(Stroke. 2003;34:932.)
© 2003 American Heart Association, Inc.
Original Contributions |
From Stanford Medical School (R.A.C.), Stanford Stroke Center (M.M.G., D.C.T.), and Department of Neurology and Neurological Sciences, Stanford University Medical Center (D.C.T.), Palo Alto, Calif.
Correspondence to David C. Tong, MD, Stanford Stroke Center, 701 Welch Rd, Palo Alto, CA 94304. E-mail dct{at}stanford.edu
| Abstract |
|---|
|
|
|---|
Methods A retrospective analysis was performed on all patients entered in the Stanford Stroke Center database during 19972001 who were clinically diagnosed with a TIA and who had also undergone a DWI scan
3 days after symptom onset. The relationship between DWI-detected findings and patients clinical presentation was then analyzed.
Results Seventy-five patients experiencing 78 TIAs who also underwent DWI within 3 days of symptom onset were identified. DWI-detected abnormalities were present in 16 of 78 cases (21%). Patients with positive DWI scans were 9.6 times more likely to have had symptom duration
1 hour, 16 times more likely to have had motor deficits, and 25 times more likely to have had aphasia than patients with negative DWI scans. The combination of all 3 symptoms was 100% specific for an abnormality on DWI. In 7 of 16 cases (44%), a DWI abnormality was present on both DWI and conventional imaging (T2-weighted imaging or fluid-attenuated inversion recovery [FLAIR]). In all of these cases the DWI clarified the extent or acuity of the lesion (n=7) or identified additional lesions not detected by conventional imaging (n=9).
Conclusions In TIA patients, symptom duration
1 hour, motor deficits, and aphasia were each independently correlated with detecting an abnormality with DWI. DWI was also helpful in differentiating between chronic versus acute lesions. These data may be of value in identifying those TIA patients for whom MRI evaluation with DWI is of greatest clinical utility.
Key Words: ischemic attack, transient magnetic resonance imaging, diffusion-weighted
| Introduction |
|---|
|
|
|---|
Diffusion-weighted MRI (DWI) is an established MRI technique that is very sensitive to acute cerebral ischemia.24 In clinical practice, DWI has been shown to be superior to conventional MRI and CT.57 In addition, DWI has the ability to differentiate between acute and chronic ischemia,810 which could be of substantial value in patients with prior cerebrovascular disease and new transient neurological symptoms. In contrast, conventional MRI cannot differentiate between acute and chronic infarcts, making it difficult to distinguish acute from chronic lesions in patients with previous infarction.11
DWI is now frequently used in the evaluation of patients who have experienced cerebral ischemia. However, while the superiority of using DWI over other imaging modalities in acute stroke has been studied extensively, its value in the evaluation of patients experiencing TIA has received significantly less attention.1215
The use of DWI in this situation could be of substantial clinical benefit because it is often difficult to determine by conventional means whether a patient has actually suffered from a TIA. Clinical history, examination, and conventional imaging frequently cannot accurately determine whether transient symptoms are due to cerebral ischemia, making determination of the exact nature of an individual patients transient symptoms problematic.
In this study we sought to determine the utility of DWI in patients with a clinical diagnosis of TIA. In addition, the relationship between specific TIA characteristics and DWI positivity was explored in an effort to identify those features associated with an increased probability of DWI positivity. This information could be of significant value in optimizing the use of DWI in the assessment of TIA patients.
| Subjects and Methods |
|---|
|
|
|---|
3 days after symptom onset. This comprehensive database consists of all patients evaluated by the Stroke Service at Stanford University Medical Center. Entries into the database are completed at the time of hospital discharge. Data were gathered regarding age; sex; symptom type, number, and date; time of symptom onset; time to symptom resolution; history of previous TIA(s) or stroke(s); and presence of vascular risk factors (eg, hypertension, diabetes mellitus, hypercholesterolemia, history of tobacco use). The date and time of DWI and the presence of a DWI abnormality were also recorded. Symptom duration was defined as the summation of time for all neurological episodes for a given patient.
