This Article Abstract Full Text (PDF) All Versions of this Article: 38/5/1482    most recent STROKEAHA.106.477380v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Redgrave, J. N.E. Articles by Rothwell, P. M. Search for Related Content PubMed PubMed Citation Articles by Redgrave, J. N.E. Articles by Rothwell, P. M. Pubmed/NCBI databases Medline Plus Health Information Stroke Transient Ischemic Attack Related Collections CT and MRI Computerized tomography and Magnetic Resonance Imaging Risk Factors for Stroke

(Stroke. 2007;38:1482.)
© 2007 American Heart Association, Inc.

Original Contributions

Systematic Review of Associations Between the Presence of Acute Ischemic Lesions on Diffusion-Weighted Imaging and Clinical Predictors of Early Stroke Risk After Transient Ischemic Attack

Jessica N.E. Redgrave, MRCP; Shelagh B. Coutts, MD; Ursula G. Schulz, DPhil; Dennis Briley, MD Peter M. Rothwell, PhD

From the Stroke Prevention Research Unit (J.N.R, U.G.S., P.M.R.), Department of Clinical Neurology, Radcliffe Infirmary, Oxford, UK; the Department of Clinical Neurosciences (S.B.C.), University of Calgary, Alberta, Canada; and the Department of Neurology (D.B.), Stoke Mandeville Hospital, Aylesbury, UK.

Correspondence to Prof Peter M. Rothwell, Stroke Prevention Research Unit, Department of Clinical Neurology, Radcliffe Infirmary, Woodstock Rd, Oxford, OX2 6HE. E-mail peter.rothwell{at}clneuro.ox.ac.uk

	Abstract

Top Abstract Introduction Method Results Discussion References

 
Background and Purpose— Early risk of stroke after a transient ischemic attack can be reliably predicted with risk scores based on clinical features of the patient and of the ischemic event, but it is unclear how these features correlate with findings on brain imaging.

Methods— We performed a systematic review of the literature and identified all previous studies which reported patient characteristics and the nature of transient ischemic attack symptoms in relation to appearances on diffusion-weighted imaging (DWI). We then performed a meta-analysis of the associations between the components of the risk scores and positive DWI. Authors were contacted for additional unpublished data.

Results— Nineteen studies were identified by the systematic review, and additional unpublished data were obtained from 11 of these studies. On meta-analysis, several components of the risk scores were associated with positive DWI, including symptom duration 60 minutes (13 studies, odds ratio [OR], 1.50; 95% CI, 1.16 to 1.96; P=0.004), dysphasia (9 studies, OR, 2.25; 95% CI, 1.57 to 3.22; P<0.001), dysarthria (8 studies, OR, 1.73; 95% CI, 1.11 to 2.68; P=0.03) and motor weakness (9 studies, OR, 2.20; 95% CI, 1.56 to 3.10; P<0.001). However patient age, sex, hypertension and diabetes were not associated with the presence of DWI lesions. From an etiologic perspective, atrial fibrillation (9 studies, OR, 2.75; 95% CI, 1.78 to 4.25; P<0.001) and ipsilateral 50% carotid stenosis (10 studies, OR, 1.93; 95% CI, 1.34 to 2.76; P=0.001) were associated with positive DWI.

Conclusions— Presence of acute ischemic lesions on DWI correlates with several clinical features known to predict stroke risk after transient ischemic attack. Large studies (sample size >1000) will therefore be required to determine the independent prognostic value of DWI and its interactions with these clinical characteristics.

Key Words: diffusion-weighted imaging • prognosis • transient ischemic attack

	Introduction

Top Abstract Introduction Method Results Discussion References

 
The risk of stroke after a transient ischemic attack (TIA) is up to 10% in the first 7 days.^1–4 Risk scores (eg, ABCD and California score) have been developed to help identify patients at highest early risk of stroke after a TIA.^4,5 These scores incorporate age, blood pressure, diabetes, and the nature of ischemic symptoms and are intended for initial triage in primary care and for public education about the characteristics of high-risk events. However, additional potentially prognostic information is available once patients have presented to medical attention and been investigated, such as data on carotid stenosis and acute ischemia on brain imaging. Prognostic scores for use in secondary care clearly need to incorporate such information.

