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Basal Ganglia Location of Subependymal Giant Cell Astrocytomas in Two Infants
Basal Ganglia Location of Subependymal Giant Cell Astrocytomas in Two Infants Ug˘ur Isxık, MD*, Alp Dinc¸er, MD†, ¨ zek, MD§ Aydın Sav, MD‡, and Memet M. O Subependymal giant cell astrocytomas are benign tumors that constitute one of the primary features of tuberous sclerosis. Two infants with tuberous sclerosis had very unusual subependymal giant cell astrocytomas, confirmed on biopsy in one of the infants. In both cases, contrast-enhanced cranial magnetic resonance imaging suggested a calcified intra-axial mass with diffuse basal ganglia involvement extending into the lateral ventricle. Computed tomography confirmed calcification in both cases. The first patient had right temporal lobectomy for intractable epilepsy. Biopsy of the basal ganglia lesion in that case suggested subependymal giant cell astrocytoma. In infants, subependymal giant cell astrocytomas can present with unusual morphology and may feature diffuse basal ganglia involvement and severe calcification. Ó 2010 by Elsevier Inc. All rights reserved. ¨ zek MM. Basal ganglia location Isxık U, Dinc¸er A, Sav A, O of subependymal giant cell astrocytomas in two infants. Pediatr Neurol 2010;42:157-159.
Introduction Subependymal giant cell astrocytomas are rare brain tumors that typically occur in the walls of the lateral ventricles and tend to cause unilateral hydrocephalus by obstructing the foramen of Monro [1]. Most of these tumors are diag-
From the *Department of Pediatrics, Division of Pediatric Neurology, † Department of Radiology, and ‡Department of Pathology, Acibadem University, Istanbul, Turkey; and §Department of Neurosurgery, Division of Pediatric Neurosurgery, Marmara University, Istanbul, Turkey.
Ó 2010 by Elsevier Inc. All rights reserved. doi:10.1016/j.pediatrneurol.2009.09.008 0887-8994/10/$—see front matter
nosed in the first or second decade of life. Only a few cases have been reported of subependymal giant cell astrocytomas with intra-axial extension [2,3]. Presented here are the cases of two infants with such tumors. Both were very large calcified lesions affecting the basal ganglia with unusual appearance on magnetic resonance imaging.
Case Reports Case 1 A 13-month-old girl presented with infantile spasms that had started at 1 month of age. Video electroencephalographic monitoring indicated that the spasms were triggered by right temporal neocortical seizures. Magnetic resonance imaging at 11 months had revealed a large basal ganglia lesion with calcification. This was confirmed with unenhanced computed tomography of the brain. The cranial magnetic resonance imaging revealed multiple tubers and subependymal nodules (Fig 1A). There was no enhancement of the brain lesion with intravenous contrast. The patient also had hypopigmented skin lesions and a cardiac rhabdomyoma. Ophthalmologic examination and abdominal ultrasound revealed no abnormalities. The patient had right temporal lobe resection with electrocorticography, and a biopsy of the large basal ganglia lesion was obtained. Her seizure frequency decreased by more than 90% after the surgery. In terms of pathologic and immunohistochemical findings, the sample was well circumscribed and heavily calcified, and the tumor cells encompassed a broad spectrum of astroglial phenotypes. The major characteristic findings included polygonal cells with abundant glassy cytoplasm and very uniform small cells set in a fibrillary background. Most of the nuclei had a fine granular chromatin pattern and distinctive nucleoli (Fig 1B). There was no evidence of mitosis, necrosis, or vascular endothelial proliferation; no mast cells were observed. Patchy areas of lymphocytic infiltration were detected. The tumor featured extensive microcalcifications. Occasional tumor cells were binucleate or multinucleate and phenotypically resembled neurons. The tissue was processed for conventional histologic examination with formalin fixation followed by paraffin embedding. Gomori silver impregnation revealed no reticulin framework. Immunohistochemical staining was performed using the streptavidin–biotin complex technique with the following antibodies: glial fibrillary acidic protein (GFAP; BioGenex, San Ramon, CA), S-100 protein (BioGenex), chromogranin (BioGenex), synaptophysin (BioGenex), neurofilament protein (70,160,200 kD; DakoCytomation, Glostrup, Denmark; Carpinteria, CA), desmin (Novocastra, Newcastle Upon Tyne, UK), smooth muscle actin (Novocastra), Ki-67 (BioGenex), and p53 (ScyTek, Logan, UT). The tumor cells exhibited variable immunoreactivity with GFAP (Fig 1C) and S-100 protein, and no reactivity with synaptophysin, chromogranin, desmin, or actin. Focal areas of tumor tissue indicated mild reaction with neurofilament protein. The proliferative index, as measured with Ki-67 (MIB-1), was 1%. There was no reactivity with mutant p53 protein. Based on the combined morphologic and immunohistochemical findings, the histopathologic diagnosis was subependymal giant cell astrocytoma.
