Nuclide Imaging and Computed Tomography in Cerebral Vascular Disease Lee C. Chiu, James H. Christie, and Rolf L. Schapiro This report presents our experience with computed tomographic and radionuclide scans in 2 2 4 patients w i t h ischemic or hemorrhagic infarcts or intracerebral hematomas secondary to cerebral occlusive vascular diseases. The results vary according to the site of vascular occlusion. The radionuclide angiograms and static scintigrams show four distinct patterns in cases of occlusion of the middle cerebral artery. Computed tomographic scans exhibit less variation in appearance and have a higher sensitivity in cases of recent ischemic infarction. The "'tentorial confluence sign" is an important finding on static scintigrams in patients w i t h occipital infarction; if this sign is not present, this diagnosis should be suspect.
Earlier reports have established the value of computed tomography and radionuclide scans in the evaluation of cerebral infarction, t 3 In individual cases, however, each of these modalities may render nondiagnostic or false negative findings; combining both types of examinations and comparing results yield a greater likelihood of an accurate diagnosis of cerebrovascular disease. Computed tomography is clearly more valuable than radionuclide scans in the diagnosis and follow-up of hemorrhagic infarcts or parenchymal hematomas.
DIONUCLIDE ANGIOGRAPHY rms part of our routine examination of patients with suspected cerebral infarction. Focal changes in blood flow are demonstrated, after antecubital vein bolus injections of ~176 sodium pertechnetate in doses of 20-25 mCi. The scintillation camera is set to image either the frontal or vertex views. Sequential images are obtained at 2-sec intervals for a total of 32 sec. Subsequently, static brain images are obtained at variable time intervals 10 min to 4 hr after injection. The computed tomographic (CT) scans were obtained on the CT 1000 EMI scanner. Onethird of the patients were examined utilizing an 80 x 80 matrix, with the remainder being examined with the use of a 160 x 160 matrix. All studies were monitored carefully, and, whenever it was considered desirable, patients were rescanned after the infusion of contrast material. In this series, one-fourth of the entire patient population was thus scanned both before and after the infusion of contrast material.
We reviewed the CT and radionuclide scan findings in 226 patients with ischemic cerebrovascular accidents (CVA) who were examined by both modalities. The diagnoses of CVA were confirmed by angiography, autopsy, or long-term clinical follow-up 4.
From the Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa. Lee C. Chiu, M.D.: Associate Professor, Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa; J a m e s H. Christie, M.D.: Professor, Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa; Rolf L. Schapiro, M.D.: Professor, Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa. Reprint requests should be addressed to Lee C. Chiu, M.D., Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242. 9 1977 by Grune & Stratton, lnc. Seminars in Nuclear Medicine, Vol. Vl I, No. 2 (April), 1977
COMPARISON
OF STATIC
BRAIN
SCAN
AND
COMPUTED TOMOGRAPHIC SCAN OBSERVATIONS WITH RADIONUCLIDE PERFUSION PATTERNSs'6
In our experience as well as in that of others, the middle cerebral a r t e r y ( M C A ) and its branches are the vessels most frequently involved in intracranial ischemic disease/ The following discussion relates the static nuclear scan and CT scan findings to these perfusion patterns. Normal perfusion (38%). A p p r o x i m a t e l y one-third of our patients had both normal perfusion on nuclide angiography and normal findings on the subsequent static images. CT scans on these patients were uniformly abnormal. Onehalf of the CT scans showed decreased density with poorly defined margins on the affected side, while the remainder showed inhomogeneous density alterations with well-defined margins.
Decreased perfusion (55%) (Figs. 1A and 2A). Approximately one-half of our patients with acute CVA showed diminished perfusion on the affected side with normal static scans. However, this combination of findings was restricted to the first week after the clinical insult, with all radionuclide findings on later examinations being normal. Slightly more com17 5
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Fig. 1. These examinations are on a 69-yr-old male 9 days after onset of left hemiparesis and coma. (A) There is decreased perfusion on the right side during the arterial phase (arrows) returning to normal in the venous phase. (B) The 2-hr scan shows increased activity in the area supplied by the right middle cerebral artery (MCA). A finger-shaped pattern of activity is best seen on the right lateral view. (C) The computed tomographic (CT) scan shows a large irregular area of patchily decreased density in the right hemisphere. The pineal gland is shifted slightly to the left, and there is complete obliteration of the right lateral ventricle. A t autopsy, the right M C A was occluded by a thrombus, and herniation of the uncus and the right cingulate gyrus was present,
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Fig. 2. The scans were performed 6 days after the sudden onset of left hemiparesis in this 64-yr-old man w h o had a 2-yr history of a mild residual right hemiparesis secondary to an old embolic infarction. This was related to earlier cardiac valve surgery. Carotid arteriography revealed an embolus in the right MCA. (A) There is reduced perfusion of the right hemisphere in the arterial and venous phases (arrows). (B) The 2-hr scan shows a crescent-shaped area of increased activity parallel to the right convexity (arrows) on the posterior projection. (C) There is an area of decreased density with ill-defined margins in the area of distribution of the right MCA, and the lateral ventricle is obliterated. The wen-defined area of decreased density surrounding the darker central area in the left hemisphere reflects an old M C A infarction.
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mon is the combination of reduced perfusion on radionuclide angiography coupled with abnormal findings also present on the static radionuclide brain images. This combination of abnormalities is likely to be demonstrated late in the first week after the clinical insult and persists for approximately 4 wk thereafter. In this group of patients, CT scans show areas of diminished density, which do not assume a specific or characteristic configuration or pattern. The demonstration of reduced perfusion on radionuctide angiography, coupled with a negative static image, generally favors a cerebrovascular accident. However, brain contusion can also present as a perfusion deficiency without concomitant positive findings on a static radionuclide brain scan.
Delayed increased perfusion, flip-flop phenomenon (6%). Occasional patients are encountered in whom the radionuclide angiogram shows a unilateral delay and reduction in perfusion during the arterial phase, which is followed by increased perfusion of the affected hemisphere during the venous phase. This observation has been referred to as the flip-flop phenomenon) The subsequent static brain scintigram may be either negative or positive. CT scans on patients showing this flip-flop phenomenon on radionuclide imaging generally show an area of abnormally decreased density on the affected side; the central portions of these lesions especially tend to be of very homogeneous density. Figure 4A shows an example of the flip-flop phenomenon with initial-decreased perfusion, followed by a gradual increase in activity, which ultimately, during the washout phase, exceeds that of the normal side. Analogous findings have been demonstrated on carotid angiography, suggesting the development of collateral blood flow from the normal side (Fig. 4C).
Increased perfusion or luxury perfusion 9-11 (2%). Six of our 174 patients who had susFig. 3, Eleven days prior to admission, this 62-yr-old hypertensive woman experienced the sudden onset of right hemiparesis and motor aphasia. Carotid arteriography showed occlusions of several branches of the left M C A . The perfusion is normal. (A) The 2-hr scan shows t w o areas of increased uptake in the left parietal lobe (arrows). (B) There is an area of decreased density with in-defined margins in the left hemisphere.
tained acute CVA showed a seemingly paradoxical pattern of regionally increased perfusion during the arterial phase, with a subsequent return to normal, slightly diminished or slightly increased perfusion in the same area. The subsequent static images on all six patients were also abnormal.
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Fig. 4. This 65-yr-old male suddenly developed a right hemiparesis and confusion of speech 6 days prior to these examinations. (A) There is decreased perfusion on the left during the arterial phase (arrows) and increased perfusion in the venous phase (arrows). Serial late static scans are normal. (B) There is an irregularly marginated area of patchily decreased density in the distribution of the left M C A and a mass effect with extrinsic deformity of the left lateral ventricle. (C) Carotid arteriography shows complete occlusion at the origin of the left M C A (arrow). There was good opacification of the M C A branches during the venous phase presumably due to retrograde collateral filling from the anterior cerebral artery.