Diffusion-weighted MR-brain–imaging (DWI) is highly sensitive to ischemic changes, and a substantial proportion of TIA patients have acute ischemic lesions on DWI.^6,7 Recent studies have suggested that TIA patients with positive DWI are at high early risk of stroke.^8,9 In order to plan appropriately powered studies to develop prognostic scores that would incorporate the results of brain imaging, we need to understand how the presence of DWI lesions in patients with TIA relates to the clinical features in the existing risk scores and to other prognostic variables, such as atrial fibrillation and carotid stenosis.^10,11 We therefore performed a systematic review of studies which reported clinical features in relation to DWI appearances after a TIA and performed a meta-analysis of the associations between the components of the risk scores and likely etiology, and positive DWI.

	Method

Top Abstract Introduction Method Results Discussion References

 
We searched Medline using index terms (‘TIA’ OR ‘transient ischemic’ OR ‘transient ischaemic’; AND ‘DWI’ OR ‘diffusion weighted’ OR ‘apparent diffusion’ OR ‘ADC’) limited to studies in humans (last search on October 31, 2006). Studies were included if baseline patient characteristics or the nature of TIA symptoms were reported separately for patients with positive versus negative DWI or if these data might have been available from the authors. We also hand-searched the bibliographies of the retrieved articles and the contents pages (1999 to present) of the 2 most frequent journals identified by the electronic search.

For each study, we recorded inclusion and exclusion criteria, the definitions of TIA and a positive DWI scan, whether a neurologist had assessed the patients, whether all DWI lesions were symptomatic, details of the scan protocol, and the mean time interval between TIA and DWI. The proportion of patients with positive DWI and the prevalence of positive DWI in relation to components of the risk scores (age, blood pressure, diabetes, nature and duration of ischemic symptoms) and likely TIA etiology (atrial fibrillation, 50% ipsilateral carotid stenosis) were recorded. We contacted authors to request unpublished data if these data were not available in the published article. We also included unpublished data from our own study of patients attending a specialist clinic, which currently includes 200 patients with TIA.^12,13

Analysis
Odds ratios were calculated for positive versus negative DWI for each clinical feature under investigation, and estimates from individual studies were combined using the Mantel–Haenszel method. If there were no patients in one of the subgroups, 0.5 was added to all 4 cells in the 2x2 table to enable graphic representation and CI estimation.¹⁴ Heterogeneity between estimates from individual studies was determined (² test). Results were stratified according to the delay between TIA and DWI (<24 hours versus >24 hours). SPSS (version 12.0) and in-house meta-analysis software were used for analysis.

	Results

Top Abstract Introduction Method Results Discussion References

 
Sixty-five potentially relevant articles were identified, of which 19 met our inclusion criteria,^{6–9,12,15–28} including two Japanese studies which were translated into English. The most frequent journals of publication were Stroke (n=5) and American Journal of Neuroradiology (n=3). The studies were published between 1999 and 2006 and are summarized in the Table. Twelve studies stated that the patients were recruited consecutively,^{6,12,15,17,19–25,27} usually from stroke units, acute hospital admissions, or neurology out-patients. All studies used the TIA definition of "ischemic symptoms lasting <24 hours." Two studies excluded posterior circulation events,^16,29 and one study excluded anterior circulation events.²⁰ Four studies excluded patients if the delay to scan was above a certain threshold (6 hours,¹⁵ 24 hours,¹⁶ 3 days,⁷ and 14 days¹⁸). In 13 studies, a vascular neurologist made the diagnosis of TIA, but the speciality of the attending physician was not stated in the remaining 6 studies.^{16,17,19,20,23,25}

View this table: [in this window] [in a new window]   Summary of Studies in Systematic Review

A magnet strength of 1.5 T was used in all but two studies (1.0 T²³ and 3.0 T⁸). Slice thickness was 4 to 7 mm in 11 studies,^{6,7,9,12,15–17,19,21,25,27} 3 mm in one study²⁰ and not stated in the remaining studies. Interslice gap was zero in 3 studies,^6,15,27 1 to 2 mm in 6 studies^{9,16,17,19,21,25} and >2 mm in one study.⁷ A positive scan was usually defined as increased signal on DWI, but 10 studies stated that lesions must also have reduced apparent diffusion coefficient.^{6–8,16,18,19,24–27}