Communications should be addressed to: _ ¨ nu¨ Cad. Okur Sok; No:20 Dr. Is xık; Kozyatag˘ı Acıbadem Hastanesi; Ino Kozyatag˘ı, Istanbul 34742, Turkey. E-mail: [email protected] Received May 13, 2009; accepted September 8, 2009.
Is xık et al: SEGA in Basal Ganglia 157
Figure 1. Case 1, a 13-month-old girl with subependymal giant cell astrocytoma. (A) T1-weighted magnetic resonance imaging without contrast administration reveals a hyperintense lesion involving the basal ganglia diffusely, as well as severe dysplasia of the cortex overlying the basal ganglia and multiple tubers. (B) The mass contained polygonal tumor cells with abundant cytoplasm, as well as scattered microcalcifications and diffuse lymphocytes. Hematoxylin and eosin stain. Original magnification 200) (C) Most of the tumor cells reacted with glial fibrillary acidic protein. Streptavidin-biotin complex. Original magnification 200.
Case 2 A 7-month-old boy had started having seizures at 2 months of age. The seizures were characterized by bilateral arm and eyelid clonus. Video electroencephalographic monitoring indicated that the seizures started in the right temporoparietal area. The magnetic resonance imaging findings were similar to those observed in Case 1, namely, a large basal ganglia lesion that did not enhance with contrast (Fig 2). Cranial computed tomography revealed a hyperdense lesion in the right basal ganglia, suggesting calcification. Wood’s lamp examination revealed two hypopigmented lesions, but ophthalmologic examination, cardiac examinations (both echocardiography and electrocardiography), and abdominal ultrasound revealed no abnormalities. The patient had genetic testing for tuberous sclerosis and this demonstrated a nonsense mutation, p.Arg228X, confirming the diagnosis of tuberous sclerosis with the TSC1 gene. He was initially started on valproic acid, but it did not control the seizures and the regimen was changed to a combination of vigabatrin and oxcarbazepine. As of writing, after 1 year of treatment the patient was having rare seizures.
