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Case report: A small temporal lobe glioma detected only by magnetic resonance imaging
Clinical Radiology (1989) 40, 528-529
Case Report: A Small Temporal Lobe_Glioma Detected Only by Magnetic Resonance Imaging K. YANAKA,
Y. Y O S H I I ,
T. N O S E
a n d Y. M A K I
Department o f Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Ibaraki 305, Japan
The authors were able to demonstrate a very small glioma (1.0 x 0.8 cm in size) of the temporal lobe using M R I . They discuss the relative merits of CT and M R I in the diagnosis of gliomas in terms of their size. CT fails to detect tumours less than 2.0 x 1.5 cm in size which are not calcified. So far, M R I has revealed a tumour as small as 1.0 x 0.8 cm. Therefore, M R I is superior to CT for detecting small gliomas.
Since 198 l, several a u t h o r s h a v e r e p o r t e d the s u p e r i o r i t y of magnetic resonance imaging (MRI) over other imaging techniques. Certain limitations of computed tomography ( C T ) in the d i a g n o s i s o f lesions o f the c e n t r a l n e r v o u s s y s t e m h a v e also b e e n p o i n t e d o u t ( D a v i s et al., 1976). Recently, reports have appeared of MR imaging of brain t u m o u r s u n r e v e a l e d by C T ( G r ~ f i n v o n Einsiedel & L6effler, 1982; L a s t e r et al., 1985). I n this p a p e r , a v e r y s m a l l m i x e d g l i o m a is d e s c r i b e d w h i c h was o n l y d e t e c t e d by M R I , a n d the d e t e c t a b i l i t y o f g l i o m a is discussed in t e r m s o f t u m o u r size b e t w e e n M R I a n d C T .
Fig. 1 A small glioma in the mesial aspect of the left temporal lobe is seen as a high signal intensity area: A low signal intensity area in the centre of the lesion indicates calcification.
CASE REPORT A 29-year-old male presented with a history of partial complex seizures for 18 years. He had been healthy until aged ll, when he developed focal seizures of his right arm which gradually increased in severity. Despite anticonvulsant medication with drugs such as phenytoin, phenobarbital and valproic acid, his seizures remained incompletely controlled. In 1981, he was referred to a neurological department for further examinations, and a CT scan and angiogram were carried out. Both were negative. In 1986 because of more frequent attacks, he was referred to the University of Tsukuba Hospital. Plain skull radiographs were non-contributory. A C T examination carried out before and after tissue enhancement and performed in both axial and coronal planes showed a small area of calcification, 0.5 x 0.4 cm in size, in the mesial part of the left temporal lobe. Even with a double-dose technique, no enhancement could be demonstrated. The left carotid angiogram showed no arteriovenous malformation or 'tumour stain', and was interpreted as normal. However, the electroencephalogram (EEG) showed slow waves and a spike focus in the mesial aspect of the left temporal lobe. A MRI scan was carried out (Hitachi resistive magnet, 0.15 Tesla magnetic field) using a spin echo (SE) pulse sequence with a repetition time (TR) of 2000 msec and an echo time (TE) of 50 msec. A small area (1.0 x 0.8 cm in size) of high intensity was demonstrated in the mesial aspect of the left temporal lobe (Fig. 1). A reduced intensity area was seen within this area with inversion recovery (IR 1400/60; 1400 msec: TR, 60 msec: TE). No abnormality was visible with the saturation recovery sequence (SR 700/30). Multiple spin echo sequences using SE with three different echo times (2000/40, 2000/80, 2000/120) were obtained, and the well-circumscribed lesion was shown in all three as an area of high signal intensity. On the basis of these results, the lesion was diagnosed as a gIioma. At operation, a well-encapsulated tumour was found, composed of yellow soft tissue and containing small foci of calcification within it. A total removal was accomplished. HistologiCorrespondence and reprint requests to: Yoshihiko Yoshii, Department of Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Tennodai, Tsukuba City, Ibaraki 305, Japan
cally, the tumour tissue consisted ofoligodendrogliai cells and clumps of astrocytes. The final diagnosis was a mixed glioma.