The median number of patients per study was 61 (range 14 to 129) and the median mean delay to scan was 37 hours (Table; <24 hours in 6 studies,^{6–8,16,20,25} >24 hours in 9 studies^{9,12,17–19,21–23,27} and not stated in 4 studies^15,24,26,28). The proportion of patients with positive DWI ranged from 16% to 67% across the 19 studies (Table). Seven studies stated that all patients with positive DWI had lesions that were in an appropriate vascular territory for the presenting symptoms,^{17,18,20,22,23,25,26} 4 studies included a minority of patients with potentially asymptomatic lesions^6,12,21,27 and the remaining 8 studies did not give these data.

Several studies recorded additional details of the DWI lesions (eg, size, number and location), but with the exception of one study,¹⁷ only the presence or absence of a DWI lesion(s) were reported in relation to clinical characteristics. Rovira et al¹⁷ reported no association between DWI lesion size and symptom duration in 39 patients.

There were no associations between positive DWI (Figure 1) and age 60 (9 studies, odds ratio [OR], 1.26; 95% CI, 0.91 to 1.75; P=0.24), male sex (13 studies, OR, 1.14; 95% CI, 0.88 to 1.48; P=0.37), previous hypertension (usually defined as being on treatment; 14 studies, OR, 0.90; 95% CI, 0.69 to 1.18; P=0.51), current raised blood pressure (>160 systolic or >95 diastolic^18,22 or >140 or 90^8,16,26,27; 8 studies, OR, 1.08; 95% CI, 0.79 to 1.47; P=0.71) or diabetes (13 studies, OR, 0.82; 95% CI, 0.57 to 1.20; P=0.38). However, dysphasia (9 studies, OR, 2.25; 95% CI, 1.57 to 3.22; P<0.001), motor weakness (9 studies, OR, 2.20; 95% CI, 1.56 to 3.10; P<0.001) and dysarthria (8 studies, OR, 1.73; 95% CI, 1.11 to 2.68; P=0.03) were strongly associated with positive DWI (Figure 2). Duration 60 minutes was also positively associated with DWI lesions (13 studies, OR, 1.50; 95% CI, 1.16 to 1.96; P=0.004; Figure 2) as were atrial fibrillation (9 studies, OR, 2.75; 95% CI, 1.78 to 4.25; P<0.001) and ipsilateral carotid stenosis 50% (10 studies, OR, 1.83; 95% CI, 1.26 to 2.65; P=0.003; Figure 3).

View larger version (19K): [in this window] [in a new window]   Figure 1. Patients characteristics. Meta-analysis of associations between clinical characteristics and positive DWI (u/d=unpublished data). Probability values given for the significance (sig) and heterogeneity (het) of pooled odds ratios.

View larger version (19K): [in this window] [in a new window]   Figure 2. Characteristics of the TIA. Meta-analysis of associations between clinical characteristics and positive DWI (u/d=unpublished data). Probability values given for the significance (sig) and heterogeneity (het) of pooled odds ratios.

View larger version (17K): [in this window] [in a new window]   Figure 3. Etiology of the TIA. Meta-analysis of associations between clinical characteristics and positive DWI (u/d=unpublished data). Probability values given for the significance (sig) and heterogeneity (het) of pooled odds ratios.

	Discussion

Top Abstract Introduction Method Results Discussion References

 
Our meta-analysis has shown that certain clinical features which are known to predict a high early risk of stroke after a TIA are also associated with the presence of acute ischemic lesions on DWI. In general, it was the characteristics of the TIA (eg, duration, motor weakness, dysphasia, dysarthria) and the underlying etiology (carotid stenosis and atrial fibrillation) rather than traditional vascular risk factors (age, sex, diabetes, hypertension, and blood pressure) that were associated with a positive DWI.

