Lacunar stroke or lacunar cerebral infarct (LACI) is the most common type of ischemic stroke, resulting from the occlusion of small penetrating arteries that provide blood to the brains deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed, may be described as having lacunar stroke syndrome (LACS). Much of the current knowledge of lacunar strokes comes from C. Miller Fishers cadaver dissections of post-mortem stroke patients. He observed "lacunae" (empty spaces) in the deep brain structures after occlusion of 200–800 μm penetrating arteries and connected them with five classic syndromes. These syndromes are still noted today, though lacunar infarcts are diagnosed based on clinical judgment and radiologic imaging. Signs and symptoms
Each of the five classical lacunar syndromes has a relatively distinct symptom complex. Symptoms may occur suddenly, progressively, or in a fluctuating (e.g., the capsular warning syndrome) manner. Occasionally, cortical infarcts and intracranial hemorrhages can mimic lacunar infarcts, but true cortical signs (aphasia, visuospatial neglect, gaze deviation, and visual field defects) are always absent in lacunar strokes. The classic syndromes are as follows:

Silent lacunar infarction
A silent lacunar infarction (SLI) is one type of silent stroke which usually shows no identifiable outward symptoms, and is thus termed "silent." Because stroke is a clinical diagnosis (that is, it is defined by clinical symptoms), there is debate about whether SLI are considered to be strokes, even though the pathophysiology is presumably the same. Individuals who have a SLI are often completely unaware they have had a stroke.
Occasionally, atheroma in the parent artery blocks the orifice of the penetrating artery (luminal atheroma), or atheroma involves the origin of the penetrating artery (junctional atheroma). Alternatively, hypoperfusion is believed to be the mechanism when there is stenosis of the penetrating artery. When no evidence of small vessel disease is found on histologic examination, an embolic cause is assumed, either artery-to-artery embolism or cardioembolism. In one recent series, 25% of patients with clinical radiologically defined lacunes had a potential cardiac cause for their strokes. More recent advances have also suggested these mechanisms may play a combined role in the aetiology of lacunar infarction. The most current theory indicates endothelial dysfunction and increased permeability of the blood-brain barrier first allow leakage of blood contents, promoting gliosis and white matter hyper-intensities on magnetic resonance imaging. Moreover, focal narrowing of brain vessels and impairment of their ability to dilate in response to various stimuli may lead to a decreased cerebral blood flow and ultimately lacunar stroke.Advanced age, chronic hypertension, smoking and diabetes mellitus are risk factors. It is unclear whether there is an association with alcohol consumption, elevated cholesterol, or history of prior stroke. Lacunar strokes may result from carotid artery pathology or microemboli from the heart as in atrial fibrillation. Patients often recover well, but if there is enough white matter disease from lacunar pathology, one can see a subcortical dementia such as Binswanger disease.