BRAIN CT SCAN IN ACUTE ISCHEMIC STROKE: EARLY SIGNS AND FUNCTIONAL OUTCOME

BRAIN CT SCAN IN ACUTE ISCHEMIC STROKE:

EARLY SIGNS AND FUNCTIONAL OUTCOME

Nicola Tambasco,1,* Francesco Corea,1 Roberto Luccioli,2

Ettore Ciorba,2 Lucilla Parnetti,1 and Virgilio Gallai1

1Dipartimento di Neuroscienze, Universita di Perugia,

Perugia, Italy2Servizio di Neuroradiologia, Azienda Ospedaliera di Perugia,

Perugia, Italy

ABSTRACT

There is evidence that an improvement of the diagnostic abilities could have a

value for prognosis and therapy of the ischemic stroke. New neuroradiological

strategies could be used with an amelioration of the evaluation and

standardization of the ischemic damage. The value of early vascular sign

remains controversial as a predictor of patient outcome. Early parenchymal

changes are related to a poor outcome. The risk of hemorrhagic transformation

increases with trombolytic therapy and especially with the onset of therapy.

Between hemorrhagic transformation, only the large hematomas seems to be

related to early deterioration and death. Brain Computed Tomography (CT)

examination can give information about prognosis and therapeutic choice.

Key Words: Computed tomography; CT scan; Stroke; Acute stroke; Ischemic

stroke; Early signs

INTRODUCTION

Stroke is the first cause of disability and the second cause of death in adults in

the Western industrialized countries. There is evidence that an improvement of the

*Corresponding author. Fax: þ39 075 5783870; E-mail: [email protected]

687

DOI: 10.1081=CEH-120015345 1064-1963 (Print); 1525-6006 (Online)

Copyright # 2002 by Marcel Dekker, Inc. www.dekker.com

CLINICAL AND EXPERIMENTAL HYPERTENSION

Vol. 24, Nos. 7 & 8, pp. 687–696, 2002

©2002 Marcel Dekker, Inc. All rights reserved. This material may not be used or reproduced in any form without the express written permission of Marcel Dekker, Inc.

MARCEL DEKKER, INC. • 270 MADISON AVENUE • NEW YORK, NY 10016

Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

diagnostic abilities could have a value for prognosis and therapy. In this context,

neuroradiology has meaningfully improved stroke observation and evaluation

giving the possibility to standardize the studies on pharmacotherapy of the ischemic

stroke. For its relative facility of execution, availability and the cost effectiveness,

CT is the first step in the early diagnosis of acute stroke. In fact, since 1980 the CT

scan has provided an accurate assessment to: exclude a non-vascular lesion as the

cause of a manifestation and to determine whether the stroke is an ischemic

infarction or an intracranial hemorrhage.[1] The first important evidence in favour of

performing a CT scan in all stroke patients is to improve the quality of secondary

prevention prescribing antiplatelet treatment to all patients with infarction verified

by scan.[2]

Then, different studies have pointed out the availability of new strategies in

the treatment of acute stroke in evaluating the infarction, age, extension of the

lesion and eventually have documented on its underlying mechanism.

NEURORADIOLOGICAL STROKE EVALUATION

The characteristic aspect of a cerebral ischemia is represented by the

identification of a zone of the cerebral parenchyma with reduction of the

attenuation to the x-ray passage. The infarction involves a whole or a part of a

vascular territory. The aspect and the extension are related to the time of

observation. Virtually the ischemic infarcts are at most visible and have the

greatest definition from the 4th day to the 10th day from onset. After three months

variations of the neuroradiological definition in comparison to those made at 7–10

days are not observed.[3] Thus, serial neuroimaging studies do not alter the

classification of stroke for which an initial diagnosis has already been made.[4] On

the other hand, a percentage of stroke cases are not visible at CT examination and

not even at magnetic resonance imaging scan.[5]

If the timing to observe an ischemic lesion is standardized, different factors

can influence the early CT-detection of stroke: some depend on the adopted

instruments and technics, others on the reliability between the observers, and

increasingly on the time between onset and observation of the stroke and on the

severity of the symptoms. Wardlaw stresses the importance that a simplification

and a clarification of the early signs and a clearer description of the infarct extent

are all factors that may improve recognition of early infarction.[6] The importance

of early neuroradiological confirmation of stroke is clearly evidencied in a

consecutive series of 993 stroke patients, in which visible infarction at CT scan,

seen within the first 24 hours or later, is a negative prognostic factor, where primary

outcome measures were dependency or death at six months.[7] Addictionally, it was

suggested that an independent predictor of early improvement of the clinical

condition consisted in the absence of early hypodensity at the first scan made

within 6 hours from onset.[8] Probably brain CT visibility of an ischemic stroke is

associated with poor outcome, in patients with the same clinical conditions.