DWI scans were performed as previously described.16 In brief, MRI was performed with the use of echo-planar imaging on a 1.5-T magnet (Signa; General Electric). Multislice whole-brain DWI was performed with the following variables: 16 slices; repetition time, 8100 ms; echo time, 110 ms; slice thickness, 5 mm; gap, 2.5 mm; 128x128 matrix; and field of view, 24 cm. B values were 0 and 829 s/mm2. Diffusion-weighted images were acquired in the x, y, and z directions and were processed to generate trace apparent diffusion coefficient maps. A DWI scan was considered positive if the scan revealed an area of hyperintensity on DWI and hypointensity on apparent diffusion coefficient maps relative to the normal brain, signifying acute cerebral ischemia. All scans were reviewed by the treating neurologist and a board-certified neuroradiologist during the patients hospitalization. All MRI readers had extensive experience with the interpretation of DWI scans.
Statistical Analysis
Symptom duration, number, and time from symptom onset to MRI between patients with positive and negative DWI scans were compared. The Mann-Whitney test was used for these analyses. Yates corrected
2 and Fisher exact analyses were used for analysis of contingency tables as appropriate. Logistic regression analysis was used to test for independence among predictors for positive DWI. Significance was determined at the P<0.05 level. Sensitivity, specificity, and positive and negative predictive value for a positive DWI scan were assessed by cross tabulation. We calculated 95% CIs using the efficient-score method, corrected for continuity.17,18 Statistical analyses were performed with the use of a commercially available computer program (SPSS 10.0; SPSS Inc).
| Results |
|---|
|
|
|---|
DWI was positive in 16 of 78 cases (21%). Patients with positive DWI scans had a significantly longer duration of symptoms than patients with negative DWI scans (Table 1; P=0.025). The mean duration of TIA symptoms for patients with a positive DWI scan was 5.2±8.0 hours (median, 2.0 hours). The mean duration of symptoms in patients with a negative DWI scan was 2.8±5.7 hours (median, 0.5 hour). The shortest total symptom duration in a patient with a positive DWI scan was 40 seconds. Patients with TIAs lasting
1 hour were significantly more likely to have a positive scan than those with symptoms lasting <1 hour (Figure 1, Table 2; P=0.007). By univariate analysis, patients with positive DWI scans experienced significantly more frequent motor symptoms (Table 2; P=0.027) and aphasia (Table 2; P=0.005) during their TIAs than patients with negative DWI scans.
|
|
|
A stepwise multiple logistic regression analysis was performed with positive DWI scans as the outcome variable and duration of symptoms (continuous and dichotomous), motor symptoms, and aphasia as potential predictors of DWI positivity. Longer symptom duration, motor symptoms, and aphasia were found to be independently correlated with a positive DWI scan. Patients with a positive DWI scan were 9.6 times more likely (95% CI, 1.7 to 56; P=0.011) to have had symptom duration
1 hour, 16 times more likely (95% CI, 1.8 to 140; P=0.014) to have had motor deficits, and 25 times more likely (95% CI, 3.3 to 190; P=0.0018) to have had aphasia.
The combination of symptoms lasting
1 hour, motor deficits, and aphasia was 100% specific (95% CI, 93% to 100%) for a positive DWI scan, with a 100% positive predictive value (95% CI, 46% to 100%). Similarly, having either symptoms lasting
1 hour, motor deficits, or aphasia was 100% sensitive (95% CI, 76% to 100%) for DWI positivity with a 100% negative predictive value (95% CI, 72% to 100%). In addition, the absence of each of these clinical characteristics was 100% specific (95% CI, 76% to 100%) for a negative DWI scan (Table 3).
|
There was no difference in the presence of sensory symptoms between the 2 groups (Table 2; P=0.71). In addition, there was no association between having a positive or negative DWI scan and the presence of dysarthria, ataxia, headache, vertigo, syncope/presyncope, dizziness not otherwise specified, nausea/vomiting, diplopia, and other visual disturbances (Table 2). Risk factors for experiencing a TIA such as increasing age, male sex, diabetes, hypertension, high cholesterol, smoking, and prior history of stroke or TIA were not significantly associated with DWI scan results (Table 2).
