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The chronic expanding intracerebral hematoma
Cmpuferized Medml Ima,&‘and Graphm, Vol. 14, No. I, pp. 61-65, Printed in the U.S.A. All rights reserved.
THE CHRONIC
1990 Copyright
EXPANDING
INTRACEREBRAL
0X95-61 1 l/90 $3.00 + .OO 0 1990 Pergamon Press plc
HEMATOMA
Leon A. Weisberg, Antonio Stazio and Debra Elliott Department of Neurology and Psychiatry of the Tulane Medical School, Department of Neurology Veterans Administration Hospital of New Orleans and the Charity Hospital of New Orleans
of the
(Received 5 May 1989)
Abstract-Three normotensive patients presented with seizures and CT showed an intracerebral hematoma. Although these patients had no more seizures and developed no other neurological deficit, repeat CT scans (performed 2 to 3 weeks later) showed hematoma enlargement. Angiogram was performed in 2 cases and showed no evidence of vascular malformation or neoplasm. Six weeks to 6 months later, CT showed that the hematoma had changed from a hyperdense to an isodense appearance and in two cases slight enhancement occurred. During a follow-up interval of 6 to 24 months, no other neurological episodes have occurred. The etiology of the chronic expanding intracerebral hematomas was not delineated in these 3 patients. Key Words:
Intracerebral hematoma, Seizures, Progressive neurological deficit, Ring enhancement, bosed anteriovenous malformation
CASE
INTRODUCTION
Angiography, Throm-
REPORT
Case I
Parenchymal or intracerebral hematoma (ICH) usually present with sudden onset of focal neurological deficit. Maximal severity is usually reached immediately or within several hours of the initial clinical ictus. Seizures may occur with subcortical white matter hematomas of any etiology, but seizures are more common if the ICH is caused by vascular malformation, aneurysm or neoplasm (1, 2, 3). The concept of the “chronic expanding intracerebral hematoma” has been recently introduced (4-7). These patients may present with seizures or progressive neurological deficit. CT may show superficial subcortical white matter hematoma and the hematoma may enhance. Angiography may show an avascular mass lesion or be normal. In one series (4) surgery was performed and a chronic encapsulated hematoma with surrounding collagen membrane were the characteristic findings in these patients. Of these 10 patients, two had cryptic vascular malformation (4). The present study reports the clinical and CT findings in three patients who fulfilled the diagnostic criteria for “chronic expanding intracerebral hematomas.” These patients did not undergo surgical hematoma evacuation. They were followed with serial CT scans which subsequently showed spontaneous decrease in hematoma size.
A 40-year-old alcoholic man had been sober for over 18 months. He was attending an Alcoholic Anonymous meeting and had a generalized major motor seizure. He did not appear to injure his head. He rapidly recovered consciousness. Blood pressure and neurological examination were entirely normal. Laboratory studies showed no coagulation disturbances. Initial CT (Fig. 1) showed a superficial right temporal-parietal hematoma. Electroencephalogram (EEG) showed a right hemisphere slow wave pattern. The patient was treated with phenytoin, 300 mg per day. CT was repeated 3 weeks later (Fig. 2) and showed increased hematoma size. There was increased mass effect and surrounding edema. The lesion appeared to enhance slightly. He had no further seizures. Because he was neurologically asymptomatic, he was continued on anticonvulsant medication and no operation was performed. Eight months later, CT (Fig. 3) showed resolution of hyperdense appearance of the hematoma, but there was still slight enhancement.
Case 2 A 42-year-old woman had a generalized major motor seizure. Following the seizure, she had no abnormal neurological signs. Blood pressure was normal. EEG showed a right hemispheric slow wave focus with interspersed spike discharges. CT showed a right temporal-parietal hyperdense noncalcified lesion with slight peripheral enhancement. She was
Address Correspondence to: Leon A. Weisberg, M.D., Department of Neurology and Psychiatry, Tulane Medical Center, 14 15 Tulane Avenue, New Orleans, LA 70 112. 61
Computerized
Medical
Imaging
and Graphics
January-February/l990,
Volume
14, Number
1
mained neurologically asymptomatic. Six weeks later CT showed hematoma resolution and disappearance of the enhancement. She was continued on anticonvulsants and had good seizure control for 2 years. DISCUSSION
Fig. 1. Initial CT shows right (reader’s left) hyperdense temporal-parietal nonhomogeneous hyperdense nonenhancing round lesion with surrounding hypodense region. There is slight ventricular compression.
