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Published online before print April 10, 2002, 10.1148/radiol.2233011017
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(Radiology 2002;223:667-671.)
© RSNA, 2002

Neuroradiology

Proximal and Distal Hyperattenuating Middle Cerebral Artery Signs at CT: Different Prognostic Implications1

Diederik M. Somford, MD, Paul J. Nederkoorn, MD, Dirk R. Rutgers, MD, L. Jaap Kappelle, MD, Willem P. T. M. Mali, MD and Jeroen van der Grond, PhD

1 From the Department of Radiology (D.M.S., D.R.R., W.P.T.M.M., J.v.d.G.), Department of Neurology (L.J.K.), and the Julius Center for Patient Oriented Research (P.J.N.), University Medical Center Utrecht, E01.132, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands. Received June 8, 2001; revision requested August 1; revision received August 30; accepted October 1. Address correspondence to J.v.d.G. (e-mail: j.vandergrond@azu.nl).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To determine whether a proximal (M1-segment) or distal (M2- and/or M3-segment) hyperattenuating middle cerebral artery (MCA) sign in patients with ischemic infarction in the territory of the MCA indicates a worse short-term prognosis than that in patients without a hyperattenuating MCA sign.

MATERIALS AND METHODS: We retrospectively reviewed the records of 352 patients who were diagnosed with ischemic brain infarction in the territory of the MCA. Of these patients, 186 patients met our final criteria and were included in this study. Nonenhanced computed tomography (CT) was performed for the entire brain, with a 5-mm section thickness in all patients, within 24 hours after symptom onset. The presence and location of a hyperattenuating MCA sign was correlated with neurologic deficit at discharge from the hospital (ie, short-term prognosis) by using the {chi}2 test to detect differences between patient groups.

RESULTS: Patients with a hyperattenuating MCA sign at CT have a worse short-term prognosis than do patients without a hyperattenuating MCA sign (P < .05). Patients with a proximal hyperattenuating MCA sign have a significantly (P < .01) worse short-term prognosis than do patients with a distal hyperattenuating MCA sign.

CONCLUSION: A proximal hyperattenuating MCA sign is a reliable predictor of poor short-term prognosis in patients who experience acute stroke.

© RSNA, 2002

Index terms: Arteries, middle cerebral, 174.4312, 174.4352 • Brain, infarction, 174.4352 • Cerebral blood vessels, abnormalities, 174.4312, 174.4352


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
In patients who experience acute stroke, areas of cerebral infarction are often not visualized at computed tomography (CT) during the first hours after onset of symptoms (1,2). However, hyperattenuation of the middle cerebral artery (MCA) may be of diagnostic and prognostic value, since it has been reported to be associated with poor short- (3–6) and long-term prognosis in patients with ischemic stroke (7). A hyperattenuating middle cerebral artery sign has been reported to be associated with a larger volume of infarction at follow-up CT (3,7–11), although its absence does not exclude such a development (9). An association between a hyperattenuating MCA sign and the location of infarction has also been found. Patients with a hyperattenuating MCA sign developed cortical and larger deep MCA infarctions more often (8). However, investigators in other studies (8,12–14) have reported that the value of a hyperattenuating MCA sign as a predictor of poor prognosis is controversial. As far as cause of occlusion is concerned, a hyperattenuating MCA sign is nonspecific in differentiating embolic from thrombotic occlusions (8,15).

An important study on hyperattenuating MCA signs was performed by Manelfe et al (12), who investigated a population of 603 patients with hemispheric ischemic stroke, with all patients receiving thrombolytic therapy or placebo in the first European Cooperative Acute Stroke Study (ECASS 1). By using a logistic regression model, they found initial neurologic severity and early parenchymal ischemic changes at CT to be predictors of worse outcome; however, in this context, they could not establish the hyperattenuating MCA sign as an independent predictor of poor long-term prognosis. We hypothesize that this finding (that the hyperattenuating MCA sign is not an independent predictor of long-term outcome) could have been caused by the fact that proximal (M1-segment) and distal (M2- and/or M3-segment) hyperattenuating MCA signs were pooled in this study. Since it can be expected that proximal and distal hyperattenuating MCA signs (which represent occlusions of the M1 segment and the M2 and/or M3 segment, respectively) have different effects on prognosis, differentiation of these two subgroups may be important (16). The aim of our study was to determine whether a proximal (M1-segment) or distal (M2- and/or M3-segment) hyperattenuating MCA sign in patients with ischemic infarction in the territory of the MCA indicates a worse short-term prognosis than that of patients without a hyperattenuating MCA sign.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
We retrospectively reviewed the records of 352 patients who were diagnosed with ischemic brain infarction in the territory of the MCA from January 1, 1994, to April 16, 1999. Records were compiled from our hospital’s stroke database, which is an accumulation of records from all patients who present with symptoms of stroke or who undergo follow-up stroke consultation at our hospital. Next, we (D.M.S., L.J.K.) obtained the histories of these 352 patients from the medical records of our hospital. Nonenhanced CT was performed in all patients by using a 5-mm section thickness for the entire brain. The CT scans of these patients were reevaluated if a hyperattenuating MCA sign was present. Patient history was reviewed for the following exclusion criteria: (a) first CT scan obtained more than 24 hours after onset of symptoms, (b) CT scan obtained at another hospital prior to admission to our hospital, (c) insufficient history known to researcher, (d) presence of disseminated cancer or widespread local cancer, or (e) neurosurgery or thrombolytic therapy performed.

