CLINICAL IMAGING 1991;15:176-181


Magnetic resonance (MR) images of 12 patients with angiographically proven middle cerebral artery (MCA) occlusion were analyzed, retrospectively. In three of the 12 patients, cerebral infarctions related to the MCA occlusions were not evident. Two of the three patients were cases of atherosclerotic occlusion and the remaining patient had an acute thromboembolism. In all of the occluded Ml portions of the MCA the flow void was absent and there were isointense linear structures, with or without a hyperintense component in the Sylvian vallecula, on Tl-weighted images. For nine of the 12 patients, the absence of flow void in the ipsilateral Sylvian fissure was evident on the T2-weighted images. Therefore, even in cases with no evidence of a cerebral infarction, the presence of flow void in the Sylvian vallecula and Sylvian fissure must be searched for in routine reviews of MR images. If MR imaging can be obtained on an emergency basis, appropriate interventional therapy may be immediately initiated. KEY WORDS:

Middle cerebral artery; Arterial occlusion; Magnetic resonance imaging Magnetic resonance (MR) imaging is useful to detect occlusions in the major vessels. Most reports on MR imaging of these occlusions involved findings in the internal carotid arteries and in the vertebrobasilar system [l-3]. Cerebral infarction is usually present From the Department of Radiology, Kyushu Rosai Hospital, Fukuoka, Japan. Address reprint requests to: Akira Uchino, MD, Department of Radiology, Kyushu University Hospital, Maidashi 3-l-1, Higashiku, Fukuoka 812, Japan. Received June 1990; revised February 1991; accepted April 1991. 0 1991 by Elsevier Science Publishing Co., Inc.

655 Avenue of the Americas, New York, NY 10010 0699/7071191/$3.50


in cases of We report clusion in associated

a middle cerebral artery (MCA) occlusion. MR findings of middle cerebral artery oc12 patients, three of whom did not have findings of cerebral infarction.



From February 1988 through April 1990, we examined 12 patients with angiographically proven MCA occlusion, using MR imaging. These 12 included 11 men and one woman, the age range being 20 to 73 years (mean, 58 years]. Six of these 12 had right MCA occlusion and in the other six, there was a left MCA occlusion. Of the 12 occlusions there were ten related to atherosclerosis, one to thromboembolism, and one to angiitis. The time between onset of clinical symptoms and MR imaging varied from 4 hours to 13 years [Table 1). All these patients were examined using the 1.5-T GE Signa system. The imaging parameters were 4001 20/2 for Tl-weighted images and 2000/80/l for T2weighted images, using a 5 mm section thickness with a 2.5 mm interslice gap, a 24-cm field of view, and a 256 x 256 matrix. Flow compensation techniques were not used.

RESULTS The MR findings are presented in Table 1.Cerebral infarctions related to MCA occlusions observed in nine patients were located in the basal ganglia, insular cortex, corona radiata, centrum semiovale. In two of the 12 patients, there were no parenchymal abnormalities related to the MCA occlusion. Intraventricular hemorrhage was noted in the other patient. Signal intensities related to the occluded MCA in




the Sylvian vallecula were grossly isointense to the brain parenchyma, on the Tl-weighted images. In three chronic cases, a hyperintense component was also present. On the T2-weighted images, flow void of the MCA branches in the Sylvian fissure was absent in nine patients and in the remaining three patients, flow void was present but the caliber of the arteries had decreased.




