| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 1999;30:1076-1082.)
© 1999 American Heart Association, Inc.
Original Contributions |
Attenuated Corticomedullary Contrast: An Early Cerebral Computed Tomography Sign Indicating Malignant Middle Cerebral Artery Infarction
A Case-Control Study
From the Department of Neurology (H-P.H., E.D., A.K., B.P., E.S.), Institute of Computed Tomography (A.P.), and Institute of Biostatistics (G.H.), University of Innsbruck (Austria).
Correspondence to Hans-Peter Haring, MD, Department of Neurology, University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria. E-mail hans-peter.haring{at}uibk.ac.at
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Background and Purpose—No neuroradiological markers have been characterized that support a timely decision for decompressive surgery in malignant middle cerebral artery (MCA) infarction (mMCAI). This case-control study was designed to analyze whether early cerebral CT (CCT) scanning provides reliable information for the prospective selection of stroke patients at risk of developing mMCAI.
Methods—Thirty-one pairs (n=62) were formed with cases (mMCAI) and controls (acute but not malignant MCA infarction) closely matched in terms of age, sex, and stroke etiology. CCT was performed within 18 hours of stroke onset and analyzed by a blinded neuroradiologist according to a defined panel of 12 CCT criteria.
Results—In terms of predicting mMCAI, the criteria of
extended MCA territory hypodensities >67% and >50%, hemispheric
brain swelling, midline shift, and hyperdense MCA sign exhibited high
specificity (100%, 93.5%, 100%, 96.7%, and 83.9%, respectively)
but low sensitivity (45.2%, 58.1%, 12.9%, 19.4%, and 70.9%,
respectively). Two criteria yielded high sensitivity
(subarachnoid space compressed, 100%; cella media compressed,
80.6%) but low specificity (29% and 74.2%, respectively). The
criterion of attenuated corticomedullary contrast
yielded both high specificity (96.8%) and sensitivity (87.1%). The
latter remained as the crucial criterion [Exp(B)=90.8; 95% CI, 5.8 to
1427.5] in a 2-tailed logistic regression analysis with the
strongest correlating parameters (Spearman correlation
factor 
0.6 or 
-0.6).
Conclusions—The analysis of CCT scans within 18 hours of stroke onset revealed an attenuated corticomedullary contrast as the crucial CCT criterion, which, with both sufficient sensitivity and specificity, predicted mMCAI with 95% certainty.
Key Words: case-control study • cerebral infarction • middle cerebral artery • tomography, x-ray computed
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
Total middle cerebral artery (MCA) territory infarcts may be distinguished from the diverse group of ischemic MCA strokes. Epidemiological data indicate that this particular stroke type accounts for 3% to 15% of all ischemic supratentorial infarctions.1 2 3 This subgroup is characterized by a distinct pattern of etiological, pathomorphological, and clinical features.3 Internal carotid artery (ICA) occlusions, ICA dissections, and cardiogenic embolism are the most frequent causes, and the subsequent development of large space-occupying brain edema resulting in tentorial and foraminal herniation is usually responsible for the fatal course in the majority of patients.3 4 The mortality rate in such patients approximates 78%, which is 3 to 4 times higher than in the general ischemic supratentorial stroke population.3 4 In consideration of these characteristics, the term malignant middle cerebral artery territory infarction (mMCAI) was coined.4
Recent experimental and clinical series suggest that decompressive surgery might be a life-saving emergency measure, reducing mortality significantly without elevated morbidity.5 6 However, the rapid course of the space-occupying lesion requires urgent diagnostic and therapeutic decisions. Cerebral CT (CCT) is a mainstay in the emergency diagnostic workup of acute stroke patients and conveys important information within a few hours after the ictus.7 8 9 The initiation of thrombolytic intervention is guided by early CCT signs, among others.7 8 9 In contrast, no neuroradiological markers have been characterized that support the decision for decompressive surgery in a timely manner.
