A lacunar infarct is an ischemic stroke that occurs when blood flow is blocked to one of the brain’s tiny, deep penetrating arteries. This blockage causes the death of a small area of brain tissue in the subcortical regions, such as the basal ganglia or thalamus. The term “lacunar” comes from the Latin word lacuna, meaning a small pit or lake, referring to the small cavity left behind after the body reabsorbs the damaged tissue. Lacunar infarcts are common, accounting for approximately 25% of all ischemic strokes worldwide.
The Specific Mechanism of Lacunar Infarct
Lacunar infarcts occur deep within brain structures, affecting areas like the internal capsule, thalamus, and brainstem. These areas are supplied by slender, perforating arteries that branch directly from larger cerebral arteries. These small vessels are considered “end-arteries,” meaning they lack the redundant backup blood supply, or collateral circulation, found elsewhere in the brain.
The tiny size of these vessels, typically between 40 and 800 micrometers in diameter, makes them vulnerable to a distinct set of diseases. The primary mechanism of obstruction is often a process called lipohyalinosis, which involves the thickening and degeneration of the vessel wall due to a buildup of fatty and hyaline material. This thickening narrows the artery’s inner channel, severely restricting blood flow.
Another common pathological mechanism is microatheroma, the formation of a small atherosclerotic plaque directly within the penetrating artery. Unlike larger strokes caused by clots traveling from the heart or neck arteries, lacunar strokes result from localized disease within the small vessel itself. The resulting lesion is less than 15 millimeters in diameter, distinguishing it from larger strokes.
Primary Causes and Driving Risk Factors
The conditions that damage these small penetrating arteries are systemic and chronic, with high blood pressure being the most significant factor. Sustained, poorly controlled hypertension directly leads to the vessel wall thickening characteristic of lipohyalinosis. This chronic pressure alters the structure of the small arteries, making them prone to occlusion.
Diabetes mellitus is the second major condition that accelerates this microvascular damage. High blood sugar levels contribute to the deterioration of the vessel lining, promoting both lipohyalinosis and microatheroma formation. Diabetic individuals face a significantly higher risk of developing a lacunar stroke.
Other cardiovascular risk factors also contribute to small vessel disease. High cholesterol (hyperlipidemia) promotes the buildup of fatty deposits that form microatheromas within the vessel walls. Lifestyle factors like smoking further damage the arterial lining and increase the likelihood of plaque formation. Aggressive management of these conditions is necessary to reduce the risk of a first or recurrent lacunar infarct.
Common Clinical Syndromes
Because lacunar infarcts are small and occur in deep structures where nerve fibers are tightly packed, they produce specific neurological deficits known as lacunar syndromes. The location of the blockage determines the symptoms, which lack the higher-level cognitive signs seen in larger strokes, such as aphasia or visual field loss.
The most common presentation is Pure Motor Hemiparesis, marked by sudden weakness affecting the face, arm, and leg on one side of the body, without sensory loss. This syndrome results from an infarct in the posterior limb of the internal capsule or the pons. Pure Sensory Stroke is another common presentation, resulting from a lesion in the thalamus that causes numbness or abnormal sensation across one side of the body.
A third distinct syndrome is Ataxic Hemiparesis, which combines weakness on one side of the body with clumsiness or poor coordination, often affecting the leg more than the arm. This is usually due to an infarct in the pons or the internal capsule. Finally, Dysarthria-Clumsy Hand Syndrome presents as difficulty with speaking clearly and noticeable clumsiness in the hand, particularly for fine motor tasks like writing, while strength in the limbs is largely preserved.
Confirmation and Long-Term Outlook
Diagnosis begins with a clinical assessment of the specific lacunar syndrome, but imaging is required for confirmation. A computed tomography (CT) scan is typically the first test to rule out a brain hemorrhage, though it may not clearly show the small lacunar lesion acutely. Magnetic Resonance Imaging (MRI) is the preferred method, as it is more sensitive and can visualize the tiny infarcts deep within the brain.
The initial prognosis following a lacunar infarct is favorable, with many patients experiencing better functional recovery compared to those who have suffered a larger stroke. However, the long-term outlook is challenging because the risk of recurrence is similar to that of other stroke types. Repeated lacunar infarcts are a significant concern, as they can accumulate damage over time.
Multiple lacunar infarcts contribute to the burden of small vessel disease in the brain. This widespread damage can lead to vascular cognitive impairment, which may progress to vascular dementia. The most important long-term strategy is aggressive secondary prevention, focusing on strict control of blood pressure, blood sugar, and cholesterol to prevent future events.