DISCUSSION T h e s u p e r i o r i t y o f M R I o v e r C T in the d e t e c t i o n o f c e r e b r a l lesions i n c l u d i n g n e o p l a s m s is n o w well d o c u m e n t e d (Gr/ifin v o n E i n s i e d e l & L6ffler, 1982; B r a n d Z a w a d z k i et al., 1983; M c G i n n i s et al., 1983; A a r o n et al., 1984; L a s t e r et al., 1985; M c L a c h l a n et al., 1985; J a b b a r i et al., 1986; L e s s e r et al., 1986; S t o n e et al., 1986). D e s p i t e t e c h n i c a l a d v a n c e s , C T s c a n n i n g m a y n o t r e v e a l lesions o f the f l o o r o f the skull d u e to b o n e artifacts. U n l e s s a g l i o m a p r o d u c e s d e n s i t y c h a n g e s , a m a s s effect o r causes a b r e a k d o w n in t h e b l o o d b r a i n b a r r i e r , C T m a y n o t s h o w a n y s t r u c t u r a l a b n o r m a l i t i e s ( B o l e n d e r et al., 1983). By c o n t r a s t , M R I is p a r t i c u l a r l y suited f o r r e v e a l i n g lesions o f the p o s t e r i o r a n d m i d d l e f o s s a e ( Y o u n g et al., 1981; B y d d e r et al., 1983; M c G i n n i s et al., 1983). D a v i s et al., (1976), in r e v i e w i n g the role o f C T in i n t r a c r a n i a l d i a g n o s i s , e m p h a s i s e d t h a t o n e o f its l i m i t a t i o n s was the size o f t h e lesion. A l t h o u g h t h e y f o u n d t h a t n e o p l a s m s c o u l d be d e t e c t e d w i t h a n a c c u r a c y o f a p p r o x i m a t e l y 98 % t h o s e w i t h a d i a m e t e r o f less t h a n 1.5 c m w e r e e x c l u d e d . R e c e n t l y , several a u t h o r s h a v e r e p o r t e d the M R i m a g ing o f g l i o m a s u n r e v e a l e d by C T (Gr/ifin v o n Einsiedel a n d L6ffler, 1982; L a s t e r et al., 1985; J a b b a r i et al., 1986). H o w e v e r , m o s t o f the t u m o u r s w e r e l a r g e r t h a n 1.5 c m in d i a m e t e r . T a b l e 1 r e v i e w s e x p e r i e n c e w i t h C T a n d M R ! in
A SMALL TEMPORAL LOBE GLIOMA
529
Table 1 - Small gliomas detected by CT and MRI
Author
Case
CT
MRI
Size (cm)
Pa~thology
Aaron et al. (1984)
1 2 3 4 5 6 7 8 9 10
LDA Calc HDA HDA Normal Normal Normal LDA LDA Calc
Prolonged T1, T2 Prolonged T2 Prolonged T1, T2 Prolonged T 1, T2 Prolonged T2 Prolonged T2 Prolonged T2 Prolonged T2 Prolonged T1, T2 Prolonged T1, T2
1.5 × 2.5 1.0 × 1.5 2.5 × 3.0 2.5 x 2.5 2.0 x 1.5 2.0 x 1.5 1.0 x 1.5 2.5 x 3.0 2.0 x 2.5 1.0 x 0.8
Mixed glioma Mixed glioma Mixed glioma Glioma Astrocytoma Glioma Glioma Glioma Glioma Mixed glioma
Laster et al. (1985) Jabbari et al. (1986) Price et al. (1986) Present case
Calc, calcified lesion; HDA, high density area; LDA, low density area.
d e t e c t i n g s m a l l g l i o m a s in t e r m s o f t h e i r size. C T reveals focal c a l c i f i c a t i o n s b e t t e r t h a n M R i m a g i n g ( S u n d a r e s a n et al., 1980); e v e n v e r y s m a l l calcified lesions c a n be d e t e c t e d b y C T . H o w e v e r , r e v i e w o f the l i t e r a t u r e a n d personal experience confirm that CT does not image t u m o u r s s m a l l e r t h a n 2.0 × 1.5 c m in size i f u n c a l c i f i e d . By c o n t r a s t , a t u m o u r as s m a l l as 1.0 × 0.8 c m c a n be s h o w n by M R I . P r i c e et al. (1986) a n d S m i t h et al. (1985) r e p o r t e d t h a t the T 2 - w e i g h t e d s e q u e n c e ( c o r r e s p o n d i n g to o u r SE) is s u p e r i o r t o t h e T l - w e i g h t e d for i d e n t i f y i n g t h e site a n d d e t e r m i n i n g the n a t u r e o f i n t r a c r a n i a l t u m o u r s . T h e a u t h o r s c o n f i r m the s u p e r i o r i t y o f the T 2 - w e i g h t e d sequences. In the series r e v i e w e d in T a b l e 1, all 10 p a t i e n t s s h o w e d a b n o r m a l i t i e s w i t h the T 2 - w e i g h t e d s e q u e n c e s , w h e r e a s o n l y five s h o w e d a b n o r m a l i t i e s w i t h T 1 - w e i g h t e d sequences.
