Treatment and prognosis
Typically, tissue plasminogen activator may be administered within 3 to 4.5 hours of stroke onset if the patient is without contraindications (i.e. a bleeding diathesis such as recent major surgery or cancer with brain metastases). High dose aspirin can be given within 48 hours. For long term prevention of recurrence, medical regimens are typically aimed towards correcting the underlying risk factors for lacunar infarcts such as hypertension, diabetes mellitus and cigarette smoking. Anticoagulants such as heparin and warfarin have shown no benefit over aspirin with regards to five-year survival.Patients who have lacunar strokes have a greater chance of surviving beyond thirty days (96%) than those with other types of stroke (85%), and better survival beyond a year (87% versus 65-70%). Between 70% and 80% are functionally independent at 1 year, compared with fewer than 50% otherwise.Occupational therapy and physical therapy interventions are used in the rehabilitation of lacunar stroke. A physiotherapy program will improve joint range of motion of the paretic limb using passive range of motion exercises. When increases in activity are tolerated, and stability improvements are made, patients will progress from rolling to side-lying, to standing (with progressions to prone, quadruped, bridging, long-sitting and kneeling for example) and learn to transfer safely (from their bed to a chair or from a wheel chair to a car for example). Assistance and ambulation aids are used as required as the patient begins walking and lessened as function increases.
This type of stroke often causes lesions in the surrounding brain tissue that are visibly detected via neuroimaging techniques such as MRI and computed axial tomography (CT scan). Silent strokes, including silent lacunar infarctions, have been shown to be much more common than previously thought, with an estimated prevalence rate of eleven million per year in the United States. Approximately 10% of these silent strokes are silent lacunar infarctions. While dubbed "silent" due to the immediate lack of classic stroke symptoms, SLIs can cause damage to the surrounding brain tissue and can affect various aspects of a persons mood, personality, and cognitive functioning. A SLI or any type of silent stroke places an individual at greater risk for future major stroke. Pathophysiology
According to Koffler et al., lacunes are derived from an "occlusion of a single deep penetrating artery that arises directly from  the constituents of the circle of Willis, cerebellar arteries, and basilar artery". Other lesions that are associated with lacunes appear in the "deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%)". These lesions are less common within other brain regions such as the cerebellum, cerebral white matter and anterior limb of the internal capsule.The two proposed mechanisms are microatheroma and lipohyalinosis. At the beginning, lipohyalinosis was thought to be the main small vessel pathology, but microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis).