DOI: 10.1148/radiol.2411040573
(Radiology 2006;241:315-318.)
© RSNA, 2006
The MCA Dot Sign1
Sanjay K. Shetty, MD
1 From the Department of Radiology, Massachusetts General Hospital, 55 Fruit St, FND 215, Boston, MA 02114. Received March 3, 2004; revision requested May 28; revision received June 16; accepted August 27.
Address correspondence to the author, Department of Radiology, Beth Israel Medical Center, Boston, MA 02114 (e-mail: sshetty{at}bidmc.harvard.edu).
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APPEARANCE
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The middle cerebral artery (MCA) dot sign is a punctate focus of hyperattenuation located in the sylvian fissure and is seen on a noncontrast computed tomographic (CT) scan of the head (1).
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EXPLANATION
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The punctate hyperattenuation of the MCA dot sign (Figs 1 and 2) represents a thromboembolus within a segmental branch of the MCA located within the sylvian fissure (M2 or M3 segment). The sign appears when this high-attenuation structure is viewed in cross section, since the occluded vessel courses in a plane perpendicular to the transverse plane of imaging. While normal vessels on a noncontrast study are expected to display soft-tissue attenuation, thromboembolus and the occluded vessel will have increased attenuation. This hyperattenuation along the course of the MCA has been correlated microscopically with blood clots that demonstrate accumulation of erythrocytes, fibrin, and cellular debris (2).

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Figure 1a: Images of an 81-year-old female patient with atrial fibrillation who presented with left facial droop, slurred speech, and left lower-extremity weakness. (a) Initial noncontrast transverse head CT scan demonstrates a hyperattenuating dot (arrow) in right sylvian fissure, which is more opaque than any structure in ipsilateral or contralateral sylvian fissurethe MCA dot sign. (b) Three-dimensional CT reformation obtained after the bolus administration of intravenous contrast material confirms acute occlusion (arrow) of the distal M1 segment of the MCA; the MCA dot sign seen on the noncontrast CT scan represents propagation of this thrombus in an M2 branch vessel.
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Figure 1b: Images of an 81-year-old female patient with atrial fibrillation who presented with left facial droop, slurred speech, and left lower-extremity weakness. (a) Initial noncontrast transverse head CT scan demonstrates a hyperattenuating dot (arrow) in right sylvian fissure, which is more opaque than any structure in ipsilateral or contralateral sylvian fissurethe MCA dot sign. (b) Three-dimensional CT reformation obtained after the bolus administration of intravenous contrast material confirms acute occlusion (arrow) of the distal M1 segment of the MCA; the MCA dot sign seen on the noncontrast CT scan represents propagation of this thrombus in an M2 branch vessel.
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Figure 2a: Images of a 65-year-old female patient who presented with an expressive aphasia. (a) Initial noncontrast transverse head CT scan demonstrates the MCA dot sign (arrow) in the left sylvian fissure. Associated hypoattenuation of left insular cortex and subinsular region corresponds to subacute infarction. (b) Three-dimensional CT reformation obtained after bolus administration of intravenous contrast material demonstrates acute occlusion (arrow) of the M2 segment of the left MCA. (c) Diffusion-weighted transverse image (b = 1000 sec/mm2) from a concurrently performed magnetic resonance (MR) imaging study shows restricted diffusion (arrow) in the left insular cortex. (d) Subsequent transverse fluid-attenuated inversion-recovery MR image (10000/126/2200 [repetition time msec/echo time msec/inversion time msec]) obtained 4 days later demonstrates corresponding increase in T2 hyperintensity, confirming the infarction.
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Figure 2b: Images of a 65-year-old female patient who presented with an expressive aphasia. (a) Initial noncontrast transverse head CT scan demonstrates the MCA dot sign (arrow) in the left sylvian fissure. Associated hypoattenuation of left insular cortex and subinsular region corresponds to subacute infarction. (b) Three-dimensional CT reformation obtained after bolus administration of intravenous contrast material demonstrates acute occlusion (arrow) of the M2 segment of the left MCA. (c) Diffusion-weighted transverse image (b = 1000 sec/mm2) from a concurrently performed magnetic resonance (MR) imaging study shows restricted diffusion (arrow) in the left insular cortex. (d) Subsequent transverse fluid-attenuated inversion-recovery MR image (10000/126/2200 [repetition time msec/echo time msec/inversion time msec]) obtained 4 days later demonstrates corresponding increase in T2 hyperintensity, confirming the infarction.
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Figure 2c: Images of a 65-year-old female patient who presented with an expressive aphasia. (a) Initial noncontrast transverse head CT scan demonstrates the MCA dot sign (arrow) in the left sylvian fissure. Associated hypoattenuation of left insular cortex and subinsular region corresponds to subacute infarction. (b) Three-dimensional CT reformation obtained after bolus administration of intravenous contrast material demonstrates acute occlusion (arrow) of the M2 segment of the left MCA. (c) Diffusion-weighted transverse image (b = 1000 sec/mm2) from a concurrently performed magnetic resonance (MR) imaging study shows restricted diffusion (arrow) in the left insular cortex. (d) Subsequent transverse fluid-attenuated inversion-recovery MR image (10000/126/2200 [repetition time msec/echo time msec/inversion time msec]) obtained 4 days later demonstrates corresponding increase in T2 hyperintensity, confirming the infarction.