This case-control study was designed to analyze whether early CCT scanning provides reliable information for the prospective selection of acute ischemic stroke patients at risk to develop mMCAI.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
During a 3-year period between January 1993 and December 1995, 1230 patients with an acute ischemic stroke in the ICA territory were admitted to the neurological department of the University of Innsbruck. Among this population, 31 patients with mMCAI were selected for this study. The diagnosis of mMCAI was established on the basis of previously introduced clinical and neuroradiological characteristics4 : (1) hemiplegia, fixed head and eye deviation, and rapid deterioration of consciousness; (2) angiographically or sonographically documented ICA and/or MCA trunk occlusion; (3) space-occupying brain edema causing tentorial herniation within 24 to 96 hours after admission. Four patients whose exact time of stroke onset remained unclear were not eligible for this study. The same was true for 1 additional patient in whom neither angiographic nor sonographic tests were available. Thus, the entire percentage of mMCAI patients in the study period was 2.9% (n=36). This rate is substantially lower than the 15% reported in the community-based Oxfordshire Community Stroke Project but strikingly close to the more recent data of the Austin Hospital Stroke Registry (3%) and the Lausanne Stroke Registry (3.2%).1 2 3
According to the principles of a case-control study, each mMCAI patient
(case) was assigned a control.10 The latter were randomly
selected acute MCA infarction (aMCAI) stroke patients without a
malignant course. Thus, 31 pairs (n=62) were formed, with cases and
controls closely matched in terms of age, sex, and stroke etiology
(Table 1
). The diagnosis of cardiogenic embolism was based on
both a history of cardiac disease and the evidence of
intracavitary thrombi by transthoracic and/or
transesophageal echocardiography.
Atherothrombotic occlusions in patients with extended
atherosclerosis and a vascular risk profile included
both intracranial and extracranial (ie, artery-to-artery embolism)
arterial occlusive diseases.
|
All patients underwent CCT scanning within 18 hours after stroke
onset. A repeated CCT was performed 24 to 36 hours later. The follow-up
CCT was performed to confirm the ischemic nature and the extent
of the brain lesion but was not used for data acquisition. The initial
CCT scans were evaluated by a neuroradiologist who was aware of the
clinical diagnosis of an ischemic stroke but blinded in terms
of the individual subsequent course of each patient (ie, mMCAI versus
aMCAI) and was also unaware of the results of the repeated CCT scans.
To achieve a quasi-standardized diagnostic procedure, the
analysis of the CCT scans was performed according to a panel of
12 defined criteria, which are summarized in Table 2. These
direct and indirect neuroradiological features are routinely used to
recognize focal parenchymal ischemia (ie, MCA territory
hypodensity, attenuated corticomedullary contrast
[CMC]), edema formation (ie, compressed cella media and/or
subarachnoid space [SAS], midline shift, hemispheric brain
swelling,), and vessel occlusion (hyperdense MCA sign). In part, they
have been used in previous studies of early CCT changes in acute
ischemic stroke.7 8 9 11 12 13 14 15 16 17 18 19 In accordance with the
clinical experience of the authors that early loss of CMC has been
associated with poor outcome in ischemic and traumatic brain
injuries, this CCT criterion was additionally introduced.
|
By means of a post hoc analysis, cases and controls were
compared with respect to each CCT criterion with the use of
cross-tabulations. Statistical significance was computed with a
2-tailed 
2 test and defined as
P<0.001. Logistic regression analysis was used to
analyze the linear relation between any CCT criterion and the
study groups.10
|
Results |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
The predominant etiologies included embolism, local thrombosis, and dissection, with a nonsignificant imbalance between the study groups (Table 1
). The overall mortality
among cases was 65% compared with 5.2% among controls.
The results of the pairwise comparisons of the 12 defined CCT criteria
are presented in the order listed in Table 2. The raw data are depicted as
cross-tabulations in Table 3. Thirteen
patients had their CCT scan <6 hours after stroke onset, and 49
patients had their CCT scan 6 to 18 hours after stroke onset; the
respective figures are given separately in Table 3.
|
Nine initial CCT scans did not exhibit any hypodensity in the MCA
territory (Table 3), which was associated with the subsequent
development of mMCAI in only a single case (11.1%). In contrast, all
14 patients (100%) with a MCA territory hypodensity >67% on the
initial examination suffered a malignant course. These 2
parameters were significantly different between cases and
controls (P<0.001), which was not the case for the
remaining 2 parameters of this group (ie, MCA hypodensity
<33% and MCA hypodensity >33% but <67%).
