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CT evidence of grey matter calcification secondary to radiation therapy
Compulrrid
Tomographv
Pergamon
Press 1977. Vol. 1. pp. 103~ 110
Punted in Great Britain
CT EVIDENCE OF GREY MATTER CALCIFICATION SECONDARY TO RADIATION THERAPY K. FRANCISLEEand JUNGHo SUH Thomas Jefferson University Hospital, Philadelphia, PA 19107. U.S.A. (Received
24 September
1976)
Abstract-There are four previously reported cases of post-irradiation calcification in the basal ganglia as demonstrated on the conventional skull roentgenograms. We have described two additional cases with grey matter calcification, which were demonstrated 10 and 14yr after radiation therapy for an optic glioma and a medulloblastoma, respectively. The calcification was clearly demonstrated on CT scan, although it was not apparent on the skull roentgenogram. The exact pathogenesis of this condition is not clear. ‘It appears, however, to be related to radiation vasculitis of the small vessels of the brain with resultant hyalinization and calcification. A long-term follow up study would be necessary to evaluate the significance and implication of post-irradiation calcification of the grey matter. CT is the most sensitive method of demonstrating the intracranial calcification in uiuo. Calcification
Roentgenogram
Grey matter
Radiation vasculitis
Post-irradiation
INTRODUCTION
Harwood-Nash and Reilly [S] reported on two children with basal ganglia calcification subsequent to radiation therapy to the head. Since then, Kramer and Lee [9] and Numaguchi et al. [15] have described one case each of post-irradiation calcification in the grey matter. The calcification was demonstrated on the skull roentgenograms taken 10 months to 9 yr after irradiation of the head for various neoplastic conditions of the four reported cases. During the past two years, we have seen two additional patients with post-irradiation calcification in the grey matter as demonstrated by CT (ACTA scan). Computed tomography has proven to be extremely helpful in demonstrating both salient and subtle calcification in the brain. CASE
REPORTS
Case 1. A 12 year old girl
At the age of 2, she was found to have glioma of the right optic nerve at surgery, and radiation therapy was given with a tumor dose of 5,500 rad to the suprasellar region through 5 x 5 cm portal using the rotational technique (Fig. 1). She became totally blind in the right eye, but her left vision was normal. At the age of 9, her vision started deteriorating in the left eye with intermittent headaches, and a pneumoencephalogram showed evidence of an empty sella with no recurrent tumor (Fig. 2). At the age of 12, a CT scan was obtained to determine the cause of the headaches and blurred vision. An extensive calcification was noted in the basal ganglia and posteromedial aspect of the thalamus bilaterally on CT (Fig. 3). In retrospect, there is very subtle calcification in the right basal ganglia in the semiaxial view of the skull (Fig. 4). Case 2. A 16 year old boy
At the age of 2, the patient was found to have medulloblastoma at surgery. A course of Cobalt 60 treatment was given to the posterior fossa with the tumor dose of 4,700 rad. Approximately 4,300 rad to the supratentorial region and 4,000 rad to the entire spinal 103
104
K. FRANCISLEE and JUNG Ho SUH
