CHAPTER
The Radionuclide Cerebral Angiogram in Stroke Diagnosis JOHN F. ROCKETT, M.D.
The results of nuclear angiography in confirming the early diagnosis of stroke are reported in this presentation. METHODS AND MATERIALS
The charts of all patients admitted to the Baptist Memorial Hospital in Memphis, Tennessee, between August, 1974 and February, 1975 with acute cerebrovascular accidents were reviewed. Seventy-eight patients who had radionuclide cerebral studies and adequate clinical and laboratory data for the diagnosis of acute stroke form the basis of this communication. All patients had nuclear studies within 10 days of the onset of symptoms. The age range was from 38 years to 87 years. Those with transient ischemic attacks and residua from earlier cerebrovascular accidents were excluded from this report. Division into internal carotid and vertebrobasilar groups was made on the basis of clinical and contrast angiographic evidence. All patients were studied with the Anger scintillation camera following the intravenous injection of 15 to 20 millicuries of 99mTc-pertechnetate in a 1- to 2-ml. bolus. The patient's chart was reviewed prior to administering the radiopharmaceutical to determine the appropriate position for the radionuclide cerebral angiogram. If occipital lobe pathology or a vertebrobasilar arterial abnormality was suspected, the patient was studied in the posterior projection. Otherwise, the subject was positioned to obtain an anterior view of the head and neck. When the isotope was demonstrated in the carotid arteries, eight rapid serial scintiphotographs were recorded on hand-pulled Polaroid film at 2-second intervals. Initially, symmetrical streams of radioactivity are seen in the neck in the normal radionuclide cerebral angiogram (Fig. 18.1). This activity primarily represents the first arterial transit of the radiopharmaceutical through the right and left carotid arteries. Arterial, capillary, and venous phases are seen as the isotope passes 245
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18
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through the intracerebral circulation. The right and left middle cerebral arterial areas and overlapping anterior cerebral arterial areas are demonstrated. Symmetrical and homogeneous perfusion is present during the arterial and capillary phases in the hemispheres. Asymmetrical activity when seen during the venous portion of the dynamic study is usually due to a dominant transverse sinus. The static brain scan is then obtained from 1 to 3 hours after the radionuclide cerebral angiogram has been performed depending upon clinical information and findings on the nuclear cerebral angiogram. RESULTS
The typical abnormality on the nuclear cerebral angiogram in a patient with an acute stroke was a reduction of tracer activity in an arterial distribution compared to the opposite side. The reduced perfusion usually persisted throughout the study (Fig. 18.2). In this 56-yearold male, occlusion of the M-1 segment of the left middle cerebral artery was demonstrated. Decreased activity in the left middle cerebral arterial distribution was present throughout the dynamic study. Contrast arteriography verified the findings shown by rapid sequential scintiphotography (Fig. 18.3).
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FIG. 18.1. Normal anterior radionuclide cerebral angiogram. Numbers denote time range in seconds.
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247
In some individuals with cerebral vascular occlusive disease, late in the dynamic study, the involved hemisphere showed greater activity than the normal hemisphere. This apparently was due to delayed filling of the abnormal area of the brain by collateral vessels. Another abnormal perfusion pattern seen in patients with acute stroke was vascular displacement due to an intracerebral hemorrhage. An example of the scintiphotographic changes in a hemorrhagic stroke victim is shown in Figure 18.4. The individual was a 61-year-old hypertensive female who had suffered a sudden onset of severe left frontal headache, nausea, and vomiting. She had become aphasic and while attempting to walk, fell, striking her head on the floor. She had been maintained on oral sodium warfarin for a year following a pulmonary embolus. Upon her admission to the hospital, the attending neurosurgeon asked for immediate radionuclide studies of the brain. Absence of deep left frontal activity persisted throughout the anterior radionuclide cerebral angiogram. The left middle cerebral vessels appeared displaced laterally, and the anterior cerebral arteries were felt to be slightly shifted to the right. Peripheral depression of the convexity branches of the left middle cerebral artery was also suspected. Postflow images were interpreted as normal.
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FIG. 18.2. Middle cerebral artery obstruction. Anterior radionuclide cerebral angiogram demonstrating left middle cerebral artery occlusion. Arrows point to the lesion site. N um bers denote time range in seconds.
