1. Luminal infarcts are small (0.2-15 mm) non-cortical cerebral infarcts that result from obstruction of a single penetrating vessel of a large cerebral artery. Most of these penetrating vessels branch at an acute angle from the ring of Willis, the main trunk of the middle cerebral artery, and the basilar artery. Most of the luminal foci are located in the basal ganglia (nucleus accumbens, pallidum, thalamus, and caudate nucleus), subcortical white matter (internal capsule and corona radiata), and pontine brain. 2. The mechanisms of obstruction in several small penetrating arteries are as follows: (1) Lipohyaline degeneration of the penetrating vessels is a common cause, especially in small infarcts (3-7 mm in length). (2) Tiny atheromatous plaques starting in the middle cerebral artery, the ring of Willis, or in the distal basilar artery or in the proximal part of the penetrating vessels of the vertebral arteries. This mechanism has been confirmed by serial sections of the basilar artery. (3) In some cases, not verified by pathology, tiny emboli are suspected to be the cause of these small infarcts. 3, Luminal spaces account for 15-26% of ischemic strokes. 4, Two of the three mechanisms are associated with chronic vascular disease due to systemic hypertension, and other possible risk factors include diabetes mellitus and possibly smoking. 5. Approximately 20 lacunar syndromes have been described. Five conditions are highly recognized as radiologically indicative of lacunar infarction: pure motor paralysis; pure sensory stroke; ataxic mild hemiparesis, sensorimotor stroke, and dysarthria-awkward hand syndrome. In general, lacunar syndromes lack cortical symptoms such as aphasia, dyscognition, neglect, disuse or hemianopia. Monoplegia, xyloplegia, coma, decreased level of consciousness and seizures are also usually not seen. 6. The in vivo diagnosis of lacunar infarction relies on clinical manifestations consistent with the ischemic lesions found on CT or MRI. Brain imaging is also important to detect other potentially life-threatening conditions such as hemorrhage or subdural hematoma. The underlying stroke mechanism still needs to be looked for, with the aim of ruling out those recurrent factors that can be corrected. 7. The prognosis of patients with ischemic stroke is generally improved if alteplase (recombinant tissue-type fibrinogen activator or rt-PA) is given intravenously within 4.5 hours of symptom onset. The available evidence supports the benefit of intravenous thrombolysis in patients with luminal infarction. Most patients with acute ischemic stroke who are not candidates for thrombolysis should be treated with aspirin. 8. Compared with other types of infarction, lacunar infarction has a better short-term prognosis (within one year of onset). Prevention – The limited effectiveness of treatment in the acute phase of lacunar infarction suggests that secondary prevention should become a major focus of treatment. Intensive medical interventions and risk factor management, including antihypertensive therapy, antiplatelet coagulation therapy and statin therapy are recommended for patients with ischemic stroke or transient ischemic attack.