There was no difference in the rate of DWI positivity between patients with single versus multiple symptom episodes (Table 1; P=0.95). Furthermore, there was no significant difference in mean time from symptom onset to MRI between positive and negative DWI groups (Table 1; P=0.89). Positive scans were identified as early as 1.3 hours and as late as 42 hours after symptom onset (Figure 2).
|
In 7 of 16 cases (44%), the DWI abnormality was present on both DWI and conventional imaging (T2-weighted imaging or fluid-attenuated inversion recovery [FLAIR]). However, in all cases the DWI clarified the extent or acuity of the lesion (n=7) or identified additional lesions not detected by conventional imaging (n=9).
| Discussion |
|---|
|
|
|---|
1 hour, motor weakness, and aphasia independently predict positive DWI lesions. Moreover, in this analysis the combination of all 3 symptoms was always associated with a lesion on DWI. Our results substantiate the hypothesis that longer symptom duration is associated with an increased likelihood of a positive DWI scan, consistent with some prior studies.1214 Similar observations have been reported for CT imaging.1921 A relationship between symptom duration and DWI positivity makes theoretical sense since longer duration of symptoms would be expected to result in a higher probability of persistent parenchymal damage that could be detected by MRI.
However, symptom duration alone may be an inadequate determinant of DWI positivity. For example, the minimum symptom duration in a patient with positive DWI scan reported in our study was 40 seconds. This is significantly lower than the shortest duration of 10 minutes previously reported.12,13 In addition, 10% of patients with symptom duration of <5 minutes demonstrated a positive DWI scan. Thus, symptom duration alone appears to be an imperfect predictor of DWI scan positivity.
Although there was no difference in time from symptom onset to scan for positive and negative DWI groups, we found that after 42 hours all scans were negative. These data suggest that the yield of DWI scanning is optimal if <2 days pass between symptoms and MRI scanning. This is consistent with previous studies that reported a lack of a corresponding lesion on conventional follow-up MRI in at least one fifth of TIA patients with acute DWI abnormalities, particularly in those with brain stem ischemia.12,22 This suggests that early imaging of TIA patients may significantly increase diagnostic yield and that it may be appropriate to rapidly perform DWI in TIA patients presenting early after symptom onset.
We found that sensory symptoms were not associated with a positive DWI scan. They are often viewed as "soft" symptoms because they are subjective. In addition, sensory symptoms may be associated with a broad range of possible etiologies such as hyperventilation, seizure, migraine, or multiple sclerosis.23,24 This may explain why patients presenting with sensory symptoms did not have a greater likelihood of abnormal DWI imaging. The same reasoning may hold true for other nonspecific symptoms such as dizziness or nausea that were not associated with positive DWI scans. In addition, the latter symptoms are often associated with brain stem lesions, which are known to be more difficult to detect with MRI than hemispheric abnormalities.
Somewhat surprisingly, there was no relationship between the number of neurological symptoms and the probability of DWI positivity. Theoretically, it would seem that more frequent symptoms would lead to a greater chance of DWI-detected abnormalities. Repeated ischemia would be expected to result in a higher probability of persistent MRI-detectable neurological injury because of the cumulative damage believed to occur after recurrent ischemic insults. However, it has recently been reported that brief ischemic insults may actually be associated with ischemic tolerance.25 This leads to greater resistance to permanent ischemic injury and thus could lead to a lower likelihood of detecting ischemia by MRI.
We also found that DWI is frequently helpful even in patients in whom conventional MRI could detect the symptomatic lesion. This finding expands on prior data from acute stroke studies that have reported that DWI helps to accurately determine acuity of an ischemic lesion.26 This unique characteristic of DWI may be particularly helpful in the frequent scenario of recurrent transient symptoms in patients with a preexisting neurological deficit related to a prior stroke. In these cases, DWI is uniquely able to clarify the diagnosis, significantly aiding the clinician to arrive at the correct diagnosis. Moreover, DWI frequently detects additional lesions not seen on conventional imaging, which could influence subsequent management.26
DWI may also detect lesions not directly associated with the patients clinical presentation. For example, in Figure 3, the patient presented with sensory symptoms, yet several lesions are evident that would not usually be associated with the patients symptoms. This could lead to alterations in the diagnostic impression and subsequent management of the patient. One study reported that more than one third of their positive DWI scans led to a change in the suspected anatomic location, vascular location, or mechanism of the TIA.12 Thus, as with acute stroke, DWI may help to optimize management of TIAs by altering the diagnostic impression of both the location and mechanism of ischemia.
|
Our study is subject to some limitations. Caution is always required when interpreting data obtained retrospectively from a database because of the possibility of selection bias. The relatively small size of this study could also result in type II error when analyzing subgroups. In addition, the number of patients with positive DWI scans may have been underestimated because the treating clinician could have categorized a patient with transient symptoms as a stroke if the DWI were positive even if clinically the patients symptoms lasted <24 hours. Such misclassifications could artificially lower the number of TIA patients with positive DWI scans detected in our study.