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The nuclear cerebral angiogram appeared to detect a hypovascular mass deep in the left frontal region, most likely an intracerebral hemorrhage. It was thought a small left subdural or extradural hematoma might also be present. The neurosurgeon was immediately notified of these impressions, but before carotid arteriography could be performed, 2-hour postinjection static brain images were made. No definite abnormalities were detected by the conventional brain scintiphotos. A left direct carotid arteriogram (Fig. 18.5) showed the hypovascular left frontal mass. The acute left-sided subdural hematoma which had caused the depression of the peripheral vessels on the radionuclide cerebral angiogram was also visualized.
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FIG. 18.3. Left direct common carotid angiogram. Anterioposterior view, showing occlusion of the left middle cerebral artery.
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249
The same day, a 20-ml. deep left frontal intracerebral hemorrhage and a 15-ml. acute subdural hematoma were surgically evacuated. A definite abnormality in perfusion during the arterial phase of the neck vessels and/or arterial-capillary phases of the cranial vessels was present in 47 of the 78 patients (60%) with acute strokes. The deficit had to persist on at least two successive scintiphotos to be considered significant. In 29 individuals with acute strokes, the radionuclide cerebral angiograms were abnormal, and the conventional brain images were negative (Table 18.1). Abnormalities were present on both radionuclide studies in 12 patients. The static brain scan detected two infarcts in patients with normal radionuclide cerebral angiograms. One was a small middle cerebral stroke, the other an anterior cerebral branch infarct. Six additional stroke victims in whom no brain scan was requested had vascular deficits detected by the dynamic study.
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FIG. 18.4. Intracerebral hemorrhage and acute subdural hematoma. D2-D8, scintiphotos from anterior radionuclide cerebral angiogram, taken at 2-second intervals, show avascular left frontal lesion and peripheral compression of convexity branches of the left middle cerebral artery. Arrows point to the abnormalities. PF-A, post "flow"-anterior view; and PF-LL, post "flow"-left lateral view, appeared normal. A, anterior; P, posterior; LL, left lateral; and RL, right lateral 1 hour post-injection static brain scans fail to demonstrate any abnormal areas.
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TABLE 18.1 Radionuclide Cerebral Angiogram (NCA)-Brain Scan Correlation
NCA NCA NCA NCA NCA
Results
No.
+ + + -
29
scan scan-tscan+ no scan no scan
12 2 6 2
Static brain scans were not performed in two patients with false negative isotopic perfusion studies. The nuclear cerebral angiograms were not technically satisfactory in 6 of the 78 patients in this series. These studies were assumed to be normal. Radionuclide angiography was interpreted as abnormal in 45 of 68 patients with acute strokes involving the internal carotid artery or its branches (Table 18.2). Only two dynamic studies in patients with vertebrobasilar system
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FIG. 18.5. Left direct common carotid angiogram showing left frontal intracerebral hemorrhage and left acute subdural hematoma.
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TABLE
18.2
Stroke Distribution Carotid System
Radionuclide cerebral angiogram abnormal Radionuclide cerebral angiogram normal Total TABLE
Vertebrobasilar System
45
2
23
8
68
10
18.3
Acute Stroke Per Cent Detected
Radionuclide cerebral angiogram abnormal Radionuclide cerebral angiogram and/or brain scan abnormal
Carotid System
Vertebrobasilar System
66% 69%
20% 20%
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disease were abnormal. One patient had unilateral vertebral artery disease. The other individual had a posterior cerebral artery occlusion. The static brain images failed to detect any additional strokes in those with negative radionuclide angiography. Eight patients with vertebrobasilar system strokes failed to show a perfusion defect on cerebral angioscintiphotography. Static brain images were abnormal in 14 of 70 (20%) patients with acute strokes. Patients had nuclear studies an average of 2.8 days after the onset of symptoms. All abnormal brain scans were in regions of the brain supplied by the internal carotid artery. One patient with a posteror cerebral infarct had positive dynamic and static studies. Her right posterior cerebral artery originated from the carotid system, rather than the basilar artery. The detection rate of acute strokes in this series is shown in Table 18.3. The radionuclide cerebral angiogram was abnormal in 660/0 of acute carotid system strokes. Blood flow abnormalities were seen in 200/0 of patients with strokes in the vertebrobasilar distribution. The two abnormal brain scans in patients with normal nuclide angiography raised the detection rate in acute carotid system strokes by nuclide studies to 69%. No additional vertebrobasilar cerebrovascular accidents were detected on static brain scans. Of the 31 stroke patients who had arteriographically proven cerebral vascular disease, 23 had abnormal radionuclide cerebral angiograms (74%). Contrast arteriography detected vascular lesions in the neck in six patients that had normal anterior radionuclide cerebral angiograms. The carotid obstruction was less than 70% of the arterial lumen. Verte-
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DISCUSSION
The radionuclide cerebral angiogram provides an assessment of the cerebral circulation that is unattainable by other noninvasive radiologi-
FIG. 18.6. Bilateral anterior cerebral occlusions. Anterior radionuclide cerebral angiogram portraying reduction of radioactive transit through the anterior cerebral arteries. (Arrows) denote the reduced activity. On the 8- to 10-second scintiphoto the region has filled, probably by collateral vessels. Static scintiphotos at 1 hour were negative. RL, right lateral; A, anterior; and LL, left lateral projections.