There are several possible explanations for the associations between patient and event characteristics and positive DWI. Clinical diagnosis of TIA is not completely reliable,³⁰ and some patients with an apparent TIA will have a nonvascular etiology. Therefore, the presence of a potentially causal vascular pathology, such as AF or carotid stenosis, makes it more likely that the diagnosis of TIA was correct—and hence the DWI is positive. However, it is also possible that AF and carotid stenosis might be associated with a more severe ischemic insult, which could also increase the rate of positive DWI. In the case of carotid stenosis, reduced perfusion may alter the diffusion properties of brain tissue on the ipsilateral side³¹ and might also influence the temporal evolution of DWI lesions³² as well as susceptibility to ischemia in the first place. It is uncertain why motor weakness and dysphasia are associated with a positive DWI. Again, it is possible that they simply indicate a greater likelihood of a correct diagnosis of TIA although in most of the studies in the meta-analysis the diagnosis of TIA was made by a vascular neurologist. It is also theoretically possible that some cerebral locations are more susceptible to infarction than others (eg, attributable to reduced collateral circulation) and that this relates to presenting symptoms.

Three studies have reported prognostic data for TIA patients^8,9,28 in relation to DWI appearances at baseline. However, all 3 were relatively small and were not powered to determine the independent prognostic value of DWI lesions. Cucchiara et al studied 61 patients but identified only 2 strokes at 90-day follow-up.²⁸ Purroy et al⁹ (83 patients) found that patients with both a positive DWI and a symptom duration >60 minutes were at greater risk of recurrent TIA or stroke at 90-days than patients with neither (OR, 5.02; 95% CI, 1.37 to 18.3; P=0.02). Coutts et al⁸ (106 patients) found that TIA patients with both a positive DWI and intracranial vessel occlusion were more likely to have recurrent stroke at 90 days than patients with neither (OR, 8.9; 95% CI, 1.6 to 49.6; P=0.01).

It has been proposed that TIA be redefined as ischemic symptoms lasting <1 hour without evidence of acute infarction.³³ This stems from the fact that the majority of TIAs resolve within 1 hour and a significant proportion of patients with TIAs have infarcts on brain imaging. We have found that symptom duration 60 minutes is associated with the presence of acute ischemic lesions on DWI in patients with TIA. However, positive DWI is also associated with dysphasia, dysarthria, weakness, atrial fibrillation and large artery atherosclerosis, all of which have prognostic significance after a TIA.^5,10 Therefore, a risk stratification tool which incorporates these other important clinical features as well as symptom duration is likely to be most useful in the prognostication of patients with TIA.

In all 19 studies, the proportion of TIAs lasting 60 minutes (30% to 83%) was greater than that found in the general population of patients with TIA,³⁴ suggesting that there may have been some selection bias. For example, studies which scanned patients acutely generally recruited patients from the emergency department and may have included patients with more severe symptoms than studies which recruited from outpatient clinics and tended to scan patients after a delay. However, studies which scanned late may also have been subject to bias because TIA patients with early recurrent stroke were excluded, some silent recurrent lesions³⁵ may have been included, and some very transient lesions on DWI may have been missed. Another source of heterogeneity might be variation in the definition of ‘positive DWI’ and whether lesions in a vascular territory different to that expected from the clinical history were included. However, several studies did not provide all these data.

Extrapolation from studies in patients with acute stroke suggests that DWI parameters other than simply the presence or absence of acute ischemic lesions may be associated with prognosis in patients with TIA. For example, there is some evidence that lesion size or volume is associated with worse short-term outcome after ischemic stroke^19,36 although this association may not be independent of age and stroke severity.³⁷ In addition, multiple acute ischemic lesions on DWI in patients with acute stroke, often indicating embolic etiology,^38,39 are associated with recurrent silent DWI lesions on follow-up.^35,40 In this review, the majority of studies only reported clinical or follow-up data in relation to DWI lesion presence, and the prognostic relevance of size and pattern of lesions on DWI after a TIA is unclear.