Indeed, the incidence of positive DWI scans in our study is lower than in prior reports. We found that 21% of our TIA patients had DWI abnormalities versus 48%,12 35%,13 67%,14 and 37%15 of patients in other studies. However, such a bias should also tend to identify a greater population of bona fide TIA patients, thereby increasing the accuracy of the findings by reducing the number of individuals with transient neurological symptoms not due to cerebral ischemia. However, only prospective studies with complete case ascertainment can hope to clarify this issue.
Other explanations for differences in the prevalence of DWI-detected abnormalities in our series include differences in the patient populations studied, differences in the time to MRI scan, and variations in both the type and severity of neurological symptoms between different studies. As illustrated in this study, the type of neurological symptom may have a profound effect on the probability of DWI positivity. Similarly, the relationship between symptom severity and DWI positivity has not been adequately evaluated. It seems likely that symptom severity would have a substantial effect on DWI positivity. However, this hypothesis is difficult to test retrospectively. Prospective studies quantifying the severity of the transient neurological deficit may be better able to adequately assess this possibility.
Finally, it should be emphasized that the observations in this study are preliminary and require prospective validation. Because of the multiple comparisons performed, the possibility of a false-positive relationship is increased. Therefore, the associations identified should be considered hypothesis generating only and validated prospectively. Nevertheless, a number of the relationships identified appear biologically plausible and potentially clinically useful.
Conclusions
In conclusion, we found that symptom duration
1 hour, motor deficits, and aphasia were associated with DWI positivity. In addition, DWI substantially aided in identifying new lesions in patients with chronic cerebral ischemia. These relationships may help in clinical decision making regarding the use of acute neuroimaging in TIA patients. However, further studies with larger study populations and prospective case ascertainment will be needed to validate these observations. Such studies may also help to identify additional clinical characteristics associated with DWI positivity. Additional studies will also be necessary to determine whether DWI alone can help to differentiate patients with TIAs versus other causes of transient neurological symptoms. Such studies are currently under way at our institution. Only in this way can the true utility of DWI in patients with transient neurological symptoms be fully elucidated. Nevertheless, our data suggest that DWI is a powerful tool that can be of substantial value in the evaluation of patients experiencing TIAs.
| Acknowledgments |
|---|
Received July 3, 2002; revision received September 27, 2002; accepted October 22, 2002.
| References |
|---|
|
|
|---|
2. Neumann-Haefelin T, Moseley ME, Albers GW. New magnetic resonance imaging methods for cerebrovascular disease: emerging clinical applications. Ann Neurol. 2000; 47: 559570.[CrossRef][Medline] [Order article via Infotrieve]
3. Moseley ME, Cohen Y, Mintorovitch J, Chileuitt L, Shimizu H, Kucharczyk J, Wendland MF, Weinstein PR. Early detection of regional cerebral ischemia in cats: comparison of diffusion- and T2-weighted MRI and spectroscopy. Magn Reson Med. 1990; 14: 330346.[Medline] [Order article via Infotrieve]
4. Baird AE, Warach S. Magnetic resonance imaging of acute stroke. J Cereb Blood Flow Metab. 1998; 18: 583609.[CrossRef][Medline] [Order article via Infotrieve]
5. Yoneda Y, Tokui K, Hanihara T, Kitagaki T, Tabuchi M, Mori E. Diffusion-weighted magnetic resonance imaging: detection of ischemic injury 39 minutes after onset in a stroke patient. Ann Neurol. 1999; 45: 794797.[CrossRef][Medline] [Order article via Infotrieve]
6. Abdalla M, Boguslawska R, Poniatowska R. Hyperacute infarction: early CT findings. Med Sci Monit. 2000; 6: 10271030.[Medline] [Order article via Infotrieve]
7. Yuh WT, Crain MR, Loes DJ, Greene GM, Ryals TJ, Sato Y. MR imaging of cerebral ischemia: findings in the first 24 hours. AJNR Am J Neuroradiol. 1991; 12: 621629.[Abstract]
8. Marks MP, de Crespigny A, Lentz D, Enzmann DR, Albers GW, Moseley ME. Acute and chronic stroke: navigated spin-echo diffusion-weighted MR imaging. Radiology. 1996; 199: 403408.