axis were given. The patient did well except for occasional headache and minor seizure disorder. The CT scan in 1975 showed calcification in the basal ganglia and cerebral cortex (Fig. 5). DISCUSSION About one half of the patients with parathyroid disorders (e.g. idiopathic, post operative, and pseudo-hypoparathyroidism) demonstrated basal ganglia calcification on skull roentgenograms [14, lo]. Calcification in the grey matter may also occur in carbon monoxide or lead poisoning, Fahr’s syndrome (familial cerebrovascular ferrcFcalcinosis) [l, 2,6,7,12]. Other causes of basal ganglia and paraventricular calcification include tuberous sclerosis, toxoplasmosis, cytomegalic inclusion disease, amaurotic idiocy, and idiopathic cerebral calcification [S, 8,12,15-J. Microscopic description of bilateral basal ganglia calcification was first made by Virchow [17]. In 1935 Fritzsche [7] was the first to report roentgenologic appearance of basal ganglia calcification in 3 siblings. Its occurrence in idiopathic hypoparathyroidism was described by Eaton, Camp and Love in 1939 [4]. Basal ganglia calcification in pseudohypoparathyroidism was first reported by Sprague, Hains, and Power [16] in 1945. Its occurrence subsequent to radiation therapy was first described by Harwood-Nash and Reilly [S] in 1970. Intrathecal administration of Methotrexate may produce intracranial calcification L-141.Kramer and Lee [9] described a case with diffuse calcification in the basal ganglia and cerebral cortex subsequent to irradiation and methotrexate (intrathecal) treatment for acute lymphocytic leukemia (Table 1). Nakagaki et al. [13] described monkey brain damage from radiation in the therapeutic range. At six months after 6,000 rad, widely scattered punctate necrotic lesions, 1 mm or less, were demonstrated, whereas, 1 yr later almost complete mineralization of necrotic lesions with innumerable minute deposits of calcium and iron were observed. Vasculitis and telangiectasis were also present. The pathogenesis of calcification in the grey matter is not clear. Microscopically, vasculitis, fibroblastic process, hyalinization, and calcification were observed in the brains of both humans and animals following irradiation to the heads (Fig. 6). The possibility of an autoimmune reaction localized to the irradiated demyelinated tissue Table 1. Reported cases of basal ganglia calcification subsequent to radiation therapy CaSC
NO.
Sex
Author
Pathology
and
site
Radiation therapy source. field size and dose
Duration radiation
following therapy
Serum calcium and phosphorus lW&
I.
Harwood-Nash and Reilly. 1970
9
F
Gliohlastoma multlforme in the suprasellar region
External cobalt 60, 5 x 5cm’ 4,500 tad/4 weeks and 4,500 rad/4 weeks 3 yr later
3 Y’
Normal
2.
Harwood-Nash and Reilly, 1970
3
M
Histiocytosis x involving multiple areas of the
200 kV X-ray various ports 3COrad x 3. 1,250 rad next year and 1,700 rad following year
9 Yr
Normal
3.
Kramer Lee, 1974
10
M
CNS involvement of lymphocytic leukemia
External cobalt 550 rad and methotrexate
4.
Numaguchi 1974
9
F
Astrocytoma in the thalamic region
5
Lee and 1976
Sub,
12
F
6.
Lee and 1976
Suh,
16
M
and
et al.
IO month
Normal
Supervoltage 2 meV resonant transformer, 7 x 7cm” 6.ooO r&d/h weeks
6 yr
Normal
Spongmblastoma polare, R,ghr optic nerve
External cobalt 60 5 x 5cmz 5.500 rad/5 weeks
IOyr
Normal
Medulloblastoma cerebellar vermis
Total bran and spine axis 4,ooO tad, 4.700 rad to vermis/ 4: weeks
14yr
Normal
60
JO5
Fig. 1. Case 1 (at age 2). Radiation dosimetry. CoGo with 180”rotational technique and a wedge filter provided 5500 rad in 25 treatments during a period of 5 weeks. Fig. 2. Case 1 (at age 10). The initial pneumoencephalogram (not shown) demonstrated a suprasellar tumor which was proved to be optic glioma. Seven years later, a second pneumoencephalogram showed no evidence of tumor mass, the third ventricle being fully expanded (a large arrow). An empty sella (intrasellar herniation of the subarachnoid space) was demonstrated (small arrows) A “J” shaped sella is still evident. 3v: 3rd ventricle.
106
Fig. 3. Jase 1 (at age 12). 10 yr after radiation therapy. A CT (ACTA) shows der lse hlOIllOgene:OU calcifications in the grey matter; lenticular nucleus (lateral arrows) and post erior aspect of the thalamus (lower arrows), bilaterally. Fig. 4. Case 1 (same time as Fig. 3). A semiaxial view of the skull, in retrospect, shows very faint linear calcification in the right basal ganglia (arrows).