Large studies of DWI in patients with TIA are now required in order to reliably determine the prognostic value of all of the above DWI characteristics and to afford sufficient power to determine what they add to established clinical risk factors for early stroke.^4,5 Given the number of potentially prognostic clinical and DWI characteristics, and their nonindependence and potential for complex interaction as identified in this review, sample sizes of at least 1000 patients with acute TIA are likely to be required. Indeed, to determine the independent predictive value of 10 variables, and to allow for several interaction terms, a sample size of 2000 is required based on an expected event rate of 10% at 30 days.⁴¹

In conclusion, several clinical characteristics with proven prognostic significance are associated with the presence of acute ischemic lesions on DWI after TIA. Future studies of DWI will need to be appropriately powered to adjust for clinical features and the underlying etiology in order to determine how best to incorporate DWI into clinical risk scores.

	Acknowledgments

 
We would like to thank the following for providing unpublished data for the meta-analysis: K. Sander (former Winbeck, Technical University of Munich; 60 cases¹⁶), J. Marx (University of Mainz; 14 cases²⁰), H. Takayama (Mihara Memorial Hospital, Japan; 19 cases²⁴), C. Lamy (Department of Neurology, St. Anne’s Hospital, Paris; 98 cases²⁷), L. Restrepo (Department of Neurology, John Hopkins Hospital, Baltimore; 22 cases²⁶), F. Purroy (University of Barcelona; 83 cases⁹), H. Ay (Department of Neurology, Massachusetts General Hospital; 144 cases^21,25), B. Cucchiara (University of Pennsylvania; 61 cases²⁸), A. Demchuk, and VISION study group (University of Calgary; 106 cases⁸). We also thank Kaori Flossmann for translating the Japanese studies.

Sources of Funding

This work was supported by grant number TSA 2004/12 received from The Stroke Association.

Disclosures

None.

Received November 6, 2006; revision received November 24, 2006; accepted December 5, 2006.

	References

Top Abstract Introduction Method Results Discussion References

 
1. Lovett JK, Dennis MS, Sandercock PA, Bamford J, Warlow CP, Rothwell PM. Very early risk of stroke after a first transient ischemic attack. Stroke. 2003; 34: e138–e140.[Medline] [Order article via Infotrieve]

2. Hill MD, Yiannakoulias N, Jeerakathil T, Tu JV, Svenson LW, Schopflocher DP. The high risk of stroke immediately after transient ischemic attack: a population-based study. Neurology. 2004; 62: 2015–2020.[Abstract/Free Full Text]

3. Coull AJ, Lovett JK, Rothwell PM. Population based study of early risk of stroke after transient ischaemic attack or minor stroke: implications for public education and organisation of services. BMJ. 2004; 328: 326.[Abstract/Free Full Text]

4. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000; 284: 2901–2906.[Abstract/Free Full Text]

5. Rothwell PM, Giles MF, Flossmann E, Lovelock CE, Redgrave JN, Warlow CP, Mehta Z. A simple score (ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack. Lancet. 2005; 366: 29–36.[CrossRef][Medline] [Order article via Infotrieve]

6. Kidwell CS, Alger JR, Di Salle F, Starkman S, Villablanca P, Bentson J, Saver JL. Diffusion MRI in patients with transient ischemic attacks. Stroke. 1999; 30: 1174–1180.[Abstract/Free Full Text]

7. Crisostomo RA, Garcia MM, Tong DC. Detection of diffusion-weighted MRI abnormalities in patients with transient ischemic attack: correlation with clinical characteristics. Stroke. 2003; 34: 932–937.[Abstract/Free Full Text]

8. Coutts SB, Simon JE, Eliasziw M, Sohn CH, Hill MD, Barber PA, Palumbo V, Kennedy J, Roy J, Gagnon A, Scott JN, Buchan AM, Demchuk AM. Triaging transient ischemic attack and minor stroke patients using acute magnetic resonance imaging. Ann Neurol. 2005; 57: 848–854.[CrossRef][Medline] [Order article via Infotrieve]

9. Purroy F, Montaner J, Rovira A, Delgado P, Quintana M, Alvarez-Sabin J. Higher risk of further vascular events among transient ischemic attack patients with diffusion-weighted imaging acute ischemic lesions. Stroke. 2004; 35: 2313–2319.[Abstract/Free Full Text]

10. Lovett JK, Coull AJ, Rothwell PM. Early risk of recurrence by subtype of ischemic stroke in population-based incidence studies. Neurology. 2004; 62: 569–573.[Abstract/Free Full Text]