treated with phentoin, 300 mg per day, and had no further seizures. Three weeks later, CT showed hematoma enlargement with more intense peripheral rim enhancement. The patient refused angiography. Three months later she had no neurological symptoms and had no further seizures. Four months later, CT showed complete hematoma resolution; however there was slight nodular enhancement. She had no further seizures during a six month follow-up. Case 3 A 4 l-year-old woman had several brief staring spells preceded by an olfactory aura. Later she had a generalized seizure; postictally she had no focal neurological signs. Blood pressure was normal. CT showed a hyperdense noncalcified temporal region subcortical hematoma. There was no enhancement. She was treated with phenytoin, 300 mg per day, and had no further seizures. Two weeks later, CT showed increased hematoma size and more mass effect with slight peripheral enhancement. Angiogram showed no vascular malformation or neoplasm. She re-
There have been several reports describing the clinical and CT findings of the “chronic expanding intracerebral hematoma” (4-7). These patients had no clinical evidence of coagulation disturbances and no risk factors for intracranial hemorrhage (e.g., alcoholism, endocarditis, arteritis). These young patients did not have systemic arterial hypertension. The clinical features of these patients with “chronic expanding ICH” were separated into two groups; (a) seizures, (b) progressive neurological deficit and papilledema. Because the clinical and CT findings simulated the presentation of a neoplasm or vascular malformation, surgical evacuation was performed. Two types of chronic ICH have been reported; (a) liquefied chronic hematoma, (b) solid clot with surrounding peripheral capsule. In patients with chronic expanding ICH, it is important to perform a thorough histological search for an underlying neoplasm or vascular malformation (8,9). In one series of ten patients with chronic expanding ICH, two had arteriovenous malformations identified by histological findings. In patients with ICH, blood extravasates from arterioles into the brain parenchyma. This usually occurs over an interval of several minutes (10). There are rare reports of continued active bleeding with CT visualization of hematoma enlargement over a more prolonged interval (11). With progressive hematoma enlargement, continued neurological deterioration would be expected. In our 3 cases, the hematoma enlargement was observed over an interval of several weeks; however the patients remained neurologically stable. In rare cases of trauma-related ICH, there may be delayed hematoma enlargement. This results from impaired cerebral autoregulation with increased cerebral blood flow into an edematous and necrotic brain tissue (12). Since our three patients had seizures and may have hit their heads (although there were no external signs of head trauma), this is a possible explanation of hematoma enlargement. We consider this to be unlikely because hematoma enlargement occurred 2 to 3 weeks after the initial ictus rather than within 24 to 72 hours. In one series of 10 patients with “chronic expanding ICH,” CT showed the lesion to be hyperdense with surrounding hypodense component. In two cases, there was interspersed calcifications. In 7 of 10 cases, there was an enhancing peripheral rim.
Chronic expanding intracerebral hematoma 0 L. A.
WEISBERG et al.
63
(a)
Fig. 2. Repeat CT scan was performed 3 weeks later. This shows that the hematoma is larger in size with slightly more ventricular compression (a). The hyperdense component at one level (b) shows slight diffuse enhancement (c).
Computerized
Medical
Imaging
and Graphics
(4
January-February/
1990, Volume
14, Number
:
(b)
Fig. 3. Repeat CT scan performed six months later. This shows slight residual hyperdense lesion (a) with nodular enhancement (b). There is no surrounding hypodense region or mass effect.
Since all patients had early surgical hematoma evacuation, serial CT scan findings before surgery were not reported. The finding of peripheral ring enhancement associated with a spontaneous or hypertensive hematoma has been previously well documented (13, 14). The peripheral enhancing rim is usually seen 7 to 28 days after the acute hematoma develops. When the enhancement occurs, the following changes have usually occurred; (a) the hyperdense hematoma is decreasing in density and size, (b) surrounding edema has decreased, (c) mass effect is usually reduced. In the CT scans of the ten patients with “chronic expanding ICH,” edema and mass effect were prominent findings (4). In our patients, we visualized peripheral ring enhancement on both the initial and follow-up CT (2 and 3 weeks later) in 2 patients; whereas in the other patient enhancement was not seen on the initial scan and only nodular (rather than peripheral rim) enhancement was seen on the early follow-up scan. In this patient, enhancement was still seen on the scan which was performed 6 months
later. This pattern of an isodense nodular enhancing lesion was similar to that previously reported in intracranial gliosis ( 15). Our three patients presented with seizures and none developed neurological deficit. The hematomas were located in the temporal-parietal white matter. The finding of a normal angiogram does not exclude an occult vascular malformation. Without a longer follow-up period or histological findings, the precise mechanism of the expanding ICH cannot be determined. In some of the previously reported cases of “chronic expanding ICH,” the presence of a thick surrounding fibrous capsule with a central region of clot (in various stages of resolution) would be unlikely to spontaneously resolve; however certain hematomas do resolve without surgery. If the patients are neurologically stable, nonsurgical management may be sufficient if angiography shows no underlying pathological condition. Despite the good outcome in our three cases, it must be remembered that the etiology of the hematomas is not known.
