Neuroradiology
•
Cerebral Hypervascularity and Early Venous Opacification in Status Epilepticus
•
DISCUSSION
CASE REPORT
The association of seizure activity with hyperemia has been reported (7). In cats, a close correlation was shown,between regional perfusion and electroencephalographic (EEG) activity (1). In monkeys, an average of 260 % increase in cerebral blood flow occurred during induced seizures (10). Brodersen et al. (2) extended these observations to man, measuring a transient doubling in cerebral blood flow during electroconvulsive therapy in anesthetized patients. Among published reports of arteriograms in focal epilepsy (4, 5, 11, 12), there are two cases (4) in which vascular hyperemia was described, and another (5) in which both vascular hyperemia and early draining veins were noted. Holmquest and Launey (4) described capillary blush in patients in focal status epilepticus. Jaffe et al. (5) reported a right temporal blush and early filling veins with concurrent EEG evidence of right temporal activity. In these patients no pathological study was reported. Our patient had seizure activity at the time of arteriography.' Postmortem examination excluded all causes of hyperemia except for the small astrocytoma-the probable epileptogenic focus and cause of the progressive weakness. The diffuse hyperemia was considerably out of proportion to the size and grade of the tumor. For this reason, we postulate a direct relationship between seizure activity and its consequent metabolic demands, and the angiographic demonstration of hypervascularity and early venous opacification.
A 60-year-old man was brought to the emergency room following an automobile accident. He was comatose, with clonic movements of the right face, arm, and hand. History from the family physician described progressive weakness in the right arm and face and mild expressive aphasia during the preceding 7 months. Four months before admission, a brain scan showed no abnormality; arteriography was refused at that time. On the day of admission, seizures were poorly controlled by means of diazepam and phenobarbital, and emergency arteriography was performed to determine the possible presence of a surgically correctable epileptogenic focus (8). A left internal carotid arteriogram (Figs. 1-4) demonstrated an extensive area of hypervascularity with numerous early draining veins in the left frontal, temporal, and parietal lobes. No mass effect, midline shift, or occlusion of vessels was seen. The right internal carotid arteriogram showed no abnormalities. Focal seizure activity continued intermittently. Two days after admission, a brain scan recorded normal static image but increased flow to the left cerebral hemisphere. The patient died four days after admission. The cause of death established by autopsy was acute myocardial infarction. The formalin-fixed brain weighed 1320 g, and no abnormalities in size or distribution of major branches of the arterial and venous circulation were found. Barely perceptible enlargement and firmness of the left middle frontal gyrus were noted. Coronal sections of this gyrus showed obliteration of the architecture by a poorly defined, white tumor (Fig. 5). Infiltration was minimal and did not extend into the inferior and superior frontal gyri nor into deep white matter. The maximum diameter of involved area was 21 mm. The astrocytic nature of this well-differentiated tumor was confirmed histologically (Fig. 6), and no abnormal vascularity could be seen. Sections of the entire brain disclosed no other tumor. Vascular malformation, contusion, and infarction were not apparent.
1. Baldy-Moulinier M, Ingvar DH: EEGfrequency content related to regional blood flow of cerebral cortex in cat. Exp Brain Res 5: 55-60, Feb 1968 2. Brodersen P, Paulson OB, Bolwig TG, et al: Cerebral hyperemia in electrically induced epileptic seizures. Arch Neurol 28:334338, May 1973 3. Ferris EJ, Gabriele OF, Hipona FA, et al: Early venous filling in cranial angiography. Radiology 90:553-557, Mar 1968 4. Holmquest DL, Launey WS Jr: Abnormal scintiangiographic findings associated with seizure activity. Radiology 111: 147-150, Apr 1974 5. Jaffe ME, McHenry LC Jr, Goldberg HI: Regional cerebral blood flow measurement with small probes. II. Application of the method. Neurology 20:225-237, Mar 1970 6. Lassen NA: The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet 2:1113-1115,19 Nov 1966 7. Meyer JS, Gotoh F, Favale E: Cerebral metabolism during epileptic seizures in man. Electroencephalogr Clin Neurophysiol 21: 10-22,Ju11966 8. Oxbury JM, Whitty CWM: Causes and consequences of status epilepticus in adults. A study of 86 cases. Brain 94:733-744, 1971 9. Peterson HO, Kieffer SA: Introduction to Neuroradiology. Hagerstown, Md., Harper & Row, 1972, pp. 91-105 10. Plum F, Posner JB, Troy B: Cerebral metabolic and circulatory responses to induced convulsions in animals. Arch Neurol 18: 1-13, Jan 1968 11. Vermess M, Stein SC, Ajmone-Marsan C, et al: Angiography in "idiopathic" focal epilepsy. Am J Roentgenol 115:120-125, May 1972 12. Waddington MM: Angiographic changes in focal motor epilepsy. Neurology 20:879-888, Sep 1970
A Case Report 1 Eugene J. McDonald, Jr., M.D., Philip C. Goodman, M.D., Surl L. Nielsen, M.D., and David P. Winestock, M.D. Cerebral hyper perfusion and early draining veins directly resulting from status eplleptlcus can be demonstrated angiographically. Postmortem examination of the brain excluded other possible causes of hyperemia and early venous drainage. INDEX TERMS:
Cerebral blood vessels, flow dynamics • Epilepsy
Radiology 117:87-88, October 1975
•
•
