Published online before print September 18, 2003, doi: 10.1161/01.STR.0000094581.18411.97
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(Stroke. 2003;34:2451.)
© 2003 American Heart Association, Inc.
Original Contributions |
Editorial Comment—Transient Cerebral Ischemia Demands Urgent Evaluation
Department of Emergency Medicine, Southern General Hospital, Glasgow, UK
Patients suffering a transient ischemic attack (TIA) are at high risk of stroke in the days and weeks following the index event: the risk even at 2 days is more than 5% in studies from the United States1 and the United Kingdom.2
Johnston and Easton take this concept further and have not only considered those with TIA (as conventionally defined, with no deficit at 24 hours3) but have also examined patients who have had a 
50% improvement in NIHSS scores despite a continuing neurological deficit. Their aim was to identify whether the crucial factor in the increased early risk of stroke with TIA is the reversible, labile nature of the neurological deficit, which could be a marker for an underlying unstable atherosclerotic plaque in the cerebral circulation.
The authors utilized the NINDS tPA dataset4 to test their hypothesis. One of the exclusion criteria for the NINDS study was "rapidly improving symptoms," so it is likely that a number of patients with TIA who would otherwise have been eligible for NINDS were excluded, which may account for the small number of TIA patients in the study. NINDS was also restricted to those eligible patients for thrombolysis randomization within 3 hours of symptom onset, which again limits the applicability of the results of this study. Many patients with TIA will not present within this time frame,1,2 but their physicians want to know how aggressive the initial investigation of these patients should be.
The methods used in this study were robust. The authors attempted to include all possible patients who may have had a neurological deterioration (unless due to symptomatic intracranial hemorrhage) after initial improvement by defining deterioration as an increase of 1 point or more on the NIHSS. While this may appear to be trivial, the actual deterioration detected was 6 NIHSS points (mean), which is clinically important. No data were presented on the time course of subsequent deterioration, but other work suggests that half of all patients who will deteriorate will do so within 2 days of the index TIA.1
A higher proportion of the TIA group received tPA compared with the non-TIA group (83% versus 47%, P<0.0001), although there was no difference in tPA administration rates between those who did deteriorate as compared with those who did not. These findings suggest that tPA may be more likely to lead to reversal of the observed deficit, but that it is no more likely to prevent a deterioration over the ensuing 90 days. These 90 days are a window of opportunity for physicians to evaluate potential causes for transient cerebral ischemia and consider other therapies to improve outcome.5
The suggested underlying theory of an unstable atherosclerotic plaque undergoing rupture, followed by thrombosis and then resolution, is pathophysiologically attractive. Statins have been shown to play a significant role in plaque stabilization after myocardial infarction and they may fulfill this role in the cerebral vasculature patients as well.6 Significant early improvement may also be caused by an increase in collateral cerebral blood flow locally, but this effect may be offset by reductions in flow secondary to local infarct related edema.
It is clear from these data that the artificial dichotomy between TIA (as traditionally defined) and stroke that has some spontaneous functional recovery is unnecessary.3 Even a functional recovery of 30% to 50% on the initial NIHSS is associated with up to nearly twice the odds of subsequent deterioration compared with no recovery. All patients with evidence of early functional recovery following a probable ischemic neurological deficit, of >10 minutes’ duration,1 are at risk of subsequent deterioration and require urgent evaluation. The authors have identified that TIA is an independent predictor of subsequent deterioration and it is likely that as a TIA represents "maximum improvement," it also gives the potential for most clinically apparent neurological deterioration.
Further studies are required to confirm the data of Johnston and Easton, but their elegant work should prompt us to examine whether the current services provided to patients with unstable cerebral ischemia are appropriate.7 Many countries and states have fewer neurologists than they should. In the United Kingdom, the specialty of stroke medicine is now established but requires a significant increase in numbers of specialist physicians to provide a uniformly available and effective service.8,9
Patients with symptoms and signs suggestive of unstable cerebral ischemia should have immediate cerebral imaging, either computed tomography (CT) or magnetic resonance imagine (MRI).5 While this may be possible in many centers in the United States, the relative lack of radiologists and traditional differences in practice in other countries often delay acute cerebral imaging. While there are accepted standards and guidelines for cranial CT imaging after trauma,10 radiologists are sometimes reluctant to undertake emergency imaging for patients with cerebral ischemia.
Apart from the issue of imaging, what should the emergency physician or family physician do with patients with acutely recovered cerebral ischemia? Despite national recommendations for rapid-access clinics for patients with TIA,11 it remains unclear whether these patients would have better outcomes from hospital admission or clinic assessment. It is clear that many patients do not present for some time after the development of symptoms suggestive of cerebral ischemia.12 Obvious electrolyte abnormalities should be identified and hypoglycemia must be excluded. Atrial fibrillation must be identified and therapy instituted if required. The decision to anticoagulate may be difficult and may require hospital admission for brain imaging and echocardiography. In the absence of a cardioembolic source, the carotid arteries should be urgently imaged using Doppler ultrasound and if a high-grade stenosis is identified, an urgent vascular surgery referral is required.5
Further collaboration among stroke physicians, neurologists, epidemiologists, family physicians, radiologists, and emergency physicians, for both research and service delivery, is a necessary first step to improve the long-term outcome of patients with unstable cerebral ischemia.
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References |
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 Top References |
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- 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] - Lovett JK, Dennis MS, Sandercock PAG, Bamford J, Warlow CP, Rothwell PM. Very early risk of stroke after a first transient ischemic attack. Stroke. 2003; 34: e138–e140.
[Abstract/Free Full Text] - Albers GW, Caplan LR, Easton JD, Fayad PB, Mohr JP, Saver JL, et al. Transient ischemic attack: proposal for a new definition. N Engl J Med. 2002; 347: 1713–1716.
[Free Full Text] - The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995; 333: 1581–1587.
[Abstract/Free Full Text] - Johnston SC. Clinical practice: transient ischemic attack. N Engl J Med. 2002; 347: 1687–1692.
[Free Full Text] - Libby P, Aikawa M. New insights into plaque stabilisation by lipid lowering. Drugs. 1998; 56 (suppl 1): 9–13.[CrossRef][Medline] [Order article via Infotrieve]
- Burgin WS, Staub L, Chan W, Wein TH, Felberg RA, Grotta JC, et al. Acute stroke care in non-urban emergency departments. Neurology. 2001; 57: 2006–2012.
[Abstract/Free Full Text] - Bath P, Lees K, Dennis M, Smithard D, Bone I, Grosset D, et al. Should stroke medicine be a separate subspecialty? BMJ. 1997; 315: 1167–1168.
[Free Full Text] - Hankey GJ. Should stroke medicine be a separate subspecialty? Stroke services should be coordinated by physicians who are expert and interested. BMJ. 1998; 316: 629.
[Free Full Text] - Udstuen GJ, Claar JM. Imaging of acute head injury in the adult. Semin Ultrasound CT MR. 2001; 22: 135–147.[CrossRef][Medline] [Order article via Infotrieve]
- Intercollegiate Working Party for Stroke. National Clinical Guidelines for Stroke. London, UK: Royal College of Physicians; 2000.
- Castaldo JE, Nelson JJ, Reed JF III, Longenecker JE, Toole JF. The delay in reporting symptoms of carotid artery stenosis in an at-risk population. Arch Neurol. 1997; 54: 1267–1271.[Abstract]
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