Child's Nerv Syst (1992) 8:383-388
NlllI S 9 Springer-Verlag 1992
Central neurocytoma: its differentiation from intraventrieular oligodendroglioma Siu Tsan Yuen 1, Ching Fai Fung 2, Thomas H.K. Ng 1, and Suet Yi Leung 1 1 Department of Pathology and 2 Division of Surgical Neurology, Department of Surgery, Queen Mary Hospital, University of Hong Kong, Hong Kong Received May 20, 1991/Revised January 5, 1992
Abstract. Two patients with intraventricular t u m o u r s are presented. B o t h h a d similar features on light microscopic examination. O n the basis of the specific i m m u n o h i s t o chemical staining patterns and the ultrastructural findings, one was diagnosed as a central n e u r o c y t o m a while the other was diagnosed as an intraventricular oligodendroglioma. The possibility of central n e u r o c y t o m a should be considered in all y o u n g patients including children presenting with an intraventricular lesion. Definitive diagnosis requires electron microscopic and i m m u n o h i s t o chemical studies.
Key words: Intraventricular n e o p l a s m - Central neurocytoma - Oligodendroglioma
Intraventricular n e u r o c y t o m a is a rare t u m o u r ; to date, only 30-odd cases have been reported in the world literature. It was first described by H a s s o u n et al. in 1982, w h o presented two cases [3]. Subsequently, several reports have appeared in the literature [1, 2, 4 - 8 , 1 1 - 1 3 ] . Because it has only recently been recognised and because of its close resemblance to intraventricular oligodendroglioma, it is possible that cases are missed and misdiagnosed. I n addition, it has never been described in pediatric patients. We report two cases of intraventricular tumours, one of central n e u r o c y t o m a in a 6-year-old b o y and the other of intraventricular o l i g o d e n d r o g l i o m a in an adult patient, trying to highlight their i m p o r t a n t features and the m e t h o d in differential diagnosis.
Case 1 A 6-year-old Chinese boy was referred to the Neurosurgical Division of Queen Mary Hospital for progressive tremor of both hands. The child had had apparently normal psychomotor development until the age of 4 years, when he was noted to have increasing difficulty in fine movement and deteriorating handwriting. Performance in school work had also deteriorated.
Correspondence to." S.T. Yuen
Examination On admission, the child was alert, well nourished and obese. His intellectual performance was normal. There was no papilloedema and muscle power was normal. Truncal ataxia and dysdiadochokinesia were demonstrated. Jerk reflexes were brisk with normal plantar reflex.
Investigation Computerised tomography revealed an extensive intraventricular tumour with ill-defined margin and variable enhancement after contrast injection. Obstructive hydrocephalus was noted. Magnetic resonance imaging gave a similar finding (Fig. 1).
Operation The child received a ventriculo-peritoneal shunt soon after admission. Right frontal craniotomy was performed. The tumour was approached through the lateral ventricule method. The whole lateral ventricle was covered by thick whitish tumour mass, soft and necrotic. No margin could be identified between normal brain tissue and the tumour. Biopsy was taken and further removal was considered impossible. The child recovered uneventfully from the operation and external irradiation was given after the operation.
Case 2 A 33-year-old man was referred to the Neurosurgical Division of Queen Mary Hospital for the investigation of unsteady gait. He was apparently well until 3 months ago when he started to have progressive hand tremor. This was soon followed by progressive unsteady gait and he was unable to work as a mechanic.
Examination Physical examination revealed bilateral papilloedema and gross impairment of cognitive function. The patient walked with a reeling gait and truncal ataxia was demonstrated. All jerk reflexes were brisk.
384
Fig. 1. Case 1: MRI scan of brain showing large intraventricular turnout with ill-defined margin and variable signal intensities
Fig. 2. Case 2: Computerised tomogram showing intraventricular tumour with calcification and patchy contrast enhancement
Investigation Computerised tomography of the brain revealed a large intraventricular tumour with calcification and patchy contrast enhancement (Fig. 2).
Operation Craniotomy was performed. The tumour was approached through the occipital horn of the fight lateral ventricle. It was vascular with no clear margin. Gross total removal was performed. However, the patient's condition deteriorated on the 3rd day after operation due to secondary haemorrhage, and he died after further exploration.