CT scans in four of these patients showed a central increased density or blush within the overall low density lesion; on rescanning after infusion of contrast material, a ring of increased density was demonstrated in the central portions of the overall low density lesion (Figs. 5B, 5C). It is interesting to note that the four blushing infarcts were all found within 9-16 days after the clinical insult. The remaining two
cases showed the usual area of reduced density without a blush. The demonstration of luxury perfusion or a blushing infarct is apparently restricted to a relatively short time period after the clinical insult. The blush is not demonstrated on CT scans obtained on a restudy of the patient a few months later, although the lesion persists as an area of homogeneously reduced density. Radionuclide brain scans at
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Fig. 5. This 45-yr-old woman has a 2-wk history of aphasia, confusion, and right hemiparesis. (A) Focal hyperperfusion is present in the left cerebral hemisphere (arrows); a static scan not shown showed a corresponding abnormal fan-shaped pattern, {B) In the distribution of the left MCA is a poorly defined area of diminished density, After injection of contrast material (lower photos), this area increases markedly in density (blush). (C)The angiogram demonstrates increased perfusioo during the arterial and venous phases consistent with luxury perfusion.
comparably delayed time intervals are normal and do not show any residual abnormalities. In our experience, the presence of luxury perfusion and blushing infarcts on radionuclide and CT scans as a manifestation of vascular disease is difficult to interpret. All these cases were initially diagnosed as neoplasms with tumor vascularity, despite the fact that the clinical presentation was suggestive of infarction. Final diagnoses were made by biopsy in one case, and five patients had arteriography which revealed occlusion of the MCA in three patients and of the posterior cerebral artery in two patients. Luxury perfusion was also identified on one arteriograph (Fig. 5D); the term "luxury perfusion" was coined by Lassen ~2when he described his observations following intracarotid injection of ~3~Xe in saline into patients with cerebral in-
farction. He proposes that regional cerebral perfusion is regulated in part by local metabolic requirements of the brain tissue. In acute infarction, local hyperemia produces localized metabolic acidosis, which in turn results in loss of the normal autoregulatory mechanism. Inappropriate vascular dilatation then occurs in the a b s e n c e o f a d e c r e a s e in c e r e b r a l blood pressure, so that the volume of blood supplied to the area exceeds that required by the local metabolic conditions. STATIC BRAIN SCAN AND COMPUTED TOMOGRAPHIC SCAN FINDINGS IN MIDDLE CEREBRAL ARTERY DISEASE
Fairly characteristic patterns were observed on CT and static radionuclide scans in 174 ischemic infarcts. The findings are in part de-
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termined'by the site of vascular occlusion in terms of various branches of the MCA.
Static Radionuclide Scan Findings in Occlusion of Major Branches of the Middle Cerebral Artery Four different patterns are encountered. 1. Normal static scan (18%). The static brain scan was normal in 31 cases, and the abnormality was only detected on the radionuclide angiogram in terms of one or another of the abnormalities described in the above section. 2. Static brain scan showing a finger-shaped area of uptake (56%) (Fig. 1B). This pattern was encountered in 98 patients and is best demonstrated on the lateral view in which the fingershaped area of excessive uptake corresponds to the Sylvian triangle. H o w e v e r , e x c e s s i v e activity can also be seen on the anterior view in the area of the MCA distribution (Fig. IB). 3. Static brain scan showing crescent-shaped excessive uptake (21%) (Fig. 2B). This pattern was present in 36 cases, and is best recognized on the anterior or posterior view as an area of i n c r e a s e d u p t a k e p a r a l l e l l i n g the c o n v e x contour of the calvarium. Lateral views are generally negative, or alternatively may reveal very faintly increased uptake in the temporal region. This pattern is similar to that seen in subdural hematomas. 4. Static brain scan showing multiple areas of uptake (5%) (Fig. 3A). This pattern of multifocal excessive uptake was present in nine patients, and is best identified on the lateral view. Probably, this appearance is the result of multiple occlusions of branches of the MCA.
CHIU, CHRISTIE, AND SCHAPIRO
diminished density with irregular, ill-defined margins in the region of the MCA distribution (Figs. 1C, 2C, 3B, 4B). The absorption range is 2 8 EMI units less than the contralateral control region. Generally, differentiation from neoplasm and other lesions is readily achieved. In cases of large infarcts, a mass effect may appear with displacement or obliteration of the ventricular system (Figs. 1C, 2C, 4B). This effect is not encountered in cases with small infarcts. Following the first week, very little change is to be expected in the density alterations encountered during the first week. Some possible changes which might occur include diminution in the area of decreased density, sharper definition of the margin of the lesion, and some loss of the patchiness of the lesion or improved homogeneity of the density distribution. In an old infarct, the lesion is homogeneous
) A. Axial view 4-5 cm above OM line"
B. Axial vmw 6-8 cm above OM line"
C. Lt. lateral
Computed Tomographic Scan Findings in Occlusion o f Major Branches o f the Middle Cerebral Artery The CT scan is especially valuable in the evaluation of ischemic infarcts within the first week of the clinical insult, and, during this time period, appears to have considerably greater sensitivity than the radionuclide scan. In our series, the earliest positive CT scan was obtained 4 hr after accidental occlusion of the MCA during the course of a carotid angiogram. During the first week following occlusion of a major branch of the MCA, the typical lesion presents as a nonhomogeneous, patchy area of
D. Anterior
E. Posterior
Fig. 6. The distributions of the anterior, middle, and posterior cerebral arteries are shown in the low axial (A), high axial (B), left lateral (C), anterior (D), and posterior (E)views. Major branches of the M C A are identified as anterior temporal artery (AT), orbital frontal artery (OF), prerolandic artery (PR), rolandic artery (R), posterior temporal artery (PT), parietoangular artery (PA), basal ganglia (BG), anterior cerebral artery (AC), middle cerebral artery (MC), posterior cerebral artery (PC), and orbitomeatal line (OM).
CEREBRAL VASCULAR DISEASE
Fig. 7. These examinations were obtained 8 days following admission of this 72-yr-old male w i t h a left hemiplegia and unconsciousness. (A) There is increased uptake in the region supplied by the orbital frontal branch of the right M C A . (B) There is an ill-defined area of diminished density in the right frontal lobe. A t autopsy, there was occlusion of several major branches of the right M C A ,
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and has absorption characteristics that are identical to those of cerebrospinal fluid (Fig. 2C), and such old lesions are always well marginated. The loss of brain substance may be manifest in dilatation of the ipsilateral ventricles. At this stage, the radionuclide angiogram is negative except in three patients whose lesions have converted into large cysts causing displacement of vessels. The static brain scans are always negative.