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brobasilar disease or bilateral carotid lesions were present in these six false negative isotopic patients. An anterior projection nuclear angiogram failed to detect a posterior cerebral artery occlusion. The radionuclide perfusion study was not technically satisfactory for interpretation in one patient with an abnormal radiocontrast arteriogram. This tracer examination was counted as a false negative study. Three patients with acute strokes in the middle cerebral distribution had abnormal radionuclide cerebral angiograms and normal contrast angiograms. The tracer study detected a vascular lesion while the radiographic examination did not. Division of the patients into hemorrhagic and ischemic strokes could not always be made from the clinical information available. In five of seven patients with proved intracerebral hemorrhages, vascular displacement was present on the radionuclide cerebral angiogram.
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253
cal techniques, including computed tomography (6). It can detect abnormalities, particularly occlusive vascular lesions, that are not shown on the static brain images. For example, in this study, 35 of 47 patients with isotopic perfusion defects either had normal static images or did not have brain scans performed. Use of the radionuclide cerebral angiogram approximately doubles the isotopic detection rate of cerebrovascular disease (2, 4). This is partly because most static brain images are negative for the first 7 to 10 days after a cerebrovascular accident. The isotopic perfusion study is most effective in detecting middle cerebral and carotid artery occlusive disease. Significant obstruction of the carotid artery, usually 70% or greater, will result in decreased blood flow (1). This degree of carotid occlusion will usually be detected by the radionuclide cerebral angiogram (10). In the present study, the nuclear cerebral angiogram detected all unilateral carotid stenoses when greater than 70% of the vessel's lumen was occluded. Some difficulty in detecting bilateral carotid ischemic lesions has also been experienced by other investigators (2, 3, 5). Low cardiac output, slow intravenous injection of the radiopharmaceutical, and interfering external carotid flow may cause one to miss bilateral carotid cerebrovas-
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FIG. 18.7. Posterior cerebral infarct. Posterior radionuclide cerebral angiogram demonstrating reduction in activity in the right occipital area. Numbers denote time range in seconds. Static scintiphotos 2 hours after injection showing abnormal concentration of radiopertechnetate in the left posterior cerebral distribution. P, posterior; RPO, right posterior oblique; RL, right lateral views. Arrows point to pathology.
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cular disease. Increased intracranial pressure also may cause slow but symmetrical passage of the radiopharmaceutical through the neck arteries. Unilateral anterior cerebral artery ischemic lesions are difficult to visualize with the dynamic radioisotopic technique. The rarer bilateral anterior cerebral occlusions are readily recognized by nuclear angiography, however (8) (Fig. 18.6). Absence of early perfusion in the anterior cerebral artery distribution was evident in this stroke victim. We did not find the radionuclide cerebral angiogram to be an effective means of detecting most vertebrobasilar vascular occlusions. Cowan and associates had a similar experience (2). Posterior cerebral strokes should usually be detected if the patient is studied in the posterior projection. This patient's posterior cerebral infarct was detected on both dynamic and static radionuclide studies (Fig. 18.7). The posterior radionuclide cerebral angiogram showed decreased activity in the right occipital region. Two-hour static brain images demonstrated the infarction in the
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FIG. 18.8. Right intracerebral hemorrhage. Anterior radionuclide cerebral angiogram showing decreased transit of the radiopertechnetate through the right hemisphere and lateral displacement of the middle cerebral vessels due to the centrosylvian mass. Arrows point to the pathology. Numbers denote time range in seconds. Imm, immediate postradionuclide cerebral angiogram; A, anterior; and RL, right lateral scintiphotos are negative.
STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
255
FIG. 18.9. Right direct common carotid angiogram. Anterioposterior view. Avascular centrosylvian mass and a lobulated aneurysm at the bifurcation of the right internal carotid artery.