Pathological findings Smear preparations from the two surgical specimens showed similar features. There were sheets of monotonous cells with small, uniform, rounded nuclei, small inconspicuous nucleoli and indistinct cytoplasm. No mitosis was seen. Paraffin sections of both specimens showed a uniform population of closely packed small cells in a fibrillary background with fine vasculature. These tumour cells were roundish, having a central regular nucleus with fine delicate chromatin and a clear cytoplasm (Fig. 3 a, b). N o mitosis was seen and there was no necrosis. HomerWright rosettes and perivascular pseudorosettes were, however, seen focally in case 1 (Fig. 3 c). Immunohistochemical studies were performed using the avidin-biotin method. In case 1, the neoplastic cells stained positive for neurofilament (Fig. 4) and synaptophysin (Fig. 5). Glial fibrillary acidic protein (GFAP) was not demonstrated inside the tumour cells. In case 2, GFAP was present in some of the tumour cells while neurofilament and synaptophysin were not demonstrated. Neurone specific enolase (NSE) was present in both cases. Electron microscopic studies were also performed using a Jeol 100SX electron microscope. In case 1, neuronal differentiation was evident, as numerous dendritic cytoplasmic processes were present and these contained bundles of microtubules. The cytoplasm contained a few dense core vesicles (Fig. 6). Synapses, however, were not identified. On the basis of these findings, the tumour was
diagnosed as a central neurocytoma. In case 2, glial filaments were present but microtubules and neurosecretory granules were not found. We reported this case as intraventricular oligodendroglioma.
Discussion Central neurocytoma is a recently recognised clinicopathological entity [3]. It affects a relatively young population with an age range of 1 5 - 5 2 years (average 28 years). However, it has never been described in children as in our case. Central neurocytoma typically arises in the lateral or III ventricle and is often associated with obstructive hydrocephalus and signs and symptoms of increased intracranial pressure, as were seen in our case. The duration of symptoms is variable, but they have usually been present for several months at the time of presentation ( 2 - 6 months). It is likely that the onset of symptoms is related to the development of obstructive hydrocephalus, and that the tumour has been present long before the symptoms start. CT and M R I scans typically reveal an intraventricular mass occupying one or both lateral ventricles, with or without III ventricular involvement. These features are well demonstrated in our case. Pathologically, these tumours typically have a uniform monotonous appearance on light microscopic examination, being composed of cells with regular small nuclei. Cellular pleomorphism and mitosis are not features of these tumours, although rare mitoses have been described. For the most part, the tumour cells are evenly distributed in a fine fibrillary stroma, but ill-defined rosettes and perivascular pseudorosettes may be present. Microcalcifications may be prominent. It is important to distinguish central neurocytoma from oligodendroglioma. Both may be intraventricular and they look remarkably similar on light microscopic examination. This is well illustrated by the two cases we report. We believe that differentiation between the two based on light microscopy and, especially, on smear and cryostat sections is very difficult. The finding of true neuroblastic rosettes, nuclei with a slightly ganglionic appearance and ill-defined cell boundaries may point slight-
385
Fig. 3. a Paraffin section of tumour in case 1 showing the closely packed small cells with regular nuclei and clear cytoplasm. (Haematoxylin & eosin, x 267). b Paraffin section of tumour in case 2 showing similar features to those in case 1. (Haematoxylin & eosin, x 133). e Other area of case I tumour showing Homer-Wright rosettes, perivascular pseudorosettes, and small areas of cell free islands of neuropil. (Haematoxylin & eosin, x 133)
386
Fig. 4. The tumour cells in case 1 stained positive for neurofilarnent. ( x 267) Fig. 5. Case 1: Immunohistochemieal staining for synaptophysin shows defnite positivity. ( x 267)
ly towards neurocytoma. Nevertheless, the final diagnosis should be confirmed by immunohistochemical and electron microscopic studies. Markers of neuroendocrine or neuronal differentiation such as neurofilament protein, chromogranin and synaptophysin are positive in neurocytoma only, while GFAP is positive in oligodendroglioma only. NSE has been shown to be non-specific [I0], as has Leu-7 [9]. Both can be present in central neurocytoma and oligodendroglioma. Synaptophysin, a pre-synaptic glycoprotein, is claimed to be the most sensitive and reliable marker [1]. The ultrastructural features of central neurocytoma clearly demonstrate neuronal differentiation, with numerous neuritic processes containing microtubules and neurosecretory granules. This has been described in previous reports [1, 2, 4-8, 11-13] and should be the basis for ultimate diagnosis. Table 1 summarises the differences between the two tumours.