688 TAMBASCO ET AL.



Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

Different Early Signs at Computed Tomography Examination

Usually in the first 24 hours from stroke onset CT does not enable the

evidence of the lesion, but it is possible to identify different early signs, subtle and

difficult to evidence, which are important to individualize location and extention of

infarction. In fact, the early CT signs may allow the prediction of further infarct

location.[9]

Vascular Hyperdensity

In a series of 19 acute ischemic patients, Pressman et al. highlighted an

increased density of the middle cerebral artery (MCA).[10] A hyperdense

intracranial artery can be considered as an early sign of arterial occlusion[11]

rather than an early CT sign of ischemic infarction; the comparison between MCA

arteries may allow the evidence of hyperdensity determined by thrombus or

embolus.[12] With density measurements it is possible to distinguish the density

profile for normal vessels, atheromatous palques and affected vessel segments in

the clinical context of acute stroke[13] (Fig. 1).

Figure 1. Brain CT showing an early hyperdensity of the M1 tract of the right MCA in a 56 year-

old man, 2 hours after onset of the right hemiparesis.

BRAIN CT SCAN IN ACUTE ISCHEMIC STROKE 689



Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

Several authors have suggested that the early MCA sign is a negative

prognostic factor,[3,14–16] but on the contrary Leys has written that in his series the

evidence of a MCA occlusion does not always predict a poor outcome.[17] The

value of isolated MCA hyperdensity as a predictor of outcome remains

controversial. This sign assumes probably importance for clinical outcome when

it is associated with other early signs.[9]

Parenchymal Hypodensity

Early CT parenchymatous signs can be detected as a low density, of several

degrees, without a clear-cut between the white and grey matter (Fig. 2).

This corresponds to an early increase in the water component in brain cells,

which is already present 1 hour after arterial occlusion. The early decrease in

density is probably related to infarction in progress and could predict irreversibile

brain damage.[9] Haring, in 1999, evidencied that the attenuated corticomedullary

contrast, if present within 18 hours of stroke onset, is strongly indicative of a

malignant MCA infarction development with both high specificity (96.8%) and

sensitivity (87.1%).[18] The deep MCA territory is rather sensitive to ischemia,

because lenticulostriate arteries supply end zone territories and account for the

Figure 2. Brain CT showing an early attenuation of the right hemisphere with brain swelling in a

67 year-old woman, 3 hours after onset of the left hemiparesis.

690 TAMBASCO ET AL.



Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

obscuration of the lentiform nucleus.[9] The hypodensity involving the insular

ribbon is another early sign that refers to a loss of the normal white–grey matter

distinction in the lateral margins of the insula.[19] The identification of this early

sign requires a good CT section and proper positioning of the patient.[9]

Edema and Mass Effect

In ischemic infarcts, the edema seen in the early stage involves both grey and

white matter and is present only in the area affected by ischemia.[20]

Experimentally, it has been shown that after the onset of ischemia a hydrostatic

pressure gradient across the capillary develops immediately and it is the driving

force for early edema fluid formation.[21] Brain edema may play a role in both early

and long progressing stroke, which is in keeping with the notion that brain edema

reaches its maximum expression within the initial five days after stroke onset.