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calcarine region of the right cerebral hemisphere. As stated earlier, this posterior cerebral vessel originated from the carotid system. The radionuclide cerebral angiogram can also detect vascular pathology not seen with contrast arteriography. The radioisotopic study visualizes the vasculature below the resolution of the contrast angiogram, or the microcirculation (9). Three acute middle cerebral stroke victims had definite vascular abnormalities demonstrated by the dynamic isotopic procedure while contrast angiography was interpreted as normal. Detection of intracerebral hemorrhages by the nuclear cerebral angiogram alone has been reported (7). We have been successful in demonstrating frontal and temporal lobe hematomas on anterior cerebral angioscintigrams. An emergency radionuclide cerebral angiogram was requested on this comatose 16-year-old female (Fig. 18.8). It showed decreased activity in the right hemisphere throughout the anterior perfusion study. The right middle cerebral complex appeared displaced
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SUMMARY
The radionuclide cerebral angiogram using intravenous radiopertechnetate has been found to be of value in confirming the early diagnosis of stroke. The isotopic perfusion study is of value in detecting ischemic carotid and middle cerebral lesions. It can also provide a rapid means of demonstrating intracerebral hemorrhages. Nuclear angiography is not recommended for detection of vertebrobasilar artery disease unless a posterior cerebral artery occlusion is suspected. REFERENCES 1. Brice, J. G., Dowsett. D. J., and Lowe, R. D., Haemodynamic effects of carotid artery stenosis. Br. Med. J., 2: 1363-1366, 1964. 2. Cowan, R. J., Maynard, C. D., Meschan. I., Janeway, R., and Shigeno, K. Value of the routine use of the cerebral dynamic radioisotope study. Radiology, 107: 111-116, 1973.
3. Fischer, R. J., and Miale, A., Jr. Evaluation of cerebral vascular disease with radionuclide angiography. Stroke, 3: 1-9, 1972. 4. Fish, M. B., Barnes, B., and Polycove, M. Cranial scintiphotographic blood flow defects in arteriographically proven cerebral vascular disease. J. Nucl. Med., 14: 558-564. 1973. 5. Moses, D. C., James, A. E., Jr., Strauss, H. W., and Wagner. H. N., Jr. Regional
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laterally. The superior sagittal sinus was never demonstrated; therefore, it was believed the cerebral circulation was slowed, probably due to increased intracranial pressure. Immediate postinjection views were normal. It was our impression that there was a large right frontal mass present, most likely an intracerebral hematoma. A low grade glioma or abscess could cause similar findings on the dynamic study. A right direct common carotid arteriogram was performed immediately. An avascular right frontal lesion and a large lobulated aneurysm at the bifurcation of the internal carotid artery were shown (Fig. 18.9). A right frontal craniotomy was then performed. The internal carotid aneurysm was clipped and the huge intracerebral hematoma evacuated. The over-all stroke detection rate of 600/0 in the present series from the Baptist Memorial Hospital would have been improved considerably if the six patients with technically inadequate studies has not been included. All six unsatisfactory examinations occurred in patients with carotid system disease. If these isotopic studies had been excluded, the radionuclide cerebral angiogram detection rate in carotid system strokes would have increased to 710/0. Other investigators in not altogether comparable studies have reported from 450/0 to 830/0 cerebrovascular disease detection with nuclear angiography (2-5, 9).
STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
7.
8.
9. 10.
cerebral blood flow estimation in the diagnosis of cerebrovascular disease. J. Nucl. Med., 13: 135-141, 1972. Pendergrass, H. P., McKusick, K. A., New, P. F. J., and Potsaid, M. S. Relative efficacy of radionuclide imaging and computed tomography of the brain. Radiology, 116: 363-366, 1975. Rockett, J. F., Kaplan, E. S., Hudson, J. S., and Moinuddin, M. Intracerebral hemorrhage demonstrated by nuclear cerebral angiogram: case report. J. Nucl. Med., 16: 459-461, 1975. Rockett, J. F., Kaplan, E. S., Ray, M., Buchignani, J. S., and Gardner, H. C. Scintiphotographic demonstration of bilateral infarction in the distribution of the anterior cerebral arteries. Radiology, 112: 135-137, 1974. Rosenthall, L., Chan, J., Sidhu, R., and Stratford, J. Combined radiocontrast and radionuclide cerebral angiography. Radiology, 92: 1223-1228, 1969. Wise, G., Brockenbrough, E. C., and Marty, R. The detection of carotid artery obstruction: a correlation with arteriography. Stroke, 2: 105-113, 1971.
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6.
