Published online before print May 27, 2004, doi: 10.1161/01.STR.0000131929.98486.54
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(Stroke. 2004;35:1780.)
© 2004 American Heart Association, Inc.
Controversies in Stroke |
Why Lacunar Syndromes Are Different and Important
From the Department of Neurology (S.M.D.), Royal Melbourne Hospital and University of Melbourne; and The National Stroke Research Institute (G.A.D.), Austin and Repatriation Medical Centre and University of Melbourne, Australia.
Correspondence to Professor Stephen M Davis, Dept of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia 3050. E-mail stephen.davis{at}mh.org.au
Key Words: lacunar infarction • embolism
The lacunar hypothesis has been one of the hallmarks of the modern understanding of the clinical categorization of the pathogenesis of stroke. Stated simply, the hypothesis implies that classical lacunar syndromes are caused by small deep brain infarcts, due to occlusion of a single penetrating artery. The underlying pathology has been documented to be either in situ microatheroma or lipohyalinosis, rather than embolism.1
The controversy arises because many clinicians remain less than convinced that embolism is not a frequent cause of lacunar infarcts and hence would not warrant a different investigative strategy from other ischemic stroke syndromes. As we see it, the established facts are as follows:
1. There is no animal model of lacunar infarction due to in situ small-vessel disease, in contrast to the embolic model quoted by Futrell.
2. The proportion of embolic sources in patients with lacunar syndromes is substantially lower than for other hemispheric ischemic strokes, as stated by Norrving.
3. MRI studies have demonstrated that variable proportions of patients presenting with classical lacunar syndromes have sometimes shown multiple concurrent infarcts or more widespread perfusion abnormalities suggesting embolism.2
4. Other evidence for a possible embolic source in some cases includes a benefit to the subset of patients with lacunar syndromes and ipsilateral high-grade carotid stenosis in the NASCET trial.3 Further, aortic arch atheroma has been shown to be a risk factor for lacunar stroke.4
While recognizing that there is some heterogeneity of mechanism within the lacunar syndromes, we believe that the concept is clinically useful, and that the evidence favors the view that the majority are due to in situ, small-vessel disease. Hence, their recognition enables clinicians to be less aggressive in the search for an embolic source, although we would suggest that exclusion of large-vessel disease and cardiac screening is appropriate. Further, there are compelling clinical and epidemiological reasons to separate lacunar from nonlacunar ischemic strokes. For example, their outcome is substantially more favorable and their location in deep white matter may have implications for therapy. Intriguingly, in the recently reported IMAGES trial, a planned subanalysis showed an unexpected benefit for lacunar syndromes.5 We encourage further trials of therapy within this group such as the current SPS3 trial of combined antiplatelet and blood pressure lowering therapy.6 It may well be that the therapeutic response in lacunar infarcts may be somewhat different than in predominantly gray matter infarcts, given the well-known differences in ischemic neurochemical cascades.7
Given the importance of small-vessel disease, particularly in Asian countries, and its relationship to both clinical stroke and cognitive decline, we strongly believe that this disease entity deserves specific recognition to focus future research initiatives. While embolism is the likely cause of a minority of lacunar infarcts, we do not see it as the key, but perhaps a small component of a combination lock.
Received April 16, 2004; accepted April 16, 2004.
References
1. Fisher CM. Lacunes: small, deep cerebral infarcts. Neurology. 1965; 15: 774–784.
2. Gerraty RP, Parsons MW, Barber A, Darby DG, Desmond PM, Tress BM, Davis SM. Examining the lacunar hypothesis with diffusion and perfusion magnetic resonance imaging. Stroke. 2002; 33: 2019–2024.
3. Inzitari D, Eliasziw M, Sharpe BL, Fox AJ, Barnett HJ. Risk factors and outcome of patients with carotid artery stenosis presenting with lacunar stroke. North American Symptomatic Carotid Endarterectomy Trial Group. Neurology. 2000; 54: 660–666.
4. Kazui S, Levi CR, Jones EF, Quang L, Calafiore P, Donnan GA. Risk factors for lacunar stroke: a case-control transesophageal echocardiographic study. Neurology. 2000; 54: 1385–1387.
5. Muir KW, Lees KR, Ford I, Davis S; Intravenous Magnesium Efficacy in Stroke (IMAGES) Study Investigators. Magnesium for acute stroke (Intravenous Magnesium Efficacy in Stroke Trial): randomised controlled trial. Lancet. 2004; 363: 439–445.[CrossRef][Medline] [Order article via Infotrieve]
6. Benavente O, Hart RG. Secondary prevention of small subcortical strokes (SPS3). Seminars in Cerebrovascular Diseases and Stroke. 2003; 3: 8–17.
7. Waxman SG. Molecular mechanisms of subcortical versus cortical infarction. In: Donnan G, Norrving B, Bamford J, Bogousslavsky J, eds. Subcortical Stroke, 2nd ed. Oxford, UK: Oxford Medical Publications; 2002: 67–83.
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