hypervascularity and early venous opacification were demonstrated by cerebral angiography in a patient in status epilepticus. The patient's death from an unrelated cause permitted careful examination of the brain and exclusion of other possible causes of hyperemia and early venous drainage (e.g., contusion, infarction, inflammation, arteriovenous malformation, high-grade malignancy) (3, 6, 8, 9). Although other investigators have noted these findings with status epilepticus (4, 5), to our knowledge this is the first reported case with pathological proof. IFFUSE
D
REFERENCES
1 From the Departments of Radiology (E. J. M., P. C. G., D. P. W.) and Pathology (S. L. N.), University of California School of Medicine and San Francisco General Hospital, San Francisco, Calif. Accepted for publication in June 1975. An additional article related to this subject will be found on page 113. Address reprint requests to Dr. Winestock. dk
87
Fig. 1. Internal carotid arteriogram, early arterial phase. Left, affected side demonstrates increased brain opacification in portions of the frontal, temporal, and parietal lobes. Fig. 2. Internal carotid arteriogram, late arterial phase. Left, affected side shows early opacification of the internal cerebral (closed arrow) and superficial cortical parietal veins (small arrowheads) and the sphenoparietal sinus (open arrow). Fig. 3. Internal carotid arteriogram, capillary phase. On the left, affected side the internal cerebral, middle cerebral, posterior frontal and parietal superficial cortical veins are already well opacified, as are the sagittal, straight and sphenoparietal sinuses. Fig. 4. Left internal carotid arteriogram, frontal view. Early opacification of the thalamostriate and internal cerebral veins is seen in this late arterial phase. Midline structures are not displaced. Fig. 5. Brain section. The slightly swollen middle frontal gyrus exhibits an indistinct gray-white junction, obliterated by an infiltrating astrocytoma (arrowheads). This appearance contrasts with the adjacent normal gyri. Fig. 6. Microscopic section of tumor. Diffuse, infiltrating astrocytoma (left) involving cortex of the gyrus on the left contrasts markedly with the minimally increased cellularity of the adjacent gyrus. (Phosphotungstic acid-hematoxylin stain, X100)
88
•
Cerebral Hypervascularity and Early Venous Opacification in Status Epilepticus
•
DISCUSSION
CASE REPORT
The association of seizure activity with hyperemia has been reported (7). In cats, a close correlation was shown,between regional perfusion and electroencephalographic (EEG) activity (1). In monkeys, an average of 260 % increase in cerebral blood flow occurred during induced seizures (10). Brodersen et al. (2) extended these observations to man, measuring a transient doubling in cerebral blood flow during electroconvulsive therapy in anesthetized patients. Among published reports of arteriograms in focal epilepsy (4, 5, 11, 12), there are two cases (4) in which vascular hyperemia was described, and another (5) in which both vascular hyperemia and early draining veins were noted. Holmquest and Launey (4) described capillary blush in patients in focal status epilepticus. Jaffe et al. (5) reported a right temporal blush and early filling veins with concurrent EEG evidence of right temporal activity. In these patients no pathological study was reported. Our patient had seizure activity at the time of arteriography.' Postmortem examination excluded all causes of hyperemia except for the small astrocytoma-the probable epileptogenic focus and cause of the progressive weakness. The diffuse hyperemia was considerably out of proportion to the size and grade of the tumor. For this reason, we postulate a direct relationship between seizure activity and its consequent metabolic demands, and the angiographic demonstration of hypervascularity and early venous opacification.
A 60-year-old man was brought to the emergency room following an automobile accident. He was comatose, with clonic movements of the right face, arm, and hand. History from the family physician described progressive weakness in the right arm and face and mild expressive aphasia during the preceding 7 months. Four months before admission, a brain scan showed no abnormality; arteriography was refused at that time. On the day of admission, seizures were poorly controlled by means of diazepam and phenobarbital, and emergency arteriography was performed to determine the possible presence of a surgically correctable epileptogenic focus (8). A left internal carotid arteriogram (Figs. 1-4) demonstrated an extensive area of hypervascularity with numerous early draining veins in the left frontal, temporal, and parietal lobes. No mass effect, midline shift, or occlusion of vessels was seen. The right internal carotid arteriogram showed no abnormalities. Focal seizure activity continued intermittently. Two days after admission, a brain scan recorded normal static image but increased flow to the left cerebral hemisphere. The patient died four days after admission. The cause of death established by autopsy was acute myocardial infarction. The formalin-fixed brain weighed 1320 g, and no abnormalities in size or distribution of major branches of the arterial and venous circulation were found. Barely perceptible enlargement and firmness of the left middle frontal gyrus were noted. Coronal sections of this gyrus showed obliteration of the architecture by a poorly defined, white tumor (Fig. 5). Infiltration was minimal and did not extend into the inferior and superior frontal gyri nor into deep white matter. The maximum diameter of involved area was 21 mm. The astrocytic nature of this well-differentiated tumor was confirmed histologically (Fig. 6), and no abnormal vascularity could be seen. Sections of the entire brain disclosed no other tumor. Vascular malformation, contusion, and infarction were not apparent.