257
The Radionuclide Cerebral Angiogram in Stroke Diagnosis JOHN F. ROCKETT, M.D.
The results of nuclear angiography in confirming the early diagnosis of stroke are reported in this presentation. METHODS AND MATERIALS
The charts of all patients admitted to the Baptist Memorial Hospital in Memphis, Tennessee, between August, 1974 and February, 1975 with acute cerebrovascular accidents were reviewed. Seventy-eight patients who had radionuclide cerebral studies and adequate clinical and laboratory data for the diagnosis of acute stroke form the basis of this communication. All patients had nuclear studies within 10 days of the onset of symptoms. The age range was from 38 years to 87 years. Those with transient ischemic attacks and residua from earlier cerebrovascular accidents were excluded from this report. Division into internal carotid and vertebrobasilar groups was made on the basis of clinical and contrast angiographic evidence. All patients were studied with the Anger scintillation camera following the intravenous injection of 15 to 20 millicuries of 99mTc-pertechnetate in a 1- to 2-ml. bolus. The patient's chart was reviewed prior to administering the radiopharmaceutical to determine the appropriate position for the radionuclide cerebral angiogram. If occipital lobe pathology or a vertebrobasilar arterial abnormality was suspected, the patient was studied in the posterior projection. Otherwise, the subject was positioned to obtain an anterior view of the head and neck. When the isotope was demonstrated in the carotid arteries, eight rapid serial scintiphotographs were recorded on hand-pulled Polaroid film at 2-second intervals. Initially, symmetrical streams of radioactivity are seen in the neck in the normal radionuclide cerebral angiogram (Fig. 18.1). This activity primarily represents the first arterial transit of the radiopharmaceutical through the right and left carotid arteries. Arterial, capillary, and venous phases are seen as the isotope passes 245
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18
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through the intracerebral circulation. The right and left middle cerebral arterial areas and overlapping anterior cerebral arterial areas are demonstrated. Symmetrical and homogeneous perfusion is present during the arterial and capillary phases in the hemispheres. Asymmetrical activity when seen during the venous portion of the dynamic study is usually due to a dominant transverse sinus. The static brain scan is then obtained from 1 to 3 hours after the radionuclide cerebral angiogram has been performed depending upon clinical information and findings on the nuclear cerebral angiogram. RESULTS
The typical abnormality on the nuclear cerebral angiogram in a patient with an acute stroke was a reduction of tracer activity in an arterial distribution compared to the opposite side. The reduced perfusion usually persisted throughout the study (Fig. 18.2). In this 56-yearold male, occlusion of the M-1 segment of the left middle cerebral artery was demonstrated. Decreased activity in the left middle cerebral arterial distribution was present throughout the dynamic study. Contrast arteriography verified the findings shown by rapid sequential scintiphotography (Fig. 18.3).
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FIG. 18.1. Normal anterior radionuclide cerebral angiogram. Numbers denote time range in seconds.
STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
247
In some individuals with cerebral vascular occlusive disease, late in the dynamic study, the involved hemisphere showed greater activity than the normal hemisphere. This apparently was due to delayed filling of the abnormal area of the brain by collateral vessels. Another abnormal perfusion pattern seen in patients with acute stroke was vascular displacement due to an intracerebral hemorrhage. An example of the scintiphotographic changes in a hemorrhagic stroke victim is shown in Figure 18.4. The individual was a 61-year-old hypertensive female who had suffered a sudden onset of severe left frontal headache, nausea, and vomiting. She had become aphasic and while attempting to walk, fell, striking her head on the floor. She had been maintained on oral sodium warfarin for a year following a pulmonary embolus. Upon her admission to the hospital, the attending neurosurgeon asked for immediate radionuclide studies of the brain. Absence of deep left frontal activity persisted throughout the anterior radionuclide cerebral angiogram. The left middle cerebral vessels appeared displaced laterally, and the anterior cerebral arteries were felt to be slightly shifted to the right. Peripheral depression of the convexity branches of the left middle cerebral artery was also suspected. Postflow images were interpreted as normal.
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FIG. 18.2. Middle cerebral artery obstruction. Anterior radionuclide cerebral angiogram demonstrating left middle cerebral artery occlusion. Arrows point to the lesion site. N um bers denote time range in seconds.
