(Stroke. 2001;32:442.)
© 2001 American Heart Association, Inc.
Original Contributions |
From the Department of Neurology (T.G., E.S., S.K., S.B., I.F., M.J., M.K.), Justus-Liebig-University Giessen (Germany); the Department of Neurology (T.G.), UMass Memorial Health Care and University of Massachusetts Medical School, Worcester; and the Department of Neurology (S.K., I.F.), Medical University at Luebeck, Germany.
Correspondence to Prof Dr med M. Kaps, Am Steg 20, 35385 Giessen, Germany. E-mail Manfred.Kaps{at}Neuro.med.Uni-Giessen.de
| Abstract |
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MethodsForty-two patients with acute, severe hemispheric stroke were enrolled. Cranial computed tomography (CCT) and extracranial duplex sonography were performed on admission. TCCS was carried out 8±3, 16±3, 24±3, 32±3, and 40±3 hours after stroke onset. Lesion size was determined from follow-up CCT.
ResultsTwelve patients
died as the result of cerebral herniation (group 1); 28 survived (group
2). Two patients received decompressive hemicraniectomy and were
therefore excluded from further evaluation. MLS was significantly
higher in group 1 as early as 16 hours after onset of stroke.
Specificity and positive predictive values for death caused by cerebral
herniation of MLS
2.5, 3.5, 4.0, and 5.0 mm after 16, 24, 32,
and 40 hours were 1.0.
ConclusionsTCCS helps to estimate outcome as early as 16 hours after stroke onset and thus facilitates identification of patients who are unlikely to survive without decompressive craniectomy. Because of its noninvasive character and bedside suitability, sonographic monitoring of MLS might be a useful tool in management of critically ill patients who cannot undergo repeated CCT scans.
Key Words: brain edema cerebral infarction stroke outcome ultrasonography, Doppler, duplex
| Introduction |
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In a recent study, sonographic assessment of MLS 32±4 hours after stroke onset was shown to identify MCA stroke patients who are unlikely to survive.7 Furthermore, horizontal displacement of the septum pelucidum and the pineal gland, derived from cranial computed tomography (CCT) scans, is used as an inclusion criterion in a randomized trial testing hemicraniectomy versus medical therapy in severe hemispheric stroke (Derk W. Krieger, MD, personal communication, 2000).
The purpose of this study was to evaluate the temporal dynamics of MLS in hemispheric stroke patients in short intervals within the first 40 hours. We hypothesized that measurement of MLS at defined time intervals may serve as an early outcome predictor and facilitates indication for aggressive treatments such as hypothermia or decompressive hemicraniectomy.
| Subjects and Methods |
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Neurosonologic Methods
Extracranial color-coded duplex sonography of the
brain-supplying arteries was performed on admission (Hewlett Packard;
SONOS 2000 or 5500; 5.0-MHz sector and 7.5-MHz linear scanner). TCCS
was performed by 3 investigators through the transtemporal
acoustic bone window with the use of a 2.5-MHz sector scanner as
described earlier.3
Angle-corrected systolic and diastolic blood flow
velocity of the MCA and the supraclinoid part of the internal carotid
artery was obtained from the ipsilateral and contralateral sides. By
tilting the ultrasound probe
10 degrees upward, the third ventricle
could be displayed at a depth of 6 to 8 cm. This structure was easily
identified by its hyperechogenic margins, the surrounding hypoechogenic
thalami, and the hyperechogenic pineal gland. The distance between the
TCCS probe and the center of the third ventricle was measured in a line
perpendicular to the walls of the third ventricle
(Figure 1
) from both the ipsilateral (A) and contralateral
(B) sides, and the deviation from the presumed midline was calculated
by the equation
MLS=(A-B)/2.5
|
TCCS was carried out 8±3, 16±3, 24±3, 32±3, and 40±3 hours after stroke onset.