can trigger them [10,11]. In some children with infantile spasms, cortical lesions can induce both partial seizures and spasms [12,13]. The prevalence of partial seizures in cases of infantile spasms is 31% [13,14]. The patient in case 1 had not only a large basal ganglia tumor, but also an overlying cortical malformation. Once this lesion was removed, the frequency of seizures decreased. It is not clear to what extent the basal ganglia tumor contributed to this child’s seizures. To date, there have been very few reports of subependymal giant cell astrocytomas involving brain parenchyma, and no clear explanation has been presented for the
Discussion Subependymal giant cell astrocytomas are benign tumors and one of the primary features of tuberous sclerosis. These neoplasms account for 1.5% of all pediatric brain tumors [4]. The typical magnetic resonance imaging findings for subependymal giant cell astrocytoma are hyperintensity on T2-weighted images and hypointensity on T1-weighted images. Most of these tumors display extensive enhancement with contrast administration. Most subependymal giant cell astrocytomas arise adjacent to the foramen of Monro, with heterogeneous calcification that can cause obstruction. Subependymal giant cell astrocytomas not associated with tuberous sclerosis have been described in atypical locations [2,3]. In the present two cases of basal ganglia subependymal giant cell astrocytoma, the patients had developed seizures at very early ages: case 1 at 1 month and case 2 at 2 months. It is likely that both patients had congenital subependymal giant cell astrocytomas. Neonatal subependymal giant cell astrocytomas are very rare, with fewer than 20 cases reported in the literature to date [5-9]. In case 1, the patient presented with infantile spasms. Tumors rarely cause such spasms, but basal ganglia tumors
158 PEDIATRIC NEUROLOGY Vol. 42 No. 2
Figure 2. Case 2, a 7-month-old boy with subependymal giant cell astrocytoma. T1-weighted axial magnetic resonance image shows a large mass involving the right basal ganglia. The lesion is hyperintense, with some heterogeneity.
extension of these tumors [2,3]. Hon et al. [3] reported a case of subependymal giant cell astrocytoma not associated with tuberous sclerosis that featured parenchymal involvement. Mirkin et al. [6] identified a subependymal giant cell astrocytoma on prenatal ultrasound, and magnetic resonance imaging of this lesion identified it in the foramen of Monro and exhibiting mass effect. Oikawa et al. [2] also described a huge subependymal giant cell astrocytoma with parenchymal involvement. None of these cases, however, featured extensive basal ganglia involvement with severe calcification, as observed in the present two cases. The differential diagnosis for subependymal giant cell astrocytoma includes infiltrating gliomas with trapped neurons, gangliocytoma, ganglioglioma, and desmoplastic ganglioglioma. Presence of pink cytoplasm, cell processes, and frequent GFAP and S-100 positivity are also features of gemistocytic astrocytoma, but those lesions are diffuse and intra-axial and not well delineated, exophytic, or intraventricular. Morphologically, neoplastic gemistocytic astrocytes are usually smaller than those observed in subependymal giant cell astrocytomas and are diffusely distributed, rather than being arranged in a pattern [15]. Another tumor that should be considered is desmoplastic infantile ganglioglioma. These neoplasms are typically located superficially in the brain and have cystic architecture and a firm desmoplastic component. They contain GFAP-positive astrocytes that are part of such a distinctive constellation that, if ganglion cells are identified, no other diagnosis is possible. In the present patients, there was no evidence of desmoplasia and neither desmin nor actin was detected. Based on these findings, all neuronal tumors in the differential diagnosis were excluded [16,17]. Subependymal giant cell astrocytomas are typically found near the foramen of Monro, but can also arise in unusual locations. In infants, these tumors can present with very unusual morphology and may feature diffuse basal ganglia involvement and severe calcification. References [1] McLendon RE, Tien RD. Tuberous sclerosis (Bourneville’s disease). In: Bigner DD, McLendon RE, Bruner JM, editors. Russell and Ru-