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The nuclear cerebral angiogram appeared to detect a hypovascular mass deep in the left frontal region, most likely an intracerebral hemorrhage. It was thought a small left subdural or extradural hematoma might also be present. The neurosurgeon was immediately notified of these impressions, but before carotid arteriography could be performed, 2-hour postinjection static brain images were made. No definite abnormalities were detected by the conventional brain scintiphotos. A left direct carotid arteriogram (Fig. 18.5) showed the hypovascular left frontal mass. The acute left-sided subdural hematoma which had caused the depression of the peripheral vessels on the radionuclide cerebral angiogram was also visualized.
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FIG. 18.3. Left direct common carotid angiogram. Anterioposterior view, showing occlusion of the left middle cerebral artery.
STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
249
The same day, a 20-ml. deep left frontal intracerebral hemorrhage and a 15-ml. acute subdural hematoma were surgically evacuated. A definite abnormality in perfusion during the arterial phase of the neck vessels and/or arterial-capillary phases of the cranial vessels was present in 47 of the 78 patients (60%) with acute strokes. The deficit had to persist on at least two successive scintiphotos to be considered significant. In 29 individuals with acute strokes, the radionuclide cerebral angiograms were abnormal, and the conventional brain images were negative (Table 18.1). Abnormalities were present on both radionuclide studies in 12 patients. The static brain scan detected two infarcts in patients with normal radionuclide cerebral angiograms. One was a small middle cerebral stroke, the other an anterior cerebral branch infarct. Six additional stroke victims in whom no brain scan was requested had vascular deficits detected by the dynamic study.
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FIG. 18.4. Intracerebral hemorrhage and acute subdural hematoma. D2-D8, scintiphotos from anterior radionuclide cerebral angiogram, taken at 2-second intervals, show avascular left frontal lesion and peripheral compression of convexity branches of the left middle cerebral artery. Arrows point to the abnormalities. PF-A, post "flow"-anterior view; and PF-LL, post "flow"-left lateral view, appeared normal. A, anterior; P, posterior; LL, left lateral; and RL, right lateral 1 hour post-injection static brain scans fail to demonstrate any abnormal areas.
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TABLE 18.1 Radionuclide Cerebral Angiogram (NCA)-Brain Scan Correlation
NCA NCA NCA NCA NCA
Results
No.
+ + + -
29
scan scan-tscan+ no scan no scan
12 2 6 2
Static brain scans were not performed in two patients with false negative isotopic perfusion studies. The nuclear cerebral angiograms were not technically satisfactory in 6 of the 78 patients in this series. These studies were assumed to be normal. Radionuclide angiography was interpreted as abnormal in 45 of 68 patients with acute strokes involving the internal carotid artery or its branches (Table 18.2). Only two dynamic studies in patients with vertebrobasilar system
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FIG. 18.5. Left direct common carotid angiogram showing left frontal intracerebral hemorrhage and left acute subdural hematoma.
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STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
TABLE
18.2
Stroke Distribution Carotid System
Radionuclide cerebral angiogram abnormal Radionuclide cerebral angiogram normal Total TABLE
Vertebrobasilar System
45
2
23
8
68
10
18.3
Acute Stroke Per Cent Detected
Radionuclide cerebral angiogram abnormal Radionuclide cerebral angiogram and/or brain scan abnormal
Carotid System
Vertebrobasilar System
66% 69%
20% 20%
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disease were abnormal. One patient had unilateral vertebral artery disease. The other individual had a posterior cerebral artery occlusion. The static brain images failed to detect any additional strokes in those with negative radionuclide angiography. Eight patients with vertebrobasilar system strokes failed to show a perfusion defect on cerebral angioscintiphotography. Static brain images were abnormal in 14 of 70 (20%) patients with acute strokes. Patients had nuclear studies an average of 2.8 days after the onset of symptoms. All abnormal brain scans were in regions of the brain supplied by the internal carotid artery. One patient with a posteror cerebral infarct had positive dynamic and static studies. Her right posterior cerebral artery originated from the carotid system, rather than the basilar artery. The detection rate of acute strokes in this series is shown in Table 18.3. The radionuclide cerebral angiogram was abnormal in 660/0 of acute carotid system strokes. Blood flow abnormalities were seen in 200/0 of patients with strokes in the vertebrobasilar distribution. The two abnormal brain scans in patients with normal nuclide angiography raised the detection rate in acute carotid system strokes by nuclide studies to 69%. No additional vertebrobasilar cerebrovascular accidents were detected on static brain scans. Of the 31 stroke patients who had arteriographically proven cerebral vascular disease, 23 had abnormal radionuclide cerebral angiograms (74%). Contrast arteriography detected vascular lesions in the neck in six patients that had normal anterior radionuclide cerebral angiograms. The carotid obstruction was less than 70% of the arterial lumen. Verte-
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DISCUSSION
The radionuclide cerebral angiogram provides an assessment of the cerebral circulation that is unattainable by other noninvasive radiologi-
FIG. 18.6. Bilateral anterior cerebral occlusions. Anterior radionuclide cerebral angiogram portraying reduction of radioactive transit through the anterior cerebral arteries. (Arrows) denote the reduced activity. On the 8- to 10-second scintiphoto the region has filled, probably by collateral vessels. Static scintiphotos at 1 hour were negative. RL, right lateral; A, anterior; and LL, left lateral projections.