The presence of proximal and distal hyperattenuating MCA signs was defined by using the following criteria: (a) appearance of a unilateral hyperattenuating MCA at nonenhanced CT, (b) clinical symptoms of infarction in the corresponding MCA territory, (c) no CT evidence of other disorders able to cause ischemic signs, and (d) greater attenuation of the ipsilateral MCA when compared with the contralateral MCA and basilar artery. We derived these criteria from earlier publications (4,8,14–19) on the presence of the hyperattenuating MCA sign. Establishing reliable criteria is important, since the sensitivity in detecting the hyperattenuating MCA sign ranges from 26% to 61% (7,18–21). We classified each hyperattenuating MCA sign as proximal or distal; a proximal hyperattenuating MCA sign was defined as hyperattenuation of the horizontal part of the MCA (M1 segment) (Fig 1a), whereas a distal hyperattenuating MCA sign displayed hyperattenuation of the MCA in its Sylvian tract (M2 and/or M3 segment), as shown in Figure 1b. Patients who had a hyperattenuating MCA sign in both the proximal and distal MCA were classified as having a proximal hyperattenuating MCA sign.



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  		Transverse CT scans show (a) proximal and (b) distal hyperattenuating MCA signs (arrows).

 


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  		Transverse CT scans show (a) proximal and (b) distal hyperattenuating MCA signs (arrows).

 
Two independent observers evaluated the CT scans; the first observer was the radiologist who initially evaluated the CT scans. The second observer (D.M.S.) who evaluated all scans was blinded to the results of the first observer. In case of disagreement, a third observer (W.P.T.M.M. or J.v.d.G.) was consulted. Consensus was always achieved.

For all patients, we collected the following clinical data: age; sex; history of hypertension, diabetes mellitus, hypercholesterolemia, and atrial fibrillation; hematocrit level at admission; and neurologic deficit and modified Rankin score (22) at discharge.

Cardiovascular risk factors (ie, history of hypertension, diabetes mellitus, hypercholesterolemia, and atrial fibrillation) were scored as present when mentioned in a patient’s medical history. Hematocrit levels were adopted from the admission work-up.

Neurologic deficit at discharge (ie, short-term prognosis) was determined on the basis of the following points: homonymous hemianopia (ie, impairment of vision), facial function, motor function of upper and lower extremities, dysarthria, and dysphasia. These points were scored as positive when the medical records stated them as present at discharge. When their presence could not be determined reliably from the consulted records, patients were left out of the analysis on that specific point. The modified Rankin score, which represents the level of disability after a cerebrovascular accident, was determined for all patients at discharge. Good to reasonable outcome was defined as a score of 0–2, whereas poor outcome was defined as a score of 3–6, with 6 being the equivalent of death. According to the guidelines of the human research committee at our hospital, no patient approval and/or informed consent was necessary, since CT was performed as part of routine clinical examination. Also, no approval and/or informed consent was necessary for our retrospective review of clinical images and records, since patient anonymity was maintained.

For statistical review, we used logistic regression to compare patients with and without hyperattenuating MCA signs and to compare patients with distal versus proximal hyperattenuating MCA signs. In the logistic regression analysis, we adjusted for patient age, sex, hematocrit level, and the presence of hypertension, diabetes mellitus, hypercholesterolemia, or atrial fibrillation.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Within our population of 352 patients, 164 patients had one exclusion criterion in their history (Table 1). Two patients had two exclusion criteria. The remaining group of 186 patients consisted of 104 men and 82 women (mean age, 65.3 years; age range, 19–93 years). Demographic and other collected data for these patients are shown in Table 2.