Chronic
expanding
intracerebral
SUMMARY
The clinical and CT findings of three patients with nontraumatic intracerebral hematomas which subsequently enlarged in size are reviewed. There was no neuroradiographic evidence of an underlying vascular malformation or neoplasm. These patients with chronic expanding hematomas differ from the other previously reported patients because the hematoma resolved spontaneously in our cases. REFERENCES 1. Kase, C.S.; Williams, J.P.; Wyatt, D.A.; Mohr, J.P. Lobar intracerebral hematomas: clinical and CT analysis of 22 cases. Neurology 32:1146-l 150; 1982. 2. Ropper, A.H.; Davis, K.R. Lobar cerebral hemorrhages: acute clinical syndromes in 26 cases. Ann. Neurology 8141-147; 1980. 3. Mohr, J.P.; Caplan, L.P.; Melski, J.W. The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 28:754762; 1978. 4. Pozzati, E.; Giulani, G.; Gaist, G.; Piazza, G.; Vergoni, G. Chronic expanding intracerebral hematoma. J. Neurosurg. 65:61 l-614; 1986. 5. Lin, S.Z.; Shih, C.J.; Wang, Y.C. Intracerebral hematoma simulating a new growth. Surg. Neurology 21:459-464; 1984. 6. Reid, J.D.; Kommareddi, S.; Lankerani, M. Chronic expanding hematomas: a clinicopathologic entity. JAMA 244:24412442; 1980. 7. Yashon, D.; Kosnik, E.J. Chronic intracerebral hematoma. Neurosurgery 2:103-106; 1978. 8. Kramer, R.A.; Wing, SD. CT of angiographically occult cerebral vascular malformations. Radiology 123:649-655; 1977.
hematoma
0 L. A. WEISBERG et al.
65
9. Becker, D.H.; Townsend, J.J.; Kramer, R.A. Occult cerebrovascular malformations. Brain 102:249-265; 1979. H.H. Hypertensive intracerebral 10. Herbstein, D.J.; Schaumberg, hematoma. Arch. Neurology 30:4 12-4 16; 1974. 11. Kelley, R.E.; Berger, J.R.; Scheinberg, P. Active bleeding in hypertensive intracerebral hemorrhage: computed tomography findings. Neurology 32:852-856; 1982. 12. Diaz. F.G.: Yock. D.H.: Larson. D. Earlv diagnosis of delaved post:traumatic mtracerebral hematomas. i. Neurosurgery 50:217-223; 1979. R.D.; Leeds, N.E.; Naidich, T.P. Ring blush as13. Zimmerman, sociated with intracerebral hematoma. Radiology 122:70771 1; 1977. 14. Weisberg, LA. Peripheral rim enhancement in supratentorial intracerebral hematoma. Computerized Tomography 4: 145152; 1980. 15. Weisberg, L.A. Computed tomographic findings in intracranial gliosis. Neuroradiology 21:253-257; 198 1.
About the Author-DR. LEON WEISBERG is Professor of Neurology and Head of the Section of Neurology at the Tulane Medical School. He is director of the Neurology-Neurosurgery Service of the Charity Hospital of New Orleans. He is the author-of Cerebral
Computed Tomography; A Text Atlas, Essentials of Clinical Neurological and Decision Making in Adult Neurology. About the Author-DR. ANTONIO STAZIO is Associate Professor of Neurology at the Tulane Medical School. He is Head of Neurology at the Veterans Administration Hospital in New Orleans and director of the Multiple Sclerosis Clinic at the Tulane Medical School. About the Author-DR. DEBRA ELLIOTT is a graduate of the Tulane Medical School. Dr. Elliott is Assistant Professor of Neurology at the Tulane Medical School and Codirector of Neurology Residency Training Program at Tulane Medical School.