Twenty patients presented initially with MCA territory
hypodensity >50% (Table 3), which was followed by the
development of mMCAI in 18 patients (90%). In contrast, only 12 of 33
patients (36.4%) with MCA territory hypodensity <50% were in the
mMCAI group, and the remaining 21 were in the aMCAI group
(P<0.001).
Twenty-five of 33 patients (75.8%) with unilateral compression of the
cella media (Table 3) developed mMCAI, compared with only 6 of
29 patients (20.7%) without this CCT sign (P<0.001).
Fifty-three patients, including all 31 patients (58.5%) with mMCAI,
exhibited a compressed SAS (Table 3) on the initial CCT scan.
However, this finding was also associated with the nonfatal course of
aMCAI in 22 patients (41.5%). None of the 9 patients without
compressed SAS suffered a mMCAI.
A midline shift (Table 3) was present in only 7 of 62
patients and was associated with mMCAI in 6 of those (85.7%). In case
of an absent midline shift on the initial CCT scan, 25 patients
(45.5%) went on to mMCAI and the remaining 30 (54.5%) to aMCAI. This
difference was not statistically different (P=0.313).
The hyperdense MCA sign (Table 3) was found in 27 patients and
was associated with mMCAI in 22 of those (81.5%). It was absent in 35
patients and associated with mMCAI in only 9 of those (25.7%)
(P<0.001).
Only 4 patients had a brain swelling (Table 3) of the entire
affected hemisphere on the initial CCT scan, and all of them (100%)
developed mMCAI. Among the remaining 58 patients without this CCT sign,
27 (46.6%) were also associated with mMCAI, but 31 patients (53.4%)
were not. This difference was not statistically different
(P=0.039).
Twenty-eight patients exhibited an attenuated CMC (Table 3),
which was present at least throughout the entire MCA territory on
the initial CCT scan. This was related to subsequent mMCAI in 27
(96.4%) of these cases. In contrast, only 4 of the 34 patients
(11.8%) with an intact CMC developed a fatal mMCAI
(P<0.001).
Sensitivity, specificity, predictive values, and the respective odds
ratios (with 95% CIs) for the development of mMCAI are summarized in
Table 4. CCT criteria exhibiting a
specificity of 80% were extended hypodensities >67% (100%) and
>50% (93.5%) of the MCA territory, hemispheric brain swelling
(100%), midline shift (96.7%), and hyperdense MCA sign (83.9%)
(Table 4). However, the respective sensitivities were low
(45.2%, 58.1%, 12.9%, 19.4%, and 70.9%, respectively). In
contrast, 2 criteria yielded high sensitivity (SAS compressed, 100%;
cella media compressed, 80.6%) but low specificity (29% and 74.2%,
respectively). The CCT criterion of attenuated CMC remained as the only
radiological feature yielding both high specificity (96.8%) and
sensitivity (87.1%). In a 2-tailed logistic regression
analysis with the strongest correlating parameters
(Spearman correlation factor 0.6 or -0.6), an attenuated CMC
remained as the critical criterion [Exp(B)=90.8; 95% CI, 5.8 to
1427.5], thereby suggesting that this sign on the initial CCT scan may
predict the development of mMCAI with a 95% probability. The
regression analysis yielded no further significant
correlations.
|
A further subanalysis was performed with patients who underwent
CCT scanning before or after 6 hours of stroke onset. This cutoff was
chosen because of its critical therapeutic implications. Thirteen
subjects (21%) were diagnosed within 6 hours, and the remaining 49
(79%) were diagnosed later. The distribution of the CCT criteria was
not statistically different between both groups (Table 3).