Computed Tomography
CCT was performed on admission to exclude patients
with intracerebral hematoma and during the first 2
weeks to determine the size of the infarct. Diagnosis of old
territorial infarcts (>1.5 cm) and space-occupying bleeding
complications during the first 40 hours after stroke were exclusion
criteria for this study. MLS was calculated from follow-up images if
the time delay between CCT and TCCS was <6 hours, in a fashion
analogous to that of TCCS by measuring the distance between the
external tabula of the skull to the middle of the third ventricle on
both sides, with the use of the previously stated formula. CCT
examiners were blinded to TCCS findings and vice
versa.
Statistics
Sensitivity, specificity, and predictive values were
calculated from cross-tables. MLS of patients in both outcome groups
(death versus survival) were compared by a nonparametric
test for unrelated samples (Mann-Whitney
U test). Differences in sex,
age, and extracranial and intracranial vascular status were tested by
Fishers exact test. MLS values obtained from TCCS and CCT images were
compared by linear regression analysis. Significance was
assigned for values of
P<0.05.
| Results |
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Follow-up CCT demonstrated infarction of <50% of the MCA territory in 9 and >50% in 33 patients. In 5 patients, an additional anterior or posterior cerebral artery infarction was found. Sixteen of 42 patients (38.1%) were sedated and artificially ventilated during the first 48 hours.
Thirty-eight CCT images were performed within 6 hours before
or after a TCCS examination. Mean MLS was 1.18 mm (SD 1.15) on CCT
and 1.25 mm (SD 1.30) on TCCS images. The difference of MLS
between both methods was
0.75 mm in 31 (81.6%), 0.75 to
1.5 mm in 6 (15.8%), and >1.5 mm in 1 (2.6%) data pairs.
MLS values correlated well with both imaging techniques
(r=0.88;
P<0.0001).
Twelve patients (28.6%) died secondary to cerebral herniation with clinical signs of rostrocaudal deterioration such as decerebral posturing or pupil dilation and no other cause of death (group 1). Death occurred between 24 and 168 hours after onset of stroke (mean, 78.3 hours). Median SSS on admission was 10 (range, 4 to 30). Twenty-eight patients (71.4%) survived (group 2; median SSS=16; range, 4 to 35). The difference of SSS on admission was not significant between both groups (P>0.05). Two men received decompressive hemicraniectomy 27 and 30 hours after stroke and survived. Both were excluded from further statistical evaluation.
MLS monitoring was possible in 33, 29, 26, 29, and 23
patients in each 8-hour time interval. Data are
presented in
Table 1
and
Figure 2
. Missing values were due to admission after >11
hours, performance of other diagnostic or
therapeutic procedures within an examination time interval, or death.
MLS was significantly higher in patients who died compared with
survivors 16, 24, 32, and 40 hours after onset of stroke but not after
8 hours. Specificity and positive predictive values (PPV) of MLS
2.5,
3.5, 4.0, and 5.0 mm after 16, 24, 32, and 40 hours for death
caused by cerebral herniation were 1.0
(Table 2
).
|
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No statistically significant differences were found between both groups concerning sex (P>0.1), age (P>0.1), MCA occlusion (P>0.1), and carotid T occlusion (P>0.1). There was a nonsignificant trend toward a better outcome after early (within 12 hours; P=0.06) as well as late MCA recanalization (within 40 hours; P=0.06). Death caused by herniation occurred significantly more often in patients with an infarct size >50% of the MCA territory depicted by late follow-up CCT (P<0.05; Fishers exact test).
| Discussion |
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Midline Shift
The first to describe a method for measuring MLS by
means of TCCS were Seidel and
coworkers5 in 1996. Various
studies evaluated its reliability in revealing information regarding
the diameter and lateral displacement of the third ventricle. A
comparative study revealed a high correlation of the diameter of the
third ventricle depicted by CCT and TCCS
(r=0.96).33
Seidel et al34 demonstrated
a good interobserver and intraobserver reproducibility for determining
the diameter of the third ventricle on TCCS images. The correlation of
MLS apparent on CCT and TCCS in this study is in agreement with various
other studies that report correlation coefficients between 0.87 and
0.93.5 8 35
Concerning the precision of sonographic MLS measurement, Stolz et
al8 reported a ±0.89-mm,
2-SD confidence interval of TCCS findings compared with CCT. It is
likely, however, that the CCT measurements in these studies contain
some error because they were based on manual readings of the CCT scans
and thus that the precision of the sonographic MLS measurements was
underestimated.