Neuroradiological observation of mass effect in association with early hypodensity

are strongly associated with the progression of neurological deficits.[22,23]

Mechanism Size and Localization

Different factors influence the clinical presentation and the entity of the

lesion, but not always a lesion of greater entity correspond to a more serious

clinical picture. There is neuroradiological evidence that embolic infarction is

more than twice as large as one thought to be thrombotic.[3] Recently, it has been

found that there is a different evolution of infarcts if the evaluation is based on the

size of MCA territory infarction. In the ECASS study, the involvement of more

than 33% of the MCA territory and brain swelling was considered a factor

associated with early progression of stroke.[24] But it is difficult to identify the

precise entity of the infarct. It was suggested that neuroradiologists may fail to

understand what constitutes an infarct in a third of the MCA territory in fact the

boundaries of the MCA territory vary from patient to patient and it is hard to see

where a defined hypodensity swelling or loss of grey–white matter differentiation

stops.[6] On the other hand, neuroradiologists without clinical information can have

a good reliability to determine whether and to what extent the MCA territory has

became hypodense or swollen in the majority of stroke patients in the first 6

hours.[25] A simple and objective tool to evaluate early signs is based on

ASPECTS criteria which define the MCA territory in 10 areas of parenchyma

(seven cortical and three subcortical). This method presents higher sensitivity for

functional outcome than the >33 % MCA with a good reliability between

observers.[26]

Information about the location of the lesion may be more important for some

patients than infarction volume in determining the eventual clinical handicap.[3] In

fact, it is not enough to identify a part of MCA territory infarction but also to

evaluate the level of MCA occlusion in determining the prognosis of the patients.




Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

The favorable effect of good leptomeningeal circulation in conjunction with rapid

recanalization of an emobolically occluded MCA produce limited infarction and

benign outcome.[27] Different topographic patterns in MCA territory infarction are

related to individual vascular variability in supply zones, degree of primary and

secondary collateralization, and pathogenesis of infarcts.[28] Lenticular arteries

have an important role, because these are end arteries with no possibility of

anastomotic collateral blood supply.[29] A different evaluation was made by Chen,

who founded that motor and functional outcomes correlate with a combination of

delimiting sizes and primary locations of the stroke more than with absolute or

relative lesion sizes only.[30]

Clinical Presentation

A different presentation and severity of clinical conditions could have a

difference in the CT brain scan evidence. In a retrospective study it was observed

that the presence of early ischemic signs correlated more closely with the severity

of the patient’s neurologic dysfunction than the length of time from symptoms

onset in the acute setting.[31] The most widely accepted classification is

Oxfordshire Community Stroke Project (OCSP) by Bamford et al. based on

clinical presentation.[32] The OCSP classification predicts correctly the site and

size of infarct in about three quarters of patients. This may be useful in helping the

standardization of therapeutic protocol in acute phase when a hypothesis still needs

to be tested.[33] The accordance between OCSP classification and early signs of

acute stroke is not always available because this clinical classification is based on

the time of maximum deficit. Despite the progression of the symptomatology is

variable from time of onset, Tei suggests that the OCSP classification remains

reasonably important.[34] Visible infarction is more frequent in TACI.[7] In TACI

patients, the CT scan done early after stroke provide data about location of the

lesion in most patients. The percentage of visibility of TACI is about 68% within

48 hours compared to PACI (57%), LACI (22%), and POCI (38%).[35] This is

important as much as we consider that TACI patients arrive to the CT scan and

neurological examination earlier than other types of stroke.

Hemorrhagic Transformation

One of the most frequent evolutions of the ischemic lesion that impedes the

therapeutic approach is the hemorrhagic transformation (HT), a common and even

spontaneous event after ischemic infarction. The prognostic and therapeutic

implications of HT remain unclear. In fact, the clinical manifestation of HT is

various and ranges from asymptomatic to deterioration and death. The age, the

presence of early ischemic changes on CT scan,[36] large infarcts or midline

shift[37] and cardioembolism[38] are stronger risk factors for HT.

692 TAMBASCO ET AL.



Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

An increased risk is represented by the pharmacological treatment with

thrombolytic agents, especially in patients with severe hypertension. Data from

r-tPA studies evidenced that the risk of HT is three-fold increased than placebo

group with a simultaneous reduction of death and disability. The risk of

hemorrhage increases with the onset of therapy. Therapy started 3 hours following

stroke onset brings with it increased the hemorrhagic risk.[39] A retrospective study

has assessed the HT in four points: H1 (small petechiae), H2 (more confluent

petechiae), PH1 (<30% of the infarcted area with some mild space-occupying

effect) and PH2 (>30% of the infarcted area with significant space-occupying

effect, or clot remote from infarcted area). In this design, only the large hematomas

(PH2) significantly increased the risk of early deterioration and death.[40]

CONCLUSION

On the basis of previous considerations, the CT brain early signs assume day

by day greater therapeutic and prognostic implications for all the people who work

in this field as neurologists, neuroradiologists, general pratictioners, and primary

care operators. The search for a better approach to patients in terms of time,

understanding of the mechanisms that induce morphological alterations of the

brain, and an amelioration of the information can give new possibilities to the

management of stroke.