The Figure shows
representative CCT images of 3 patients with either
mMCAI or aMCAI.
|
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
This represents the first controlled study of early CCT signs associated with the subsequent development of mMCAI. From a panel of CCT criteria, a widespread attenuated CMC (ie, covering at least the entire MCA territory) has been identified as the most reliable neuroradiological feature. If present within 18 hours of stroke onset, this single CCT sign was strongly indicative (95% CI, 5.8 to 1427.5 in the logistic regression analysis) for the development of mMCAI with both high specificity (96.8%) and sensitivity (87.1%) (odds ratio, 202.5; 95% CI, 21.3 to 1925). This was in contrast to a number of other early CCT criteria (MCA >67%, MCA >50%, midline shift, hemispheric brain swelling), which were also highly specific (>80%) for a subsequent mMCAI but exhibited insufficient sensitivity (Table 4
). Two other CCT signs
(compressed SAS, compressed cella media) were sufficiently sensitive
(100%, 80.6%) but not specific (Table 4). Most direct and indirect CCT signs of cerebral ischemia reflect common pathophysiological grounds. Ischemia-induced energy breakdown of the cells is followed by an immediate transmembrane ionic shift and subsequent water accumulation. This in turn alters the x-ray attenuation in the affected tissue.8 Depending on the extent and severity of the stroke, increased radiolucency appears as hypodensity in subcortical or cortical areas or both.8 In our study, loss of the usual contrast between gray and white matter was termed attenuated CMC and considered to indicate cortical hypodensity. Reflecting impaired cortical perfusion, this CCT sign might reasonably be considered an early indicator of large territorial infarctions when widespread cortical areas are covered. Whether parenchymal hypodensity is accompanied by brain swelling as a reflection of edema depends primarily on the timing of the examination. The reason therefore lies in the superior sensitivity of CCT scanning for increased radiolucency compared with water accumulation.8
The identification of very early changes on CCT scans in acute
ischemic stroke patients has been the subject of previous
studies stressing even subtle parenchymal alterations only hours after
stroke onset in the majority of patients.11 12 13 14 15 16 17 18 19 In a
recent series of patients with MCA territory infarctions, the incidence
of positive findings was 68% in CCT scans performed within 2 hours of
stroke onset, increasing to 89% within 3 hours.19 These
data emphasize the great value of emergency CCT scanning in acute
stroke management, which is superior to MRI in this patient
population.18 In contrast to the thoroughly documented
diagnostic power of very early CCT scanning in acute
stroke, surprisingly little is known about its prognostic value. Only a
single study describes the predictive value of early CT in MCA trunk
occlusion.19 In this series, MCA territory hypodensity
>50% and local brain swelling were valuable indicators of fatal
outcome with high sensitivity (61% and 78%, respectively), high
specificity (98% and 83%, respectively), and a high positive
predictive value (85% and 70%, respectively).19 These
data are closely correlated to the results of our series, in which the
respective sensitivity, specificity, and positive predictive values for
the development of mMCAI in the case of MCA territory hypodensity
>50% were 58.1%, 93.5%, and 90% (Table 4). The criterion of
local brain swelling was not included in our standardized CCT
diagnostic checklist but was closely paralleled by our
criterion of compressed cella media. This CCT finding showed
sensitivity, specificity, and positive predictive value for mMCAI of
80.6%, 74.2%, and 75.8% (Table 4). Compared with a localized
edematous process, early hemispheric brain swelling (ie, swelling of
the entire hemisphere) exhibited a maximal (ie, 100%) specificity and
positive prediction (100%) for mMCAI but a very low sensitivity of
12.9% (Table 4). However, this can be reasonably explained by
the dynamics of ischemic brain edema formation, which usually
takes 24 to 72 hours for maximal extension.20 Therefore,
this CCT finding is highly predictive for a fatal course in those cases
in which it is present early, but it is insufficiently sensitive
for emergency CCT scanning within 24 hours after stroke onset. The same
might prove true for the early formation of a midline shift, which in
our series was associated with a high specificity and positive
predictive value (96.7% and 85.7%, respectively) for mMCAI but a
comparably low sensitivity of 19.4% (Table 4). In agreement
with these data, severe brain swelling with mass effect in terms of a
midline shift was not observed within 6 hours of stroke onset in the
European Cooperative Acute Stoke Study (ECASS)
population.21 In contrast, CCT scanning in a series of 118
acute stroke patients within 48 hours revealed a strong positive
correlation between the extent of midline shift and the risk of early
death.22 In our series, the low prevalence of midline
shift (n=7) did not allow a reasonable correlation between the extent
of the shift and stroke outcome.