The comparison between CCT and TCCS revealed a marked discrepancy in 1 of 38 examinations (TCCS, 4.35 mm; CCT, 6.1 mm). In this patient, a severe compression of the third ventricle was visible on the CCT image, which probably led to difficulties in identification of this structure on the TCCS images.
In this study, patients with large hemispheric stroke were prospectively investigated. Other midline structures such as the pineal gland or the septum pellucidum have not been monitored because of their poor display on TCCS scans. Nevertheless, there is a close correlation of the lateral displacement of the septum pellucidum and the pineal gland (r=0.82) as demonstrated on CCT.12 TCCS findings were monitored in 8-hour time intervals during the first 40 hours after onset of stroke. Extracranial vascular status was investigated on admission with duplex sonography. TCCS proved to be a reliable method in assessing intracranial vessel occlusion36 37 and was used for assessment of MCA occlusion and recanalization on follow-up.
Twelve patients died as the result of cerebral herniation; 28 survived. Death occurred after day 1 and before day 7 (mean, 3.3 days); 4 of 12 patients (33%) died within the first 48 hours. This clinical course is representative and agrees with clinicopathological16 23 24 and epidemiological studies,25 where 19% to 47% of all deaths caused by herniation occurred within 48 hours after onset of stroke. Silver and coworkers21 analyzed the course of 38 patients with malignant MCA infarction whose cause of death was transtentorial herniation. They reported no deaths occurring within the first 24 hours or after day 10. Furthermore, our results concur with a clinicopathological study, where MLS, as a measure of brain edema, reaches a maximum between day 2 and day 4 after stroke onset.23
Two patients of our cohort survived after decompressive
hemicraniectomy. MLS of one patient exceeded 3.5 mm after 24 hours
(Figure 2
), giving anecdotal evidence that hemicraniectomy
can be a life-saving therapy in space-occupying stroke.
MLS differed significantly between both outcome groups as early as 16 hours after onset of stroke. For calculation of sensitivity, specificity, and predictive values, we set limiting values for MLS to 1.25 mm after 8 hours, 2.5 mm after 16 hours, 3.5 mm after 24 hours, 4.0 mm after 32 hours, and 5.0 mm after 40 hours to obtain a maximum PPV. In agreement with our previous study,7 all patients with a MLS >4 mm after 32 hours died (PPV=1.0). In addition, the present study demonstrates that MLS is a reliable outcome measure even as early as 24 and 16 hours (PPV=1.0 and 1.0) after onset of symptoms. Nevertheless, the difference of 1.4 and 1.0 mm between the highest MLS of survivors and the lowest fatal MLS at 24 and 32 hours indicates a certain overlap between survivors and fatalities.
Besides horizontal shift, vertical displacement has also been shown to be relevant for survival. Horizontal rather than downward displacement is closely related to the level of consciousness.11 14 Downward displacement is also important, although it does not correlate well with outcome.38 39 It is clearly an advantageous coincidence that horizontal displacement can be depicted accurately by means of TCCS.
Our findings agree with those of Pullicino and
coworkers,12 who evaluated
lateral displacement of the pineal gland by using CCT scans performed
between 0 and 48 hours after the onset of clinical symptoms; they found
a specificity of 0.89 and a sensitivity of 0.46 for predicting patient
14-day mortality rates. Displacement >4 mm was associated with a
low probability of 14-day survival, although the relation between time
of stroke onset and time of CCT scan was not precisely defined. Haring
et al13 found a low
sensitivity (0.19) but a high specificity (0.97) of MLS-obtained CT
scans within the first 18 hours after stroke onset for the development
of malignant MCA infarction. In contrast, various other studies with
less clearly defined time points of measurements could not find a
positive correlation between MLS and outcome
(Table 3
).
|
We conclude that MLS measurements performed very early (ie, within the first 16 hours from stroke onset) or not strictly correlated with time after infarct fail to predict fatal outcome in patients with severe MCA infarctions.
