Lacunar stroke: mechanisms and therapeutic implications

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 Lacunar stroke: mechanisms and therapeutic implications

1. http://orcid.org/0000-0003-0031-1004Shadi Yaghi1,
2. http://orcid.org/0000-0003-2998-8481Eytan Raz2,
3. Dixon Yang2,3,
4. Shawna Cutting1,
5. Brian Mac Grory4,
6. Mitchell SV Elkind5,
7. http://orcid.org/0000-0001-8178-8597Adam de Havenon6

1. Correspondence to Dr Shadi Yaghi, Department of Neurology, Brown University Warren Alpert Medical School, Providence, RI 02903, USA; shadiyaghi@yahoo.com

Abstract

Lacunar stroke is a marker of cerebral small vessel disease and accounts for up to 25% of ischaemic stroke. In this narrative review, we provide an overview of potential lacunar stroke mechanisms and discuss therapeutic implications based on the underlying mechanism. For this paper, we reviewed the literature from important studies (randomised trials, exploratory comparative studies and case series) on lacunar stroke patients with a focus on more recent studies highlighting mechanisms and stroke prevention strategies in patients with lacunar stroke. These studies suggest that lacunar stroke is a heterogeneous disease with various mechanisms, including most commonly lipohyalinosis and less commonly atheromatous disease and cardioembolism, highlighting the importance of a careful review of brain and neurovascular imaging, a cardiac and systemic evaluation. A better understanding of pathomechanisms of neurological deterioration may lead to investigating the utility of novel treatment strategies and optimisation of short-term antithrombotic treatment strategies to reduce the risk of neurological deterioration and prevent long-term disability in patients with lacunar stroke.

http://dx.doi.org/10.1136/jnnp-2021-326308

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Introduction

Lacunar stroke is a marker of cerebral small vessel disease1 and accounts for up to 25% of ischaemic stroke. The word lacunar comes from Latin for ‘lacuna’ meaning hole, and it is used to describe a small focus of encephalomalacia containing CSF, which is the end result of liquefactive necrosis. Lacunar stroke is defined as a subcortical infarct measuring less than 20 mm in diameter, caused by occlusion of a perforator of an intracranial artery.1 In this narrative review, we aim to provide an overview of potential lacunar stroke mechanisms and diagnostic approaches, and discuss therapeutic implications targeting the underlying mechanism.

Background

The incidence of lacunar stroke varies based on the population studied from 25 to 50 per 100 000 people,2 3 comprising 15%–25% of ischaemic stroke.2–4 These numbers, however, have been declining over time, likely due to better control of vascular risk factors such as hypertension.5

Lacunar stroke shares risk factors with other stroke subtypes, namely hypertension, diabetes, advanced age, cigarette smoking and hyperlipidaemia.6 7 While studies have shown that the overall prevalence of these risk factors is similar between lacunar stroke and other stroke subtypes,8 some studies suggest that smoking, hypertension and diabetes are particularly important risk factors for lacunar stroke3 7 and that these risk factors may be more prevalent in patients with lacunar stroke.9 Among these risk factors, hypertension is most common in patients with lacunar stroke (68%), followed by diabetes (30%).3 7 9 These studies were performed when the control of risk factors, particularly hypertension, was less aggressive and more recent studies suggest that risk factors for lacunar stroke may be similar to those of other subtypes.10

In addition to conventional risk factors, rare genetic conditions, such as Cerebral Autosomal Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) can cause lacunar stroke.11 These typically have other accompanying manifestations, including a positive family history, and the diagnosis is made by clinical suspicion and confirmed by genetic testing (table 1).11