Table 1. Differences between central neurocytorna and intraventricular oligodendroglioma
Neurofilament protein Synaptophysin Glial fibrillary acidic protein Neurotubules Neurosecretory granules
Central neurocytoma
Intraventficular oligodendroglioma
+ + + +
+ -
As shown by case 1, central neurocytoma can occur in patients of the pediatric age group. The typical site, typical presentation and light microscopic features should alert one to this possibility, in view of the fact that intraventricular oligodendroglioma is also a rare tumour in
387
Fig. 6. a An electron micrograph of tumour from case 1 showing rounded nuclei with adjacent areas consisting of cell processes. ( x 1667). b Higher-power image showing the prominent microtubules and the dense core neurosecretory granules in the cell processes. ( x 26 667)
children. Immunohistochemical and electron microscopic studies should be performed to establish the correct diagnosis. Another differential diagnosis that needs to be considered is ependymoma. The perivascular anuclear zones and the location of the lesion in and around the ventricular system make ependymoma a likely diagnosis. However, there should be no epithelial surfaces seen in central neurocytoma and the perivascular cells are negative for GFAP, whereas the perivascular pseudorosettes of ependymomas are usually strongly positive. Electron microscopic study is also needed for a definitive diagnosis, because features of ependymal differentiation such as tight junction, microvilli and cilia are never seen in central neurocytoma. The entity of ependymomas of the foramen of M o n r o need a more detail discussion. This was first described by Zfilch and Schmid in 1955 [14]. These tumours are known
to occur in young adults with a remarkably good prognosis. However these tumours have never been studied systematically by immunocytochemistry or electron microscopy. Apparently, ependymomas and central neurocytomas have important features in common, including histological appearance, periventricular location and preferential occurrence in young adults. It is likely that all these ependymomas would have actually proved to be. central neurocytomas if studied in detail, as reported in one recent series [2]. Moreover, the presence of perinuclear halo in the central neurocytoma cells associated with pseudorossette formation may cause misinterpretation of this tumour as ependymoma with clear cell change, an entity the existence of which is still controversial. The actual origin of central neurocytoma remains obscure. Because of their consistent location in lateral ventricles and around the foramen of Monro, the hypothesis
388 has been p r o p o s e d that these neoplasms m a y originate f r o m the s u b e p e n d y m a l plate o f the lateral ventricles. D u r i n g development, this matrix layer gives rise to cerebral neurons, glial and e p e n d y m a l cells. This hypothesis w o u l d also a c c o u n t for their bi-potential differentiation, which was reported in one series [2]. Surgical removal remains the m o d e o f treatment. Some people w o u l d also institute postoperative radiotherapy. U p to now, the cases reported are t o o few for an accurate assessment o f the prognosis. Available d a t a suggest that these t u m o u r s follow a benign course and after surgical removal the majority o f patients have an excellent prognosis. Only one recurrence has been reported so far [5].
5. 6. 7.
8. 9. 10.
References 1. Barbosa MD, Balsitis M, Jaspan T, Lowe J (1990) Intraventricular neurocytoma: a clinical and pathological study of three cases and review of the literature. Neurosurgery 26:1045-1054 2. Deimling A, Janzer R, Kleihues P, Wiester OD (1990) Patterns of differentiation in central neurocytoma: an immunohistochemical study of eleven biopsies. Acta Neuropathol 79: 473479 3. Hassoun J, Gambarelli D, Grisoli F, Pellet W, Salamon G, Pellissicr JF, Toga M (1982) Central neurocytoma. An electron microscopic study of two cases. Acta Neuropathol 56:151 -156 4. Louis DN, Swearingen B, Linggood RM, Dickersin GR, Kretschmar C, Bhan AK, Hedley-Whyte ET (1990) Central
11.