Fig. 5. Case 2. A 16-year-old boy who had Co6’ therapy (4000-4700 rad) at the age (If 2 for med Ull’blastoma. A CT scan shows calcification in the basal ganglia (upper arrow ,‘s) and cerebral cortex (lower arrows). Fig. 6. Post-irradiation calcification in the cerebral cortex. Neuronal cell loss is accorr lpalnied by fc,ca calcifications in the deeper layers of the cerebral cortex 8 yr after X-irradiation. X 108 (Courtesy of Dr. L. J. Rubinstein).
CT evidence
of grey matter
calcification
109
with subsequent accumulation of abnormal metabolites was suggested by Lampert et Babbitt et al. [ 11 proposed that the ferrqcalcinosis is the end result of a process of circulatory disturbance resulting in local anoxia and necrosis. Harwood-Nash and Reilly [S] postulate that hypersensitivity of small vessels of the basal ganglia to radiation produces vascular damage with hypoxia resulting in calcification. We feel that radiation vasculitis and demyelination due to a localized autoimmune reaction or hypersensitivity to radiation are responsible for hyalinization and eventual calcification in the grey matter. A long term follow up study would be necessary in order to assess the significance and implication of post-irradiation calcification in the grey matter. Calcifications may not be apparent on the plain skull roentgenograms or even on the tomograms unless sufficient calcium deposit is present. With the use of computerized tomography, we are able to detect both subtle and salient intracranial calcification.
al. [lo].
SUMMARY We have described two cases of grey matter calcification subsequent to radiation therapy. CT is extremely useful in demonstrating subtle calcification in the basal ganglia and cortex. The pathogenesis of grey matter calcification following irradiation has been discussed. REFERENCES I. D. P. Babbitt, T. Tang, J. Dobbs and R. Berk, Idiopathic familial cerebrovascular ferrocalcinosis (Fahr’s disease) and review of differential diagnosis of intracranial calcification in children, Am. J. Roentgenol. 105. 352 (1969). 2. J. C. Bennett, R. H. Maffly and H. L. Steinbach. Significance of bilateral basal ganglia calcification, Radiology 72, 368 (1959). 3. J. D. Camp, Symmetrical calcification of basal ganglia, Radiology 49, 568 (1947). 4. L. M. Eaton, J. D. Camp and J. G. Love, Symmetrical cerebral calcification. particularly of basal ganglia, Arch. Neural. Psychiat. 41. 921 (1939). demonstrable reoentgenographically, 5. C. R. Fitz, C. F. Dereck, D. C. F. Harwood-Nash and J. R. Thompson. Neuroradiology of tuberous sclerosis in children, Radiology 110, 635 (1974). 6. R. L. Friede, K. R. Magee and E. W. Mack, Idiopathic non-arteriosclerotic calcification of cerebral vessels. AMA. Arch. Neural. 5, 219 (1961). 7. R. Fritzsche, Eine familiLr auftretende Form von Oligophrenie mit riientgenologisch nachweisbaren symmetrischen Kalkablagerungen im Gehirn, besonders in den Stammganglien. Schweiz. Arch. Neural. I/. Psychiat. 35, 1 (1935). 8. D. C. F. Harwood-Nash and B. J. Reilly, Calcification of basal ganglia following radiation therapy, Am. J. Roentgenal. 108. 392 (1970). 9. S. Kramer and K. F. Lee, Complications of radiation therapy central nervous system, Sentin. Roentgenol 9. 15 (1974). IO. P. Lampert, M. I. Tom and W. D. Rider, Disseminated demyelination of the brain following Cob” (Gamma) radiation, AMA Arch. Pathol. 68, 322 (1959). 11. E. V. Medill, Bilateral symmetric calcification of basal ganglia associated with parathyroid insufficiency, Bit. J. Radial. 24, 685 (1951). 12. J. C. Melchoir, C. E. Benda and P. I. Yakovlev. Familial idiopathic cerebral calcifications in childhood. AMA Am. J. Dis. Child. 99, 787 (1960). 13. H. Nakagaki, G. Brunhart, T. L. Kemper and W. F. Caveness. Monkey brain damage from radiation in the therapeutic range, J. Neurosurg. 44. 3 (1976). 14. H. Norrell, C. B. Wilson, D. E. Slagel and D. B. Clark, Leukoencephalopathy following the administration of methotrexate into the cerebrospinal fluid in the treatment of primary brain tumors, Cancer 33. 923
(1974). 15. Y. Numaguchi, J. C. Hoffman and P. J. Sones, Basal ganglia calcification as a late radiation effect, Am. J. Roentgenol. 123, 27 (1975). 16. R. G. Sprague, S. F. Haines and M. H. Power, Metabolic effects of parathyroid hormone, dihydrotachysterol and calciferol in a case of pseudo-hvpoparathvroidism. J. Lab. C/in. Med. 30. 361 (1945). 17. R Virchow, Kalk-metastasen. Vbchows ,&h: Path.. Anat. 8, 103 (1855).
