointestinal system that might not be identified on CT scanning of the abdomen,13 as well as documented regression of cutaneous malignant melanoma.14,15 Further investigations (that is with positron emission tomographs scans and gastrointestinal tract endoscopy) were not possible due to the patient’s clinical deterioration. Metastatic disease to the pituitary gland can be entirely asymptomatic (an autopsy finding) or cause a variety of symptoms including visual disturbance, hypopituitarism and DI.2,11 The higher incidence of DI in patients with pituitary metastases is thought to be related to the preferential deposition to the posterior pituitary, which receives a direct arterial supply rather than the anterior pituitary receiving blood via the portal-hypophyseal system.16 There was no evidence of DI in our patient, although DI has also been apparent in some of the previously reported patients with melanoma of the sellar region. Melanomas are recognised to have a tendency for microhaemorrhages that may have been the cause of the apoplexy-like presenting symptoms in our patient. On MRI, melanin is said to demonstrate high signal on T1weighted and low signal on T2-weighted images relative to the cerebral cortex.17 In reality a varying amount of heterogeneity may be present with melanoma deposits, due to the differential amounts of microhaemorrhages and melanin content within each lesion. Most lesions demonstrated enhancement, although some heterogeneity may again be expected.17,18 Thus, as in the present patient, unless metastatic disease from a known primary elsewhere is suspected, the diagnosis is often made on histological grounds. The prognosis from metastatic melanoma to the sellar region remains generally poor by the time patients present with symptoms attributable to pituitary spread. Average survival from the published clinical cases following diagnosis and treatment is approximately 4 months.3,4,6,8 Trans sphenoidal surgery for establishing the histological diagnosis and tumour debulking is performed in most instances, with post-operative adjuvant radio - and/or chemotherapy. Surgery can also disseminate the disease if the arachnoid layer is breached during the trans sphenoidal approach. In an eldoi:10.1016/j.jocn.2010.07.111
derly patient with widespread metastatic disease and a previous history of metastatic melanoma, consideration could be given to supportive treatment. Metastatic melanoma is becoming increasingly prevalent among Caucasian people.19 With its propensity for systemic spread, it is inevitable that more patients with sellar deposits will be reported. This report emphasises the need to consider metastatic melanoma to the pituitary gland in the differential diagnosis. References 1. Abrams H, Spiro R, Goldstein N. Metastases in carcinoma: analysis of 1000 autopsied cases. Cancer 1950;3:74–85. 2. Fassett DR, Couldwell WT. Metastases to the pituitary gland. Neurosurg Focus 2004;16:E8. 3. Guzel A, Maciaczyk J, Dohmen-Scheufler H, et al. Multiple intracranial melanoma metastases: case report and review of the literature. J Neurooncol 2009;93:413–20. 4. Leung GKK, Chow WS, Tan KCB, et al. Metastatic melanoma of the pituitary gland. Case report. J Neurosurg 2003;99:913–5. 5. Max M, Deck M, Rottenberg D. Pituitary metastasis: incidence in cancer patients and clinical differentiation from pituitary adenoma. Neurology 1981;31:998–1002. 6. McCutcheon IE, Waguespack SG, Fuller GN, et al. Metastatic melanoma to the pituitary gland. Can J Neurol Sci 2007;34:322–7. 7. Kovacs K. Metastatic cancer of the pituitary gland. Oncology 1973;27:533–42. 8. Jung SM, Hsu YY, Chuang CC, et al. A man in his mid-70s with a sellar mass. Brain Pathol 2007;17:115–6. 21. 9. Neilson JM, Moffat AD. Hypopituitarism caused by a melanoma of the pituitary gland. J Clin Pathol 1963;16:144–9. 10. Scholtz CL, Siu K. Melanoma of the pituitary. Case report. J Neurosurg 1976;45:101–3. 11. Rousseau A, Bernier M, Kujas M, et al. Primary intracranial melanocytic tumor simulating pituitary macroadenoma: case report and review of the literature. Neurosurgery 2005;57:E369. 12. Tuttenberg J, Fink W, Back W, et al. A rare primary sellar melanoma. Case report. J Neurosurg 2004;100:931–4. 13. Cox H, Sloan L. Melanoma. Report of a case apparently primary in the jejunum, the presenting symptoms resulting from metastasis in the hypophysis cerebri. J Am Med Assoc 1924;82:2021–5. 14. Avril MF, Charpentier P, Margulis A, et al. Regression of primary melanoma with metastases. Cancer 1992;69:1377–81. 15. Baldo M, Schiavon M, Cicogna PA, et al. Spontaneous regression of subcutaneous metastasis of cutaneous melanoma. Plast Reconstr Surg 1992;90:1073–6. 16. Teears RJ, Silverman EM. Clinicopathologic review of 88 cases of carcinoma metastatic to the pituitary gland. Cancer 1975;36:216–20. 17. Gaviani P, Mullins M, Braga T, et al. Improved detection of metastatic melanome by T2*-weighted imaging. Am J Neuroradiol 2006;27:605–8. 18. Isiklar I, Leeds NE, Fuller GN, et al. Intracranial metastatic melanoma: correlation between MR imaging characteristics and melanin content. AJR Am J Roentgenol 1995;165:1503–12. 19. Daryanani D, Plukker JT, de Jong MA, et al. Increased incidence of brain metastases in cutaneous head and neck melanoma. Melanoma Res 2005;15:119–24.