Clinical Scores
In our previous
study,7 we found no
significant difference in modified SSS between patients who died and
those who survived 32 hours after stroke, whereas MLS differed
significantly between both groups at this time point. This suggests
that MLS measurements might predict outcome earlier than clinical
findings. In the present study, SSS on admission again did not
correlate with outcome. These results are in accordance with findings
of other groups who could not find an association between clinical
scores on admission and fatal
outcome.13 15 16
On the contrary, Berrouschot et
al41 reported a good
correlation between an SSS <27 on admission and fatal outcome
(P<0.001) but with a moderate
sensitivity and specificity of SSS on admission for predicting cerebral
herniation of 0.73 and 0.74.
In the present study, assessment of SSS during follow-up was not possible in 16 patients because of sedation and artificial ventilation, resulting in a selection bias. Thus, we did not compare the time course of MLS and SSS. This reflects a common problem in the clinical assessment of critically ill stroke patients. Clinical scores are of limited help in predicting outcome in patients with severe MCA stroke who require ventilator therapy.
Cerebrovascular Status
Several studies have demonstrated the significance of
the cerebrovascular status as an early predictor of functional outcome.
Patency of the MCA was identified as an independent predictor of early
improvement,42 43
whereas diminished blood flow velocity or occlusion of the MCA
predicted early
deterioration.42 An
association between normalization of MCA blood flow and a better
functional outcome has been reported in several
studies.44 45 46
In the present study, the vascular status on admission failed to
predict fatal outcome. This discrepancy may be due to differences in
the chosen outcome measures. Functional outcome scores (CNS, NIHSS,
ESS, and modified Rankin scale) were used in the above-mentioned
studies, whereas we differentiated between death and survival within
the first 2 weeks because of the considerable number of severely
impaired patients on ventilator therapy who were not clinically
assessable.
In contrast to others15 47 who found a good correlation between vascular status on admission and recanalization (P<0.001 and P<0.01) and who reported a high sensitivity, specificity, PPV, and negative predictive value (NPV) (0.53, 0.83, 0.47, and 0.85) for the diagnosis of a carotid T occlusion in predicting fatal outcome, we only found a vague correlation for early (<24 hours) or late (>24 hours) recanalization of the occluded MCA (P=0.06) and no correlation for vascular findings on admission (P>0.1).
CCT Findings
Several studies indicate a good correlation between
early CCT signs of cerebral ischemia and
outcome.48 PPVs for
indicating fatal outcome range from 0.36 to
1.00.13 47 49 50
We did not assess early CCT signs because initial images were performed
at varying time points (0.75 and 17.5 hours) after stroke
onset.
On follow-up CCT, we found an association between an infarct size of >50% of the MCA territory and death (P<0.05). Although we analyzed CCT that was performed late (median, 40 hours after stroke onset), sensitivity, specificity, and predictive values for this parameter remain low. Repeated CCT scans at short intervals within the first 48 hours after stroke onset would reveal more prognostic information, but CCT monitoring is difficult to perform in critically patients.
A number of parameters that can be assessed at
bedside or on the initial CCT within the first few hours after
admission have been shown to be associated with fatal outcome in
hemispheric stroke. However, PPVs for determining fatal outcome,
crucial to assess the indication for surgical intervention, are
moderate. MLS was only found to correlate well with fatal outcome when
measurements were not performed too early and time of onset was taken
into account. In this study, MLS was measured after strictly defined
time intervals
(Table 2
). Thus, specificity and PPV of MLS was excellent in
predicting fatal outcome.
Nevertheless, evaluation of early CCT signs, cerebrovascular status, and monitoring of intracranial pressure and clinical findings (if assessable) are still generally used for deciding on a decompressive hemicraniectomy.18 29 51 52 53 Our findings suggest that TCCS monitoring of MLS, because of its noninvasive character and suitability for bedside application, is a diagnostic alternative in critically ill patients, who are not able to cooperate, not fit for repeated transportation, and cannot otherwise be monitored adequately. TCCS helps to estimate outcome as early as 16 hours after stroke onset and thus facilitates identification of patients who are unlikely to survive without decompressive craniectomy.
| Acknowledgments |
|---|
Received August 28, 2000; revision received September 27, 2000; accepted September 27, 2000.
| References |
|---|
|
|
|---|
2. Martin PJ, Evans DH, Naylor AR. Transcranial color-coded sonography of the basal cerebral circulation: reference data from 115 volunteers. Stroke. 1994;25:390396.[Abstract]
3.