Acknowledgement. We thank Professor Youichi Ishida of Gunma University for his professional advice regarding neuropathology.
REFERENCES
Aaron, J, New, PFJ, Strand, R, Beaulieu, P, Elmden, K & Brady, T (1984). NMR imaging in temporal lobe epilepsy due to gliomas. Journal of Computer Assisted Tomography, 8(4), 608 613. Bolender, NF, Cromwell, LD, Graves, V, Margolis, MT, Kerber, CW & Wendling, L (1983). Interval appearance of glioblastomas not evident in previous CT examinations. Journal of Computer Assisted Tomography, 7(4), 599-603. Brand-Zawadzki, M, Davis, PL, Crooks, LE, Mills, CM, Norman, D, Newton, TH et al. (1983). NMR demonstration of cerebral abnormalities. Comparison with CT. American Journal of Neuroradiology, 4, 117-124. Bydder, GM, Steiner, RE, Thomas, D J, Marshall, J, Gilderdale, DJ & Young, IR (1983). Nuclear magnetic resonance imaging of the posterior fossa: 50 cases. Clinical Radiology, 34, 173-188.
Davis, KR, Taveras, JM, Roberson, GH & Ackerman, RH (1976). Some limitations of computed tomography in the diagnosis of neurological diseases. American Journal of Roentgenology, 127, 111123. Gr~ifin yon Einsiedel, H & L6ffter, W (1982). Nuclear magnetic resonance imaging of brain tumors unrevealed by CT. European Journal of Radiology, 2, 226-234. Jabbari, B, Gunderson, CH, Wippold, F, Charles, C, Sherman, J, Bartoszek, D et al. (1986). Magnetic resonance imaging in partial complex epilepsy. Archives of Neurology, 43, 869 872. Laster, DW, Penry, JK, Moody, DM, Ball, MR, Witcofski, RL & Riela, AR (1985). Chronic seizure disorders: Contribution of MR imaging when CT is normal. American Journal of Neuroradiology, 6,177 180. Lesser, RP, Modic, MT, Weinstein, MA, Duchesneau, PM, Luders, H, Dinner, DS et al. (1986). Magnetic resonance imaging (1.5 Tesla) in patients with intractable focal seizures. Archives of Neurology, 43, 367 371. McGinnis, BD, Brady, TJ, New, PFJ, Buonanno, FS, Pykett, IL, DeLaPaz, RL et al. (1983). Nuclear magnetic resonance (NMR) imaging of tumors in the posterior fossa. Journal of Computer Assisted Tomography, 7, 575-584. McLachlan, RS, Nicholson, RL, Black, S, Cart, T & Blume, WT (1985). Nuclear magnetic resonance imaging, a new approach to the investigation of refractory temporal lobe epilepsy. Epilepsia, 26(6), 555-562. Price, AC, Runge, VM, Allen, JH, Partin, CL & James, AE (1986). Primary glioma: Diagnosis with magnetic resonance imaging. Journal of Computer Assisted Tomography, I0, 325-334. Smith, AS, Weintein, MA, Modic, MT, Pavlicek, W, Rogers, LR, Budd, TG et al. (1985). Magnetic resonance with marked T-2 weighted images: Improved demonstration of brain lesions, tumor, and edema. American Journal of Roentgenology, 145, 949-955. Stone, JL, Hughes, JR, Barr, A, Tan, W, Russell, E & Crowell, RM (1986). Neuroradiological and electroencephalographic features in a case of temporal lobe status epilepticus. Neurosurgery, 18, 212 216. Sundaresan, N, Larsen, M, Deck, MDF & Fraser, RAR (1980). Brain tumors presenting as small calcified lesions on computerized tomography. Report of three cases. Child~ Brain, 7, 95-100. Young, IR, Burl, M, Clarke, GJ, Hall, AS, Pasmore, T, Collins, AG, et al. (1981). Magnetic resonance properties of hydrogen: imaging of the posterior fossa. American Journal of Roentgenology, I37, 895901.
