Acute lacunar infarcts seen within 4.5 hours of onset and presenting with symptoms other than just pure sensory should be considered for intravenous tissue-type plasminogen activator therapy. This is the only treatment proven to improve clinical outcome. Lacunar strokes showed the most favorable outcome following intravenous thrombolysis (The NINDS rt-PA Stroke Study Group 1995), with the lowest rate of post-thrombolysis hemorrhagic transformation. Imaging better identifies the lacunar infarct before thrombolysis than clinical lacunar syndrome (Lee 2010). Intraarterial therapy may be indicated if a large artery (middle cerebral or basilar) is found to be the cause of the lacunar infarct and the patient is seen within 6 hours. Between 24% and 37% of lacunar strokes progress and have a fluctuating course of motor deficit for the first 24 hours and up to 72 hours or 1 week. Multiple mechanisms have been considered responsible for progression: inflammatory response, glutamate excitotoxicity, stepwise occlusion of the small penetrators (Steinke 2002), and severe hypoperfusion of ischemic area with distal embolization (Caplan 2002). The only treatment proved to be effective in progressing lacunar stroke is augmentation of cerebral blood flow. Blood pressure should not be lowered and volume expanders or pressor medication can be used, if necessary. Although hyperglycemia is associated with worsened outcome in acute ischemic stroke, the impact may not be similar in lacunar versus nonlacunar infarct. Hyperglycemia has a detrimental effect on nonlacunar stroke outcome, but a moderate hyperglycemia (8-12 mmol/L) seems to be beneficial in lacunar infarct. This beneficial effect diminishes with severe hyperglycemia with more than 12 mmol/L (Uyttenboogaart 2007). Antiplatelets and neuroprotectants have limited utility as long as perfusion failure persists (Caplan 2002). A higher blood pressure during the first 24 hours after the occurrence of an acute lacunar infarct carries a better neurologic outcome (Semplicini 2003). Anticoagulation may not stop stroke progression and, in addition, it may increase the already existing risk for cerebral hemorrhages. The T2-weighted gradient-echo MRI is sensitive in detecting hemosiderin resulting from cerebral microbleeds. One study showed an increased incidence of silent microbleeds in patients with Binswanger disease (77%) and multiple lacunar infarctions (51%), indicating an advanced bleeding-prone cerebral microangiopathy (Hanyn 2003). This finding has important implications in clinical management. Rehabilitation, prevention, and treatment of medical complications are important measures.