Case 1 A 48-year old man with a history of mitral valvoplasty and atria1 fibrillation, suddenly experienced left hemiparesis and speech disturbance. Emergency MR imaging was performed four hours after the ictus. Right MCA occlusion was observed as an isointense linear structure in the Sylvian vallecula and Sylvian




FIGURE 1. Case 1. Acute thromboembolic

occlusion of right MCA in a 4%year-old man. MR imaging was performed 4 hr after clinical onset using a 1.5 T scanner. [A) Ml portion of right MCA in the Sylvian vallecula is isointense on the Tl-weighted image (arrow), thereby indicating a complete occlusion. (B) M2 portion of right MCA in the Sylvian fissure is also isointense on the Tl-weighted image (arrow]. (C) On the T&weighted image, absence of flew void is clearly evident in the right Sylvian vallecula, but, the occluded vessel is not clearly identified. (D) Absence of flow void is also clearly demonstrated in the Sylvian fissure on the T&weighted image. There is no evidence of cerebral infarction. (E) Right carotid injection shows complete occlusion of right MCA and stenosis of the right anterior cerebral artery at the origin, findings indicative of an acute thromboembolism.

fissure on the Tl-weighted images (Figure 1 A,B) and absence of flow void was seen on the T2-weighted images (Figure 1 CD). Because of a diagnosis of acute thromboembolism of the right MCA, emergency angiography was performed (Figure 1 E). Intraarterial urokinase was infused (60,000 unit/60 min) starting at 5 hr after ictus, all neurological deficits disappeared.

Case 9 A 44-year old man was admitted with a history of four transient ischemic attacks consisting of 5 min episodes of speech disturbance and left hemiparesis over the previous three months. On the Tl-weighted axial MR image through the Sylvian vallecula, the right MCA was isointense to the brain parenchyma (not shown) and absence of flow void in the right Sylvian fissure was clearly demonstrated on the T2weighted image (Figure 2A). Although there was no evidence of cerebral infarction, the MR-related diagnosis was right MCA occlusion and angiographic studies confirmed this diagnosis (Figure 2B). Case


A 56-year-old man suddenly headache. MR imaging obtained

experienced severe 3 days after the ictus

showed not only intraventricular hemmorrhage but also right MCA occlusion but without cerebral infarction (Figure 3A). Angiography revealed a right MCA occlusion and a hypoplastic Al portion of the right anterior cerebral artery (Figure 3B).

DISCUSSION MCA occlusions are usually caused by a thromboembolism and/or atherosclerosis. In most cases of an MCA occlusion, cerebral infarction occurs. As the distribution is typical, MCA occlusions can be readily diagnosed when CT scans are done. In some cases of acute thromboembolism, a hyperdense MCA can be detected by CT, even though cerebral infarction is not evident [4-61, nevertheless, the majority of cases of MCA occlusion in the absence of cerebral infarction cannot be diagnosed using only CT. MR imaging is useful to determine the presence or absence of intravascular flow. “Flow void” seen, as the absence of signal, indicates a vascular patency and a rapid flow [7-91. The absence of flow void is indicative of a vascular occlusion or blood stasis. Although there are reports on MR imaging of carotid artery occlusions and of those of the vertebral artery [l-3], MR imaging of MCA occlusions without



cerebral infarction has apparently not been documented in the English literature. In our patients, occluded MCAs were predominantly isointense to the brain parenchyma on Tlweighted images. Because the thrombus in patient 1 was fresh, it was thought to consist of oxyhemoglobin, hence it was not paramagnetic [lo]. Atheroma and arterial thrombi lack red blood cells [l]. In our 10 patients with atherosclerotic occlusion, the occluded MCA was apparently not so hyperintense as the intraparenchymal hematoma. In three patients with chronic atherosclerotic MCA occlusion, hyperintense components were observed on Tl-weighted images, presumably due to a flow-related enhancement. MCAs and their proximal branches are surrounded by cerebrospinal fluid (CSF) in the Sylvian vallecula and in the Sylvian fissure. As CSF is hyperintense on the T2-weighted images and is hypointense on the Tl-weighted images, normal MCAs are more clearly demonstrated on the T2-weighted images. The absence of a normal flow void is therefore more clearly