9. Gonzalez RG, Schaefer PW, Buonanno FS, Schwamm LH, Budzik RF, Rordorf G, Wang B, Sorensen AG, Koroshetz WJ. Diffusion-weighted MR imaging: diagnostic accuracy in patients imaged within 6 hours of stroke symptom onset. Radiology. 1999; 210: 155162.
10. Lovblad K, Laubach H, Baird A, Curtin F, Schlaug G, Edelman RR, Warach S. Clinical experience with diffusion-weighted MR in patients with acute stroke. AJNR Am J Neuroradiol. 1998; 19: 10611066.[Abstract]
11. Awad IA, Modic M, Little JR, Furlan AJ, Weinstein M. Focal parenchymal lesions in transient ischemic attacks: correlation of computed tomography and magnetic resonance imaging. Stroke. 1986; 17: 399403.
12. 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: 11741180.
13. Engelter ST, Provenzale JM, Petrella JR, Alberts MJ. Diffusion MR imaging and transient ischemic attacks. Stroke. 1999; 30: 27622763.[Medline] [Order article via Infotrieve]
14. 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: 7783.
15. 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: 919923.[Medline] [Order article via Infotrieve]
16. Thijs VN, Adami A, Neumann-Haefelin T, Moseley ME, Albers GW. Clinical and radiological correlates of reduced cerebral blood flow measured using magnetic resonance imaging. Arch Neurol. 2002; 59: 233238.
17. Newcombe RG. Two-sided confidence intervals for the single proportion: comparison of seven methods. Stat Med. 1998; 17: 857872.[CrossRef][Medline] [Order article via Infotrieve]
18. Wilson EB. Probable inference, the law of succession, and statistical inference. JASA. 1927; 22: 209212.
19. Koudstaal PJ, van Gijn J, Frenken CW, Hijdra A, Lodder J, Vermeulen M, Bulens C, Franke CL, for the Dutch TIA Study Group. TIA, RIND, minor stroke: a continuum, or different subgroups? J Neurol Neurosurg Psychiatry. 1992; 55: 9597.
20. Bogousslavsky J, Regli F. Cerebral infarct in apparent transient ischemic attack. Neurology. 1985; 35: 15011503.
21. Davalos A, Matias-Guiu J, Torrent O, Vilaseca J, Codina A. Computed tomography in reversible ischaemic attacks: clinical and prognostic correlations in a prospective study. J Neurol. 1988; 235: 155158.[CrossRef][Medline] [Order article via Infotrieve]
22. 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: 572575.
23. Duncan GW, Pessin MS, Mohr JP, Adams RD. Transient cerebral ischemic attacks. Adv Intern Med. 1976; 21: 120.[Medline] [Order article via Infotrieve]
24. Fisher CM. Concerning recurrent transient cerebral ischemic attacks. Can Med Assoc J. 1962; 86: 1091.
25. Moncayo J, de Freitas GR, Bogousslavsky J, Altieri M, van Melle G. Do transient ischemic attacks have a neuroprotective effect? Neurology. 2000; 54: 20892094.
26. Albers GW, Lansberg MG, Norbash AM, Tong DC, OBrien MW, Woolfenden AR, Marks MP, Moseley ME. Yield of diffusion-weighted MRI for detection of potentially relevant findings in stroke patients. Neurology. 2000; 54: 15621567.