12. 13. 14.
nervous system neurocytoma and neuroblastoma in adults report of eight cases. J Neurooncol 9:231-238 Nishio S, Tashima T, Takeshita I, Fukui M (1988) Intraventricular neurocytoma: clinicopathological features of six cases. Neurosurgery 22:18-22 Patil AA, McComb RD, Gelber B, McConnell J, Sasse S (1990) Intraventricular neurocytoma: a report of two cases. Neurosurgery 26:140-144 Pearl GS, Takei Y, Stefanis GS, Hoffman JC (1981) Intraventricular neuroblastoma in a patient with von Hippel-Lindau's disease. An electron microscopic study. Acta Neuropathol 53:253-256 Pearl GS, Takei Y, Bakay RAE, Davis P (1985) lntraventricular primary cerebral neuroblastoma in adults: report of three cases. Neurosurgery 16:847-849 Perentes E, Rubinstein LJ (1986) Immunohistochemical recognition of human neuroepithelial tumours by anti-Leu 7 (HNK-1) monoclonal antibody. Acta Neuropathol 69:227-233 Perentes E, Rubinstein LJ (1987) Recent application of immunoperoxidase histochemistry in human neuro-oncology: an update. Arch Pathol Lab Med 111:796- 812 Poon TP, Mangiardi JR, Matoso I, Weitzner I Jr (1988) Third ventricular primary cerebral neuroblastoma. Electron microscopic and immunohistochemical study. Surg Neurol 30: 237241 Townsend JJ, Seaman JP (1986) Central neurocytoma: a rare benign intraventricular tumour. Acta Neuropathol 71:167-170 Wilson AJ, Leafier DH, Kohout ND (1985) Differentiated cerebral neuroblastoma: a tumour in need of discovery. Hum Pathol 16:647-649 Ziilch KJ, Schmid EE (1955) Uber das Ependymom der Seitenkammern am Foramen Monroi. Arch Psychiatr Nervenkr 193:214-228
NlllI S 9 Springer-Verlag 1992
Central neurocytoma: its differentiation from intraventrieular oligodendroglioma Siu Tsan Yuen 1, Ching Fai Fung 2, Thomas H.K. Ng 1, and Suet Yi Leung 1 1 Department of Pathology and 2 Division of Surgical Neurology, Department of Surgery, Queen Mary Hospital, University of Hong Kong, Hong Kong Received May 20, 1991/Revised January 5, 1992
Abstract. Two patients with intraventricular t u m o u r s are presented. B o t h h a d similar features on light microscopic examination. O n the basis of the specific i m m u n o h i s t o chemical staining patterns and the ultrastructural findings, one was diagnosed as a central n e u r o c y t o m a while the other was diagnosed as an intraventricular oligodendroglioma. The possibility of central n e u r o c y t o m a should be considered in all y o u n g patients including children presenting with an intraventricular lesion. Definitive diagnosis requires electron microscopic and i m m u n o h i s t o chemical studies.
Key words: Intraventricular n e o p l a s m - Central neurocytoma - Oligodendroglioma
Intraventricular n e u r o c y t o m a is a rare t u m o u r ; to date, only 30-odd cases have been reported in the world literature. It was first described by H a s s o u n et al. in 1982, w h o presented two cases [3]. Subsequently, several reports have appeared in the literature [1, 2, 4 - 8 , 1 1 - 1 3 ] . Because it has only recently been recognised and because of its close resemblance to intraventricular oligodendroglioma, it is possible that cases are missed and misdiagnosed. I n addition, it has never been described in pediatric patients. We report two cases of intraventricular tumours, one of central n e u r o c y t o m a in a 6-year-old b o y and the other of intraventricular o l i g o d e n d r o g l i o m a in an adult patient, trying to highlight their i m p o r t a n t features and the m e t h o d in differential diagnosis.
Case 1 A 6-year-old Chinese boy was referred to the Neurosurgical Division of Queen Mary Hospital for progressive tremor of both hands. The child had had apparently normal psychomotor development until the age of 4 years, when he was noted to have increasing difficulty in fine movement and deteriorating handwriting. Performance in school work had also deteriorated.