About the Author-K. FRANCISLEE was born on I March. 1929, in Seoul. Korea. He received the M.D. degree in 1951 from Severance Union Medical College in Seoul, Korea, and the D.Sc. degree in neuroradiology in 1963 from Yonsei University in Seoul. He was certified by the American Board of Radiology in 1960. Dr. Lee was Director of the Radiology Research Institute of Seoul from 1963 to 1964 and has been Professor of Radiology at Thomas Jefferson University Hospital since 1971.
110
K. FRANCIS LEE and JUNG Ho SUH His professional affiliations include Society, Philadelphia County Medical Society of Neuroradiology, Radiological logy, American Roentgen Ray Society, Society of Nuclear Medicine.
American Medical Association, Pennsylvania Medical Society, Philadelphia Neurological Society, American Society of North America, American College of RadioCollege of Physicians of Philadelphia, and the Korean
Ho SUH was born in Feb. 1939, in Seoul, Korea, and received the M.D. degree in 1964 from the College of Medicine at Yonsei University in Seoul. Dr. Suh has been Assistant Professor of Radiology at Yonsei University College of Medicine since 1973. He is presently a Fellow of Neuroradiology at Thomas Jefferson University Hospital. About the Author-JuNc
Tomographv
Pergamon
Press 1977. Vol. 1. pp. 103~ 110
Punted in Great Britain
CT EVIDENCE OF GREY MATTER CALCIFICATION SECONDARY TO RADIATION THERAPY K. FRANCISLEEand JUNGHo SUH Thomas Jefferson University Hospital, Philadelphia, PA 19107. U.S.A. (Received
24 September
1976)
Abstract-There are four previously reported cases of post-irradiation calcification in the basal ganglia as demonstrated on the conventional skull roentgenograms. We have described two additional cases with grey matter calcification, which were demonstrated 10 and 14yr after radiation therapy for an optic glioma and a medulloblastoma, respectively. The calcification was clearly demonstrated on CT scan, although it was not apparent on the skull roentgenogram. The exact pathogenesis of this condition is not clear. ‘It appears, however, to be related to radiation vasculitis of the small vessels of the brain with resultant hyalinization and calcification. A long-term follow up study would be necessary to evaluate the significance and implication of post-irradiation calcification of the grey matter. CT is the most sensitive method of demonstrating the intracranial calcification in uiuo. Calcification
Roentgenogram
Grey matter
Radiation vasculitis
Post-irradiation
INTRODUCTION
Harwood-Nash and Reilly [S] reported on two children with basal ganglia calcification subsequent to radiation therapy to the head. Since then, Kramer and Lee [9] and Numaguchi et al. [15] have described one case each of post-irradiation calcification in the grey matter. The calcification was demonstrated on the skull roentgenograms taken 10 months to 9 yr after irradiation of the head for various neoplastic conditions of the four reported cases. During the past two years, we have seen two additional patients with post-irradiation calcification in the grey matter as demonstrated by CT (ACTA scan). Computed tomography has proven to be extremely helpful in demonstrating both salient and subtle calcification in the brain. CASE
REPORTS
Case 1. A 12 year old girl