REFERENCES

1. Libman, R.B.; Wirkowski, E.; Alvir, J.; Rao, T.H. Condition That Mimic Stroke in

the Emergency Departments. Arch. Neurol. 1995, 52, 1119–1122.

2. Van der Meulen, J.H.P.; Limburg, M.; van Straten, A.; Habbema, J.D.F. Computed

Tomographic Brain Scans and Antiplatelet Therapy After Stroke. A Study of the

Quality of Care in Dutch Hospitals. Stroke 1996, 27, 633–638.

3. Brott, T.; Marler, J.; Olinger, C.P.; Adams, H.P.; Tomsick, T.; Barsan, W.J.; Biller, J.;

Eberle, R.; Hertzberg, V.; Walker, M. Measurements of Acute Cerebral Infarction:

Lesion Size by Computed Tomography. Stroke 1999, 20, 871–875.

4. Salerno, S.M.; Landry, F.J.; Schick, J.D.; Schoomaker, E.B. The Effect of Multiple

Neuroimaging Studies on Classification, Treatment and Outcome of Acute Ischemic

Stroke. Ann. Int. Med. 1996, 124 (1), 21–26.

5. Alberts, M.J.; Faulstich, M.E.; Gray, L. Stroke with Negative Brain Magnetic

Resonance Imaging. Stroke 1992, 23, 663–667.

6. Wardlaw, J.M.; Dorman, P.J.; Lewis, S.C.; Sandercock, P.A.G. Can Stroke Physicians

and Neuroradiologists Identify Signs of Early Cerebral Infarction on CT? J. Neurol.

Neurosurg. Psychiatry 1999, 67, 651–653.

7. Wardlaw, J.M.; Lewis, S.C.; Dennis, M.S.; Counsell, C.; McDowall. Is Visible

Infarction on Computed Tomography Associated with an Adverse Prognosis in

Acute Ischemic Stroke. Stroke 1998, 29, 1315–1319.




Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

8. Toni, D.; Fiorelli, M.; Bastianello, S.; Falcou, A.; Ceschin, V.; Sacchetti, M.L.;

Argentino, C. Acute Ischemic Strokes Improving During the First 48 Hours of Onset:

Predictability, Outcome, and Possible Mechanisms. A Comparison with Early

Deteriorating Strokes. Stroke 1997, 22, 10–14.

9. Moulin, T.; Cattin, F.; Crepin-Leblond, T.; Tatu, L.; Chavot, D.; Piotin, M.; Viel, J.F.;

Rumbach, L.; Bonneville, J.F. Early CT Signs in Acute Middle Cerebral Artery

Infarction: Predictive Value for Subsequent Infarct Locations and Outcome.

Neurology 1996, 47, 366–375.

10. Pressman, B.D.; Tourje, E.J.; Thompson, J.R. An Early CT Sign Of Ischemic

Infarction: Increased Density in a Cerebral Artery. AJNR 1987, 8, 645–648.

11. Bastianello, S.; Pierallini, A.; Colonnese, C.; Brughitta, G.; Angeloni, U.; Antonelli,

M.; Fantozzi, L.M.; Fieschi, C.; Bozzao, L. Hyperdense Middle Cerebral Artery CT

Sign. Neuroradiology 1991, 33, 207–211.

12. Schuierer, G.; Huk, W. The Unilateral Hyperdense Middle Cerebral Artery:

An Early CT-Sign of Embolism or Thrombosis. Neuroradiology 1988, 30, 120–122.

13. Schuknecht, B.; Ratzka, M.; Hofmann, E. The ‘‘Dense Artery Sign’’—Major

Cerebral Artery Thrombo-Embolism Demonstrated by Computed Tomography.

Neuroradiology 1990, 32, 98–103.

14. Launes, J.; Ketonen, L. Dense Middle Cerebral Artery Sign: An Indicator of Poor

Outcome in Middle Cerebral Artery Area Infarction. J. Neurol. Neurosurg.