11. Fairhead JF, Mehta Z, Rothwell PM. Population-based study of delays in carotid imaging and surgery and the risk of recurrent stroke. Neurology. 2005; 65: 371–375.[Abstract/Free Full Text]

12. Schulz UG, Briley D, Meagher T, Molyneux A, Rothwell PM. Diffusion-weighted MRI in 300 patients presenting late with subacute transient ischemic attack or minor stroke. Stroke. 2004; 35: 2459–2465.[Abstract/Free Full Text]

13. Redgrave JN, Schulz UG, Briley D, Meagher T, Rothwell PM. Presence of acute ischaemic lesions on diffusion-weighted imaging (DWI) is associated with simple clinical predictors of early stroke risk after TIA. Cerebrovasc Dis. 2006; 21 (Suppl 4): 34.[CrossRef]

14. Sterne JAC, Bradburn MJ, Egger M. Systematic reviews in health care: meta-analysis in context. In: Egger M, Smith GD, Altman DG, eds. Dealing With Zero Cells. BMJ. 2001; 375–376.

15. Kamal AK, Segal AZ, Ulug AM. Quantitative diffusion-weighted MR imaging in transient ischemic attacks. AJNR Am J Neuroradiol. 2002; 23: 1533–1538.[Abstract/Free Full Text]

16. Winbeck K, Bruckmaier K, Etgen T, von Einsiedel HG, Rottinger M, Sander D. Transient ischemic attack and stroke can be differentiated by analyzing early diffusion-weighted imaging signal intensity changes. Stroke. 2004; 35: 1095–1099.[Abstract/Free Full Text]

17. Rovira A, Rovira-Gols A, Pedraza S, Grive E, Molina C, Alvarez-Sabin J. Diffusion-weighted MR imaging in the acute phase of transient ischemic attacks. AJNR Am J Neuroradiol. 2002; 23: 77–83.[Abstract/Free Full Text]

18. Kastrup A, Schulz JB, Mader I, Dichgans J, Kuker W. Diffusion-weighted MRI in patients with symptomatic internal carotid artery disease. J Neurol. 2002; 249: 1168–1174.[CrossRef][Medline] [Order article via Infotrieve]

19. Engelter ST, Provenzale JM, Petrella JR, Alberts MJ. Diffusion MR imaging and transient ischemic attacks. Stroke. 1999; 30: 2762–2763.[Medline] [Order article via Infotrieve]

20. Marx JJ, Mika-Gruettner A, Thoemke F, Fitzek S, Fitzek C, Vucurevic G, Urban PP, Stoeter P, Hopf HC. Diffusion weighted magnetic resonance imaging in the diagnosis of reversible ischaemic deficits of the brainstem. J Neurol Neurosurg Psychiatry. 2002; 72: 572–575.[Abstract/Free Full Text]

21. Ay H, Oliveira-Filho J, Buonanno FS, Schaefer PW, Furie KL, Chang YC, Rordorf G, Schwamm LH, Gonzalez RG, Koroshetz WJ. ‘Footprints’ of transient ischemic attacks: a diffusion-weighted MRI study. Cerebrovasc Dis. 2002; 14: 177–186.[CrossRef][Medline] [Order article via Infotrieve]

22. Inatomi Y, Kimura K, Yonehara T, Fujioka S, Uchino M. DWI abnormalities and clinical characteristics in TIA patients. Neurology. 2004; 62: 376–380.[Abstract/Free Full Text]

23. Nakamura T, Uchiyama S, Shibagaki Y, Iwata M. Abnormalities on diffusion-weighted magnetic resonance imaging in patients with transient ischemic attack. Rinsho Shinkeigaku. 2003; 43: 122–125.[Medline] [Order article via Infotrieve]

24. Takayama H, Mihara B, Kobayashi M, Hozumi A, Sadanaga H, Gomi S. Usefulness of diffusion-weighted MRI in the diagnosis of transient ischemic attacks. No To Shinkei. 2000; 52: 919–923.[Medline] [Order article via Infotrieve]