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  		TABLE 1. Exclusion Criteria

 

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  		TABLE 2. Baseline Patient Characteristics

 
Forty-two of 186 patients showed a hyperattenuating MCA sign on the first CT scan, resulting in a prevalence of 22.6% in our population. Eighteen patients had a proximal hyperattenuating MCA sign, whereas 24 patients had a distal hyperattenuating MCA sign. We did not find an association between different kinds of hyperattenuating MCA signs and any of the cardiovascular risk factors (see Table 2). On admission, three patients displayed hematocrit levels higher than normal range (>0.51). Among these three patients, none showed a hyperattenuating MCA sign.

Discharge took place at a mean of 24.6 days after admission for all patients, with a 95% CI of 20.6 to 28.7. The mean time to discharge was 25.1 days in the group of patients without a hyperattenuating MCA sign, 25.8 days in the group of patients with a proximal hyperattenuating MCA sign, and 21.0 days in the group of patients with a distal hyperattenuating MCA sign.

Short-term Prognosis
In our study, we found that patients with a hyperattenuating MCA sign at CT have a worse short-term prognosis than that of patients without a hyperattenuating MCA sign (P < .05). Patients with a proximal hyperattenuating MCA sign have a significantly (P < .01) worse short-term prognosis than that of patients with a distal hyperattenuating MCA sign (Table 3). When we divided the Rankin scale into two measures (good to reasonable outcome [score of 0–2] and poor outcome [score of 3–6]), we found a significant difference in distribution between the three groups (P < .005), in which patients with a proximal hyperattenuating MCA sign had the highest prevalence of a poor short-term prognosis.


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  		TABLE 3. Rankin Score at Discharge

 
Neurologic Outcome
According to our assessments of neurologic deficit, we found a significant difference in distribution between the three groups of patients. Table 4 shows that within the group of patients with a proximal hyperattenuating MCA sign, significantly more patients had impairment of vision (P < .01) and facial function (P < .001). Less pronounced but still significant was the higher frequency of loss of motor function of upper (P < .01) and lower extremities (P < .01) in this group. Table 5 shows that we did not find an association between dysarthria and type of hyperattenuating MCA sign. However, patients with a proximal hyperattenuating MCA sign developed worse dysphasia (P < .05) than that of patients with a distal hyperattenuating MCA sign. This could have been caused by the fact that in this subgroup, the left hemisphere (which is associated with dysphasia) is coincidently affected more frequently than in patients without a hyperattenuating MCA sign or in patients with a distal hyperattenuating MCA sign. Statistical analysis of the distribution of symptoms in the left or right hemisphere shows no difference between groups (the left-right ratio of the symptomatic hemisphere was 12:6 in patients with a proximal hyperattenuating MCA sign, 18:6 in patients with a distal hyperattenuating MCA sign, and 79:65 in patients without a hyperattenuating MCA sign). Therefore, any influence of this left-right distribution on the presence or absence of dysphasia or on any of the other neurologic symptoms of stroke is expected to be small.


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  		TABLE 4. Neurologic Deficit at Discharge

 

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  		TABLE 5. Dysarthria and Dysphasia at Discharge

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The most important finding in our study is the significant association between the presence of a proximal hyperattenuating MCA sign and poor short-term prognosis and worse neurologic outcome than that of patients without a hyperattenuating MCA sign or patients with a distal hyperattenuating MCA sign. Our results show that patients with a proximal hyperattenuating MCA sign experience more neurologic deficit on most points of our functional neurologic scale, which leads to poor short-term outcome, defined as a Rankin score of 3–6, in 17 of 18 cases.

The prevalence (22.6%) of a hyperattenuating MCA sign in our population is lower than that found in most other studies (6–13,17,18), in which investigators report a prevalence within a range of 17.5%–50.0%, with a median prevalence of 30.5%. The prevalence of the hyperattenuating MCA sign is known to be dependent on two factors: section thickness and delay between onset of symptoms and CT scanning (8,15–19). Our relatively low prevalence of the hyperattenuating MCA sign can be explained by the fact that we used a maximum delay of 24 hours between onset of symptoms and first CT scanning, whereas most other studies used a shorter interval. For example, Bastianello et al (17) reported a prevalence of 50% by using a maximum interval of 4 hours.