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Figure 2d: Images of a 65-year-old female patient who presented with an expressive aphasia. (a) Initial noncontrast transverse head CT scan demonstrates the MCA dot sign (arrow) in the left sylvian fissure. Associated hypoattenuation of left insular cortex and subinsular region corresponds to subacute infarction. (b) Three-dimensional CT reformation obtained after bolus administration of intravenous contrast material demonstrates acute occlusion (arrow) of the M2 segment of the left MCA. (c) Diffusion-weighted transverse image (b = 1000 sec/mm2) from a concurrently performed magnetic resonance (MR) imaging study shows restricted diffusion (arrow) in the left insular cortex. (d) Subsequent transverse fluid-attenuated inversion-recovery MR image (10000/126/2200 [repetition time msec/echo time msec/inversion time msec]) obtained 4 days later demonstrates corresponding increase in T2 hyperintensity, confirming the infarction.
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DISCUSSION
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Noncontrast CT, when used to exclude intracranial hemorrhage in an emergency setting, is an invaluable tool in the evaluation of suspected acute stroke. Beyond the detection of hemorrhage, the early noncontrast CT scans can also be used to detect the direct or indirect signs of acute ischemia or infarction itself. This is a particularly important distinction now that such information regarding thrombolysis may guide predictions of functional outcome and hemorrhagic complications (3). Unfortunately, the findings of acute infarction on noncontrast CT scans are subtle and therefore have limited reliability.
The hyperdense vessel sign, a well-recognized indicator of proximal thromboembolism within the MCA (M1 segment), is an indirect marker of acute infarction (4,5). This curvilinear area of hyperattenuation (which appears because the proximal MCA runs approximately within the transverse plane of the section) represents thromboembolic occlusion of the vessel lumen; because it is a marker of vascular occlusion rather than a direct image of the resulting parenchymal changes, the hyperdense vessel sign can be considered an indirect indicator of subsequent infarction (6). The increased attenuation of the vessel has been distinguished from atherosclerotic plaque on the basis of correlative angiograms and follow-up CT scans that demonstrate resolution following recanalization (4). The hyperdense vessel sign has been reported in between 17% and 50% of cases of MCA stroke (7). This sign is associated with poor clinical outcomes (7) and more extensive territories of infarction, although its use as an independent predictor of poor outcome is controversial (7,8). While the sign has a high specificity (approaching 100%), the failure to detect a hyperdense vessel sign in all cases of proximal MCA (M1 segment) occlusion limits its sensitivity (9).
The MCA dot sign is a variant of the hyperdense vessel sign. It represents hyperattenuating thromboembolism located distally within a branch vessel of the MCA that courses within the sylvian fissure. This can occur in the M2 segment branches, which course over the insula within the circular sulcus (a fissure that demarcates the insula from the opercula) after the trifurcation into the anterior division, posterior division, and anterior temporal artery. The sign can also appear in the more distal M3 segments, which travel horizontally between the frontal and temporal opercula to reach the cortical surface. Because these M2 and M3 segment vessels tend not to course in the transverse plane of imaging, the occluded vessel is seen in cross section, and the thromboembolus appears as a hyperattenuating dot within the sylvian fissure.
The MCA dot sign was validated with cerebral angiography as a reference standard in a series of 58 patients presenting within 8 hours of symptom onset (10). Interpretations were rendered without associated clinical information on the basis of a definition of the MCA dot sign as "hyperdensity of an arterial structure (seen as a dot) in the Sylvian fissure relative to the contralateral side or to other vessels in the Sylvian fissure" (1). To be properly applied, the MCA dot sign should have a higher attenuation than any other visible vessel. In the tested population, a single, definite MCA dot sign was seen in 16.7% of patients and a borderline sign was seen in 4.6% of patients. Detection of an MCA dot sign was correlated with angiographically confirmed M2 or M3 branch vessel clot, yielding a sensitivity value of 38%, a specificity of 100%, a positive predictive of 100%, and a negative predictive values of 68% (10).
While the hyperdense vessel sign and MCA dot sign are similar in that they both depict thromboembolism at different levels of the MCA, there are important clinical and prognostic distinctions. The MCA dot sign reflects more distal vessel occlusion and therefore suggests a smaller territory at risk. Indeed, finding the MCA dot sign in isolation (without a concurrent hyperdense vessel sign) is associated with improved short-term clinical outcome (7) and demonstrates a trend toward milder neurologic deficits and improved outcome following thrombolysis (1,10).
A potential alternative consideration for punctate hyperattenuation in the sylvian fissure is calcification associated with intracranial atherosclerosis. However, these smaller-caliber intracranial vessels are less likely to be affected by atherosclerosis than larger intracranial vessels (1), and the distinction can often be made by evaluating the degree of atherosclerosis evident elsewhere in the intracranial vasculature. The detection of a false-positive hyperdense vessel sign has been reported with an elevated hematocrit (11), although this association is controversial and, to our knowledge, has not been reported in association with the MCA dot sign.
The MCA dot sign is a relatively recent addition to the armamentarium of the radiologist interpreting noncontrast CT scans of the head in the setting of suspected acute stroke. While it shares a similar cause with the more commonly described hyperdense vessel sign, the MCA dot sign suggests a more distal thromboembolus within the MCA territory (M2 or M3 segment). Just as important, the MCA dot sign is highly specific and has important therapeutic and prognostic implications; as an indicator of more distal branch occlusion, it may help select patients more amenable to thrombolytic therapy and may predict improved prognosis relative to more proximal occlusion.
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ACKNOWLEDGMENTS
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Thanks to Mark Mullins, MD, PhD, for reviewing the manuscript.
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FOOTNOTES
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Author stated no financial relationship to disclose.
| A trainee (resident or fellow) wishing to submit a manuscript for Signs in Imaging should first write to the Editor for approval of the sign to be prepared, to avoid duplicate preparation of the same sign.
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