Psychiatry 1987, 50, 1550–1552.

15. Tomsick, T.A.; Brott, T.G.; Olinger, C.P.; Barsan, W.; Spilker, J.; Eberle, R.; Adams,

H. Hyperdense Middle Cerebral Artery: Incidence and Quantitative Significance.

Neuroradiology 1989, 31, 312–315.

16. Giroud, M.; Beuriat, P.; Becker, F.; Binnert, D.; Dumas, R. L’artere Cerebrale

Moyenne Dense: Signification etiologique et Prognostique. Rev. Neurol. 1990, 146

(3), 224–227.

17. Leys, D.; Pruvo, J.P.; Godefroy, O.; Rondepierre, Ph.; Leclerc, X. Prevalence and

Significance of Hyperdense Middle Cerebral Artery in Acute Stroke. Stroke 1992,

23, 317–324.

18. Haring, H.-P.; Dilitz, E.; Pallua, A.; Hessemberger, G.; Kampfl, A.; Pfausler, B.;

Schmutzhard, E. Attenuated Corticomedullary Contrast: An Early Cerebral

Computed Tomography Sign Indicating Malignant Middle Cerebral Artery

Infarction. Stroke 1999, 30, 1076–1082.

19. Truwit, C.L.; Barkovich, A.J.; Gean-Marton, A.; Hibri, N.; Norman, D. Loss of

Insular Ribbon: Another Early CT Sign of Acute Middle Cerebral Artery Infarction.

Radiology. 1990, 176, 801–806.

20. Savoiardo, M.; Grisoli, M. Stroke: Pathophysiology, Diagnosis and Treatment, 3rd

Ed.; Barnett, H.J.M. et al. Eds.; Churchill Livingstone, 1998; 195–226.

21. Hatashita, S.; Hoff, J.T. Biomechanics of Brain Edema in Acute Cerebral Ischemica

in Cats. Stroke 1988, 19, 91–97.

22. Davalos, A.; Cendra, E.; Teruel, J.; Martinez, M.; Genıs, D. Deteriorating Ischemic

Stroke: Risk Factors and Prognosis. Neurology 1990, 40, 1865–1869.

23. Toni, D.; Fiorelli, M.; Gentile, M.; Bastianello, S.; Sacchetti, M.L.; Argentino, C.;

Pozzilli, C.; Fieschi, C. Progressing Neurological Deficit Secondary to Acute

Ischemic Stroke. A Study on Predictability, Pathogenesis and Prognosis. Arch.

Neurol. 1995, 52, 670–675.

694 TAMBASCO ET AL.



Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

24. Hacke, W.; Kaste, M.; Fieschi, C.; Toni, D.; Lesaffre, E.; von Kummer, R.;

Boysen, G.; Bluhmki, E.; Hoxter, G.; Mahagne, M.-H.; Hennerici, M. Intravenous

Thrombolysis with Recombinant Tissue Plasminogen Activator for Acute Hemi-

spheric Stroke. JAMA 1995, 274, 1017–1025.

25. Von Kummer, R.; Holle, R.; Grzyska, U.; Hofmann, E.; Jansen, O.; Petersen, D.;

Schumacher, M.; Sartor, K. Interobserver Agreement in Assessing Early CT Signs of

Middle Cerebral Artery Infarction. AJNR 1996, 17, 1743–1748.

26. Barber, P.A.; Demchuk, A.M.; Zhang, J.; Buchan, A.M. Validity and Reliability of a

Quantitative Computed Tomography Score in Predicting Outcome of Hyperacute

Stroke Before Thrombolytic Therapy. Lancet 2000, 355, 1670–1674.

27. Ringelstein, E.B.; Biniek, R.; Weiller, C.; Ammeling, B.; Nolte, P.N.; Thron, A. Type

and Extent of Hemispheric Brain Infarction and Clinical Outcome in Early and

Delayed Middle Cerebral Artery Recanalization. Neurology 1992, 42, 289–298.

28. Min, W.K.; Park, K.K.; Kim, Y.S.; Park, H.C.; Kim, J.Y.; Park, S.P.; Suh, C.K.

Atherotrombotic Middle Cerebral Artery Territori Infarction. Topographic Diversity

with Common Occurrence of Concomitant Small Cortical and Subcortical Infarcts.