Case Report: A Small Temporal Lobe_Glioma Detected Only by Magnetic Resonance Imaging K. YANAKA,
Y. Y O S H I I ,
T. N O S E
a n d Y. M A K I
Department o f Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Ibaraki 305, Japan
The authors were able to demonstrate a very small glioma (1.0 x 0.8 cm in size) of the temporal lobe using M R I . They discuss the relative merits of CT and M R I in the diagnosis of gliomas in terms of their size. CT fails to detect tumours less than 2.0 x 1.5 cm in size which are not calcified. So far, M R I has revealed a tumour as small as 1.0 x 0.8 cm. Therefore, M R I is superior to CT for detecting small gliomas.
Since 198 l, several a u t h o r s h a v e r e p o r t e d the s u p e r i o r i t y of magnetic resonance imaging (MRI) over other imaging techniques. Certain limitations of computed tomography ( C T ) in the d i a g n o s i s o f lesions o f the c e n t r a l n e r v o u s s y s t e m h a v e also b e e n p o i n t e d o u t ( D a v i s et al., 1976). Recently, reports have appeared of MR imaging of brain t u m o u r s u n r e v e a l e d by C T ( G r ~ f i n v o n Einsiedel & L6effler, 1982; L a s t e r et al., 1985). I n this p a p e r , a v e r y s m a l l m i x e d g l i o m a is d e s c r i b e d w h i c h was o n l y d e t e c t e d by M R I , a n d the d e t e c t a b i l i t y o f g l i o m a is discussed in t e r m s o f t u m o u r size b e t w e e n M R I a n d C T .
Fig. 1 A small glioma in the mesial aspect of the left temporal lobe is seen as a high signal intensity area: A low signal intensity area in the centre of the lesion indicates calcification.
CASE REPORT A 29-year-old male presented with a history of partial complex seizures for 18 years. He had been healthy until aged ll, when he developed focal seizures of his right arm which gradually increased in severity. Despite anticonvulsant medication with drugs such as phenytoin, phenobarbital and valproic acid, his seizures remained incompletely controlled. In 1981, he was referred to a neurological department for further examinations, and a CT scan and angiogram were carried out. Both were negative. In 1986 because of more frequent attacks, he was referred to the University of Tsukuba Hospital. Plain skull radiographs were non-contributory. A C T examination carried out before and after tissue enhancement and performed in both axial and coronal planes showed a small area of calcification, 0.5 x 0.4 cm in size, in the mesial part of the left temporal lobe. Even with a double-dose technique, no enhancement could be demonstrated. The left carotid angiogram showed no arteriovenous malformation or 'tumour stain', and was interpreted as normal. However, the electroencephalogram (EEG) showed slow waves and a spike focus in the mesial aspect of the left temporal lobe. A MRI scan was carried out (Hitachi resistive magnet, 0.15 Tesla magnetic field) using a spin echo (SE) pulse sequence with a repetition time (TR) of 2000 msec and an echo time (TE) of 50 msec. A small area (1.0 x 0.8 cm in size) of high intensity was demonstrated in the mesial aspect of the left temporal lobe (Fig. 1). A reduced intensity area was seen within this area with inversion recovery (IR 1400/60; 1400 msec: TR, 60 msec: TE). No abnormality was visible with the saturation recovery sequence (SR 700/30). Multiple spin echo sequences using SE with three different echo times (2000/40, 2000/80, 2000/120) were obtained, and the well-circumscribed lesion was shown in all three as an area of high signal intensity. On the basis of these results, the lesion was diagnosed as a gIioma. At operation, a well-encapsulated tumour was found, composed of yellow soft tissue and containing small foci of calcification within it. A total removal was accomplished. HistologiCorrespondence and reprint requests to: Yoshihiko Yoshii, Department of Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Tennodai, Tsukuba City, Ibaraki 305, Japan
cally, the tumour tissue consisted ofoligodendrogliai cells and clumps of astrocytes. The final diagnosis was a mixed glioma.