Correspondence to." S.T. Yuen
Examination On admission, the child was alert, well nourished and obese. His intellectual performance was normal. There was no papilloedema and muscle power was normal. Truncal ataxia and dysdiadochokinesia were demonstrated. Jerk reflexes were brisk with normal plantar reflex.
Investigation Computerised tomography revealed an extensive intraventricular tumour with ill-defined margin and variable enhancement after contrast injection. Obstructive hydrocephalus was noted. Magnetic resonance imaging gave a similar finding (Fig. 1).
Operation The child received a ventriculo-peritoneal shunt soon after admission. Right frontal craniotomy was performed. The tumour was approached through the lateral ventricule method. The whole lateral ventricle was covered by thick whitish tumour mass, soft and necrotic. No margin could be identified between normal brain tissue and the tumour. Biopsy was taken and further removal was considered impossible. The child recovered uneventfully from the operation and external irradiation was given after the operation.
Case 2 A 33-year-old man was referred to the Neurosurgical Division of Queen Mary Hospital for the investigation of unsteady gait. He was apparently well until 3 months ago when he started to have progressive hand tremor. This was soon followed by progressive unsteady gait and he was unable to work as a mechanic.
Examination Physical examination revealed bilateral papilloedema and gross impairment of cognitive function. The patient walked with a reeling gait and truncal ataxia was demonstrated. All jerk reflexes were brisk.
384
Fig. 1. Case 1: MRI scan of brain showing large intraventricular turnout with ill-defined margin and variable signal intensities
Fig. 2. Case 2: Computerised tomogram showing intraventricular tumour with calcification and patchy contrast enhancement
Investigation Computerised tomography of the brain revealed a large intraventricular tumour with calcification and patchy contrast enhancement (Fig. 2).
Operation Craniotomy was performed. The tumour was approached through the occipital horn of the fight lateral ventricle. It was vascular with no clear margin. Gross total removal was performed. However, the patient's condition deteriorated on the 3rd day after operation due to secondary haemorrhage, and he died after further exploration.
Pathological findings Smear preparations from the two surgical specimens showed similar features. There were sheets of monotonous cells with small, uniform, rounded nuclei, small inconspicuous nucleoli and indistinct cytoplasm. No mitosis was seen. Paraffin sections of both specimens showed a uniform population of closely packed small cells in a fibrillary background with fine vasculature. These tumour cells were roundish, having a central regular nucleus with fine delicate chromatin and a clear cytoplasm (Fig. 3 a, b). N o mitosis was seen and there was no necrosis. HomerWright rosettes and perivascular pseudorosettes were, however, seen focally in case 1 (Fig. 3 c). Immunohistochemical studies were performed using the avidin-biotin method. In case 1, the neoplastic cells stained positive for neurofilament (Fig. 4) and synaptophysin (Fig. 5). Glial fibrillary acidic protein (GFAP) was not demonstrated inside the tumour cells. In case 2, GFAP was present in some of the tumour cells while neurofilament and synaptophysin were not demonstrated. Neurone specific enolase (NSE) was present in both cases. Electron microscopic studies were also performed using a Jeol 100SX electron microscope. In case 1, neuronal differentiation was evident, as numerous dendritic cytoplasmic processes were present and these contained bundles of microtubules. The cytoplasm contained a few dense core vesicles (Fig. 6). Synapses, however, were not identified. On the basis of these findings, the tumour was
diagnosed as a central neurocytoma. In case 2, glial filaments were present but microtubules and neurosecretory granules were not found. We reported this case as intraventricular oligodendroglioma.