Seidel G, Kaps M,
Gerriets T. Potential and limitations of transcranial
color-coded sonography in stroke patients.
Stroke. 1995;26:20612066.
4.
Stolz E, Kaps M,
Dorndorf W. Assessment of intracranial venous
hemodynamics in normal individuals and patients with
cerebral venous thrombosis.
Stroke. 1999;30:7075.
5. Seidel G, Gerriets T, Kaps M, Missler U. Dislocation of the third ventricle due to space occupying stroke evaluated by transcranial duplex sonography. J Neuroimaging. 1996;6:227230.[Medline] [Order article via Infotrieve]
6.
Maurer M, Shambal
S, Berg D, Woydt M, Hofmann W, Georgiadis D, Lindner A, Becker G.
Differentiation between intracerebral
hemorrhage and ischemic stroke by
transcranial color-coded duplex-sonography.
Stroke. 1998;29:25632567.
7.
Gerriets T, Stolz
E, Modrau B, Fiss I, Seidel G, Kaps M. Sonographic monitoring of
midline shift in hemispheric infarctions.
Neurology. 1999;52:4549.
8.
Stolz E, Gerriets
T, Fiss I, Babacan S, Seidel G, Kaps M. Comparison of
transcranial color-coded duplex sonography and cranial CT
measurements for determining third ventricle midline shift in
space-occupying stroke. Am J
Neuroradiol. 1999;20:15671571.
9.
Inoue Y, Takemoto
K, Miyamoto T, Yoshikawa N, Taniguchi S, Saiwai S, Nishimura Y, Komatsu
T. Sequential computed tomography scans in acute cerebral infarction.
Radiology. 1980;135:655662.
10.
Horowitz SH, Zito
JL, Donnarumma R, Patel M, Alvir J. Computed
tomographic-angiographic findings within the first five hours of
cerebral infarction. Stroke. 1991;22:12451253.
11. Ropper AH. Lateral displacement of the brain and level of consciousness in patients with an acute hemispherical mass. N Engl J Med. 1986;314:953958.[Abstract]
12.
Pullicino PM,
Alexandrov AV, Shelton JA, Alexandrova NA, Smurawska LT, Nowwis JW.
Mass effect and death from severe acute stroke.
Neurology. 1997;49:10901095.
13.
Haring HP, Dilitz
E, Pallua A, Hessenberger G, Kampfl A, Pfausler B, Schmutzhard E.
Attenuated corticomedullary contrast: an early
cerebral computed tomography sign indicating malignant middle cerebral
artery infarction: a case-control study.
Stroke. 1999;30:10761082.
14.
Ropper AH. A
preliminary MRI study of the geometry of brain displacement and level
of consciousness with acute intracranial masses.
Neurology. 1989;39:622627.
15.
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;53:309315.
16. Berrouschot J, Sterker M, Bettin S, Köster J, Schneider D. Mortality of space-occupying ("malignant") middle cerebral artery infarction under conservative intensive care. Intensive Care Med. 1998;24:620623.[Medline] [Order article via Infotrieve]
17. Konzdiola D, Fazl M. Functional recovery after decompressive craniectomy for cerebral infarction. Neurosurgery. 1988;23:143147.[Medline] [Order article via Infotrieve]
18. 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;23:15761587.[Medline] [Order article via Infotrieve]
19.
Schwab S, Steiner
T, Aschoff A, Schwarz S, Steiner HH, Jansen O, Hacke W. Early
hemicraniectomy in patients with complete middle cerebral artery
infarction. Stroke. 1998;29:18881893.
20.
Scandinavian
Stroke Study Group. Multicenter trial of hemodilution in
ischemic stroke: background and study protocol.