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brobasilar disease or bilateral carotid lesions were present in these six false negative isotopic patients. An anterior projection nuclear angiogram failed to detect a posterior cerebral artery occlusion. The radionuclide perfusion study was not technically satisfactory for interpretation in one patient with an abnormal radiocontrast arteriogram. This tracer examination was counted as a false negative study. Three patients with acute strokes in the middle cerebral distribution had abnormal radionuclide cerebral angiograms and normal contrast angiograms. The tracer study detected a vascular lesion while the radiographic examination did not. Division of the patients into hemorrhagic and ischemic strokes could not always be made from the clinical information available. In five of seven patients with proved intracerebral hemorrhages, vascular displacement was present on the radionuclide cerebral angiogram.
STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
253
cal techniques, including computed tomography (6). It can detect abnormalities, particularly occlusive vascular lesions, that are not shown on the static brain images. For example, in this study, 35 of 47 patients with isotopic perfusion defects either had normal static images or did not have brain scans performed. Use of the radionuclide cerebral angiogram approximately doubles the isotopic detection rate of cerebrovascular disease (2, 4). This is partly because most static brain images are negative for the first 7 to 10 days after a cerebrovascular accident. The isotopic perfusion study is most effective in detecting middle cerebral and carotid artery occlusive disease. Significant obstruction of the carotid artery, usually 70% or greater, will result in decreased blood flow (1). This degree of carotid occlusion will usually be detected by the radionuclide cerebral angiogram (10). In the present study, the nuclear cerebral angiogram detected all unilateral carotid stenoses when greater than 70% of the vessel's lumen was occluded. Some difficulty in detecting bilateral carotid ischemic lesions has also been experienced by other investigators (2, 3, 5). Low cardiac output, slow intravenous injection of the radiopharmaceutical, and interfering external carotid flow may cause one to miss bilateral carotid cerebrovas-
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FIG. 18.7. Posterior cerebral infarct. Posterior radionuclide cerebral angiogram demonstrating reduction in activity in the right occipital area. Numbers denote time range in seconds. Static scintiphotos 2 hours after injection showing abnormal concentration of radiopertechnetate in the left posterior cerebral distribution. P, posterior; RPO, right posterior oblique; RL, right lateral views. Arrows point to pathology.
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cular disease. Increased intracranial pressure also may cause slow but symmetrical passage of the radiopharmaceutical through the neck arteries. Unilateral anterior cerebral artery ischemic lesions are difficult to visualize with the dynamic radioisotopic technique. The rarer bilateral anterior cerebral occlusions are readily recognized by nuclear angiography, however (8) (Fig. 18.6). Absence of early perfusion in the anterior cerebral artery distribution was evident in this stroke victim. We did not find the radionuclide cerebral angiogram to be an effective means of detecting most vertebrobasilar vascular occlusions. Cowan and associates had a similar experience (2). Posterior cerebral strokes should usually be detected if the patient is studied in the posterior projection. This patient's posterior cerebral infarct was detected on both dynamic and static radionuclide studies (Fig. 18.7). The posterior radionuclide cerebral angiogram showed decreased activity in the right occipital region. Two-hour static brain images demonstrated the infarction in the
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FIG. 18.8. Right intracerebral hemorrhage. Anterior radionuclide cerebral angiogram showing decreased transit of the radiopertechnetate through the right hemisphere and lateral displacement of the middle cerebral vessels due to the centrosylvian mass. Arrows point to the pathology. Numbers denote time range in seconds. Imm, immediate postradionuclide cerebral angiogram; A, anterior; and RL, right lateral scintiphotos are negative.
STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
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FIG. 18.9. Right direct common carotid angiogram. Anterioposterior view. Avascular centrosylvian mass and a lobulated aneurysm at the bifurcation of the right internal carotid artery.