Discussion Central neurocytoma is a recently recognised clinicopathological entity [3]. It affects a relatively young population with an age range of 1 5 - 5 2 years (average 28 years). However, it has never been described in children as in our case. Central neurocytoma typically arises in the lateral or III ventricle and is often associated with obstructive hydrocephalus and signs and symptoms of increased intracranial pressure, as were seen in our case. The duration of symptoms is variable, but they have usually been present for several months at the time of presentation ( 2 - 6 months). It is likely that the onset of symptoms is related to the development of obstructive hydrocephalus, and that the tumour has been present long before the symptoms start. CT and M R I scans typically reveal an intraventricular mass occupying one or both lateral ventricles, with or without III ventricular involvement. These features are well demonstrated in our case. Pathologically, these tumours typically have a uniform monotonous appearance on light microscopic examination, being composed of cells with regular small nuclei. Cellular pleomorphism and mitosis are not features of these tumours, although rare mitoses have been described. For the most part, the tumour cells are evenly distributed in a fine fibrillary stroma, but ill-defined rosettes and perivascular pseudorosettes may be present. Microcalcifications may be prominent. It is important to distinguish central neurocytoma from oligodendroglioma. Both may be intraventricular and they look remarkably similar on light microscopic examination. This is well illustrated by the two cases we report. We believe that differentiation between the two based on light microscopy and, especially, on smear and cryostat sections is very difficult. The finding of true neuroblastic rosettes, nuclei with a slightly ganglionic appearance and ill-defined cell boundaries may point slight-
385
Fig. 3. a Paraffin section of tumour in case 1 showing the closely packed small cells with regular nuclei and clear cytoplasm. (Haematoxylin & eosin, x 267). b Paraffin section of tumour in case 2 showing similar features to those in case 1. (Haematoxylin & eosin, x 133). e Other area of case I tumour showing Homer-Wright rosettes, perivascular pseudorosettes, and small areas of cell free islands of neuropil. (Haematoxylin & eosin, x 133)
386
Fig. 4. The tumour cells in case 1 stained positive for neurofilarnent. ( x 267) Fig. 5. Case 1: Immunohistochemieal staining for synaptophysin shows defnite positivity. ( x 267)
ly towards neurocytoma. Nevertheless, the final diagnosis should be confirmed by immunohistochemical and electron microscopic studies. Markers of neuroendocrine or neuronal differentiation such as neurofilament protein, chromogranin and synaptophysin are positive in neurocytoma only, while GFAP is positive in oligodendroglioma only. NSE has been shown to be non-specific [I0], as has Leu-7 [9]. Both can be present in central neurocytoma and oligodendroglioma. Synaptophysin, a pre-synaptic glycoprotein, is claimed to be the most sensitive and reliable marker [1]. The ultrastructural features of central neurocytoma clearly demonstrate neuronal differentiation, with numerous neuritic processes containing microtubules and neurosecretory granules. This has been described in previous reports [1, 2, 4-8, 11-13] and should be the basis for ultimate diagnosis. Table 1 summarises the differences between the two tumours.
Table 1. Differences between central neurocytorna and intraventricular oligodendroglioma
Neurofilament protein Synaptophysin Glial fibrillary acidic protein Neurotubules Neurosecretory granules
Central neurocytoma
Intraventficular oligodendroglioma
+ + + +
+ -
As shown by case 1, central neurocytoma can occur in patients of the pediatric age group. The typical site, typical presentation and light microscopic features should alert one to this possibility, in view of the fact that intraventricular oligodendroglioma is also a rare tumour in
387
Fig. 6. a An electron micrograph of tumour from case 1 showing rounded nuclei with adjacent areas consisting of cell processes. ( x 1667). b Higher-power image showing the prominent microtubules and the dense core neurosecretory granules in the cell processes. ( x 26 667)