Stroke. 1995;16:885890.
21.
Silver FL, Norris
JW, Lewis AJ, Hachinski VC. Early mortality following stroke: a
prospective review. Stroke. 1984;15:492496.
22. Frank JI. Large hemispheric infarction, deterioration, and intracranial pressure. Neurology. 1995;45:12861290.[Abstract]
23. Shaw CM, Alvord EC, Berry RG. Swelling of the brain following ischemic infarction with arterial occlusion. Arch Neurol. 1959;1:161177.
24. Bounds JV, Wiebers DO, Whisnant JP, Okazaki H. Mechanisms and timing of deaths from cerebral infarction. Stroke. 1981;4:474477.
25.
Bamford J, Dennis
M, Sandercock P, Burn J, Warlow C. The frequency, causes and timing of
death within 30 days of a first stroke: the Oxfordshire community
stroke project. J Neurol
Neurosurg Psychiatry. 1990;53:824829.
26.
Engelhorn T,
Doerfler A, Kastrup A, Beaulieu C, de Crespigny A, Forsting M, Moseley
E, Faraci FM. Decompressive craniectomy, reperfusion, or a combination
of early treatment of acute "malignant" cerebral hemisphere strokes
in rats? Potential mechanisms studied by MRI. Stroke. 1999;30:14561463.
27. Doerfler A, Forsting M, Reith W, Staff C, Heiland S, Schaebitz WR, von Kummer R, Hacke W, Sartor K. Decompressive craniectomy in a rat model of "malignant" cerebral hemispheric stroke: experimental support for an aggressive approach. J Neurosurg. 1996;85:853859.[Medline] [Order article via Infotrieve]
28.
Forsting M, Reith
W, Schaebitz WR, Heiland S, von Kummer R, Hacke W, Sartor K.
Decompressive craniectomy for cerebral infarction: an experimental
study in rats. Stroke. 1995;26:259264.
29. Schwab S, Rieke K, Aschoff A, Albert F, von Kummer R, Hacke W. Hemicraniectomy in space-occupying hemispheric infarction: useful intervention or desperate activism? Cerebrovasc Dis.. 1996;6:325329.
30. Carter BS, Ogilvy CS, Candia GJ, Rosas HD, Buonanno F. One-year outcome after decompressive surgery for massive nondominant hemispheric infarction. Neurosurgery. 1997;40:11681176.[Medline] [Order article via Infotrieve]
31. Schwab S, Steiner T, Aschoff A, Schwarz S, Steiner HH, Jansen O, Hacke W. Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke. 1998;29:18881893.
32. Oro J, Amiridze N, Boyer R. Decompressive craniectomy in medically uncontrollable malignant infarctions. Mol Med. 2000;97:1720.
33. Becker G, Bogdahn U, Straßburg HM, Lindner A, Hassel W, Meixensberger J, Hofmann E. Identification of ventricular enlargement and estimation of intracranial pressure by transcranial color-coded real-time sonography. J Neuroimaging. 1994;4:1722.[Medline] [Order article via Infotrieve]
34. Seidel G, Kaps M, Gerriets T, Hutzelmann A. Evaluation of the ventricular system by transcranial duplex sonography in adults. J Neuroimaging. 1995;5:105108.[Medline] [Order article via Infotrieve]
35. Woydt M, Greiner K, Perez J, Becker G, Krone A, Roosen K. Transcranial duplex-sonography in intracranial hemorrhage: evaluation of transcranial duplex-sonography in the diagnosis of spontaneous and traumatic intracranial hemorrhage. Zentralbl Neurochir. 1996;57:129135.[Medline] [Order article via Infotrieve]
36.
Kenton AR, Martin
PJ, Abbott RJ, Moody AR. Comparison of transcranial
color-coded sonography and magnetic resonance angiography in acute
stroke. Stroke. 1997;28:16011606.
37.
Gerriets T,
Seidel G, Fiss I, Modrau B, Kaps M, Contrast-enhanced.
transcranial color-coded duplex sonography: efficiency and
validity. Neurology. 1999;52:11331137.