1. Baldy-Moulinier M, Ingvar DH: EEGfrequency content related to regional blood flow of cerebral cortex in cat. Exp Brain Res 5: 55-60, Feb 1968 2. Brodersen P, Paulson OB, Bolwig TG, et al: Cerebral hyperemia in electrically induced epileptic seizures. Arch Neurol 28:334338, May 1973 3. Ferris EJ, Gabriele OF, Hipona FA, et al: Early venous filling in cranial angiography. Radiology 90:553-557, Mar 1968 4. Holmquest DL, Launey WS Jr: Abnormal scintiangiographic findings associated with seizure activity. Radiology 111: 147-150, Apr 1974 5. Jaffe ME, McHenry LC Jr, Goldberg HI: Regional cerebral blood flow measurement with small probes. II. Application of the method. Neurology 20:225-237, Mar 1970 6. Lassen NA: The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet 2:1113-1115,19 Nov 1966 7. Meyer JS, Gotoh F, Favale E: Cerebral metabolism during epileptic seizures in man. Electroencephalogr Clin Neurophysiol 21: 10-22,Ju11966 8. Oxbury JM, Whitty CWM: Causes and consequences of status epilepticus in adults. A study of 86 cases. Brain 94:733-744, 1971 9. Peterson HO, Kieffer SA: Introduction to Neuroradiology. Hagerstown, Md., Harper & Row, 1972, pp. 91-105 10. Plum F, Posner JB, Troy B: Cerebral metabolic and circulatory responses to induced convulsions in animals. Arch Neurol 18: 1-13, Jan 1968 11. Vermess M, Stein SC, Ajmone-Marsan C, et al: Angiography in "idiopathic" focal epilepsy. Am J Roentgenol 115:120-125, May 1972 12. Waddington MM: Angiographic changes in focal motor epilepsy. Neurology 20:879-888, Sep 1970
A Case Report 1 Eugene J. McDonald, Jr., M.D., Philip C. Goodman, M.D., Surl L. Nielsen, M.D., and David P. Winestock, M.D. Cerebral hyper perfusion and early draining veins directly resulting from status eplleptlcus can be demonstrated angiographically. Postmortem examination of the brain excluded other possible causes of hyperemia and early venous drainage. INDEX TERMS:
Cerebral blood vessels, flow dynamics • Epilepsy
Radiology 117:87-88, October 1975
•
•
hypervascularity and early venous opacification were demonstrated by cerebral angiography in a patient in status epilepticus. The patient's death from an unrelated cause permitted careful examination of the brain and exclusion of other possible causes of hyperemia and early venous drainage (e.g., contusion, infarction, inflammation, arteriovenous malformation, high-grade malignancy) (3, 6, 8, 9). Although other investigators have noted these findings with status epilepticus (4, 5), to our knowledge this is the first reported case with pathological proof. IFFUSE
D
REFERENCES
1 From the Departments of Radiology (E. J. M., P. C. G., D. P. W.) and Pathology (S. L. N.), University of California School of Medicine and San Francisco General Hospital, San Francisco, Calif. Accepted for publication in June 1975. An additional article related to this subject will be found on page 113. Address reprint requests to Dr. Winestock. dk
87
Fig. 1. Internal carotid arteriogram, early arterial phase. Left, affected side demonstrates increased brain opacification in portions of the frontal, temporal, and parietal lobes. Fig. 2. Internal carotid arteriogram, late arterial phase. Left, affected side shows early opacification of the internal cerebral (closed arrow) and superficial cortical parietal veins (small arrowheads) and the sphenoparietal sinus (open arrow). Fig. 3. Internal carotid arteriogram, capillary phase. On the left, affected side the internal cerebral, middle cerebral, posterior frontal and parietal superficial cortical veins are already well opacified, as are the sagittal, straight and sphenoparietal sinuses. Fig. 4. Left internal carotid arteriogram, frontal view. Early opacification of the thalamostriate and internal cerebral veins is seen in this late arterial phase. Midline structures are not displaced. Fig. 5. Brain section. The slightly swollen middle frontal gyrus exhibits an indistinct gray-white junction, obliterated by an infiltrating astrocytoma (arrowheads). This appearance contrasts with the adjacent normal gyri. Fig. 6. Microscopic section of tumor. Diffuse, infiltrating astrocytoma (left) involving cortex of the gyrus on the left contrasts markedly with the minimally increased cellularity of the adjacent gyrus. (Phosphotungstic acid-hematoxylin stain, X100)
88