25. Ay H, Koroshetz WJ, Benner T, Vangel MG, Wu O, Schwamm LH, Sorensen AG. Transient ischemic attack with infarction: a unique syndrome? Ann Neurol. 2005; 57: 679–686.[CrossRef][Medline] [Order article via Infotrieve]

26. Restrepo L, Jacobs MA, Barker PB, Wityk RJ. Assessment of transient ischemic attack with diffusion- and perfusion-weighted imaging AJNR Am J Neuroradiol. 2004; 25: 1645–1652.[Medline] [Order article via Infotrieve]

27. Lamy C, Oppenheim C, Calvet D, Domigo V, Naggara O, Meder J, Mas J. Diffusion-weighted MR imaging in transient ischaemic attacks. Eur Radiol. 2006; 16: 1090–1095.[CrossRef][Medline] [Order article via Infotrieve]

28. Cucchiara BL, Messe SR, Taylor RA, Pacelli J, Maus D, Shah Q, Kasner SE. Is the ABCD score useful for risk stratification of patients with acute transient ischemic attack? Stroke. 2006; 37: 1710–1714.[Abstract/Free Full Text]

29. Kimura K, Minematsu K, Wada K, Yonemura K, Yasaka M, Yamaguchi T. Lesions visualized by contrast-enhanced magnetic resonance imaging in transient ischemic attacks. J Neurol Sci. 2000; 173: 103–108.[CrossRef][Medline] [Order article via Infotrieve]

30. Koudstaal PJ, Gerritsma JG, van Gijn J. Clinical disagreement on the diagnosis of transient ischemic attack: is the patient or the doctor to blame? Stroke. 1989; 20: 300–301.[Free Full Text]

31. Soinne L, Helenius J, Saimanen E, Salonen O, Lindsberg PJ, Kaste M, Tatlisumak T. Brain diffusion changes in carotid occlusive disease treated with endarterectomy. Neurology. 2003; 61: 1061–1065.[Abstract/Free Full Text]

32. Munoz Maniega S, Bastin ME, Armitage PA, Farrall AJ, Carpenter TK, Hand PJ, Cvoro V, Rivers CS, Wardlaw JM. Temporal evolution of water diffusion parameters is different in grey and white matter in human ischaemic stroke J Neurol Neurosurg Psychiatry. 2004; 75: 1714–1718.[Abstract/Free Full Text]

33. Albers GW, Caplan LR, Easton JD, Fayad PB, Mohr JP, Saver JL, Sherman DG. Transient ischemic attack–proposal for a new definition. N Engl J Med. 2002; 347: 1713–1716.[Free Full Text]

34. Levy DE. How transient are transient ischemic attacks? Neurology. 1988; 38: 674–677.[Abstract/Free Full Text]

35. Coutts SB, Hill MD, Simon JE, Sohn CH, Scott JN, Demchuk AM. Silent ischemia in minor stroke and TIA patients identified on MR imaging. Neurology. 2005; 65: 513–517.[Abstract/Free Full Text]

36. van Everdingen KJ, van Der GJ, Kappelle LJ, Ramos LM, Mali WP. Diffusion-weighted magnetic resonance imaging in acute stroke. Stroke. 1998; 29: 1783–1790.[Abstract/Free Full Text]

37. Wardlaw JM, Keir SL, Bastin ME, Armitage PA, Rana AK. Is diffusion imaging appearance an independent predictor of outcome after ischemic stroke? Neurology. 2002; 59: 1381–1387.[Abstract/Free Full Text]

38. Baird AE, Lovblad KO, Schlaug G, Edelman RR, Warach S. Multiple acute stroke syndrome: marker of embolic disease? Neurology. 2000; 54: 674–678.[Abstract/Free Full Text]

39. Kang DW, Chalela JA, Ezzeddine MA, Warach S. Association of ischemic lesion patterns on early diffusion-weighted imaging with TOAST stroke subtypes. Arch Neurol. 2003; 60: 1730–1734.[Abstract/Free Full Text]

40. Kang DW, Latour LL, Chalela JA, Dambrosia J, Warach S. Early ischemic lesion recurrence within a week after acute ischemic stroke. Ann Neurol. 2003; 54: 66–74.[CrossRef][Medline] [Order article via Infotrieve]