THE CHRONIC
1990 Copyright
EXPANDING
INTRACEREBRAL
0X95-61 1 l/90 $3.00 + .OO 0 1990 Pergamon Press plc
HEMATOMA
Leon A. Weisberg, Antonio Stazio and Debra Elliott Department of Neurology and Psychiatry of the Tulane Medical School, Department of Neurology Veterans Administration Hospital of New Orleans and the Charity Hospital of New Orleans
of the
(Received 5 May 1989)
Abstract-Three normotensive patients presented with seizures and CT showed an intracerebral hematoma. Although these patients had no more seizures and developed no other neurological deficit, repeat CT scans (performed 2 to 3 weeks later) showed hematoma enlargement. Angiogram was performed in 2 cases and showed no evidence of vascular malformation or neoplasm. Six weeks to 6 months later, CT showed that the hematoma had changed from a hyperdense to an isodense appearance and in two cases slight enhancement occurred. During a follow-up interval of 6 to 24 months, no other neurological episodes have occurred. The etiology of the chronic expanding intracerebral hematomas was not delineated in these 3 patients. Key Words:
Intracerebral hematoma, Seizures, Progressive neurological deficit, Ring enhancement, bosed anteriovenous malformation
CASE
INTRODUCTION
Angiography, Throm-
REPORT
Case I
Parenchymal or intracerebral hematoma (ICH) usually present with sudden onset of focal neurological deficit. Maximal severity is usually reached immediately or within several hours of the initial clinical ictus. Seizures may occur with subcortical white matter hematomas of any etiology, but seizures are more common if the ICH is caused by vascular malformation, aneurysm or neoplasm (1, 2, 3). The concept of the “chronic expanding intracerebral hematoma” has been recently introduced (4-7). These patients may present with seizures or progressive neurological deficit. CT may show superficial subcortical white matter hematoma and the hematoma may enhance. Angiography may show an avascular mass lesion or be normal. In one series (4) surgery was performed and a chronic encapsulated hematoma with surrounding collagen membrane were the characteristic findings in these patients. Of these 10 patients, two had cryptic vascular malformation (4). The present study reports the clinical and CT findings in three patients who fulfilled the diagnostic criteria for “chronic expanding intracerebral hematomas.” These patients did not undergo surgical hematoma evacuation. They were followed with serial CT scans which subsequently showed spontaneous decrease in hematoma size.
A 40-year-old alcoholic man had been sober for over 18 months. He was attending an Alcoholic Anonymous meeting and had a generalized major motor seizure. He did not appear to injure his head. He rapidly recovered consciousness. Blood pressure and neurological examination were entirely normal. Laboratory studies showed no coagulation disturbances. Initial CT (Fig. 1) showed a superficial right temporal-parietal hematoma. Electroencephalogram (EEG) showed a right hemisphere slow wave pattern. The patient was treated with phenytoin, 300 mg per day. CT was repeated 3 weeks later (Fig. 2) and showed increased hematoma size. There was increased mass effect and surrounding edema. The lesion appeared to enhance slightly. He had no further seizures. Because he was neurologically asymptomatic, he was continued on anticonvulsant medication and no operation was performed. Eight months later, CT (Fig. 3) showed resolution of hyperdense appearance of the hematoma, but there was still slight enhancement.
Case 2 A 42-year-old woman had a generalized major motor seizure. Following the seizure, she had no abnormal neurological signs. Blood pressure was normal. EEG showed a right hemispheric slow wave focus with interspersed spike discharges. CT showed a right temporal-parietal hyperdense noncalcified lesion with slight peripheral enhancement. She was
Address Correspondence to: Leon A. Weisberg, M.D., Department of Neurology and Psychiatry, Tulane Medical Center, 14 15 Tulane Avenue, New Orleans, LA 70 112. 61
Computerized
Medical
Imaging
and Graphics
January-February/l990,
Volume
14, Number
1
mained neurologically asymptomatic. Six weeks later CT showed hematoma resolution and disappearance of the enhancement. She was continued on anticonvulsants and had good seizure control for 2 years. DISCUSSION
Fig. 1. Initial CT shows right (reader’s left) hyperdense temporal-parietal nonhomogeneous hyperdense nonenhancing round lesion with surrounding hypodense region. There is slight ventricular compression.