At the age of 2, she was found to have glioma of the right optic nerve at surgery, and radiation therapy was given with a tumor dose of 5,500 rad to the suprasellar region through 5 x 5 cm portal using the rotational technique (Fig. 1). She became totally blind in the right eye, but her left vision was normal. At the age of 9, her vision started deteriorating in the left eye with intermittent headaches, and a pneumoencephalogram showed evidence of an empty sella with no recurrent tumor (Fig. 2). At the age of 12, a CT scan was obtained to determine the cause of the headaches and blurred vision. An extensive calcification was noted in the basal ganglia and posteromedial aspect of the thalamus bilaterally on CT (Fig. 3). In retrospect, there is very subtle calcification in the right basal ganglia in the semiaxial view of the skull (Fig. 4). Case 2. A 16 year old boy
At the age of 2, the patient was found to have medulloblastoma at surgery. A course of Cobalt 60 treatment was given to the posterior fossa with the tumor dose of 4,700 rad. Approximately 4,300 rad to the supratentorial region and 4,000 rad to the entire spinal 103
104
K. FRANCISLEE and JUNG Ho SUH
axis were given. The patient did well except for occasional headache and minor seizure disorder. The CT scan in 1975 showed calcification in the basal ganglia and cerebral cortex (Fig. 5). DISCUSSION About one half of the patients with parathyroid disorders (e.g. idiopathic, post operative, and pseudo-hypoparathyroidism) demonstrated basal ganglia calcification on skull roentgenograms [14, lo]. Calcification in the grey matter may also occur in carbon monoxide or lead poisoning, Fahr’s syndrome (familial cerebrovascular ferrcFcalcinosis) [l, 2,6,7,12]. Other causes of basal ganglia and paraventricular calcification include tuberous sclerosis, toxoplasmosis, cytomegalic inclusion disease, amaurotic idiocy, and idiopathic cerebral calcification [S, 8,12,15-J. Microscopic description of bilateral basal ganglia calcification was first made by Virchow [17]. In 1935 Fritzsche [7] was the first to report roentgenologic appearance of basal ganglia calcification in 3 siblings. Its occurrence in idiopathic hypoparathyroidism was described by Eaton, Camp and Love in 1939 [4]. Basal ganglia calcification in pseudohypoparathyroidism was first reported by Sprague, Hains, and Power [16] in 1945. Its occurrence subsequent to radiation therapy was first described by Harwood-Nash and Reilly [S] in 1970. Intrathecal administration of Methotrexate may produce intracranial calcification L-141.Kramer and Lee [9] described a case with diffuse calcification in the basal ganglia and cerebral cortex subsequent to irradiation and methotrexate (intrathecal) treatment for acute lymphocytic leukemia (Table 1). Nakagaki et al. [13] described monkey brain damage from radiation in the therapeutic range. At six months after 6,000 rad, widely scattered punctate necrotic lesions, 1 mm or less, were demonstrated, whereas, 1 yr later almost complete mineralization of necrotic lesions with innumerable minute deposits of calcium and iron were observed. Vasculitis and telangiectasis were also present. The pathogenesis of calcification in the grey matter is not clear. Microscopically, vasculitis, fibroblastic process, hyalinization, and calcification were observed in the brains of both humans and animals following irradiation to the heads (Fig. 6). The possibility of an autoimmune reaction localized to the irradiated demyelinated tissue Table 1. Reported cases of basal ganglia calcification subsequent to radiation therapy CaSC
NO.
Sex
Author
Pathology
and
site
Radiation therapy source. field size and dose
Duration radiation
following therapy
Serum calcium and phosphorus lW&
I.
Harwood-Nash and Reilly. 1970
9
F
Gliohlastoma multlforme in the suprasellar region
External cobalt 60, 5 x 5cm’ 4,500 tad/4 weeks and 4,500 rad/4 weeks 3 yr later
3 Y’
Normal
2.
Harwood-Nash and Reilly, 1970
3
M
Histiocytosis x involving multiple areas of the
200 kV X-ray various ports 3COrad x 3. 1,250 rad next year and 1,700 rad following year
9 Yr
Normal
3.