38. Reich JB, Sierra J, Camp W, Zanzonico P, Deck MDF, Plum F. Magnetic resonance imaging measurements and clinical changes accompanying transtentorial and foramen magnum brain herniation. Ann Neurol. 1993;33:159170.[Medline] [Order article via Infotrieve]
39. Plum F, Deck MD, Reich JB. Magnetic resonance imaging measurements and clinical changes accompanying transtentorial and foramen magnum brain herniation. Ann Neurol. 1993;34:749. Letter.[Medline] [Order article via Infotrieve]
40. Wijdicks EFM, Diringer MN. Middle cerebral artery territory infarction and early brain swelling: progression and effect of age on outcome. Mayo Clin Proc. 1998;73:829836.[Abstract]
41.
Berrouschot J,
Barthel H, von Kummer R, Knapp WH, Hesse S, Schneider D.
99mTechnetium-ethyl-cysteinate-dimer
single-photon emission CT can predict fatal ischemic brain
edema. Stroke. 1998;29:25562562.
42.
Toni D, Fiorelli
M, Zanette EM, Sacchetti ML, Salerno A, Argentino C, Solaro M, Fieschi
C. Early spontaneous improvement and deterioration of ischemic
stroke patients: a serial study with transcranial
Doppler ultrasonography.
Stroke. 1998;29:11441148.
43.
Goertler M, Kross
R, Baeumer M, Jost S, Grote R, Weber S, Wallesch CW.
Diagnostic impact and prognostic relevance of early
contrast-enhanced transcranial color-coded duplex
sonography in acute stroke.
Stroke. 1998;29:955962.
44. Steiger HJ. Outcome of acute supratentorial cerebral infarction in patients under 60: development of a prognostic grading system. Acta Neurochir. 1991;111:7379.[Medline] [Order article via Infotrieve]
45.
Von Kummer R,
Holle R, Rosin L, Forsting M, Hacke W. Does arterial
recanalization improve outcome in carotid territory
stroke? Stroke. 1995;26:581587.
46.
Postert T, Braun
B, Meves S, Koster O, Przuntek H, Weber S, Buttner T. Contrast-enhanced
transcranial color-coded sonography in acute hemispheric
brain infarction. Stroke. 1999;30:18191826.
47. Kucinski T, Koch C, Grzyska U, Freitag HJ, Krömer H, Zeumer H. The predictive value of early CT and angiography for fatal hemispheric swelling in acute stroke. AJNR Am J Neuroradiol.. 1998;19:839846.[Abstract]
48.
Moulin T, Cattin
F, Crépin-Leblond T, Tatu L, Chavot D, Piotin M, Viel JF, Rumbach L,
Bonneville JF. Early CT signs in acute middle cerebral artery
infarction: predictive value for subsequent infarct locations and
outcome. Neurology. 1996;47:366375.
49.
Krieger DW,
Demchuk AM, Kasner SE, Jauss M, Hantson L. Early clinical and
radiological predictors of fatal brain swelling in ischemic
stroke. Stroke. 1999;30:287292.
50. von Kummer R, Meyding-Lamadé U, Forsting M, Rosin L, Rieke K, Sator K. Sensitivity and prognostic value of early CT in occlusion of the middle cerebral artery trunk. AJNR Am J Neuroradiol. 1994;15:915.[Abstract]
51.
Schwab S, Aschoff
A, Spranger M, Albert F, Hacke W. The value of intracranial pressure
monitoring in acute stroke.
Neurology. 1996;47:393398.
52. Schwab S, Rieke K, Krieger D, Hund E, Aschoff A, von Kummer R, Hacke W. Craniectomy in space-occupying middle cerebral artery infarcts. Nervenarzt. 1995;66:430437.[Medline] [Order article via Infotrieve]
53.
Delashaw JB,
Broaddus WC, Kassell NF, Haley EC, Pendleton GA, Vollmer DG, Maggio WW,
Grady MS. Treatment of right hemispheric cerebral infarction by
hemicraniectomy. Stroke. 1990;21:874881.
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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] |
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