Radionuclide and Computed Tomographic Scan Findings in Occlusions of Cortical Branches of the Middle Cerebral A rt ery The areas of vascular supply provided by the major branches of the MCA are diagrammatically prescribed in Fig. 6. Representative scan findings consequent to occlusions of the orbital frontal artery (Figs. 7A, 7B), the ascending frontal parietal arteries (Figs. 8A, 8B), the posterior temporal artery, and parietal angular artery (Figs. 9A, 9B) are illustrated. Whenever an occlusion occurs in the cortical branches of the MCA, the radionuclide scan may reflect this by excessive uptake some distance from the midline. This is due to the fact that the distribution of the cortical branches of the MCA does not extend to the midline. Rather, the anterior and posterior cerebral arteries supply these regions. Furthermore, the probability of detecting a lesion due to occlusion of these cortical branches by radionuclide scanning is relatively low. Serial CT scanning offers the greatest likelihood of detecting a cortical infarct or a lesion due to occlusion of a single cortical branch of the MCA. During the first 1 or 2 days after the clinical insult, the CT scan is likely to be normal, but repeat scanning 4-10 days after the infarct will render the lesion detectable. This is attributable to the fact that edema of the brain begins 2-6 hr after infarction, but it does not become maximal until 2 5 days after the infarct. ]z,]3 Subsequent resolution of the edema again renders the likelihood of demonstrating the lesion by CT scanning less likely. An exception to this rule occurs when the infarcts remain as residual cavities greater than 1 cm in size and become filled with fluid of the same density as cerebrospinal fluid; when this occurs, late CT scans will demonstrate small areas of decreased
Fig. 8. These examinations were performed 16 days after admission of this markedly hypertensive, disoriented, agitated, and drowsy 53-yr-old white man. (A) There is excessive activity in the peripheral portion of the area of distribution of the left M C A . (B) There is an area of diminished density in the left posterior frontal area. Carotid arteriography showed occlusion of the rolandic branch of the left M C A .
Fig. 9. This 66-yr-old w o m a n had a left hemiparesis and aphasia for 9 days prior to admission. (A) A t the periphery of the right parietal lobe, there is a wedge shaped area of activity. A repeat examination 8 w k later was normal. (B) An area of decreased density is noted in the right posterior parietal lobe.
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Fig. 10. This 58-yr-old male w i t h a 3-too history of headaches was a d m i t t e d 12 days prior to these examinations following the sudden onset of aphasia and weakness of the left side of the face. (A) Excessive activity is present above the right sphenoid sinus. (B) There is a small area of diminished density deep in the right temporal region corresponding to location of the basal ganglia.
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Fig. 11. This 68-yr-old male became confused, aphasic, and dizzy 10 days prior to admission. (A) There is abnormal a c t i v i t y adjacent to t h e midline at the anterior frontal area corresponding to the distribution of the right anterior cerebral artery. (B) The CT scan shows a corresponding area of diminished density in the right frontal lobe.
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Fig. 12. This 55-yr-old male developed a sudden right homonymous hemianopsia 15 days prior to admission. (A) There is increased uptake just to the left of the midline on the posterior view. On the lateral view, the excessive activity extends to the c o n f l u e n c e of t h e sinuses ( p o s i t i v e t e n t o r i a l confluence sign). (B) An area of decreased density is present in the left occipital lobe. (C) There is occlusion of the left posterior cerebral artery (arrow).
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189
Fig. 13, A 67-yr-old male with left homonymous hemianopsia and a history of progressive headaches and lethargy. (A) An area of excessive activity is present in the right occipital region distinct from the tentorium. Absence of the tentorial confluence suggests a neoplasm rather than infarct, (B) There is an irregular area of decreased density in the right occipital area that after infusion of contrast material presents as a right parietal occipital mass surrounded by edema, A glioma was found at surgery.
density. In summary, then, cortical infarcts are difficult to identify on radionuclide scans and on CT scans are most readily visualized during the acute phase 4-10 days after clinical infarction has occurred.
Radionuclide and Computed Tomographic Findings in Occlusion of the Deep Branches of the Middle Cerebral Art ery The lenticulostriate arteries are the first deep branches of the proximal segment of the MCA group supplying the basal ganglia. Infarcts due to occlusion of these vessels are reflected orr the lateral view of the radionuclide scan as "comma-shaped" or reversed comma-shaped activity above the region of the sphenoid sinus adjacent to the Sylvian fissure. In the anterior view, this excessive activity is clearly demarcated from the peripheral activity (Fig. 10A). CT scans reflect infarcts due to occlusion of the lenticulostriate arteries as diminished density in the area of the basal ganglia.
STATIC BRAIN SCAN AND COMPUTED TOMOGRAPHIC SCAN FINDINGS IN OCCLUSION OF THE ANTERIOR CEREBRAL ARTERY
Occlusions of the anterior cerebral artery are rare but produce quite characteristic changes on radionuclide scans. Because of the proximity of the contralateral anterior cerebral artery, no abnormality can be demonstrated on the early anterior radionuclide angiographic images. However, decreased or absent activity during the capillary phase, with abnormal uptake in the paramedian area or subsequent static anterior scans are characteristic. CT scans are less specific, but show abnormally diminished density in the frontal area. (Fig. 11A, B) STATIC BRAIN SCAN AND COMPUTED TOMOGRAPHIC FINDINGS IN OCCLUSIONS OF THE VERTEBROBASILAR ARTERY
Occlusion of the Posterior Cerebral A rtery In our series, there were 28 patients who had occlusions of a posterior cerebral artery. The
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Fig. 14. A 65-yr-old man with nystagmus, marked ataxia and a 10day history of nausea, vomiting, headaches, and inability to walk. (A) There is increased activity in the right p o s t e r i o r fossa. (B) There is diminished density in the right cerebellar hemisphere, A subsequent vertebral angiogram revealed an occlusion of the right posterior inferior cerebellar artery.
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Fig. 15. This 68-yr-old hypertensive man experienced a sudden aphasia and left hemiparesis. (A) Changes consistent with infarction of the right basal ganglia are present. (B) This CT scan was performed 9 mo later and shows a small well-defined area of diminished density corresponding to the region of the right basal ganglia, This finding is consistent with an old infarct of the lacunar type,
anterior and posterior radionuclide angiograms are of no value; however, decreased or absent perfusion during the capillary phase can be demonstrated on dynamic vertex views. Static radionuclide scans were positive in 23 cases, and, typically, the posterior view shows a wedge-shaped area of increased activity that is adjacent to the midline and extends down to the torcular herophili and to the medial transverse sinus. On the lateral view, this increased uptake assumes the form of a tapering crescent or triangle that blends with the normal activity of the posterior sagittai and transverse sinuses (Fig. 12A). This configuration is quite typical, and we refer to it as the "tentorial confluence" sign. 4 If the excessive uptake is not confluent with the activity of the tentorial region (Fig. 13A), the lesion is not likely due to occlusion of the posterior cerebral artery, and another etiology must be strongly considered. CT scans were positive in 26 patients and showed diminished density in the occipital region (Fig. 12B). If a patient has an initially
positive radionuclide scan and the tentorial confluence sign is absent, it is essential that a CT scan with intravenous contrast material enhancement ~4,~5be undertaken in the effort to confirm the presence of a neoplasm (Fig. 13B). Occlusion of Other Branch es o f th e Basilar Artery
Radionuclide scan findings are nonspecific and do not differentiate between infarcts and neoplasms. Infarcts in this area present as nonspecific lesions of the posterior fossa (Fig. 14A). CT scans show diminished density in the posterior fossa (Fig. 14B); occasionally, the fourth ventricle is obliterated, but obstructive hydrocephalus was not demonstrated in any of the 22 cases in our experience. This absence of obstructive hydrocephalus provides some help in differentiating infarcts from neoplastic spaceoccupying lesions. Detection of lesions in this area is rendered difficult on the conventional axial projection because of the overlying dense
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Fig. 16. This 64-yr-old woman had episodic hypotension, progressive stupor, and recurring major motor seizures. (A) Symmetric bands of increased uptake correspond to the "watershed" between the distributions of the anterior cerebral artery and the MCA, (B) Two symmetric areas of decreased density (arrows) correspond to the watershed
zone.
occipital bone. Additional coronal views can be helpful in confirming the diagnosis.