Stroke 2000, 31, 2055–2061.

29. Bozzao, L.; Fantozzi, L.M.; Bastianello, S.; Bozzao, A.; Fieschi, C. Early Collateral

Blood Supply and Late Parenchymal Brain Damage in Patients with Middle Cerebral

Artery Occlusion. Stroke 1989, 20, 735–740.

30. Chen, C.-L.; Tang, F.K.; Chen, H.-C.; Chung, C.-Y.; Wong, M.K. Brain Lesion Size

and Location: Effects on Motor Recovery and Functional Outcome in Stroke

Patients. Arch. Phys. Med. Rehab. 2000, 81, 447–452.

31. Scott, J.N.; Buchan, A.M.; Sevick, R.J. Correlation of Neurologic Disfunction with

CT Findings in Early Acute Stroke. Can. J. Neurol. Sci. 1999, 26, 182–189.

32. Adams, H.P. Jr.; Bendixen, B.H.; Kappelle, L.J.; et al. and the TOAST Investigators.

Classification of Subtype of Acute Ischemic Stroke: Definitions for Use in a

Multicenter Clinical Trial. Stroke 1993, 24, 35–41.

33. Mead, G.E.; Lewis, S.C.; Wardlaw, J.M.; Dennis, M.S.; Warlow, C.P. How Well Does

the Oxfordshire Community Stroke Project Classification Predict the Site and Size

of the Infarct on Brain Imaging? J. Neurol. Neurosurg. Psychiatry 2000, 68,

558–562.

34. Bamford, J.M. The Role of the Clinical Examination in the Subclassification of

Stroke. Cerebrovasc. Dis. 2000, 10 (4), 2–4.

35. Lindgren, A.; Norrving, B.; Rudling, O.; Johansson, B.B. Comparison of Clinical

and Neuroradiological Findings in First-Ever Stroke: A Population-Based Study.

Stroke 1994, 25, 1371–1377.

36. Larrue, V.; von Kummer, R.; del Zoppo, G.; Bluhmki, E. Hemorrhagic

Transformation in Acute Ischemic Stroke. Potential Contributing Factors in the

European Cooperative Acute Stroke Study. Stroke 1997, 28, 957–960.

37. Okada, Y.; Yamaguchi, T.; Minematsu, K.; Miyashita, T.; Sawada, T.; Sadoshima, S.;

Fujishima, M.; Omae, T. Hemorrhagic Transformation in Cerebral Embolism. Stroke

1989, 20, 598–603.

38. Alexandrov, A.V.; Black, S.E.; Ehrlich, L.E.; Caldwell, C.B.; Norris, J.W. Predictors

of Hemorrhagic Transformation Occuring Spontaneously and on Anticoagulant in

Patients with Acute Ischemic Stroke. Stroke 1997, 28, 1198–1202.




Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

39. Hacke, W.; Brott, T.; Caplan, L.; Meier, D.; Fieschi, C.; von Kummer, R.;

Donnan, G.; Heiss, W.-D.; Wahlgren, N.G.; Spranger, M.; Boysen, G.; Marler, J.R.

Thrombolysis in Acute Ischemic Stroke: Controlled Trials and Clinical Experience.

Neurology 1999, 53 (4), S3–S14.

40. Fiorelli, M.; Bastianello, S.; von Kummer, R.; del Zoppo, G.J.; Larrue, V.;

Lesaffre, E.; Ringleb, A.P.; Lorenzano, S.; Manelfe, C.; Bozzao, L. Hemorrhagic

Transformation Within 36 Hours of a Cerebral Infarct. Relationships with Early

Clinical Deterioration and 3-Month Outcome in the European Cooperative Acute

Stroke Study I (ECASS I) Cohort. Stroke 1999, 30, 2280–2284.

696 TAMBASCO ET AL.



Clin

Exp

Hyp

erte

ns D

ownl

oade

d fr

om in

form

ahea

lthca

re.c

om b

y U

nive

rsita

ets-

und

Lan

desb

iblio

thek

Due

ssel

dorf

on

03/1

7/13

For

pers

onal

use

onl

y.

Documents

BRAIN CT SCAN IN ACUTE ISCHEMIC STROKE: EARLY SIGNS AND FUNCTIONAL OUTCOME