Small arteries beneath brain. 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). 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<unk> s. More recent advances have also suggested these mechanisms may play a combined role in the aetiology of<unk>  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<unk> . 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<unk> .<unk> s 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<unk>  pathology, one can see a subcortical dementia such as Binswanger disease.
Lacunar stroke
Watershed stroke
Posterior circulation infarct
Posterior cerebral artery syndrome
Middle cerebral artery syndrome
Anterior cerebral artery syndrome
Silent stroke
ROSAH syndrome