STATIC BRAIN SCAN A N D COMPUTED TOMOGRAPHIC SCAN FINDINGS IN LACUNAR INFARCTS A N D WATERSHED INFARCTS
Acute lacunar infarcts cannot be identified on CT or radionuclide scans, unless they are quite large. The lesion must be greater than 1 cm in diameter before it can be recognized. 15 Such large lacunar infarcts will present as small areas of excessive uptake on radionuclide scans (Fig. 15A), and, on CT scans, they may present as irregular areas of decreased density with the
same absorption as cerebrospinal fluid (Fig. 15B). Watershed infarcts occur in boundary zones wherein the distributions of the anterior, middle, and posterior cerebral arteries overlap. The manifestations on radionuclide scans are usually pathognomonic, with linear bands of excessive uptake occurring in these junctional regions (Fig. 16A). On CT scans, localized areas of decreased density are present in areas corresponding to those of increased uptake on the radionuclide scan. PATHOPHYSIOLOGICAL CORRELATION
In the period following an acute arterial occlusion, an ischemic infarct shows a transient
CEREBRAL VASCULAR DISEASE
increase in the number of neutrophilic leukocytes. 1~ Edema of the brain begins within 2-6 hr after arterial occlusion and becomes maximal in 2-5 days. 17.18Cerebral anoxia results in swelling and vacuole formation of both gray and white matter of the brain. CT scans do not permit distinction between the infarcted brain area and the adjacent edematous brain p a r e n c h y m a , since both present as areas of diminished density. Neuronal degeneration occurs when the blood-brain barrier breaks down and plasma proteins leak into the injured brain tissue. Subsequently, repair commences as glial proliferation, macrophage reaction, and ultimately fibrogliosis occur. ~z,13 Heyman ~~ has shown that the uptake of the radiopharmaceuticals is related to m a c r o p h a g e activity that is most pronounced approximately 1 wk after the clinical insult. At this time, the static scintigram becomes positive, but, 60 days later, the
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radionuclide scan is likely to be negative, since fibrogliosis is taking place. As was indicated above, shortly after infarction, the necrotic brain tissue and adjacent brain edema are reflected on the CT scan as an area of inhomogeneous decreased density with an absorption range of 2-12 EMI units; normal brain tissue is in the range of 12-28 EMI units; this area of patchy reduction in density usually has an ill-defined margin. As phagocytic activity affects removal of the necrotic tissue, cystic degeneration produces an area of encephalomalacia, or a dense neuroglial scar is formed. Consequently, an infarct more than 4 wk old presents on the CT scan as an area of decreased density with an absorption identical to that of cerebrospinal fluid; at this time, the density characteristics are quite homogeneous, and the lesion generally has a well-defined margin. If there has been loss of a significant quantity of brain substance, there may be associated dilata-
Fig. 17. This B8-yr-old man presented with a history of sudden onset of right paresis and sensory deficit 9 days prior to these examinations. (A) There is abnormal activity in the left hemisphere. (B) There is a dense lesion surrounded by a zone of diminished density, Multiple occlusions of major branches of the left M C A were demonstrated on arteriography,
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cortex. Consequently, on radionuclide scans, these lesions tend to present remote to the peripheral activity and to the midline. Interpretation of such lesions is rendered more difficult, since hemorrhagic infarcts or hematomas simulate neoplasms, abscesses, or other lesions? Empirically, radionuclide brain scans become positive within 1 wk of a hemorrhagic infarct or intracerebral hematoma in approximately 50% of patients. More than 6 wk after the cerebral hemorrhage, the radionuclide image returns to normal. Ambrose' noted that infarcted brain tissue presents as a region of less than normal density on CT scans, while intracerebral hemorrhage shows greater than normal density on CT scans. Whenever both alterations in density occur sim u l t a n e o u s l y , h e m o r r h a g i c i n f a r c t i o n is considered likely. 2~ Usually, the increased density is located at the periphery of an area of decreased density (Figs. 17A, 17B); sometimes, there is also a central focus of increased density
Fig. 18. This 72-yr-old male suddenly became comatose with a left hemiparesis. The large well-defined area of increased density on the CT scan is consistent with an intracerebral hematoma. (Radionuclide scans in this case w e r e normal.)
tion of the ventricles and widening of the fissures and sulci.
Considerations Pertaining to So-called Hemorrhagic Infarct and Intracerebral Hematoma In ischemic infarcts, areas o f excessive u p t a k e on radionuclide scans usually correspond to the anatomic area supplied by the specific artery that has been occluded. This anatomic correlation between the excessive uptake on the scintiscan and the vascular supply is less likely to be maintained when hemorrhagic infarction occurs with or without formation of an intracerebral hematoma. This is attributable to the fact that the hemorrhage associated with the infarct can readily dissect brain tissue and thus cross the boundaries of the volume of brain supplied by a specific vessel. Hematomas tend to form deeper in the brain and spare the
Fig. 19. This 69-yr-old male w i t h a history of hypertension presented with a left hemiparesis and had bloody cerebrospinal fluid. There is an area of increased density in the right temporal reading, suggesting a hemorrhage into the region of the basal ganglia. Blood casts are present in both lateral ventricles and in the fourth ventricle. (Radionuclide scans were normal in this case.)
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that presumably reflects a central accumulation of blood. On CT scans, cerebral h e m a t o m a s are usually rounded with a slightly elongated shape (Fig. 18). While the contour may be somewhat irregular, the margins are well-defined and appear to be surrounded by a rim of tissue of diminished density. If t h e r e is e x t e n s i v e extravasation of blood, the latter may penetrate into the ventricular system (Fig. 19). As was indicated above, radionuclide scans tend to miss hemorrhagic infarcts during the first week after occurrence of the clinical insult. The CT scan, on the other hand, is extremely sensitive and will detect the abnormality immediately after bleeding occurs. Serial CT scans obtained after a period of time show gradual diminution of the extravasated blood. It is worthwhile to review one additional difference between the manner in which mani-
f e s t a t i o n s o f i s c h e m i c disease p r e s e n t on radionuclide and CT scans. Since CT scans generally render a relatively detailed image of the brain anatomy, distortions imposed by the infarct on the normal anatomic configuration of the brain can be recognized in addition to the focal alterations in tissue densities. The Sylvian fissure can normally be identified as a structure of diminished density. Edema associated with an infarct frequently renders recognition of this structure impossible. Localized changes in brain volume often result in displacement of the choroid plexus or in displacement and deformation of the ventricular system. These alterations diminish with time, as the brain edema subsides and the extravasated blood is resorbed. Ventricular dilatation is a common finding that increases with time; this is attributable to localized or generalized atrophy of brain tissue associated with infarction.