DISCUSSION T h e s u p e r i o r i t y o f M R I o v e r C T in the d e t e c t i o n o f c e r e b r a l lesions i n c l u d i n g n e o p l a s m s is n o w well d o c u m e n t e d (Gr/ifin v o n E i n s i e d e l & L6ffler, 1982; B r a n d Z a w a d z k i et al., 1983; M c G i n n i s et al., 1983; A a r o n et al., 1984; L a s t e r et al., 1985; M c L a c h l a n et al., 1985; J a b b a r i et al., 1986; L e s s e r et al., 1986; S t o n e et al., 1986). D e s p i t e t e c h n i c a l a d v a n c e s , C T s c a n n i n g m a y n o t r e v e a l lesions o f the f l o o r o f the skull d u e to b o n e artifacts. U n l e s s a g l i o m a p r o d u c e s d e n s i t y c h a n g e s , a m a s s effect o r causes a b r e a k d o w n in t h e b l o o d b r a i n b a r r i e r , C T m a y n o t s h o w a n y s t r u c t u r a l a b n o r m a l i t i e s ( B o l e n d e r et al., 1983). By c o n t r a s t , M R I is p a r t i c u l a r l y suited f o r r e v e a l i n g lesions o f the p o s t e r i o r a n d m i d d l e f o s s a e ( Y o u n g et al., 1981; B y d d e r et al., 1983; M c G i n n i s et al., 1983). D a v i s et al., (1976), in r e v i e w i n g the role o f C T in i n t r a c r a n i a l d i a g n o s i s , e m p h a s i s e d t h a t o n e o f its l i m i t a t i o n s was the size o f t h e lesion. A l t h o u g h t h e y f o u n d t h a t n e o p l a s m s c o u l d be d e t e c t e d w i t h a n a c c u r a c y o f a p p r o x i m a t e l y 98 % t h o s e w i t h a d i a m e t e r o f less t h a n 1.5 c m w e r e e x c l u d e d . R e c e n t l y , several a u t h o r s h a v e r e p o r t e d the M R i m a g ing o f g l i o m a s u n r e v e a l e d by C T (Gr/ifin v o n Einsiedel a n d L6ffler, 1982; L a s t e r et al., 1985; J a b b a r i et al., 1986). H o w e v e r , m o s t o f the t u m o u r s w e r e l a r g e r t h a n 1.5 c m in d i a m e t e r . T a b l e 1 r e v i e w s e x p e r i e n c e w i t h C T a n d M R ! in
A SMALL TEMPORAL LOBE GLIOMA
529
Table 1 - Small gliomas detected by CT and MRI
Author
Case
CT
MRI
Size (cm)
Pa~thology
Aaron et al. (1984)
1 2 3 4 5 6 7 8 9 10
LDA Calc HDA HDA Normal Normal Normal LDA LDA Calc
Prolonged T1, T2 Prolonged T2 Prolonged T1, T2 Prolonged T 1, T2 Prolonged T2 Prolonged T2 Prolonged T2 Prolonged T2 Prolonged T1, T2 Prolonged T1, T2
1.5 × 2.5 1.0 × 1.5 2.5 × 3.0 2.5 x 2.5 2.0 x 1.5 2.0 x 1.5 1.0 x 1.5 2.5 x 3.0 2.0 x 2.5 1.0 x 0.8
Mixed glioma Mixed glioma Mixed glioma Glioma Astrocytoma Glioma Glioma Glioma Glioma Mixed glioma
Laster et al. (1985) Jabbari et al. (1986) Price et al. (1986) Present case
Calc, calcified lesion; HDA, high density area; LDA, low density area.
d e t e c t i n g s m a l l g l i o m a s in t e r m s o f t h e i r size. C T reveals focal c a l c i f i c a t i o n s b e t t e r t h a n M R i m a g i n g ( S u n d a r e s a n et al., 1980); e v e n v e r y s m a l l calcified lesions c a n be d e t e c t e d b y C T . H o w e v e r , r e v i e w o f the l i t e r a t u r e a n d personal experience confirm that CT does not image t u m o u r s s m a l l e r t h a n 2.0 × 1.5 c m in size i f u n c a l c i f i e d . By c o n t r a s t , a t u m o u r as s m a l l as 1.0 × 0.8 c m c a n be s h o w n by M R I . P r i c e et al. (1986) a n d S m i t h et al. (1985) r e p o r t e d t h a t the T 2 - w e i g h t e d s e q u e n c e ( c o r r e s p o n d i n g to o u r SE) is s u p e r i o r t o t h e T l - w e i g h t e d for i d e n t i f y i n g t h e site a n d d e t e r m i n i n g the n a t u r e o f i n t r a c r a n i a l t u m o u r s . T h e a u t h o r s c o n f i r m the s u p e r i o r i t y o f the T 2 - w e i g h t e d sequences. In the series r e v i e w e d in T a b l e 1, all 10 p a t i e n t s s h o w e d a b n o r m a l i t i e s w i t h the T 2 - w e i g h t e d s e q u e n c e s , w h e r e a s o n l y five s h o w e d a b n o r m a l i t i e s w i t h T 1 - w e i g h t e d sequences.