treated with phentoin, 300 mg per day, and had no further seizures. Three weeks later, CT showed hematoma enlargement with more intense peripheral rim enhancement. The patient refused angiography. Three months later she had no neurological symptoms and had no further seizures. Four months later, CT showed complete hematoma resolution; however there was slight nodular enhancement. She had no further seizures during a six month follow-up. Case 3 A 4 l-year-old woman had several brief staring spells preceded by an olfactory aura. Later she had a generalized seizure; postictally she had no focal neurological signs. Blood pressure was normal. CT showed a hyperdense noncalcified temporal region subcortical hematoma. There was no enhancement. She was treated with phenytoin, 300 mg per day, and had no further seizures. Two weeks later, CT showed increased hematoma size and more mass effect with slight peripheral enhancement. Angiogram showed no vascular malformation or neoplasm. She re-
There have been several reports describing the clinical and CT findings of the “chronic expanding intracerebral hematoma” (4-7). These patients had no clinical evidence of coagulation disturbances and no risk factors for intracranial hemorrhage (e.g., alcoholism, endocarditis, arteritis). These young patients did not have systemic arterial hypertension. The clinical features of these patients with “chronic expanding ICH” were separated into two groups; (a) seizures, (b) progressive neurological deficit and papilledema. Because the clinical and CT findings simulated the presentation of a neoplasm or vascular malformation, surgical evacuation was performed. Two types of chronic ICH have been reported; (a) liquefied chronic hematoma, (b) solid clot with surrounding peripheral capsule. In patients with chronic expanding ICH, it is important to perform a thorough histological search for an underlying neoplasm or vascular malformation (8,9). In one series of ten patients with chronic expanding ICH, two had arteriovenous malformations identified by histological findings. In patients with ICH, blood extravasates from arterioles into the brain parenchyma. This usually occurs over an interval of several minutes (10). There are rare reports of continued active bleeding with CT visualization of hematoma enlargement over a more prolonged interval (11). With progressive hematoma enlargement, continued neurological deterioration would be expected. In our 3 cases, the hematoma enlargement was observed over an interval of several weeks; however the patients remained neurologically stable. In rare cases of trauma-related ICH, there may be delayed hematoma enlargement. This results from impaired cerebral autoregulation with increased cerebral blood flow into an edematous and necrotic brain tissue (12). Since our three patients had seizures and may have hit their heads (although there were no external signs of head trauma), this is a possible explanation of hematoma enlargement. We consider this to be unlikely because hematoma enlargement occurred 2 to 3 weeks after the initial ictus rather than within 24 to 72 hours. In one series of 10 patients with “chronic expanding ICH,” CT showed the lesion to be hyperdense with surrounding hypodense component. In two cases, there was interspersed calcifications. In 7 of 10 cases, there was an enhancing peripheral rim.
Chronic expanding intracerebral hematoma 0 L. A.
WEISBERG et al.
63
(a)
Fig. 2. Repeat CT scan was performed 3 weeks later. This shows that the hematoma is larger in size with slightly more ventricular compression (a). The hyperdense component at one level (b) shows slight diffuse enhancement (c).
Computerized
Medical
Imaging
and Graphics
(4
January-February/
1990, Volume
14, Number
:
(b)
Fig. 3. Repeat CT scan performed six months later. This shows slight residual hyperdense lesion (a) with nodular enhancement (b). There is no surrounding hypodense region or mass effect.
Since all patients had early surgical hematoma evacuation, serial CT scan findings before surgery were not reported. The finding of peripheral ring enhancement associated with a spontaneous or hypertensive hematoma has been previously well documented (13, 14). The peripheral enhancing rim is usually seen 7 to 28 days after the acute hematoma develops. When the enhancement occurs, the following changes have usually occurred; (a) the hyperdense hematoma is decreasing in density and size, (b) surrounding edema has decreased, (c) mass effect is usually reduced. In the CT scans of the ten patients with “chronic expanding ICH,” edema and mass effect were prominent findings (4). In our patients, we visualized peripheral ring enhancement on both the initial and follow-up CT (2 and 3 weeks later) in 2 patients; whereas in the other patient enhancement was not seen on the initial scan and only nodular (rather than peripheral rim) enhancement was seen on the early follow-up scan. In this patient, enhancement was still seen on the scan which was performed 6 months
later. This pattern of an isodense nodular enhancing lesion was similar to that previously reported in intracranial gliosis ( 15). Our three patients presented with seizures and none developed neurological deficit. The hematomas were located in the temporal-parietal white matter. The finding of a normal angiogram does not exclude an occult vascular malformation. Without a longer follow-up period or histological findings, the precise mechanism of the expanding ICH cannot be determined. In some of the previously reported cases of “chronic expanding ICH,” the presence of a thick surrounding fibrous capsule with a central region of clot (in various stages of resolution) would be unlikely to spontaneously resolve; however certain hematomas do resolve without surgery. If the patients are neurologically stable, nonsurgical management may be sufficient if angiography shows no underlying pathological condition. Despite the good outcome in our three cases, it must be remembered that the etiology of the hematomas is not known.