False-positive hyperattenuating MCA signs have been documented in patients with calcified atherosclerosis (9,10,12, 13,18) or high hematocrit levels (12,14). In the present study, we did not find an association between the presence of a hyperattenuating MCA sign and cardiovascular risk factors when compared with patients without a hyperattenuating MCA sign. Three patients had high hematocrit levels. These three patients did not display a hyperattenuating MCA sign; therefore, it seems unlikely that high hematocrit levels influenced our results by causing false-positive hyperattenuating MCA signs. In individual cases, however, hematocrit levels should be taken into account.

Differentiation between proximal and distal hyperattenuating MCA signs turned out to be crucial to our results. On nonenhanced CT scans, the MCA may appear hyperattenuating due to thromboembolic occlusion, which has been shown in patients with a hyperattenuating MCA sign who underwent angiography (3,5,8, 15,17,23–25) or autopsy (3,24). In most cases, the hyperattenuating MCA sign disappears within a few days (5,15,17,25,26) or after thrombolytic therapy (8), confirming its direct relation to thromboembolic occlusion, which resolves after recanalization (23,27,28). The hyperattenuating appearance of the MCA caused by calcification, however, will persist on follow-up CT scans (8,15,17). In the past, the hyperattenuating MCA sign has been described as a reliable predictor of thromboembolic occlusion of the MCA, with specificity close to 100% but with a low sensitivity (7,8,10,13,18). This fact supports our findings, since a proximal occlusion of the MCA is likely to produce more neurologic deficit than a distal occlusion would.

Our data partly confirm the results of Manelfe et al (12). In their study, no relationship between the hyperattenuating MCA sign and long-term prognosis was found. However, we used a logistic multivariate model, thereby controlling the effects of age, sex, thrombolytic treatment, initial severity of neurologic deficit, and early parenchymal ischemic changes at CT (12). When a univariate model was used (ie, not controlling baseline function or mass effect), the hyperattenuating MCA sign (proximal and distal combined) was a significant predictor.

In a recent study by Barber et al (16), it was shown that patients who showed a proximal hyperattenuating MCA sign after acute stroke and who received intravenous tissue plasminogen activator were either dead or dependent after 3 months (16). Patients with a distal hyperattenuating MCA sign were independent in 64% of cases (16). It has been suggested that intravenous thrombolysis is ineffective in cases of proximal MCA occlusion and is more effective in occlusions of the M2 and/or M3 segment (16). Our data show that these findings cannot be ascribed only to the effectiveness of intravenous thrombolysis, since patients with a proximal hyperattenuating MCA sign who receive no thrombolytic treatment have a worse outcome than that of patients with a distal hyperattenuating MCA sign.

Our study was designed to evaluate the clinical outcome of patients who experience stroke with and without hyperattenuating MCA signs. We excluded patients who received thrombolytic therapy to avoid understating the effects of therapy on the prognosis of patients with occlusions (which were represented by the hyperattenuating MCA sign), because thrombolytic therapy resolves clots in an early phase of stroke evolution.

The main limitation of our study was that we could not study the predictive value of the hyperattenuating MCA sign in long-term prognosis. Although short-term prognosis is a reasonable measure for clinical outcome, long-term prognosis remains the standard. Moreover, because of the retrospective design of our study, we were not able to establish initial neurologic deficit in all patients and therefore could not use these data in our analysis.

In conclusion, we found the proximal hyperattenuating MCA sign to be a reliable predictor of poor short-term prognosis in patients who experience acute stroke with an occlusion of the M1 segment of the MCA. On the contrary, the distal hyperattenuating MCA sign, which represents an occlusion in the M2 segment or a more distal location, does not implicate poor outcome. Differentiation of the hyperattenuating MCA sign in proximal and distal manifestations is important in the individual patient and has clinical significance, since it facilitates early estimation of prognosis. We believe that future investigations of the hyperattenuating MCA sign and its subsequent predictive value in long-term prognosis should differentiate proximal and distal locations.


   FOOTNOTES
 
Abbreviation: MCA = middle cerebral artery

Author contributions: Guarantor of integrity of entire study, J.v.d.G.; study concepts, L.J.K., W.P.T.M.M., J.v.d.G.; study design, all authors; literature research, D.M.S., J.v.d.G.; clinical studies, P.J.N., L.J.K.; data acquisition, D.R.R., L.J.K.; data analysis/interpretation, D.M.S., P.J.N., D.R.R., J.v.d.G.; statistical analysis, D.M.S., J.v.d.G.; manuscript preparation, all authors; manuscript definition of intellectual content, D.M.S., J.v.d.G.; manuscript editing, D.M.S., D.R.R., J.v.d.G.; manuscript revision/review and final version approval, all authors.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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