REFERENCES
1. Ambrose J: Computerized X-ray scanning of the brain. J. Neurosurg 40:679-695, 1974 2. Deland FH: Scanning in cerebral vascular disease. Semin Nucl Med 1:31, 1971 3. Paxton R, Ambrose J: The E.M.I. scanner: A brief review of the first 650 patients. Br J Radiol 47:530, 1974 4. Chiu LC, Fodor LB, Cornell, SH, et al: Computed tomography and scintigraphy in ischemic stroke. Am .l Roentgenol, 127:481, 1976 5. Rosenthall L, Martin RH: Cerebral transit of pertechnetate given intravenously. Radiology 94:521, 1970 6. Rosenthall L: Intravenous and intracarotid radionuclide cerebral angiography. Semin Nucl Med 1:70, 1971 7. Merrit H: Textbook of Neurology. Philadelphia, Lea & Febiger, 1968, pp 36-76 8. Fish MB, Pollycove M, O'Reilly S: Vascular characterization of brain lesions by rapid sequential cranial scintiphotography. J Nucl Med 9:249, 1968 9. Strauss HW, James AE, Hurley P J: Nuclear cerebral angiography. Usefulness in the differential diagnosis of cerebrovascular disease and tumor. Arch Intern Med 131:211, 1973 10. Snow M, Keyes W Jr: The luxury-perfusion syndrome following a cerebrovascular accident demonstrated by radionuclide angiography. J Nucl Med 15:907, 1974 11. Soin JS, Burdine JA: Acute cerebral vascular accident associated with hyper-perfusion. Radiology 118:109, 1976
12. Lassen NA: The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localized within the brain. Lancet 2:113, 1966 13. O'Brien MD, Jordan MM, Waltz AG: lschemic cerebral edema and the blood-brain barrier. Arch Neurol 30:461, 1974 14. Yock DH Jr, Marshall WH Jr: Recent ischemic brain infarcts at computed tomography: Appearance preand post-contrast infusion. Radiology 117:599, 1975 15. New F J, Scott WR: Infarcts, in Computed Tomography of the Brain and Orbit. Baltimore, Williams & Wilkins, 1975, pp 332-361 16. Adams RD, Sidman RL: Introduction Neuropathology. New York, McGraw-Hill, 1968
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17. Baker HL, Campbell JK, Houser SW: Computer assisted tomography of the head: An early evaluation. Mayo Clin Proc 49:17, 1974 18. Glasgow JL, Currier RD: Brain scans at varied intervals following C.V.A. J Nucl Med 6:902, 1965 19. Heyman A: Brain scanning, in Siekert, RG, Whisnant, JP (eds): Cerebral Vascular Disease: Sixth International Conference. New York, Grune & Stratton, 1968. 20. Cronqvust S, Brismar J, Kjellin K, et al: Computer assisted tomography in cerebrovascular lesions. Acta Radiol Diagn 16:135, 1975
Earlier reports have established the value of computed tomography and radionuclide scans in the evaluation of cerebral infarction, t 3 In individual cases, however, each of these modalities may render nondiagnostic or false negative findings; combining both types of examinations and comparing results yield a greater likelihood of an accurate diagnosis of cerebrovascular disease. Computed tomography is clearly more valuable than radionuclide scans in the diagnosis and follow-up of hemorrhagic infarcts or parenchymal hematomas.
DIONUCLIDE ANGIOGRAPHY rms part of our routine examination of patients with suspected cerebral infarction. Focal changes in blood flow are demonstrated, after antecubital vein bolus injections of ~176 sodium pertechnetate in doses of 20-25 mCi. The scintillation camera is set to image either the frontal or vertex views. Sequential images are obtained at 2-sec intervals for a total of 32 sec. Subsequently, static brain images are obtained at variable time intervals 10 min to 4 hr after injection. The computed tomographic (CT) scans were obtained on the CT 1000 EMI scanner. Onethird of the patients were examined utilizing an 80 x 80 matrix, with the remainder being examined with the use of a 160 x 160 matrix. All studies were monitored carefully, and, whenever it was considered desirable, patients were rescanned after the infusion of contrast material. In this series, one-fourth of the entire patient population was thus scanned both before and after the infusion of contrast material.
We reviewed the CT and radionuclide scan findings in 226 patients with ischemic cerebrovascular accidents (CVA) who were examined by both modalities. The diagnoses of CVA were confirmed by angiography, autopsy, or long-term clinical follow-up 4.
From the Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa. Lee C. Chiu, M.D.: Associate Professor, Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa; J a m e s H. Christie, M.D.: Professor, Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa; Rolf L. Schapiro, M.D.: Professor, Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa. Reprint requests should be addressed to Lee C. Chiu, M.D., Department of Radiology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242. 9 1977 by Grune & Stratton, lnc. Seminars in Nuclear Medicine, Vol. Vl I, No. 2 (April), 1977
COMPARISON
OF STATIC
BRAIN
SCAN
AND
COMPUTED TOMOGRAPHIC SCAN OBSERVATIONS WITH RADIONUCLIDE PERFUSION PATTERNSs'6
In our experience as well as in that of others, the middle cerebral a r t e r y ( M C A ) and its branches are the vessels most frequently involved in intracranial ischemic disease/ The following discussion relates the static nuclear scan and CT scan findings to these perfusion patterns. Normal perfusion (38%). A p p r o x i m a t e l y one-third of our patients had both normal perfusion on nuclide angiography and normal findings on the subsequent static images. CT scans on these patients were uniformly abnormal. Onehalf of the CT scans showed decreased density with poorly defined margins on the affected side, while the remainder showed inhomogeneous density alterations with well-defined margins.
Decreased perfusion (55%) (Figs. 1A and 2A). Approximately one-half of our patients with acute CVA showed diminished perfusion on the affected side with normal static scans. However, this combination of findings was restricted to the first week after the clinical insult, with all radionuclide findings on later examinations being normal. Slightly more com17 5
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Fig. 1. These examinations are on a 69-yr-old male 9 days after onset of left hemiparesis and coma. (A) There is decreased perfusion on the right side during the arterial phase (arrows) returning to normal in the venous phase. (B) The 2-hr scan shows increased activity in the area supplied by the right middle cerebral artery (MCA). A finger-shaped pattern of activity is best seen on the right lateral view. (C) The computed tomographic (CT) scan shows a large irregular area of patchily decreased density in the right hemisphere. The pineal gland is shifted slightly to the left, and there is complete obliteration of the right lateral ventricle. A t autopsy, the right M C A was occluded by a thrombus, and herniation of the uncus and the right cingulate gyrus was present,
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Fig. 2. The scans were performed 6 days after the sudden onset of left hemiparesis in this 64-yr-old man w h o had a 2-yr history of a mild residual right hemiparesis secondary to an old embolic infarction. This was related to earlier cardiac valve surgery. Carotid arteriography revealed an embolus in the right MCA. (A) There is reduced perfusion of the right hemisphere in the arterial and venous phases (arrows). (B) The 2-hr scan shows a crescent-shaped area of increased activity parallel to the right convexity (arrows) on the posterior projection. (C) There is an area of decreased density with ill-defined margins in the area of distribution of the right MCA, and the lateral ventricle is obliterated. The wen-defined area of decreased density surrounding the darker central area in the left hemisphere reflects an old M C A infarction.
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mon is the combination of reduced perfusion on radionuclide angiography coupled with abnormal findings also present on the static radionuclide brain images. This combination of abnormalities is likely to be demonstrated late in the first week after the clinical insult and persists for approximately 4 wk thereafter. In this group of patients, CT scans show areas of diminished density, which do not assume a specific or characteristic configuration or pattern. The demonstration of reduced perfusion on radionuctide angiography, coupled with a negative static image, generally favors a cerebrovascular accident. However, brain contusion can also present as a perfusion deficiency without concomitant positive findings on a static radionuclide brain scan.
Delayed increased perfusion, flip-flop phenomenon (6%). Occasional patients are encountered in whom the radionuclide angiogram shows a unilateral delay and reduction in perfusion during the arterial phase, which is followed by increased perfusion of the affected hemisphere during the venous phase. This observation has been referred to as the flip-flop phenomenon) The subsequent static brain scintigram may be either negative or positive. CT scans on patients showing this flip-flop phenomenon on radionuclide imaging generally show an area of abnormally decreased density on the affected side; the central portions of these lesions especially tend to be of very homogeneous density. Figure 4A shows an example of the flip-flop phenomenon with initial-decreased perfusion, followed by a gradual increase in activity, which ultimately, during the washout phase, exceeds that of the normal side. Analogous findings have been demonstrated on carotid angiography, suggesting the development of collateral blood flow from the normal side (Fig. 4C).
