Treatment Approaches to Lacunar Stroke

Abstract

Lacunar strokes are appropriately named for their ability to cavitate and form ponds or "little lakes" (Latin: lacune -ae meaning pond or pit is a diminutive form of lacus meaning lake). They account for a substantial proportion of both symptomatic and asymptomatic ischemic strokes. In recent years, there have been several advances in the management of large vessel occlusions. New therapies such as non-vitamin K antagonist oral anticoagulants and left atrial appendage closure have recently been developed to improve stroke prevention in atrial fibrillation; however, the treatment of small vessel disease-related strokes lags frustratingly behind. Since Fisher characterized the lacunar syndromes and associated infarcts in the late 1960s, there have been no therapies specifically targeting lacunar stroke. Unfortunately, many therapeutic agents used for the treatment of ischemic stroke in general offer only a modest benefit in reducing recurrent stroke while adding to the risk of intracerebral hemorrhage and systemic bleeding. Escalation of antithrombotic treatments beyond standard single antiplatelet agents has not been effective in long-term lacunar stroke prevention efforts, unequivocally increasing intracerebral hemorrhage risk without providing a significant benefit. In this review, we critically review the available treatments for lacunar stroke based on evidence from clinical trials. For several of the major drugs, we summarize the adverse effects in the context of this unique patient population. We also discuss the role of neuroprotective therapies and neural repair strategies as they may relate to recovery from lacunar stroke.

Keywords: Cerebrovascular diseases; cerebral small vessel disease; lacunar stroke; stroke.

Figure 1.. Lacunar Stroke.

Recent small subcortical infarct (yellow arrow) appears bright on the DWI sequence and dark on the ADC sequence. In the early subacute phase, there may be a corresponding WMH seen on T2 FLAIR. A small subcortical infarct may involute over time and form a fluid-filled cavity or lacune seen on the contralateral hemisphere of this patient (red arrow). Note the presence of a surrounding T2 hyperintense rim which is a useful finding to help distinguish a lacune from a dilated perivascular space. DWI: diffusion-weighted imaging; ADC: apparent diffusion coefficient; WMH: white matter hyperintensity; FLAIR: fluid-attenuated inversion recovery.

Figure 2.. Lobar Lacune.

Lobar lacunes are a recently described entity which can be observed on T1 and T2 FLAIR sequences (blue arrows). This brain scan was taken from a patient with probable CAA. Consistent with this example, lobar lacunes are more associated with CAA than other cerebral small vessel diseases. Notably, on the SWI sequence, multiple posterior cortical microbleeds (red arrows) are seen; however, there is no microbleed corresponding to the lobar lacune. FLAIR: fluid-attenuated inversion recovery; CAA: cerebral amyloid angiopathy; SWI: susceptibility-weighted imaging. Images were graciously provided by Elif Gökçal.

Figure 3.. Cerebral Microinfarct.

Cerebral microinfarcts are less than 3 mm in diameter. They are hyperintense on T2 FLAIR (left, inset) and hypointense on T1 (right).

Figure 4.. Safety of Therapies for Lacunar Stroke.

This schematic highlights the major therapies that have been trialed in lacunar stroke. The harmful therapies (left side) should be avoided in most lacunar stroke patients. The safe therapies are listed on the right side.