A lacunar infarct, often called a lacunar stroke, is a type of ischemic stroke caused by the blockage of tiny arteries deep within the brain’s subcortical structures. These events account for approximately 25% of all ischemic strokes. While the immediate effects may be less extensive than a major stroke involving larger vessels, a lacunar infarct is still a serious medical emergency requiring immediate attention. Prompt medical intervention is necessary to limit acute damage and aggressively manage underlying conditions that increase the risk of future vascular events.
What Exactly Is a Lacunar Infarct?
A lacunar infarct is defined by its small size and specific location, typically measuring less than 15 millimeters in diameter. These infarcts occur when a small, penetrating end-artery becomes blocked, disrupting blood flow to deep brain areas like the basal ganglia, thalamus, and internal capsule. The name “lacunar” comes from the Latin word lacuna, meaning “pit” or “pond,” referring to the small cavity left after the damaged tissue resolves.
The primary cause of these blockages is chronic damage to the vessel walls, known as small vessel disease. Uncontrolled high blood pressure is the strongest predisposing factor, leading to a thickening and hardening of the small artery walls (lipohyalinois). This pathology differentiates lacunar infarcts from larger strokes, which are usually caused by clots traveling from the heart or neck arteries. In some cases, a lacunar infarct may also be caused by a tiny clot lodging at the opening of the small artery, known as branch atheromatous disease.
How Symptoms Manifest
Symptoms arise when the blockage occurs in a location controlling specific long tracts of nerve fibers, such as those responsible for movement or sensation. Unlike large strokes, which often cause widespread deficits, lacunar infarcts typically cause isolated, predictable patterns of symptoms. These distinct presentations are known as lacunar syndromes, and they depend on the precise location of the injury.
One common pattern is pure motor hemiparesis, involving weakness of the face, arm, and leg on one side of the body without sensory changes or cognitive impairment. Another is pure sensory stroke, characterized by numbness or altered sensation on one side without motor weakness. Other recognized syndromes include ataxic hemiparesis (combining weakness with poor coordination) and dysarthria-clumsy hand syndrome (causing slurred speech and difficulty with fine motor tasks).
Immediate Treatment and Ongoing Management
The first priority in treating a lacunar infarct is similar to any acute ischemic stroke: prompt restoration of blood flow and stabilization. If a patient arrives within the narrow time window (typically four and a half hours of symptom onset), they may be candidates for intravenous thrombolysis using tissue plasminogen activator (tPA) to dissolve the clot. Once the immediate danger passes, the focus shifts entirely to preventing recurrence, as the infarct signals a widespread problem with the brain’s small vessels.
Secondary prevention centers on aggressive management of underlying vascular risk factors. Control of high blood pressure is the most impactful intervention; guidelines often recommend aiming for a systolic blood pressure target below 130/80 mmHg. Patients are also typically prescribed an antiplatelet agent, such as aspirin, to prevent new clots. Aggressive management of diabetes and high cholesterol with statin therapy is routinely initiated to protect the entire vascular system.
Long-Term Prognosis and Recurrence Risk
The long-term outlook following a single lacunar infarct is often favorable compared to other types of stroke, with many patients achieving good functional recovery. However, this recovery should not imply the event is insignificant. The seriousness of a lacunar infarct lies in its role as a warning sign of underlying, progressive small vessel disease.
Patients who have experienced one lacunar infarct face a significantly increased risk of future strokes, with the recurrence rate reaching approximately 22.4% over five years. The accumulation of multiple lacunar infarcts over time, even asymptomatic ones, can lead to progressive cognitive decline and is a leading cause of vascular dementia. The long-term prognosis depends entirely on controlling the risk factors that caused the infarct.