The presence of the hyperdense MCA sign is, with few exceptions,
specific for MCA trunk occlusion and a corresponding large territory
infarction.19 23 24 The prognostic significance of this
finding, however, is less unequivocally characterized. The majority of
studies point to a close relation between a positive hyperdense MCA
sign and fatal outcome after an ischemic
stroke.21 25 26 27 28 This is in agreement with our results, in
which the presence of the hyperdense MCA sign revealed reasonably high
specificity (83.9%) and positive predictive value (81.5%) for mMCAI
(Table 4). The insufficient sensitivity of 70.9% may reflect
the limited prevalence of only 40% to 60% of this CCT sign in
angiographically demonstrated MCA trunk
occlusions.19 23 24 25 27 29 30 31 However, in one recent
series, the prognostic value of the hyperdense MCA sign was strikingly
low, with sensitivity, specificity, and positive predictive value of
only 44%, 51%, and 32%, respectively.19 This
discrepancy might be due to the different timing of CCT scanning (5
hours versus 18 hours after stroke onset), which clearly affects
the prevalence of this finding.19 21 23 24 27 29 30 32
One possible weakness in the design of our study was the fact that the neuroradiologist was blinded to the subsequent course (ie, mMCAI versus aMCAI) of each patient but not to the clinical diagnosis of an ischemic stroke. This may have increased the number of positive findings on the initial CCT scans. However, the respective figures in our series correlate well with the results of a previous study in which 89% of all patients showed early CCT changes as early as 3 hours after stroke onset.19
Our study was primarily designed to identify early CCT criteria that may reliably be used to discriminate acute stroke patients with a malignant course from those with a nonmalignant course. Such criteria could be critical in supporting the decision of whether a patient with aMCAI should undergo decompressive surgery as a life-saving measure. Among our 31 patients with mMCAI, 11 patients underwent decompressive craniectomy after a median interval of 1.8 days (range, 0 to 6 days) after stroke onset, and the remaining 20 continued on full-scale intensive care. Three-month mortality among the operated patients was 41.6% compared with 80% in the conservatively treated group (overall mortality independent of therapy, 65.6%). These data correlate with the results of the only prospective controlled trial on hemicraniectomy in acute space-occupying ischemic stroke.6 This supports the notion that decompressive surgery may be a life-saving emergency measure in this particular stroke subtype. It was not the intention of this study to test therapeutic measures, but these data emphasize the clinical importance of the earliest possible and reliable neuroradiological features which, in association with clinical signs and symptoms, might be helpful for emergency differential diagnostic and therapeutic decisions. CCT scanning within 6 hours or 6 to 18 hours after stroke onset revealed no statistically significant differences in our series. However, the number of patients analyzed early was too small (n=13) to allow reliable statistical analysis from this subgroup. In this regard, the retrospective analysis of the CCT scans must be critically noted, which we regarded as a sufficient approach to provide a first predicative data set. Nevertheless, the results need to be confirmed in a prospective analysis, which might increase the sensitivity of time-related CCT changes.
It is noteworthy that our results might also be helpful in recognizing
stroke patients who, despite suspicious clinical signs and symptoms,
are not high-risk candidates for mMCAI if their CCT scans are lacking
the required criteria. An intact CMC and a normal SAS in particular
yielded high negative predictive values (Table 4). As a
limitation, it must be noted, however, that no controlled data of the
reliability of initial clinical signs and symptoms are available and
that our study was not designed to address this question.
