Brain Trauma Stroke
Vertebrobasilar (VB) territory TIAs were previously thought to have a better prognosis than carotid territory events and are sometimes managed less aggressively. However, a systematic review of 37 published cohort studies and five unpublished studies reporting the risk of stroke after a TIA or minor stroke by territory of presenting event found no major differences in prognosis between VB events and carotid events, but a higher very early risk of stroke.31
Aetiology
Common causes of TIA include a cardiac source of embolism as occurs in atrial fibrillation, thrombus formation and embolism from an unstable plaque in the internal carotid artery (so-called large atherosclerosis [LAA]), and thrombosis of a deep penetrating cerebral artery causing a lacunar infarction.
It is likely that prognosis in the acute phase after brain ischaemia depends on the underlying pathology, but this question has been studied more in stroke than in TIA.32
In one prospective cohort of 388
patients with TIA, the mechanism of TIA was studied in relation to stroke outcome at three months. Stroke risk was highest among those with LAA, lowest in those with lacunar or small-vessel disease and intermediate in those with cardio-embolic or undetermined cause of TIA.33
of cerebral infarction (see Figure 3). It has therefore been proposed that DWI may identify TIA patients with an active ‘vascular process’ such as a source of emboli or LAA disease, signifying a high risk of further thromboembolism and thus recurrent stroke.
This hypothesis has been tested in a number of studies, although these have been hampered by small size and sometimes retrospective design. For instance, Prabhakaran et al. described a retrospective cohort study of 146 patients with TIA, of whom 37 (25%) had abnormalities on DWI; the presence of these abnormalities was found to be independently associated with a higher risk of in-hospital recurrent TIA or stroke (odds ratio 11.2; p
Purroy et al. described a cohort of 83 consecutive TIA patients attending an ED who were scanned with DWI, with abnormalities identified in 27. The combination of DWI abnormalities and symptoms lasting over an hour was found to be predictive of stroke (hazard ratio [HR] 5.0, 1.4–18.3; p=0.015) or a combined end-point of stroke and other vascular events (HR 3.8, 1.1–13.0; p=0.029).38
Coutts et
al. described a cohort of 180 patients with TIA or minor ischaemic stroke presenting to an ED, all of whom had DWI within 12 hours. Stroke risk at 90 days was 18.2% in the 99 patients with DWI abnormalities compared with 2.5% in those without (p
In another study of 343 consecutive TIA patients who were admitted to a stroke unit, a similar relationship between aetiological mechanism and stroke recurrence at three months was also found.34
Brain Imaging
Some early studies suggested that the presence of infarction on CT in patients with TIA predicts an increased risk of subsequent stroke, although others have failed to confirm this finding. However, interpretation of these results is difficult because the delay between the event and scanning was variable and acute and old infarcts were not reliably distinguished. However, more recent studies that have performed CT soon after TIA and reliably distinguished new and old infarction have shown that the presence of new infarction does carry a higher risk of early stroke.35,36
There is considerable interest in the role of MRI, and DWI in particular, in predicting stroke risk after TIA. DWI is a radiological technique that measures the diffusion of water molecules in different tissues in the body and is very sensitive to the early phase
1. Johnston SC, N Engl J Med, 2002;347:1687–92. 2. Rothwell PM, et al., Lancet, 2005;366:1773–83. 3. Rothwell PM, et al., Lancet, 2004;363:1925–33. 4.
Advisory Council for the National Institute of Neurological and Communicative Disorders and Stroke II, Stroke, 1975;6:564–616.
5. Hatano S, Bull World Health Organ, 1976;54:541–53. 6. Easton JD, et al., Stroke, 2009;40:2276–93. 7. Nor AM, et al., Lancet Neurol, 2005;4:727–34. 8. Hand PJ, et al., Stroke, 2006;37:769–75. 9. Dawson J, et al., QJM, 2009;102:43–9. 10. Prabhakaran S, et al., Cerebrovasc Dis, 2008;26:630–35. 11. Dennis M, et al., J Neurol Neurosurg Psychiatry, 1992;55:437–40. 12. Gallmetzer P, et al., Neurology, 2004;62:2160–64. 13. Quinette P, et al., Brain, 2006;129:1640–58.
14. Hodges JR, et al., Brain, 1990;113:639–57. 15. Bartsch T, et al., Lancet Neurol, 2010;9:205–14. 16. Siddiqi N, et al., Age Ageing, 2006;35:350–64. 17. Francis J, et al., JAMA, 1990;263:1097. 18. Voetsch B, et al., Arch Neurol, 2004;61:496–504. 19. Rothwell PM, Cerebrovasc Dis, 2003;16(Suppl. 3):2–10. 20. Giles MF, et al., Lancet Neurol, 2007;6:1063–72. 21. Johnston SC, et al., JAMA, 2000;284:2901–6. 22. Hill MD, et al., Neurology, 2004;62:2015–20. 23. Gladstone DJ, et al., CMAJ, 2004;1707:1099–1104. 24. Rothwell PM, et al., Lancet, 2005;366:29–36. 25. Johnston SC, et al., Lancet, 2007;369:283–92. 26. Royston P, et al., Br Med J, 2009;338:b604. 27. Giles MF, et al., Stroke, 2010;41:667–73. 28. Department of Health, National Stroke Strategy,
Although the association between DWI and early risk of stroke is clear, it is uncertain what additional prognostic information over and above clinical scores and aetiology it provides. Indeed, focal motor weakness, speech disturbance and symptoms lasting longer than one hour are all associated with DWI lesions in patients with TIA,40
while
DWI abnormalities are associated with large-vessel disease. Larger studies are therefore needed to address the interplay between the prognostic information available from clinical features and imaging. n
Matthew F Giles is a Consultant Physician and Geriatrician at the John Radcliffe Hospital in Oxford and a Senior Research Fellow in the Stroke Prevention Research Unit at NIHR Biomedical Research Centre, University of Oxford. His main research interests are transient ischaemic attack and minor stroke, with a particular focus on risk prediction tools and early management. He is an investigator with the Oxford Vascular Study (OXVASC) and his publications include the ABCD system and the EXPRESS Study.
London: Crown, 2007.
29. National Stroke Foundation, Available at:
www.strokefoundation.com.au/ (accessed April 2010).
30. Hankey GJ, et al., J Neurol Neurosurg Psychiatry, 1991;54:793–802.
31. Flossman E, et al., Brain, 2003;126:1940–54. 32. Lovett JK, et al., Neurology, 2004;62:569–74. 33. Purroy F, et al., Stroke, 2007;38:3225–9. 34. Calvet D, et al., Stroke, 2009;40:187–92. 35. Sciolla R, et al., Stroke, 2008;39:297–302. 36. Douglas CD, et al., Stroke, 2003;34:2894–9. 37. Prabhakaran S, et al., Arch Neurol, 2007;64:1105–9. 38. Purroy F, et al., Stroke, 2004;35:2313–19. 39. Coutts SB, et al., Int J Stroke, 2008;3:3–10. 40. Redgrave JN, et al., Stroke, 2007;38:1482–8.
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