Chronic
expanding
intracerebral
SUMMARY
The clinical and CT findings of three patients with nontraumatic intracerebral hematomas which subsequently enlarged in size are reviewed. There was no neuroradiographic evidence of an underlying vascular malformation or neoplasm. These patients with chronic expanding hematomas differ from the other previously reported patients because the hematoma resolved spontaneously in our cases. REFERENCES 1. Kase, C.S.; Williams, J.P.; Wyatt, D.A.; Mohr, J.P. Lobar intracerebral hematomas: clinical and CT analysis of 22 cases. Neurology 32:1146-l 150; 1982. 2. Ropper, A.H.; Davis, K.R. Lobar cerebral hemorrhages: acute clinical syndromes in 26 cases. Ann. Neurology 8141-147; 1980. 3. Mohr, J.P.; Caplan, L.P.; Melski, J.W. The Harvard Cooperative Stroke Registry: a prospective registry. Neurology 28:754762; 1978. 4. Pozzati, E.; Giulani, G.; Gaist, G.; Piazza, G.; Vergoni, G. Chronic expanding intracerebral hematoma. J. Neurosurg. 65:61 l-614; 1986. 5. Lin, S.Z.; Shih, C.J.; Wang, Y.C. Intracerebral hematoma simulating a new growth. Surg. Neurology 21:459-464; 1984. 6. Reid, J.D.; Kommareddi, S.; Lankerani, M. Chronic expanding hematomas: a clinicopathologic entity. JAMA 244:24412442; 1980. 7. Yashon, D.; Kosnik, E.J. Chronic intracerebral hematoma. Neurosurgery 2:103-106; 1978. 8. Kramer, R.A.; Wing, SD. CT of angiographically occult cerebral vascular malformations. Radiology 123:649-655; 1977.
hematoma
0 L. A. WEISBERG et al.
65
9. Becker, D.H.; Townsend, J.J.; Kramer, R.A. Occult cerebrovascular malformations. Brain 102:249-265; 1979. H.H. Hypertensive intracerebral 10. Herbstein, D.J.; Schaumberg, hematoma. Arch. Neurology 30:4 12-4 16; 1974. 11. Kelley, R.E.; Berger, J.R.; Scheinberg, P. Active bleeding in hypertensive intracerebral hemorrhage: computed tomography findings. Neurology 32:852-856; 1982. 12. Diaz. F.G.: Yock. D.H.: Larson. D. Earlv diagnosis of delaved post:traumatic mtracerebral hematomas. i. Neurosurgery 50:217-223; 1979. R.D.; Leeds, N.E.; Naidich, T.P. Ring blush as13. Zimmerman, sociated with intracerebral hematoma. Radiology 122:70771 1; 1977. 14. Weisberg, LA. Peripheral rim enhancement in supratentorial intracerebral hematoma. Computerized Tomography 4: 145152; 1980. 15. Weisberg, L.A. Computed tomographic findings in intracranial gliosis. Neuroradiology 21:253-257; 198 1.
About the Author-DR. LEON WEISBERG is Professor of Neurology and Head of the Section of Neurology at the Tulane Medical School. He is director of the Neurology-Neurosurgery Service of the Charity Hospital of New Orleans. He is the author-of Cerebral
Computed Tomography; A Text Atlas, Essentials of Clinical Neurological and Decision Making in Adult Neurology. About the Author-DR. ANTONIO STAZIO is Associate Professor of Neurology at the Tulane Medical School. He is Head of Neurology at the Veterans Administration Hospital in New Orleans and director of the Multiple Sclerosis Clinic at the Tulane Medical School. About the Author-DR. DEBRA ELLIOTT is a graduate of the Tulane Medical School. Dr. Elliott is Assistant Professor of Neurology at the Tulane Medical School and Codirector of Neurology Residency Training Program at Tulane Medical School.