In conclusion, our results suggest that CCT scanning within 18 hours of stroke onset may help in the early identification of patients who may develop mMCAI. In particular, an attenuated CMC may be the crucial CCT criterion. Moreover, diagnostic reliability can be enhanced when the initial CCT scan is thoroughly screened for additional features, such as extended MCA hypodensity, hemispheric brain swelling, midline shift, and a hyperdense MCA sign.
Received January 5, 1999; revision received February 12, 1999; accepted February 12, 1999.
|
References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Bamford J, Sandercock P, Dennis M, Burn J, Warlow C. A prospective study of acute cerebrovascular diseases in the community: the Oxfordshire Community Stroke Project 1981–86, I: methodology, demography and incident cases of first ever stroke. J Neurol Neurosurg Psychiatry. 1988;51:1373–1380.
2. Donnan GA, Levi CR. Large and panhemispheric infarcts. In: Bogousslavsky J, Caplan L, eds. Stroke Syndromes. New York, NY: Cambridge University Press; 1995:300–330.
3.
Heinsius T, Bogousslavsky J, Van Melle G. Large
infarcts in the middle cerebral artery territory: etiology and outcome
patterns. Neurology. 1998;50:341–350.
4.
Hacke W, Schwab S, Horn M, Spranger M, de Georgia M,
von Kummer R. "Malignant" middle cerebral artery territory
infarction: clinical course and prognostic signs. Arch
Neurol. 1996;53:309–15.
5.
Forsting M, Reith W, Schäbitz W-R, Heiland S,
von Kummer R, Hacke W, Sartor K. Decompressive craniectomy for cerebral
infarction: an experimental study in rats. Stroke. 1995;26:259–264.
6. Rieke K, Schwab S, Krieger D, von Kummer R, Aschoff A, Schuchardt V, Hacke W. Decompressive surgery in space-occupying hemispheric infarction: results of an open, prospective trial. Crit Care Med. 1995;23:1576–1587.[Medline] [Order article via Infotrieve]
7. Von Kummer R, Nolte PN, Schnittger H, Thron A, Ringelstein EB. Detectability of hemispheric ischemic infarction by computed tomography within 6 hours after stroke. Neuroradiology. 1996;38:31–33.[Medline] [Order article via Infotrieve]
8. Unger E, Littlefield J, Gado M. Water content and water structure in CT and MRI signal changes: possible influence in detection of early stroke. AJNR Am J Neuroradiol. 1988;9:687–691.[Abstract]
9. Von Kummer R, Bozzao L, Manelfe C. Early CT Diagnosis of Hemispheric Brain Infarction. Berlin, Germany: Springer-Verlag; 1995:1–101.
10. Harms V. Korrelation und Regression. In: Harms V, ed. Biomathematik, Statistik und Dokumentation. 6th ed. Kiel, Germany: Völlig neu berarbeitete Auflage; 1992:126–141.
11. Aulich A, Wende S, Fenske A, Lange S, Steinhoff A. Diagnosis and follow-up studies in cerebral infarcts. In: Lanksch W, Kazner E, eds. Cranial Computerized Tomography. Berlin, Germany: Springer; 1976:273–283.
12.
Inoue Y, Takemoto K, Miyamoto T, Yoshikawa N, Taniguchi
S, Saiwai S, Nishimura Y, Komatsu T. Sequential computed tomography in
acute cerebral infarction. Radiology. 1980;135:655–662.
13.
Wall SD, Brant-Zawadzki M, Jeffrey RB, Barnes B. High
frequency CT findings within 24 hours after cerebral infarction.
AJR Am J Roentgenol. 1982;138:307–311.
14.
Tomura N, Uemura K, Inugami A, Fujita H, Higano S,
Shishido F. Early CT findings in cerebral infarction.
Radiology. 1988;168:463–467.
15. Bozzao L, Bastianello S, Fantozzi LM, Angeloni U, Argentino C, Fieschi C. Correlation of angiographic and sequential CT findings in patients with evolving cerebral infarction. AJNR Am J Neuroradiol. 1989;10:1215–1222.[Abstract]
16.
Truwit CL, Barkovich AJ, Gean –Marton A, Hibri N,
Norman D. Loss of the insular ribbon: another early CT sign of acute
middle cerebral artery infarction. Radiology. 1990;176:801–806.