children. Immunohistochemical and electron microscopic studies should be performed to establish the correct diagnosis. Another differential diagnosis that needs to be considered is ependymoma. The perivascular anuclear zones and the location of the lesion in and around the ventricular system make ependymoma a likely diagnosis. However, there should be no epithelial surfaces seen in central neurocytoma and the perivascular cells are negative for GFAP, whereas the perivascular pseudorosettes of ependymomas are usually strongly positive. Electron microscopic study is also needed for a definitive diagnosis, because features of ependymal differentiation such as tight junction, microvilli and cilia are never seen in central neurocytoma. The entity of ependymomas of the foramen of M o n r o need a more detail discussion. This was first described by Zfilch and Schmid in 1955 [14]. These tumours are known
to occur in young adults with a remarkably good prognosis. However these tumours have never been studied systematically by immunocytochemistry or electron microscopy. Apparently, ependymomas and central neurocytomas have important features in common, including histological appearance, periventricular location and preferential occurrence in young adults. It is likely that all these ependymomas would have actually proved to be. central neurocytomas if studied in detail, as reported in one recent series [2]. Moreover, the presence of perinuclear halo in the central neurocytoma cells associated with pseudorossette formation may cause misinterpretation of this tumour as ependymoma with clear cell change, an entity the existence of which is still controversial. The actual origin of central neurocytoma remains obscure. Because of their consistent location in lateral ventricles and around the foramen of Monro, the hypothesis
388 has been p r o p o s e d that these neoplasms m a y originate f r o m the s u b e p e n d y m a l plate o f the lateral ventricles. D u r i n g development, this matrix layer gives rise to cerebral neurons, glial and e p e n d y m a l cells. This hypothesis w o u l d also a c c o u n t for their bi-potential differentiation, which was reported in one series [2]. Surgical removal remains the m o d e o f treatment. Some people w o u l d also institute postoperative radiotherapy. U p to now, the cases reported are t o o few for an accurate assessment o f the prognosis. Available d a t a suggest that these t u m o u r s follow a benign course and after surgical removal the majority o f patients have an excellent prognosis. Only one recurrence has been reported so far [5].
5. 6. 7.
8. 9. 10.
References 1. Barbosa MD, Balsitis M, Jaspan T, Lowe J (1990) Intraventricular neurocytoma: a clinical and pathological study of three cases and review of the literature. Neurosurgery 26:1045-1054 2. Deimling A, Janzer R, Kleihues P, Wiester OD (1990) Patterns of differentiation in central neurocytoma: an immunohistochemical study of eleven biopsies. Acta Neuropathol 79: 473479 3. Hassoun J, Gambarelli D, Grisoli F, Pellet W, Salamon G, Pellissicr JF, Toga M (1982) Central neurocytoma. An electron microscopic study of two cases. Acta Neuropathol 56:151 -156 4. Louis DN, Swearingen B, Linggood RM, Dickersin GR, Kretschmar C, Bhan AK, Hedley-Whyte ET (1990) Central
11.
12. 13. 14.
nervous system neurocytoma and neuroblastoma in adults report of eight cases. J Neurooncol 9:231-238 Nishio S, Tashima T, Takeshita I, Fukui M (1988) Intraventricular neurocytoma: clinicopathological features of six cases. Neurosurgery 22:18-22 Patil AA, McComb RD, Gelber B, McConnell J, Sasse S (1990) Intraventricular neurocytoma: a report of two cases. Neurosurgery 26:140-144 Pearl GS, Takei Y, Stefanis GS, Hoffman JC (1981) Intraventricular neuroblastoma in a patient with von Hippel-Lindau's disease. An electron microscopic study. Acta Neuropathol 53:253-256 Pearl GS, Takei Y, Bakay RAE, Davis P (1985) lntraventricular primary cerebral neuroblastoma in adults: report of three cases. Neurosurgery 16:847-849 Perentes E, Rubinstein LJ (1986) Immunohistochemical recognition of human neuroepithelial tumours by anti-Leu 7 (HNK-1) monoclonal antibody. Acta Neuropathol 69:227-233 Perentes E, Rubinstein LJ (1987) Recent application of immunoperoxidase histochemistry in human neuro-oncology: an update. Arch Pathol Lab Med 111:796- 812 Poon TP, Mangiardi JR, Matoso I, Weitzner I Jr (1988) Third ventricular primary cerebral neuroblastoma. Electron microscopic and immunohistochemical study. Surg Neurol 30: 237241 Townsend JJ, Seaman JP (1986) Central neurocytoma: a rare benign intraventricular tumour. Acta Neuropathol 71:167-170 Wilson AJ, Leafier DH, Kohout ND (1985) Differentiated cerebral neuroblastoma: a tumour in need of discovery. Hum Pathol 16:647-649 Ziilch KJ, Schmid EE (1955) Uber das Ependymom der Seitenkammern am Foramen Monroi. Arch Psychiatr Nervenkr 193:214-228