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calcarine region of the right cerebral hemisphere. As stated earlier, this posterior cerebral vessel originated from the carotid system. The radionuclide cerebral angiogram can also detect vascular pathology not seen with contrast arteriography. The radioisotopic study visualizes the vasculature below the resolution of the contrast angiogram, or the microcirculation (9). Three acute middle cerebral stroke victims had definite vascular abnormalities demonstrated by the dynamic isotopic procedure while contrast angiography was interpreted as normal. Detection of intracerebral hemorrhages by the nuclear cerebral angiogram alone has been reported (7). We have been successful in demonstrating frontal and temporal lobe hematomas on anterior cerebral angioscintigrams. An emergency radionuclide cerebral angiogram was requested on this comatose 16-year-old female (Fig. 18.8). It showed decreased activity in the right hemisphere throughout the anterior perfusion study. The right middle cerebral complex appeared displaced
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SUMMARY
The radionuclide cerebral angiogram using intravenous radiopertechnetate has been found to be of value in confirming the early diagnosis of stroke. The isotopic perfusion study is of value in detecting ischemic carotid and middle cerebral lesions. It can also provide a rapid means of demonstrating intracerebral hemorrhages. Nuclear angiography is not recommended for detection of vertebrobasilar artery disease unless a posterior cerebral artery occlusion is suspected. REFERENCES 1. Brice, J. G., Dowsett. D. J., and Lowe, R. D., Haemodynamic effects of carotid artery stenosis. Br. Med. J., 2: 1363-1366, 1964. 2. Cowan, R. J., Maynard, C. D., Meschan. I., Janeway, R., and Shigeno, K. Value of the routine use of the cerebral dynamic radioisotope study. Radiology, 107: 111-116, 1973.
3. Fischer, R. J., and Miale, A., Jr. Evaluation of cerebral vascular disease with radionuclide angiography. Stroke, 3: 1-9, 1972. 4. Fish, M. B., Barnes, B., and Polycove, M. Cranial scintiphotographic blood flow defects in arteriographically proven cerebral vascular disease. J. Nucl. Med., 14: 558-564. 1973. 5. Moses, D. C., James, A. E., Jr., Strauss, H. W., and Wagner. H. N., Jr. Regional
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laterally. The superior sagittal sinus was never demonstrated; therefore, it was believed the cerebral circulation was slowed, probably due to increased intracranial pressure. Immediate postinjection views were normal. It was our impression that there was a large right frontal mass present, most likely an intracerebral hematoma. A low grade glioma or abscess could cause similar findings on the dynamic study. A right direct common carotid arteriogram was performed immediately. An avascular right frontal lesion and a large lobulated aneurysm at the bifurcation of the internal carotid artery were shown (Fig. 18.9). A right frontal craniotomy was then performed. The internal carotid aneurysm was clipped and the huge intracerebral hematoma evacuated. The over-all stroke detection rate of 600/0 in the present series from the Baptist Memorial Hospital would have been improved considerably if the six patients with technically inadequate studies has not been included. All six unsatisfactory examinations occurred in patients with carotid system disease. If these isotopic studies had been excluded, the radionuclide cerebral angiogram detection rate in carotid system strokes would have increased to 710/0. Other investigators in not altogether comparable studies have reported from 450/0 to 830/0 cerebrovascular disease detection with nuclear angiography (2-5, 9).
STROKE DIAGNOSIS RADIONUCLIDE CEREBRAL ANGIOGRAM
7.
8.
9. 10.
cerebral blood flow estimation in the diagnosis of cerebrovascular disease. J. Nucl. Med., 13: 135-141, 1972. Pendergrass, H. P., McKusick, K. A., New, P. F. J., and Potsaid, M. S. Relative efficacy of radionuclide imaging and computed tomography of the brain. Radiology, 116: 363-366, 1975. Rockett, J. F., Kaplan, E. S., Hudson, J. S., and Moinuddin, M. Intracerebral hemorrhage demonstrated by nuclear cerebral angiogram: case report. J. Nucl. Med., 16: 459-461, 1975. Rockett, J. F., Kaplan, E. S., Ray, M., Buchignani, J. S., and Gardner, H. C. Scintiphotographic demonstration of bilateral infarction in the distribution of the anterior cerebral arteries. Radiology, 112: 135-137, 1974. Rosenthall, L., Chan, J., Sidhu, R., and Stratford, J. Combined radiocontrast and radionuclide cerebral angiography. Radiology, 92: 1223-1228, 1969. Wise, G., Brockenbrough, E. C., and Marty, R. The detection of carotid artery obstruction: a correlation with arteriography. Stroke, 2: 105-113, 1971.
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