FIGURE 2. Case 9. Atherosclerotic occlusion of right MCA in a 44year-old man with TIAs. (A) Absence of flow void in the right Sylvian fissure is evident on the T2-weighted image. There is no evidence of a cerebral infarction. (B) Right carotid injection shows complete occlusion of right MCA at its Ml portion, Well-developed leptomeningeal collaterals via right anterior cerebral artery are indicative of a gradually occluding MCA.



detected on TZ-weighted images. Because occluded MCAs are predominantly isointense to brain parenchyma, they are more clearly identified on the Tlweighted images. In routine MR imaging, pulsating blood and CSF can cause phase-shift artifacts. These artifacts frequently obscure anatomical details of the Sylvian vallecula, particularly on the T&weighted images. Although the flow compensation technique (gradient moment nulling) markedly reduces this artifact, this technique does produce a paradoxical enhancement of the slow vascular flow that can lead to an erroneous diagnosis of thromboembolism [ 111. This phenomenon can also be observed in instances of a more rapid arterial flow that is parallel to the imaging plane. Using gradient echo imaging, patent vessels are hyperintense, acute thrombus-containing paramagnetic deoxyhemoglobin is hypointense, and subacute thrombus is hyperintense, on the T&weighted images [12]. The absence of flow void or decreased arterial caliber in the Sylvian fissure on the T2-weighted images

FIGURE 3. Case 3. Right MCA occlusion presumably due to atherosclerosis in a 56-year-old man. MR imaging was obtained three days after ictus. (A) On the T2-weighted image, the absence of flow void in the right Sylvian fissure is evident. A hypointense hematoma is located in the right lateral ventricle, and the arrow indicates the bleeding point. (B) Right carotid injection shows complete occlusion of the

B right MCA and a hypoplastic Al portion of the right anterior cerebral artery. Left carotid injection shows well-developed leptomeningeal collaterals to the right MCA via the right anterior cerebral artery (not shown).

TABLE 1. Data on Patients with MCA Occlusion MR Findings Case no.


Etiology of MCA occlusion

Interval from ictus to MlU


48/M/R 63/M/L

Thromboembolism Atherosclerosis

4 hr 2 days

3 4

56/M/R 20/F/R

Atherosclerosis Angitis

3 days




23 days




1 month




1 month




1 month



44/M/R 65/M/L

Atherosclerosis Atherosclerosis

3 months 9 years




12 years




13 years


11 days

o Signal intensities were compared with intensities of brain parenchyma b Presence or absence of flow void was judged on T&weighted images. c In this case, intraventricular hemorrhage was present.

Signal intensity of occluded MCAO

Location of infarct None Basal gangliaCorona radiata NoneC Basal gangliaCentrum semiovale Insular cortexCorona radiata Insular cortexCentrum semiovale Insular cortexCentrum semiovale Corona radiataCentrum semiovale None Basal gangliaCorona radiata Basal gangliaCentrum semiovale Corona radiataCentrum semiovale on Tl-weighted


Flow void in the sylvian fissureb

Isointense Isointense

Absent Absent

Isointense Isointense

Absent Present



Isointense, Hyperintense Isointense

Absent Present



Isointense Isointense, Hyperintense Isointense, Hyperintense (not performed)