Kramer Lee, 1974
10
M
CNS involvement of lymphocytic leukemia
External cobalt 550 rad and methotrexate
4.
Numaguchi 1974
9
F
Astrocytoma in the thalamic region
5
Lee and 1976
Sub,
12
F
6.
Lee and 1976
Suh,
16
M
and
et al.
IO month
Normal
Supervoltage 2 meV resonant transformer, 7 x 7cm” 6.ooO r&d/h weeks
6 yr
Normal
Spongmblastoma polare, R,ghr optic nerve
External cobalt 60 5 x 5cmz 5.500 rad/5 weeks
IOyr
Normal
Medulloblastoma cerebellar vermis
Total bran and spine axis 4,ooO tad, 4.700 rad to vermis/ 4: weeks
14yr
Normal
60
JO5
Fig. 1. Case 1 (at age 2). Radiation dosimetry. CoGo with 180”rotational technique and a wedge filter provided 5500 rad in 25 treatments during a period of 5 weeks. Fig. 2. Case 1 (at age 10). The initial pneumoencephalogram (not shown) demonstrated a suprasellar tumor which was proved to be optic glioma. Seven years later, a second pneumoencephalogram showed no evidence of tumor mass, the third ventricle being fully expanded (a large arrow). An empty sella (intrasellar herniation of the subarachnoid space) was demonstrated (small arrows) A “J” shaped sella is still evident. 3v: 3rd ventricle.
106
Fig. 3. Jase 1 (at age 12). 10 yr after radiation therapy. A CT (ACTA) shows der lse hlOIllOgene:OU calcifications in the grey matter; lenticular nucleus (lateral arrows) and post erior aspect of the thalamus (lower arrows), bilaterally. Fig. 4. Case 1 (same time as Fig. 3). A semiaxial view of the skull, in retrospect, shows very faint linear calcification in the right basal ganglia (arrows).
Fig. 5. Case 2. A 16-year-old boy who had Co6’ therapy (4000-4700 rad) at the age (If 2 for med Ull’blastoma. A CT scan shows calcification in the basal ganglia (upper arrow ,‘s) and cerebral cortex (lower arrows). Fig. 6. Post-irradiation calcification in the cerebral cortex. Neuronal cell loss is accorr lpalnied by fc,ca calcifications in the deeper layers of the cerebral cortex 8 yr after X-irradiation. X 108 (Courtesy of Dr. L. J. Rubinstein).
CT evidence
of grey matter
calcification
109
with subsequent accumulation of abnormal metabolites was suggested by Lampert et Babbitt et al. [ 11 proposed that the ferrqcalcinosis is the end result of a process of circulatory disturbance resulting in local anoxia and necrosis. Harwood-Nash and Reilly [S] postulate that hypersensitivity of small vessels of the basal ganglia to radiation produces vascular damage with hypoxia resulting in calcification. We feel that radiation vasculitis and demyelination due to a localized autoimmune reaction or hypersensitivity to radiation are responsible for hyalinization and eventual calcification in the grey matter. A long term follow up study would be necessary in order to assess the significance and implication of post-irradiation calcification in the grey matter. Calcifications may not be apparent on the plain skull roentgenograms or even on the tomograms unless sufficient calcium deposit is present. With the use of computerized tomography, we are able to detect both subtle and salient intracranial calcification.
al. [lo].