Increased perfusion or luxury perfusion 9-11 (2%). Six of our 174 patients who had susFig. 3, Eleven days prior to admission, this 62-yr-old hypertensive woman experienced the sudden onset of right hemiparesis and motor aphasia. Carotid arteriography showed occlusions of several branches of the left M C A . The perfusion is normal. (A) The 2-hr scan shows t w o areas of increased uptake in the left parietal lobe (arrows). (B) There is an area of decreased density with in-defined margins in the left hemisphere.
tained acute CVA showed a seemingly paradoxical pattern of regionally increased perfusion during the arterial phase, with a subsequent return to normal, slightly diminished or slightly increased perfusion in the same area. The subsequent static images on all six patients were also abnormal.
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Fig. 4. This 65-yr-old male suddenly developed a right hemiparesis and confusion of speech 6 days prior to these examinations. (A) There is decreased perfusion on the left during the arterial phase (arrows) and increased perfusion in the venous phase (arrows). Serial late static scans are normal. (B) There is an irregularly marginated area of patchily decreased density in the distribution of the left M C A and a mass effect with extrinsic deformity of the left lateral ventricle. (C) Carotid arteriography shows complete occlusion at the origin of the left M C A (arrow). There was good opacification of the M C A branches during the venous phase presumably due to retrograde collateral filling from the anterior cerebral artery.
CT scans in four of these patients showed a central increased density or blush within the overall low density lesion; on rescanning after infusion of contrast material, a ring of increased density was demonstrated in the central portions of the overall low density lesion (Figs. 5B, 5C). It is interesting to note that the four blushing infarcts were all found within 9-16 days after the clinical insult. The remaining two
cases showed the usual area of reduced density without a blush. The demonstration of luxury perfusion or a blushing infarct is apparently restricted to a relatively short time period after the clinical insult. The blush is not demonstrated on CT scans obtained on a restudy of the patient a few months later, although the lesion persists as an area of homogeneously reduced density. Radionuclide brain scans at
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Fig. 5. This 45-yr-old woman has a 2-wk history of aphasia, confusion, and right hemiparesis. (A) Focal hyperperfusion is present in the left cerebral hemisphere (arrows); a static scan not shown showed a corresponding abnormal fan-shaped pattern, {B) In the distribution of the left MCA is a poorly defined area of diminished density, After injection of contrast material (lower photos), this area increases markedly in density (blush). (C)The angiogram demonstrates increased perfusioo during the arterial and venous phases consistent with luxury perfusion.
comparably delayed time intervals are normal and do not show any residual abnormalities. In our experience, the presence of luxury perfusion and blushing infarcts on radionuclide and CT scans as a manifestation of vascular disease is difficult to interpret. All these cases were initially diagnosed as neoplasms with tumor vascularity, despite the fact that the clinical presentation was suggestive of infarction. Final diagnoses were made by biopsy in one case, and five patients had arteriography which revealed occlusion of the MCA in three patients and of the posterior cerebral artery in two patients. Luxury perfusion was also identified on one arteriograph (Fig. 5D); the term "luxury perfusion" was coined by Lassen ~2when he described his observations following intracarotid injection of ~3~Xe in saline into patients with cerebral in-
farction. He proposes that regional cerebral perfusion is regulated in part by local metabolic requirements of the brain tissue. In acute infarction, local hyperemia produces localized metabolic acidosis, which in turn results in loss of the normal autoregulatory mechanism. Inappropriate vascular dilatation then occurs in the a b s e n c e o f a d e c r e a s e in c e r e b r a l blood pressure, so that the volume of blood supplied to the area exceeds that required by the local metabolic conditions. STATIC BRAIN SCAN AND COMPUTED TOMOGRAPHIC SCAN FINDINGS IN MIDDLE CEREBRAL ARTERY DISEASE
Fairly characteristic patterns were observed on CT and static radionuclide scans in 174 ischemic infarcts. The findings are in part de-
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termined'by the site of vascular occlusion in terms of various branches of the MCA.
Static Radionuclide Scan Findings in Occlusion of Major Branches of the Middle Cerebral Artery Four different patterns are encountered. 1. Normal static scan (18%). The static brain scan was normal in 31 cases, and the abnormality was only detected on the radionuclide angiogram in terms of one or another of the abnormalities described in the above section. 2. Static brain scan showing a finger-shaped area of uptake (56%) (Fig. 1B). This pattern was encountered in 98 patients and is best demonstrated on the lateral view in which the fingershaped area of excessive uptake corresponds to the Sylvian triangle. H o w e v e r , e x c e s s i v e activity can also be seen on the anterior view in the area of the MCA distribution (Fig. IB). 3. Static brain scan showing crescent-shaped excessive uptake (21%) (Fig. 2B). This pattern was present in 36 cases, and is best recognized on the anterior or posterior view as an area of i n c r e a s e d u p t a k e p a r a l l e l l i n g the c o n v e x contour of the calvarium. Lateral views are generally negative, or alternatively may reveal very faintly increased uptake in the temporal region. This pattern is similar to that seen in subdural hematomas. 4. Static brain scan showing multiple areas of uptake (5%) (Fig. 3A). This pattern of multifocal excessive uptake was present in nine patients, and is best identified on the lateral view. Probably, this appearance is the result of multiple occlusions of branches of the MCA.
CHIU, CHRISTIE, AND SCHAPIRO
diminished density with irregular, ill-defined margins in the region of the MCA distribution (Figs. 1C, 2C, 3B, 4B). The absorption range is 2 8 EMI units less than the contralateral control region. Generally, differentiation from neoplasm and other lesions is readily achieved. In cases of large infarcts, a mass effect may appear with displacement or obliteration of the ventricular system (Figs. 1C, 2C, 4B). This effect is not encountered in cases with small infarcts. Following the first week, very little change is to be expected in the density alterations encountered during the first week. Some possible changes which might occur include diminution in the area of decreased density, sharper definition of the margin of the lesion, and some loss of the patchiness of the lesion or improved homogeneity of the density distribution. In an old infarct, the lesion is homogeneous
) A. Axial view 4-5 cm above OM line"
B. Axial vmw 6-8 cm above OM line"
C. Lt. lateral
Computed Tomographic Scan Findings in Occlusion o f Major Branches o f the Middle Cerebral Artery The CT scan is especially valuable in the evaluation of ischemic infarcts within the first week of the clinical insult, and, during this time period, appears to have considerably greater sensitivity than the radionuclide scan. In our series, the earliest positive CT scan was obtained 4 hr after accidental occlusion of the MCA during the course of a carotid angiogram. During the first week following occlusion of a major branch of the MCA, the typical lesion presents as a nonhomogeneous, patchy area of
D. Anterior
E. Posterior
Fig. 6. The distributions of the anterior, middle, and posterior cerebral arteries are shown in the low axial (A), high axial (B), left lateral (C), anterior (D), and posterior (E)views. Major branches of the M C A are identified as anterior temporal artery (AT), orbital frontal artery (OF), prerolandic artery (PR), rolandic artery (R), posterior temporal artery (PT), parietoangular artery (PA), basal ganglia (BG), anterior cerebral artery (AC), middle cerebral artery (MC), posterior cerebral artery (PC), and orbitomeatal line (OM).
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Fig. 7. These examinations were obtained 8 days following admission of this 72-yr-old male w i t h a left hemiplegia and unconsciousness. (A) There is increased uptake in the region supplied by the orbital frontal branch of the right M C A . (B) There is an ill-defined area of diminished density in the right frontal lobe. A t autopsy, there was occlusion of several major branches of the right M C A ,
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and has absorption characteristics that are identical to those of cerebrospinal fluid (Fig. 2C), and such old lesions are always well marginated. The loss of brain substance may be manifest in dilatation of the ipsilateral ventricles. At this stage, the radionuclide angiogram is negative except in three patients whose lesions have converted into large cysts causing displacement of vessels. The static brain scans are always negative.