Absent Absent Absent Absent



seems to be a most reliable finding of MCA occlusion or high-grade stenosis. However, a fresh thrombus containing intracellular deoxyhemoglobin or methemoglobin can give a “pseudo-flow void” appearance on high-field-strength T&weighted images [2]. Patients with acute thromboembolism, as was the case in patient 1,can be saved by giving an intraarterial infusion of urokinase or streptokinase. Treatment later than 6 hr after ictus is not effective and can even be dangerous [ 131. A correct diagnosis of thromboembolism immediately after clinical onset can be lifesaving. CT is sometimes useful, but MR imaging is even more so. In patients with chronic occlusion as in our case 9 and 3 patients, knowledge of the presence of MCA occlusion is vital for the physician. Systemic hypotension is untoward in such cases. In cases of transient ischemic attack (TIA), as was our case 9 with a superficial temporal artery, an MCA anastomosis can often prevent cerebral infarction [ 141. Moyamoya disease is a rare cerebrovascular occlusive disease, most prevalent in the Japanese, living in Japan. The adult type of moyamoya disease is frequently discovered after the occurrence of intraventricular hemmorrhage [15], as in our case 3 patient with unilateral involvement and only MCA occluded. Thus, atherosclerotic change was suspected. To our knowledge, such a case has not previously been documented with MR imaging. MR angiography has made significant progress [lS] but cost of the equipment limits its acquisition by many institutions. As routine MR imaging is now a pertinent, noninvasive diagnostic modality for evaluating MCA occlusions, we wish to stress that even in the absence of cerebral infarction, the presence of a normal flow void in the Sylvian vallecula and in the Sylvian fissure must be searched for in the routine reviews of MR images.





REFERENCES 1. Katz BH, Quencer

imaging of 10:345-350.

RM, Kaplan JO, Hinks RS, Post MJD. MR intracranial carotid occlusion. AJNR 1989;

2. Heinz ER, Yeates AE, Djang WT. Significant extracranial carotid stenosis: detection on routine cerebral MR images. Radiology 1989;170:843-848, 3. Uchino A, Ohnari N, Ohno M. MR imaging of intracranial vertebral artery occlusion. Neuroradiology 1989;31:403-407. 4. Yock DH Jr. CT demonstration Assist Tomogr 1981:5:190-196.

of cerebral

emboli. J Comput

5. Pressman BD, Tourje EJ, Thompson JR. An early CT sign of ischemic infarction: increased density in a cerebral artery. AJNR 1987;8:645-648. 6. Schuierer G, Huk W. The unilateral hyperdense middle cerebral artery: an early CT sign of embolism or thrombosis. Neuroradiology 1988:30:120-122, 7. Kaufman L. Crooks LE, Sheldon PE, Rowan W, Miller T. Evaluation of NMR imaging for detection and quantification of obstructions in vessels. Invest Radio1 1982;17:554-560. M, Crooks LE, et al.Nuclear mag8. Mills CM, Brant-Zawadzki netic resonance: principles of blood flow imaging. AJR 1984;142:165-170. 9. Bradley WG Jr, Waluch V. Blood flow: magnetic imaging. Radiology 1985:154:443-450.


10. Gomori JM, Grossman RI, Goldberg HI, Zimmerman RA, Bilaniuk LT. Intracranial hematomas: imaging by high-field MR. Radiology 1985:157:87-93. 11. Elster AD. Motion artifact suppression technique (MAST) for cranial MR imaging: superiority over cardiac gating for reducing phase-shift artifacts AJNR 1988;9:671-674. 12. Yousem DM, Balakrishnan J, Debrun GM, Bryan RN. Hyperintense thrombus on GRASS MR images: potential pitfall in flow evaluation AJNR 1990:11:51-58. 13. Theron J, Courtheoux P, Casasco A, et al. Local intraarterial fibrinolysis in the carotid territory. AJNR 1989:10:753-765 14. Day AL. Indications for surgical intervention in middle cerebral artery 0bstruction.J Neurosurg 1984:60:296-304. 1.5. Pia HW, Langmaid C, Zierski J, (eds). Spontaneous bra1 Haematoma. Berlin: Springer-Verlag, 1980.


16. Keller PJ, Drayer BP, Fram EK, Williams KD, Dumoulin CL, Souza SP: MR angiography with two-dimensional acquisition and three-dimensional display: work in progress. Radiology 1989; 173:527-532.

MR imaging of middle cerebral artery occlusion without cerebral infarction.

Magnetic resonance (MR) images of 12 patients with angiographically proven middle cerebral artery (MCA) occlusion were analyzed, retrospectively. In t...
4MB Sizes 0 Downloads 0 Views