Acknowledgement. We thank Professor Youichi Ishida of Gunma University for his professional advice regarding neuropathology.
REFERENCES
Aaron, J, New, PFJ, Strand, R, Beaulieu, P, Elmden, K & Brady, T (1984). NMR imaging in temporal lobe epilepsy due to gliomas. Journal of Computer Assisted Tomography, 8(4), 608 613. Bolender, NF, Cromwell, LD, Graves, V, Margolis, MT, Kerber, CW & Wendling, L (1983). Interval appearance of glioblastomas not evident in previous CT examinations. Journal of Computer Assisted Tomography, 7(4), 599-603. Brand-Zawadzki, M, Davis, PL, Crooks, LE, Mills, CM, Norman, D, Newton, TH et al. (1983). NMR demonstration of cerebral abnormalities. Comparison with CT. American Journal of Neuroradiology, 4, 117-124. Bydder, GM, Steiner, RE, Thomas, D J, Marshall, J, Gilderdale, DJ & Young, IR (1983). Nuclear magnetic resonance imaging of the posterior fossa: 50 cases. Clinical Radiology, 34, 173-188.
Davis, KR, Taveras, JM, Roberson, GH & Ackerman, RH (1976). Some limitations of computed tomography in the diagnosis of neurological diseases. American Journal of Roentgenology, 127, 111123. Gr~ifin yon Einsiedel, H & L6ffter, W (1982). Nuclear magnetic resonance imaging of brain tumors unrevealed by CT. European Journal of Radiology, 2, 226-234. Jabbari, B, Gunderson, CH, Wippold, F, Charles, C, Sherman, J, Bartoszek, D et al. (1986). Magnetic resonance imaging in partial complex epilepsy. Archives of Neurology, 43, 869 872. Laster, DW, Penry, JK, Moody, DM, Ball, MR, Witcofski, RL & Riela, AR (1985). Chronic seizure disorders: Contribution of MR imaging when CT is normal. American Journal of Neuroradiology, 6,177 180. Lesser, RP, Modic, MT, Weinstein, MA, Duchesneau, PM, Luders, H, Dinner, DS et al. (1986). Magnetic resonance imaging (1.5 Tesla) in patients with intractable focal seizures. Archives of Neurology, 43, 367 371. McGinnis, BD, Brady, TJ, New, PFJ, Buonanno, FS, Pykett, IL, DeLaPaz, RL et al. (1983). Nuclear magnetic resonance (NMR) imaging of tumors in the posterior fossa. Journal of Computer Assisted Tomography, 7, 575-584. McLachlan, RS, Nicholson, RL, Black, S, Cart, T & Blume, WT (1985). Nuclear magnetic resonance imaging, a new approach to the investigation of refractory temporal lobe epilepsy. Epilepsia, 26(6), 555-562. Price, AC, Runge, VM, Allen, JH, Partin, CL & James, AE (1986). Primary glioma: Diagnosis with magnetic resonance imaging. Journal of Computer Assisted Tomography, I0, 325-334. Smith, AS, Weintein, MA, Modic, MT, Pavlicek, W, Rogers, LR, Budd, TG et al. (1985). Magnetic resonance with marked T-2 weighted images: Improved demonstration of brain lesions, tumor, and edema. American Journal of Roentgenology, 145, 949-955. Stone, JL, Hughes, JR, Barr, A, Tan, W, Russell, E & Crowell, RM (1986). Neuroradiological and electroencephalographic features in a case of temporal lobe status epilepticus. Neurosurgery, 18, 212 216. Sundaresan, N, Larsen, M, Deck, MDF & Fraser, RAR (1980). Brain tumors presenting as small calcified lesions on computerized tomography. Report of three cases. Child~ Brain, 7, 95-100. Young, IR, Burl, M, Clarke, GJ, Hall, AS, Pasmore, T, Collins, AG, et al. (1981). Magnetic resonance properties of hydrogen: imaging of the posterior fossa. American Journal of Roentgenology, I37, 895901.