17.
Horowitz SH, Zoto JL, Donnarumma R, Patel M, Alvir
J. Computed tomographic–angiographic findings within the first
five hours of cerebral infarction. Stroke. 1991;22:1245–1253.
18.
Mohr JP, Biller J, Hilal SK, Yuh WTC, Chang DN,
Tatemichi TK, Tali E, Nguyen H, Mun I, Adams HP Jr, Grisman K, Marler
JR. Magnetic resonance vs computed tomographic imaging in acute stroke.
Stroke. 1995;26:807–812.
19. Von Kummer R, Meyding-Lamadè U, Forsting M, Rosin L, Rieke K, Hacke W, Sartor K. Sensitivity and prognostic value of early computed tomography in middle cerebral artery trunk occlusion. AJNR Am J Neuroradiol. 1994;15:9–15.[Abstract]
20. Haring H-P, Aichner FT. Treatment of intracranial hypertension in acute ischemic stroke. In: Castillo J, Dàvalos A, Toni D, eds. Management of Acute Ischemic Stroke. Barcelona, Spain: Springer-Verlag; 1997:109–126.
21.
Hacke W, Kaste M, Fieschi C, Toni D, Lesaffre E, von
Kummer R, Boysen G, Bluhmki E, Höxter G, Mahagne MH, Hennerici M,
for the ECASS Study Group. Intravenous
thrombolysis with recombinant tissue
plasminogen activator for acute hemispheric
stroke: the European Cooperative Acute Stroke Study (ECASS).
JAMA. 1995;274:1017–1025.
22.
Pullicino PM, Alexandrov AV, Shelton JA, Alexandrova
NA, Smurawska LT, Norris JW. Mass effect and death from severe acute
stroke. Neurology. 1997;49:1090–1095.
23. Bastianello S, Pierallini A, Collonese C, Brughitta G, Angeloni U, Antonelli M, Fantozzi LM, Fieschi C, Bozzao L. Hyperdense middle cerebral artery sign: comparison with angiography in the acute phase of ischemic supratentorial infarction. Neuroradiology. 1991;33:207–211.[Medline] [Order article via Infotrieve]
24. Tomsick TA, Brott TG, Chambers AA, Fox AJ, Gaskill MF, Lukin RR, Pleatman CW, Wiot JG, Bourekas E. Hyperdense middle cerebral artery sign on CT: efficacy in detecting middle cerebral artery thrombosis. AJNR Am J Neuroradiol. 1990;11:473–477.[Abstract]
25.
Gàcs G, Fox AJ, Barnett HJM, Vinuela F. CT
visualization of intracranial arterial thromboembolism.
Stroke. 1983;14:756–764.
26.
Launes J, Ketonen L. Dense middle cerebral artery sign:
an indicator of poor outcome in middle cerebral artery infarction.
J Neurol Neurosurg Psychiatry. 1987;50:1550–1552.
27. Schuierer G, Huk W. The unilateral hyperdense middle cerebral artery: an early CT-sign of embolism or thrombosis. Neuroradiology. 1988;30:120–122.[Medline] [Order article via Infotrieve]
28. Zorzon M, Mase G, Pozzi-Muzelli F, Biasutti E, Antonutti L, Iona L, Cazzato G. Increased density in the middle cerebral artery by nonenhanced computed tomography: prognostic value in acute cerebral infarction. Eur J Neurol. 1993;33:256–259.
29.
Pressmann BD, Tourje EJ, Thompson JR. An early CT sign
of ischemic infarction: increased density in a cerebral artery.
AJR Am J Roentgenol. 1987;149:583–586.
30.
Leys D, Pruvo JP, Godefroy O, Rondepierre P, Leclerce
X. Prevalence and significance of hyperdense middle cerebral artery in
acute stroke. Stroke. 1992;23:317–324.
31. Tomsick T, Brott T, Barsan W, Broderick J, Haley EC, Spilker J. Thrombus localization with emergency cerebral CT. AJNR Am J Neuroradiol. 1992;13:257–263.[Abstract]
32.