41. Peduzzi P, Concato J, Kemper E, Holford TR, Feinstein AR. A simulation study of the number of events per variable in logistic regression analysis. J Clin Epidemiol. 1996; 49: 1373–1379.[CrossRef][Medline] [Order article via Infotrieve]

This article has been cited by other articles:

				O. C. Sheehan, A. Merwick, L. A. Kelly, N. Hannon, M. Marnane, L. Kyne, P. M.E. McCormack, J. Duggan, A. Moore, J. Moroney, et al. Diagnostic Usefulness of the ABCD2 Score to Distinguish Transient Ischemic Attack and Minor Ischemic Stroke From Noncerebrovascular Events: The North Dublin TIA Study Stroke, November 1, 2009; 40(11): 3449 - 3454. [Abstract] [Full Text] [PDF]

				A. W. Asimos, W. D. Rosamond, A. M. Johnson, M. F. Price, K. M. Rose, C. V. Murphy, C. H. Tegeler, and A. Felix Early Diffusion Weighted MRI as a Negative Predictor for Disabling Stroke After ABCD2 Score Risk Categorization in Transient Ischemic Attack Patients Stroke, October 1, 2009; 40(10): 3252 - 3257. [Abstract] [Full Text] [PDF]

				A. Fothergill, T. J.H. Christianson, R. D. Brown Jr, and A. A. Rabinstein Validation and Refinement of the ABCD2 Score: A Population-Based Analysis Stroke, August 1, 2009; 40(8): 2669 - 2673. [Abstract] [Full Text] [PDF]

				J. D. Easton, J. L. Saver, G. W. Albers, M. J. Alberts, S. Chaturvedi, E. Feldmann, T. S. Hatsukami, R. T. Higashida, S. C. Johnston, C. S. Kidwell, et al. Definition and Evaluation of Transient Ischemic Attack: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease: The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke, June 1, 2009; 40(6): 2276 - 2293. [Abstract] [Full Text] [PDF]

				M. Mlynash, J-M Olivot, D. C. Tong, M. G. Lansberg, I. Eyngorn, S. Kemp, M. E. Moseley, and G. W. Albers Yield of combined perfusion and diffusion MR imaging in hemispheric TIA Neurology, March 31, 2009; 72(13): 1127 - 1133. [Abstract] [Full Text] [PDF]

				H. Ay, E. M. Arsava, S. C. Johnston, M. Vangel, L. H. Schwamm, K. L. Furie, W. J. Koroshetz, and A. G. Sorensen Clinical- and Imaging-Based Prediction of Stroke Risk After Transient Ischemic Attack: The CIP Model Stroke, January 1, 2009; 40(1): 181 - 186. [Abstract] [Full Text] [PDF]

				D. Calvet, E. Touze, C. Oppenheim, G. Turc, J.-F. Meder, and J.-L. Mas DWI Lesions and TIA Etiology Improve the Prediction of Stroke After TIA Stroke, January 1, 2009; 40(1): 187 - 192. [Abstract] [Full Text] [PDF]

				J. L. Saver Proposal for a Universal Definition of Cerebral Infarction Stroke, November 1, 2008; 39(11): 3110 - 3115. [Abstract] [Full Text] [PDF]

				J R Selvarajah, C J Smith, S Hulme, R F Georgiou, A Vail, P J Tyrrell, and on behalf of the NORTHSTAR Collaborators Prognosis in patients with transient ischaemic attack (TIA) and minor stroke attending TIA services in the North West of England: The NORTHSTAR Study J. Neurol. Neurosurg. Psychiatry, January 1, 2008; 79(1): 38 - 43. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) All Versions of this Article: 38/5/1482    most recent STROKEAHA.106.477380v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Redgrave, J. N.E. Articles by Rothwell, P. M. Search for Related Content PubMed PubMed Citation Articles by Redgrave, J. N.E. Articles by Rothwell, P. M. Pubmed/NCBI databases Medline Plus Health Information Stroke Transient Ischemic Attack Related Collections CT and MRI Computerized tomography and Magnetic Resonance Imaging Risk Factors for Stroke