This article has been cited by other articles:
![]() |
F. Purroy, R. Begue, A. Quilez, G. Pinol-Ripoll, J. Sanahuja, L. Brieva, E. Seto, and M. I. Gil The California, ABCD, and Unified ABCD2 Risk Scores and the Presence of Acute Ischemic Lesions on Diffusion-Weighted Imaging in TIA Patients Stroke, June 1, 2009; 40(6): 2229 - 2232. [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] |
||||
![]() |
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] |
||||
![]() |
S. Prabhakaran, J. Y. Chong, and R. L. Sacco Impact of Abnormal Diffusion-Weighted Imaging Results on Short-term Outcome Following Transient Ischemic Attack Arch Neurol, August 1, 2007; 64(8): 1105 - 1109. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. N.E. Redgrave, S. B. Coutts, U. G. Schulz, D. Briley, and P. M. Rothwell 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 Stroke, May 1, 2007; 38(5): 1482 - 1488. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. C. Tong and L. R. Caplan Determining future stroke risk using MRI: New data, new questions Neurology, February 6, 2007; 68(6): 398 - 399. [Full Text] [PDF] |
||||
![]() |
C. Oppenheim, C. Lamy, E. Touze, D. Calvet, M. Hamon, J.-L. Mas, and J.-F. Meder Do transient ischemic attacks with diffusion-weighted imaging abnormalities correspond to brain infarctions? AJNR Am. J. Neuroradiol., September 1, 2006; 27(8): 1782 - 1787. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Pinero, A. Gonzalez, A. Mayol, E. Martinez, J.R. Gonzalez-Marcos, F. Boza, A. Cayuela, and A. Gil-Peralta Silent Ischemia after Neuroprotected Percutaneous Carotid Stenting: A Diffusion-Weighted MRI Study AJNR Am. J. Neuroradiol., June 1, 2006; 27(6): 1338 - 1345. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. M. Rothwell and S. C. Johnston Transient Ischemic Attacks: Stratifying Risk Stroke, February 1, 2006; 37(2): 320 - 322. [Full Text] [PDF] |
||||
![]() |
A. L. Krol, S. B. Coutts, J. E. Simon, M. D. Hill, C.-H. Sohn, A. M. Demchuk, and for the VISION Study Group Perfusion MRI Abnormalities in Speech or Motor Transient Ischemic Attack Patients Stroke, November 1, 2005; 36(11): 2487 - 2489. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. B. Coutts, M. D. Hill, J. E. Simon, C. -H. Sohn, J. N. Scott, A. M. Demchuk, and for the VISION Study Group Silent ischemia in minor stroke and TIA patients identified on MR imaging Neurology, August 23, 2005; 65(4): 513 - 517. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Adams, R. Adams, G. Del Zoppo, and L. B. Goldstein Guidelines for the Early Management of Patients With Ischemic Stroke: 2005 Guidelines Update A Scientific Statement From the Stroke Council of the American Heart Association/American Stroke Association Stroke, April 1, 2005; 36(4): 916 - 923. [Full Text] [PDF] |
||||
![]() |
K Winbeck, T Etgen, H G von Einsiedel, M Rottinger, and D Sander DWI in transient global amnesia and TIA: proposal for an ischaemic origin of TGA J. Neurol. Neurosurg. Psychiatry, March 1, 2005; 76(3): 438 - 441. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. G. Schulz, D. Briley, T. Meagher, A. Molyneux, and P. M. Rothwell Diffusion-Weighted MRI in 300 Patients Presenting Late With Subacute Transient Ischemic Attack or Minor Stroke Stroke, November 1, 2004; 35(11): 2459 - 2465. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Winbeck, K. Bruckmaier, T. Etgen, H. G. von Einsiedel, M. Rottinger, and D. Sander Transient Ischemic Attack and Stroke Can Be Differentiated by Analyzing Early Diffusion-Weighted Imaging Signal Intensity Changes Stroke, May 1, 2004; 35(5): 1095 - 1099. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Inatomi, K. Kimura, T. Yonehara, S. Fujioka, and M. Uchino DWI abnormalities and clinical characteristics in TIA patients Neurology, February 10, 2004; 62(3): 376 - 380. [Abstract] [Full Text] [PDF] |
||||
![]() |
Diffusion-Weighted Imaging Could Aid TIA Diagnosis Journal Watch (General), May 27, 2003; 2003(527): 5 - 5. [Full Text] |
||||
![]() |
Diffusion-Weighted Imaging May Aid TIA Diagnosis Journal Watch Neurology, May 22, 2003; 2003(522): 2 - 2. [Full Text] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2003 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |