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(Stroke. 2007;38:1482.)
© 2007 American Heart Association, Inc.
Original Contributions |
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 |
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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 Authors were contacted for additional unpublished data.
Results— Nineteen studies were identified by the systematic review, and additional unpublished data were obtained from 11 of these studies.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 |
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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 |
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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 |
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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 studies9,16,17,19,21,25 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 studies9,12,17–19,21–23,27 and not stated in 4 studies15,24,26,28). 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 lesions6,12,21,27 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 diastolic18,22 or >140 or
908,16,26,27; 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).
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| Discussion |
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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 patients8,9,28 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 stroke19,36 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 |
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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 |
|---|
|
|
|---|
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.
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.
4. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000; 284: 2901–2906.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
34. Levy DE. How transient are transient ischemic attacks? Neurology. 1988; 38: 674–677.
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.
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.
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.
38. Baird AE, Lovblad KO, Schlaug G, Edelman RR, Warach S. Multiple acute stroke syndrome: marker of embolic disease? Neurology. 2000; 54: 674–678.
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.
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]
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