binstein’s pathology of tumors of the nervous system. Vol. 1. 6th ed. London: Arnold; New York: Oxford University Press, 1998:353-6. [2] Oikawa S, Sakamato K, Kobayashi N. A neonatal huge giant cell astrocytoma: case report. Neurosurgery 1994;35:748-50. [3] Hon SF, Wong GKC, Zhu XL, Ng HK, Sin NC, Poon WS. Surgical treatment of a neonate with refractory seizures secondary to congenital giant cell astrocytoma: case report and literature review. Hong Kong Med J 2006;12:222-4. [4] Shepherd CW, Scheithauer BW, Gomez MR, Altermatt HJ, Katzmann JA. Subependymal giant cell astrocytoma: a clinical, pathological and flow cytometric study. Neurosurgery 1991;28:864-8. [5] Raju GP, Urion DK, Sahin M. Neonatal subependymal giant cell astrocytoma: new case and review of literature. Pediatr Neurol 2007;36: 128-31. [6] Mirkin LD, Ey EH, Chaparro M. Congenital subependymal giantcell astrocytoma: case report with prenatal ultrasonogram. Pediatr Radiol 1999;29:776-80. [7] Medhkour A, Traul D, Husain M. Neonatal subependymal giant cell astrocytoma. Pediatr Neurosurg 2002;36:271-4. [8] Painter MJ, Pang D, Ahdab-Barmada M, Bergman I. Connatal brain tumors in patients with tuberous sclerosis. Neurosurgery 1984;14: 570-3. [9] Hahn JS, Bejar R, Gladson CL. Neonatal subependymal giant cell astrocytoma associated with tuberous sclerosis: MRI, CT, and ultrasound correlation. Neurology 1991;41:124-8. [10] RamachandranNair R, Ochi A, Akiyama T, et al. Partial seizures triggering infantile spasms in the presence of a basal ganglia glioma. Epileptic Disord 2005;7:378-82. [11] Gastaut H, Gastaut JL, Regis H, et al. Computerized tomography in the study of West’s syndrome. Dev Med Child Neurol 1978; 20:21-7. [12] Yamamoto N, Watanabe K, Negoro T, et al. Partial seizures evolving to infantile spasms. Epilepsia 1988;29:34-40. [13] Ohtsuka Y, Murashima I, Asano T, Oka E, Ohtahara S. Partial seizures in West syndrome. Epilepsia 1996;37:1060-7. [14] Donat JF, Wright FS. Simultaneous infantile spasms and partial seizures. J Child Neurol 1991;6:246-50. [15] Hirose T, Scheithauer BW, Lopes MB, et al. Tuber and subependymal giant cell astrocytoma associated with tuberous sclerosis: an immunohistochemical, ultrastructural, and immunoelectron and microscopic study. Acta Neuropathol 1995;90:387-99. [16] Sharma M, Ralte A, Arora R, Santosh V, Shankar SK, Sarkar C. Subependymal giant cell astrocytoma: a clinicopathological study of 23 cases with special emphasis on proliferative markers and expression of p53 and retinoblastoma gene proteins. Pathology 2004;36:139-44. [17] Burger PC, Scheithauer BW. Tumors of the central nervous system. AFIP atlas of tumor pathology. 4th series, fascicle 7. Washington, DC: American Registry of Pathology in collaboration with the Armed Forces Institute of Pathology, 2007:114-8.
Is xık et al: SEGA in Basal Ganglia 159
Introduction Subependymal giant cell astrocytomas are rare brain tumors that typically occur in the walls of the lateral ventricles and tend to cause unilateral hydrocephalus by obstructing the foramen of Monro [1]. Most of these tumors are diag-
From the *Department of Pediatrics, Division of Pediatric Neurology, † Department of Radiology, and ‡Department of Pathology, Acibadem University, Istanbul, Turkey; and §Department of Neurosurgery, Division of Pediatric Neurosurgery, Marmara University, Istanbul, Turkey.
Ó 2010 by Elsevier Inc. All rights reserved. doi:10.1016/j.pediatrneurol.2009.09.008 0887-8994/10/$—see front matter
nosed in the first or second decade of life. Only a few cases have been reported of subependymal giant cell astrocytomas with intra-axial extension [2,3]. Presented here are the cases of two infants with such tumors. Both were very large calcified lesions affecting the basal ganglia with unusual appearance on magnetic resonance imaging.
Case Reports Case 1 A 13-month-old girl presented with infantile spasms that had started at 1 month of age. Video electroencephalographic monitoring indicated that the spasms were triggered by right temporal neocortical seizures. Magnetic resonance imaging at 11 months had revealed a large basal ganglia lesion with calcification. This was confirmed with unenhanced computed tomography of the brain. The cranial magnetic resonance imaging revealed multiple tubers and subependymal nodules (Fig 1A). There was no enhancement of the brain lesion with intravenous contrast. The patient also had hypopigmented skin lesions and a cardiac rhabdomyoma. Ophthalmologic examination and abdominal ultrasound revealed no abnormalities. The patient had right temporal lobe resection with electrocorticography, and a biopsy of the large basal ganglia lesion was obtained. Her seizure frequency decreased by more than 90% after the surgery. In terms of pathologic and immunohistochemical findings, the sample was well circumscribed and heavily calcified, and the tumor cells encompassed a broad spectrum of astroglial phenotypes. The major characteristic findings included polygonal cells with abundant glassy cytoplasm and very uniform small cells set in a fibrillary background. Most of the nuclei had a fine granular chromatin pattern and distinctive nucleoli (Fig 1B). There was no evidence of mitosis, necrosis, or vascular endothelial proliferation; no mast cells were observed. Patchy areas of lymphocytic infiltration were detected. The tumor featured extensive microcalcifications. Occasional tumor cells were binucleate or multinucleate and phenotypically resembled neurons. The tissue was processed for conventional histologic examination with formalin fixation followed by paraffin embedding. Gomori silver impregnation revealed no reticulin framework. Immunohistochemical staining was performed using the streptavidin–biotin complex technique with the following antibodies: glial fibrillary acidic protein (GFAP; BioGenex, San Ramon, CA), S-100 protein (BioGenex), chromogranin (BioGenex), synaptophysin (BioGenex), neurofilament protein (70,160,200 kD; DakoCytomation, Glostrup, Denmark; Carpinteria, CA), desmin (Novocastra, Newcastle Upon Tyne, UK), smooth muscle actin (Novocastra), Ki-67 (BioGenex), and p53 (ScyTek, Logan, UT). The tumor cells exhibited variable immunoreactivity with GFAP (Fig 1C) and S-100 protein, and no reactivity with synaptophysin, chromogranin, desmin, or actin. Focal areas of tumor tissue indicated mild reaction with neurofilament protein. The proliferative index, as measured with Ki-67 (MIB-1), was 1%. There was no reactivity with mutant p53 protein. Based on the combined morphologic and immunohistochemical findings, the histopathologic diagnosis was subependymal giant cell astrocytoma.
Communications should be addressed to: _ ¨ nu¨ Cad. Okur Sok; No:20 Dr. Is xık; Kozyatag˘ı Acıbadem Hastanesi; Ino Kozyatag˘ı, Istanbul 34742, Turkey. E-mail: [email protected] Received May 13, 2009; accepted September 8, 2009.
Is xık et al: SEGA in Basal Ganglia 157
Figure 1. Case 1, a 13-month-old girl with subependymal giant cell astrocytoma. (A) T1-weighted magnetic resonance imaging without contrast administration reveals a hyperintense lesion involving the basal ganglia diffusely, as well as severe dysplasia of the cortex overlying the basal ganglia and multiple tubers. (B) The mass contained polygonal tumor cells with abundant cytoplasm, as well as scattered microcalcifications and diffuse lymphocytes. Hematoxylin and eosin stain. Original magnification 200) (C) Most of the tumor cells reacted with glial fibrillary acidic protein. Streptavidin-biotin complex. Original magnification 200.
Case 2 A 7-month-old boy had started having seizures at 2 months of age. The seizures were characterized by bilateral arm and eyelid clonus. Video electroencephalographic monitoring indicated that the seizures started in the right temporoparietal area. The magnetic resonance imaging findings were similar to those observed in Case 1, namely, a large basal ganglia lesion that did not enhance with contrast (Fig 2). Cranial computed tomography revealed a hyperdense lesion in the right basal ganglia, suggesting calcification. Wood’s lamp examination revealed two hypopigmented lesions, but ophthalmologic examination, cardiac examinations (both echocardiography and electrocardiography), and abdominal ultrasound revealed no abnormalities. The patient had genetic testing for tuberous sclerosis and this demonstrated a nonsense mutation, p.Arg228X, confirming the diagnosis of tuberous sclerosis with the TSC1 gene. He was initially started on valproic acid, but it did not control the seizures and the regimen was changed to a combination of vigabatrin and oxcarbazepine. As of writing, after 1 year of treatment the patient was having rare seizures.
can trigger them [10,11]. In some children with infantile spasms, cortical lesions can induce both partial seizures and spasms [12,13]. The prevalence of partial seizures in cases of infantile spasms is 31% [13,14]. The patient in case 1 had not only a large basal ganglia tumor, but also an overlying cortical malformation. Once this lesion was removed, the frequency of seizures decreased. It is not clear to what extent the basal ganglia tumor contributed to this child’s seizures. To date, there have been very few reports of subependymal giant cell astrocytomas involving brain parenchyma, and no clear explanation has been presented for the
Discussion Subependymal giant cell astrocytomas are benign tumors and one of the primary features of tuberous sclerosis. These neoplasms account for 1.5% of all pediatric brain tumors [4]. The typical magnetic resonance imaging findings for subependymal giant cell astrocytoma are hyperintensity on T2-weighted images and hypointensity on T1-weighted images. Most of these tumors display extensive enhancement with contrast administration. Most subependymal giant cell astrocytomas arise adjacent to the foramen of Monro, with heterogeneous calcification that can cause obstruction. Subependymal giant cell astrocytomas not associated with tuberous sclerosis have been described in atypical locations [2,3]. In the present two cases of basal ganglia subependymal giant cell astrocytoma, the patients had developed seizures at very early ages: case 1 at 1 month and case 2 at 2 months. It is likely that both patients had congenital subependymal giant cell astrocytomas. Neonatal subependymal giant cell astrocytomas are very rare, with fewer than 20 cases reported in the literature to date [5-9]. In case 1, the patient presented with infantile spasms. Tumors rarely cause such spasms, but basal ganglia tumors
158 PEDIATRIC NEUROLOGY Vol. 42 No. 2
Figure 2. Case 2, a 7-month-old boy with subependymal giant cell astrocytoma. T1-weighted axial magnetic resonance image shows a large mass involving the right basal ganglia. The lesion is hyperintense, with some heterogeneity.
extension of these tumors [2,3]. Hon et al. [3] reported a case of subependymal giant cell astrocytoma not associated with tuberous sclerosis that featured parenchymal involvement. Mirkin et al. [6] identified a subependymal giant cell astrocytoma on prenatal ultrasound, and magnetic resonance imaging of this lesion identified it in the foramen of Monro and exhibiting mass effect. Oikawa et al. [2] also described a huge subependymal giant cell astrocytoma with parenchymal involvement. None of these cases, however, featured extensive basal ganglia involvement with severe calcification, as observed in the present two cases. The differential diagnosis for subependymal giant cell astrocytoma includes infiltrating gliomas with trapped neurons, gangliocytoma, ganglioglioma, and desmoplastic ganglioglioma. Presence of pink cytoplasm, cell processes, and frequent GFAP and S-100 positivity are also features of gemistocytic astrocytoma, but those lesions are diffuse and intra-axial and not well delineated, exophytic, or intraventricular. Morphologically, neoplastic gemistocytic astrocytes are usually smaller than those observed in subependymal giant cell astrocytomas and are diffusely distributed, rather than being arranged in a pattern [15]. Another tumor that should be considered is desmoplastic infantile ganglioglioma. These neoplasms are typically located superficially in the brain and have cystic architecture and a firm desmoplastic component. They contain GFAP-positive astrocytes that are part of such a distinctive constellation that, if ganglion cells are identified, no other diagnosis is possible. In the present patients, there was no evidence of desmoplasia and neither desmin nor actin was detected. Based on these findings, all neuronal tumors in the differential diagnosis were excluded [16,17]. Subependymal giant cell astrocytomas are typically found near the foramen of Monro, but can also arise in unusual locations. In infants, these tumors can present with very unusual morphology and may feature diffuse basal ganglia involvement and severe calcification. References [1] McLendon RE, Tien RD. Tuberous sclerosis (Bourneville’s disease). In: Bigner DD, McLendon RE, Bruner JM, editors. Russell and Ru-
binstein’s pathology of tumors of the nervous system. Vol. 1. 6th ed. London: Arnold; New York: Oxford University Press, 1998:353-6. [2] Oikawa S, Sakamato K, Kobayashi N. A neonatal huge giant cell astrocytoma: case report. Neurosurgery 1994;35:748-50. [3] Hon SF, Wong GKC, Zhu XL, Ng HK, Sin NC, Poon WS. Surgical treatment of a neonate with refractory seizures secondary to congenital giant cell astrocytoma: case report and literature review. Hong Kong Med J 2006;12:222-4. [4] Shepherd CW, Scheithauer BW, Gomez MR, Altermatt HJ, Katzmann JA. Subependymal giant cell astrocytoma: a clinical, pathological and flow cytometric study. Neurosurgery 1991;28:864-8. [5] Raju GP, Urion DK, Sahin M. Neonatal subependymal giant cell astrocytoma: new case and review of literature. Pediatr Neurol 2007;36: 128-31. [6] Mirkin LD, Ey EH, Chaparro M. Congenital subependymal giantcell astrocytoma: case report with prenatal ultrasonogram. Pediatr Radiol 1999;29:776-80. [7] Medhkour A, Traul D, Husain M. Neonatal subependymal giant cell astrocytoma. Pediatr Neurosurg 2002;36:271-4. [8] Painter MJ, Pang D, Ahdab-Barmada M, Bergman I. Connatal brain tumors in patients with tuberous sclerosis. Neurosurgery 1984;14: 570-3. [9] Hahn JS, Bejar R, Gladson CL. Neonatal subependymal giant cell astrocytoma associated with tuberous sclerosis: MRI, CT, and ultrasound correlation. Neurology 1991;41:124-8. [10] RamachandranNair R, Ochi A, Akiyama T, et al. Partial seizures triggering infantile spasms in the presence of a basal ganglia glioma. Epileptic Disord 2005;7:378-82. [11] Gastaut H, Gastaut JL, Regis H, et al. Computerized tomography in the study of West’s syndrome. Dev Med Child Neurol 1978; 20:21-7. [12] Yamamoto N, Watanabe K, Negoro T, et al. Partial seizures evolving to infantile spasms. Epilepsia 1988;29:34-40. [13] Ohtsuka Y, Murashima I, Asano T, Oka E, Ohtahara S. Partial seizures in West syndrome. Epilepsia 1996;37:1060-7. [14] Donat JF, Wright FS. Simultaneous infantile spasms and partial seizures. J Child Neurol 1991;6:246-50. [15] Hirose T, Scheithauer BW, Lopes MB, et al. Tuber and subependymal giant cell astrocytoma associated with tuberous sclerosis: an immunohistochemical, ultrastructural, and immunoelectron and microscopic study. Acta Neuropathol 1995;90:387-99. [16] Sharma M, Ralte A, Arora R, Santosh V, Shankar SK, Sarkar C. Subependymal giant cell astrocytoma: a clinicopathological study of 23 cases with special emphasis on proliferative markers and expression of p53 and retinoblastoma gene proteins. Pathology 2004;36:139-44. [17] Burger PC, Scheithauer BW. Tumors of the central nervous system. AFIP atlas of tumor pathology. 4th series, fascicle 7. Washington, DC: American Registry of Pathology in collaboration with the Armed Forces Institute of Pathology, 2007:114-8.
Is xık et al: SEGA in Basal Ganglia 159