Radionuclide and Computed Tomographic Scan Findings in Occlusions of Cortical Branches of the Middle Cerebral A rt ery The areas of vascular supply provided by the major branches of the MCA are diagrammatically prescribed in Fig. 6. Representative scan findings consequent to occlusions of the orbital frontal artery (Figs. 7A, 7B), the ascending frontal parietal arteries (Figs. 8A, 8B), the posterior temporal artery, and parietal angular artery (Figs. 9A, 9B) are illustrated. Whenever an occlusion occurs in the cortical branches of the MCA, the radionuclide scan may reflect this by excessive uptake some distance from the midline. This is due to the fact that the distribution of the cortical branches of the MCA does not extend to the midline. Rather, the anterior and posterior cerebral arteries supply these regions. Furthermore, the probability of detecting a lesion due to occlusion of these cortical branches by radionuclide scanning is relatively low. Serial CT scanning offers the greatest likelihood of detecting a cortical infarct or a lesion due to occlusion of a single cortical branch of the MCA. During the first 1 or 2 days after the clinical insult, the CT scan is likely to be normal, but repeat scanning 4-10 days after the infarct will render the lesion detectable. This is attributable to the fact that edema of the brain begins 2-6 hr after infarction, but it does not become maximal until 2 5 days after the infarct. ]z,]3 Subsequent resolution of the edema again renders the likelihood of demonstrating the lesion by CT scanning less likely. An exception to this rule occurs when the infarcts remain as residual cavities greater than 1 cm in size and become filled with fluid of the same density as cerebrospinal fluid; when this occurs, late CT scans will demonstrate small areas of decreased
Fig. 8. These examinations were performed 16 days after admission of this markedly hypertensive, disoriented, agitated, and drowsy 53-yr-old white man. (A) There is excessive activity in the peripheral portion of the area of distribution of the left M C A . (B) There is an area of diminished density in the left posterior frontal area. Carotid arteriography showed occlusion of the rolandic branch of the left M C A .
Fig. 9. This 66-yr-old w o m a n had a left hemiparesis and aphasia for 9 days prior to admission. (A) A t the periphery of the right parietal lobe, there is a wedge shaped area of activity. A repeat examination 8 w k later was normal. (B) An area of decreased density is noted in the right posterior parietal lobe.
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Fig. 10. This 58-yr-old male w i t h a 3-too history of headaches was a d m i t t e d 12 days prior to these examinations following the sudden onset of aphasia and weakness of the left side of the face. (A) Excessive activity is present above the right sphenoid sinus. (B) There is a small area of diminished density deep in the right temporal region corresponding to location of the basal ganglia.
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Fig. 11. This 68-yr-old male became confused, aphasic, and dizzy 10 days prior to admission. (A) There is abnormal a c t i v i t y adjacent to t h e midline at the anterior frontal area corresponding to the distribution of the right anterior cerebral artery. (B) The CT scan shows a corresponding area of diminished density in the right frontal lobe.
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Fig. 12. This 55-yr-old male developed a sudden right homonymous hemianopsia 15 days prior to admission. (A) There is increased uptake just to the left of the midline on the posterior view. On the lateral view, the excessive activity extends to the c o n f l u e n c e of t h e sinuses ( p o s i t i v e t e n t o r i a l confluence sign). (B) An area of decreased density is present in the left occipital lobe. (C) There is occlusion of the left posterior cerebral artery (arrow).
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189
Fig. 13, A 67-yr-old male with left homonymous hemianopsia and a history of progressive headaches and lethargy. (A) An area of excessive activity is present in the right occipital region distinct from the tentorium. Absence of the tentorial confluence suggests a neoplasm rather than infarct, (B) There is an irregular area of decreased density in the right occipital area that after infusion of contrast material presents as a right parietal occipital mass surrounded by edema, A glioma was found at surgery.
density. In summary, then, cortical infarcts are difficult to identify on radionuclide scans and on CT scans are most readily visualized during the acute phase 4-10 days after clinical infarction has occurred.
Radionuclide and Computed Tomographic Findings in Occlusion of the Deep Branches of the Middle Cerebral Art ery The lenticulostriate arteries are the first deep branches of the proximal segment of the MCA group supplying the basal ganglia. Infarcts due to occlusion of these vessels are reflected orr the lateral view of the radionuclide scan as "comma-shaped" or reversed comma-shaped activity above the region of the sphenoid sinus adjacent to the Sylvian fissure. In the anterior view, this excessive activity is clearly demarcated from the peripheral activity (Fig. 10A). CT scans reflect infarcts due to occlusion of the lenticulostriate arteries as diminished density in the area of the basal ganglia.
STATIC BRAIN SCAN AND COMPUTED TOMOGRAPHIC SCAN FINDINGS IN OCCLUSION OF THE ANTERIOR CEREBRAL ARTERY
Occlusions of the anterior cerebral artery are rare but produce quite characteristic changes on radionuclide scans. Because of the proximity of the contralateral anterior cerebral artery, no abnormality can be demonstrated on the early anterior radionuclide angiographic images. However, decreased or absent activity during the capillary phase, with abnormal uptake in the paramedian area or subsequent static anterior scans are characteristic. CT scans are less specific, but show abnormally diminished density in the frontal area. (Fig. 11A, B) STATIC BRAIN SCAN AND COMPUTED TOMOGRAPHIC FINDINGS IN OCCLUSIONS OF THE VERTEBROBASILAR ARTERY
Occlusion of the Posterior Cerebral A rtery In our series, there were 28 patients who had occlusions of a posterior cerebral artery. The
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Fig. 14. A 65-yr-old man with nystagmus, marked ataxia and a 10day history of nausea, vomiting, headaches, and inability to walk. (A) There is increased activity in the right p o s t e r i o r fossa. (B) There is diminished density in the right cerebellar hemisphere, A subsequent vertebral angiogram revealed an occlusion of the right posterior inferior cerebellar artery.
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Fig. 15. This 68-yr-old hypertensive man experienced a sudden aphasia and left hemiparesis. (A) Changes consistent with infarction of the right basal ganglia are present. (B) This CT scan was performed 9 mo later and shows a small well-defined area of diminished density corresponding to the region of the right basal ganglia, This finding is consistent with an old infarct of the lacunar type,
anterior and posterior radionuclide angiograms are of no value; however, decreased or absent perfusion during the capillary phase can be demonstrated on dynamic vertex views. Static radionuclide scans were positive in 23 cases, and, typically, the posterior view shows a wedge-shaped area of increased activity that is adjacent to the midline and extends down to the torcular herophili and to the medial transverse sinus. On the lateral view, this increased uptake assumes the form of a tapering crescent or triangle that blends with the normal activity of the posterior sagittai and transverse sinuses (Fig. 12A). This configuration is quite typical, and we refer to it as the "tentorial confluence" sign. 4 If the excessive uptake is not confluent with the activity of the tentorial region (Fig. 13A), the lesion is not likely due to occlusion of the posterior cerebral artery, and another etiology must be strongly considered. CT scans were positive in 26 patients and showed diminished density in the occipital region (Fig. 12B). If a patient has an initially
positive radionuclide scan and the tentorial confluence sign is absent, it is essential that a CT scan with intravenous contrast material enhancement ~4,~5be undertaken in the effort to confirm the presence of a neoplasm (Fig. 13B). Occlusion of Other Branch es o f th e Basilar Artery
Radionuclide scan findings are nonspecific and do not differentiate between infarcts and neoplasms. Infarcts in this area present as nonspecific lesions of the posterior fossa (Fig. 14A). CT scans show diminished density in the posterior fossa (Fig. 14B); occasionally, the fourth ventricle is obliterated, but obstructive hydrocephalus was not demonstrated in any of the 22 cases in our experience. This absence of obstructive hydrocephalus provides some help in differentiating infarcts from neoplastic spaceoccupying lesions. Detection of lesions in this area is rendered difficult on the conventional axial projection because of the overlying dense
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Fig. 16. This 64-yr-old woman had episodic hypotension, progressive stupor, and recurring major motor seizures. (A) Symmetric bands of increased uptake correspond to the "watershed" between the distributions of the anterior cerebral artery and the MCA, (B) Two symmetric areas of decreased density (arrows) correspond to the watershed
zone.
occipital bone. Additional coronal views can be helpful in confirming the diagnosis.
STATIC BRAIN SCAN A N D COMPUTED TOMOGRAPHIC SCAN FINDINGS IN LACUNAR INFARCTS A N D WATERSHED INFARCTS
Acute lacunar infarcts cannot be identified on CT or radionuclide scans, unless they are quite large. The lesion must be greater than 1 cm in diameter before it can be recognized. 15 Such large lacunar infarcts will present as small areas of excessive uptake on radionuclide scans (Fig. 15A), and, on CT scans, they may present as irregular areas of decreased density with the
same absorption as cerebrospinal fluid (Fig. 15B). Watershed infarcts occur in boundary zones wherein the distributions of the anterior, middle, and posterior cerebral arteries overlap. The manifestations on radionuclide scans are usually pathognomonic, with linear bands of excessive uptake occurring in these junctional regions (Fig. 16A). On CT scans, localized areas of decreased density are present in areas corresponding to those of increased uptake on the radionuclide scan. PATHOPHYSIOLOGICAL CORRELATION
In the period following an acute arterial occlusion, an ischemic infarct shows a transient
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increase in the number of neutrophilic leukocytes. 1~ Edema of the brain begins within 2-6 hr after arterial occlusion and becomes maximal in 2-5 days. 17.18Cerebral anoxia results in swelling and vacuole formation of both gray and white matter of the brain. CT scans do not permit distinction between the infarcted brain area and the adjacent edematous brain p a r e n c h y m a , since both present as areas of diminished density. Neuronal degeneration occurs when the blood-brain barrier breaks down and plasma proteins leak into the injured brain tissue. Subsequently, repair commences as glial proliferation, macrophage reaction, and ultimately fibrogliosis occur. ~z,13 Heyman ~~ has shown that the uptake of the radiopharmaceuticals is related to m a c r o p h a g e activity that is most pronounced approximately 1 wk after the clinical insult. At this time, the static scintigram becomes positive, but, 60 days later, the
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radionuclide scan is likely to be negative, since fibrogliosis is taking place. As was indicated above, shortly after infarction, the necrotic brain tissue and adjacent brain edema are reflected on the CT scan as an area of inhomogeneous decreased density with an absorption range of 2-12 EMI units; normal brain tissue is in the range of 12-28 EMI units; this area of patchy reduction in density usually has an ill-defined margin. As phagocytic activity affects removal of the necrotic tissue, cystic degeneration produces an area of encephalomalacia, or a dense neuroglial scar is formed. Consequently, an infarct more than 4 wk old presents on the CT scan as an area of decreased density with an absorption identical to that of cerebrospinal fluid; at this time, the density characteristics are quite homogeneous, and the lesion generally has a well-defined margin. If there has been loss of a significant quantity of brain substance, there may be associated dilata-
Fig. 17. This B8-yr-old man presented with a history of sudden onset of right paresis and sensory deficit 9 days prior to these examinations. (A) There is abnormal activity in the left hemisphere. (B) There is a dense lesion surrounded by a zone of diminished density, Multiple occlusions of major branches of the left M C A were demonstrated on arteriography,
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cortex. Consequently, on radionuclide scans, these lesions tend to present remote to the peripheral activity and to the midline. Interpretation of such lesions is rendered more difficult, since hemorrhagic infarcts or hematomas simulate neoplasms, abscesses, or other lesions? Empirically, radionuclide brain scans become positive within 1 wk of a hemorrhagic infarct or intracerebral hematoma in approximately 50% of patients. More than 6 wk after the cerebral hemorrhage, the radionuclide image returns to normal. Ambrose' noted that infarcted brain tissue presents as a region of less than normal density on CT scans, while intracerebral hemorrhage shows greater than normal density on CT scans. Whenever both alterations in density occur sim u l t a n e o u s l y , h e m o r r h a g i c i n f a r c t i o n is considered likely. 2~ Usually, the increased density is located at the periphery of an area of decreased density (Figs. 17A, 17B); sometimes, there is also a central focus of increased density
Fig. 18. This 72-yr-old male suddenly became comatose with a left hemiparesis. The large well-defined area of increased density on the CT scan is consistent with an intracerebral hematoma. (Radionuclide scans in this case w e r e normal.)
tion of the ventricles and widening of the fissures and sulci.
Considerations Pertaining to So-called Hemorrhagic Infarct and Intracerebral Hematoma In ischemic infarcts, areas o f excessive u p t a k e on radionuclide scans usually correspond to the anatomic area supplied by the specific artery that has been occluded. This anatomic correlation between the excessive uptake on the scintiscan and the vascular supply is less likely to be maintained when hemorrhagic infarction occurs with or without formation of an intracerebral hematoma. This is attributable to the fact that the hemorrhage associated with the infarct can readily dissect brain tissue and thus cross the boundaries of the volume of brain supplied by a specific vessel. Hematomas tend to form deeper in the brain and spare the
Fig. 19. This 69-yr-old male w i t h a history of hypertension presented with a left hemiparesis and had bloody cerebrospinal fluid. There is an area of increased density in the right temporal reading, suggesting a hemorrhage into the region of the basal ganglia. Blood casts are present in both lateral ventricles and in the fourth ventricle. (Radionuclide scans were normal in this case.)
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that presumably reflects a central accumulation of blood. On CT scans, cerebral h e m a t o m a s are usually rounded with a slightly elongated shape (Fig. 18). While the contour may be somewhat irregular, the margins are well-defined and appear to be surrounded by a rim of tissue of diminished density. If t h e r e is e x t e n s i v e extravasation of blood, the latter may penetrate into the ventricular system (Fig. 19). As was indicated above, radionuclide scans tend to miss hemorrhagic infarcts during the first week after occurrence of the clinical insult. The CT scan, on the other hand, is extremely sensitive and will detect the abnormality immediately after bleeding occurs. Serial CT scans obtained after a period of time show gradual diminution of the extravasated blood. It is worthwhile to review one additional difference between the manner in which mani-
f e s t a t i o n s o f i s c h e m i c disease p r e s e n t on radionuclide and CT scans. Since CT scans generally render a relatively detailed image of the brain anatomy, distortions imposed by the infarct on the normal anatomic configuration of the brain can be recognized in addition to the focal alterations in tissue densities. The Sylvian fissure can normally be identified as a structure of diminished density. Edema associated with an infarct frequently renders recognition of this structure impossible. Localized changes in brain volume often result in displacement of the choroid plexus or in displacement and deformation of the ventricular system. These alterations diminish with time, as the brain edema subsides and the extravasated blood is resorbed. Ventricular dilatation is a common finding that increases with time; this is attributable to localized or generalized atrophy of brain tissue associated with infarction.
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