SUMMARY We have described two cases of grey matter calcification subsequent to radiation therapy. CT is extremely useful in demonstrating subtle calcification in the basal ganglia and cortex. The pathogenesis of grey matter calcification following irradiation has been discussed. REFERENCES I. D. P. Babbitt, T. Tang, J. Dobbs and R. Berk, Idiopathic familial cerebrovascular ferrocalcinosis (Fahr’s disease) and review of differential diagnosis of intracranial calcification in children, Am. J. Roentgenol. 105. 352 (1969). 2. J. C. Bennett, R. H. Maffly and H. L. Steinbach. Significance of bilateral basal ganglia calcification, Radiology 72, 368 (1959). 3. J. D. Camp, Symmetrical calcification of basal ganglia, Radiology 49, 568 (1947). 4. L. M. Eaton, J. D. Camp and J. G. Love, Symmetrical cerebral calcification. particularly of basal ganglia, Arch. Neural. Psychiat. 41. 921 (1939). demonstrable reoentgenographically, 5. C. R. Fitz, C. F. Dereck, D. C. F. Harwood-Nash and J. R. Thompson. Neuroradiology of tuberous sclerosis in children, Radiology 110, 635 (1974). 6. R. L. Friede, K. R. Magee and E. W. Mack, Idiopathic non-arteriosclerotic calcification of cerebral vessels. AMA. Arch. Neural. 5, 219 (1961). 7. R. Fritzsche, Eine familiLr auftretende Form von Oligophrenie mit riientgenologisch nachweisbaren symmetrischen Kalkablagerungen im Gehirn, besonders in den Stammganglien. Schweiz. Arch. Neural. I/. Psychiat. 35, 1 (1935). 8. D. C. F. Harwood-Nash and B. J. Reilly, Calcification of basal ganglia following radiation therapy, Am. J. Roentgenal. 108. 392 (1970). 9. S. Kramer and K. F. Lee, Complications of radiation therapy central nervous system, Sentin. Roentgenol 9. 15 (1974). IO. P. Lampert, M. I. Tom and W. D. Rider, Disseminated demyelination of the brain following Cob” (Gamma) radiation, AMA Arch. Pathol. 68, 322 (1959). 11. E. V. Medill, Bilateral symmetric calcification of basal ganglia associated with parathyroid insufficiency, Bit. J. Radial. 24, 685 (1951). 12. J. C. Melchoir, C. E. Benda and P. I. Yakovlev. Familial idiopathic cerebral calcifications in childhood. AMA Am. J. Dis. Child. 99, 787 (1960). 13. H. Nakagaki, G. Brunhart, T. L. Kemper and W. F. Caveness. Monkey brain damage from radiation in the therapeutic range, J. Neurosurg. 44. 3 (1976). 14. H. Norrell, C. B. Wilson, D. E. Slagel and D. B. Clark, Leukoencephalopathy following the administration of methotrexate into the cerebrospinal fluid in the treatment of primary brain tumors, Cancer 33. 923
(1974). 15. Y. Numaguchi, J. C. Hoffman and P. J. Sones, Basal ganglia calcification as a late radiation effect, Am. J. Roentgenol. 123, 27 (1975). 16. R. G. Sprague, S. F. Haines and M. H. Power, Metabolic effects of parathyroid hormone, dihydrotachysterol and calciferol in a case of pseudo-hvpoparathvroidism. J. Lab. C/in. Med. 30. 361 (1945). 17. R Virchow, Kalk-metastasen. Vbchows ,&h: Path.. Anat. 8, 103 (1855).
About the Author-K. FRANCISLEE was born on I March. 1929, in Seoul. Korea. He received the M.D. degree in 1951 from Severance Union Medical College in Seoul, Korea, and the D.Sc. degree in neuroradiology in 1963 from Yonsei University in Seoul. He was certified by the American Board of Radiology in 1960. Dr. Lee was Director of the Radiology Research Institute of Seoul from 1963 to 1964 and has been Professor of Radiology at Thomas Jefferson University Hospital since 1971.
110
K. FRANCIS LEE and JUNG Ho SUH His professional affiliations include Society, Philadelphia County Medical Society of Neuroradiology, Radiological logy, American Roentgen Ray Society, Society of Nuclear Medicine.
American Medical Association, Pennsylvania Medical Society, Philadelphia Neurological Society, American Society of North America, American College of RadioCollege of Physicians of Philadelphia, and the Korean
Ho SUH was born in Feb. 1939, in Seoul, Korea, and received the M.D. degree in 1964 from the College of Medicine at Yonsei University in Seoul. Dr. Suh has been Assistant Professor of Radiology at Yonsei University College of Medicine since 1973. He is presently a Fellow of Neuroradiology at Thomas Jefferson University Hospital. About the Author-JuNc