Rieth KG, Fujiwara K, Di Chiro G, Klatzo I, Brooks RA,
Johnston GS, O'Connor CM, Mitchell LG. Serial measurements of CT
attenuation and specific gravity in experimental cerebral edema.
Radiology. 1980;135:343–348.
This article has been cited by other articles:
 |
|
 |
|
  J. A. Alawneh, R. R. Moustafa, and J.-C. Baron Hemodynamic Factors and Perfusion Abnormalities in Early Neurological Deterioration Stroke, June 1, 2009; 40(6): e443 - e450. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W W M Lam, T W H Leung, W C W Chu, D T K Yeung, L K S Wong, and W S Poon Early computed tomography features in extensive middle cerebral artery territory infarct: prediction of survival J. Neurol. Neurosurg. Psychiatry, March 1, 2005; 76(3): 354 - 357. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Dohmen, B. Bosche, R. Graf, F. Staub, L. Kracht, J. Sobesky, M. Neveling, G. Brinker, and W.-D. Heiss Prediction of Malignant Course in MCA Infarction by PET and Microdialysis Stroke, September 1, 2003; 34(9): 2152 - 2158. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. J. Thomalla, T. Kucinski, V. Schoder, J. Fiehler, R. Knab, H. Zeumer, C. Weiller, and J. Rother Prediction of Malignant Middle Cerebral Artery Infarction by Early Perfusion- and Diffusion-Weighted Magnetic Resonance Imaging Stroke, August 1, 2003; 34(8): 1892 - 1899. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J M Wardlaw, T M West, P A G Sandercock, S C Lewis, and O Mielke Visible infarction on computed tomography is an independent predictor of poor functional outcome after stroke, and not of haemorrhagic transformation J. Neurol. Neurosurg. Psychiatry, April 1, 2003; 74(4): 452 - 458. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. M. Manno, D. A. Nichols, J. R. Fulgham, and E. F. M. Wijdicks Computed Tomographic Determinants of Neurologic Deterioration in Patients With Large Middle Cerebral Artery Infarctions Mayo Clin. Proc., February 1, 2003; 78(2): 156 - 160. [Abstract] [PDF]
|
|
|
|
|
|
J. F. Arenillas, A. Rovira, C. A. Molina, E. Grive, J. Montaner, J. Alvarez-Sabin, and K.-O. Lovblad Prediction of Early Neurological Deterioration Using Diffusion- and Perfusion-Weighted Imaging in Hyperacute Middle Cerebral Artery Ischemic Stroke * Editorial Comment Stroke, September 1, 2002; 33(9): 2197 - 2205. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. E. Kasner, A. M. Demchuk, J. Berrouschot, E. Schmutzhard, L. Harms, P. Verro, J. A. Chalela, R. Abbur, H. McGrade, I. Christou, et al. Predictors of Fatal Brain Edema in Massive Hemispheric Ischemic Stroke Stroke, September 1, 2001; 32(9): 2117 - 2123. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Gerriets, E. Stolz, S. Konig, S. Babacan, I. Fiss, M. Jauss, and M. Kaps Sonographic Monitoring of Midline Shift in Space-Occupying Stroke : An Early Outcome Predictor Stroke, February 1, 2001; 32(2): 442 - 447. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Oppenheim, Y. Samson, R. Manai, T. Lalam, X. Vandamme, S. Crozier, A. Srour, P. Cornu, D. Dormont, G. Rancurel, et al. Prediction of Malignant Middle Cerebral Artery Infarction by Diffusion-Weighted Imaging Stroke, September 1, 2000; 31(9): 2175 - 2181. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. T. F. Cheung Computed Tomographic Findings and Prediction of Malignant Middle Cerebral Artery Infarction Stroke, December 1, 1999; 30 (12): 2759 - 2768. [Full Text] [PDF]
|
|
|
|
|
|
R. von Kummer Ischemic Stroke and Tissue Hypodensity on Computed Tomography Stroke, September 1, 1999; 30(9): 1974 - 1981. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||