During the past few years, the branch syndromes have been ascribed to pontine lesions, and the development of neuroimaging techniques has renewed the interest in exploring their clinical–radiological correlation. Brain imaging via MRI has helped in the diagnosis and accurate localization of lesions. From classic studies it is now accepted that the pathogenic mechanism of lacunar pontine infarction (LPI) is perforating small arterial disease or microangiopathy caused by lipohyalinosis, whereas paramedian pontine infarction (PPI) are caused by paramedian or circumferential basilar branch disease due to atheromatous branch occlusion. The importance of basilar artery disease not only in severe posterior circulation infarcts but also in minor brainstem strokes is known from previous reports. The mechanism of PPI is probably local occlusion of the mouths of paramedian perforators through the atheromatous basilar artery (basilar branch occlusion). Infrequent basilar artery diseases such as dissection, aneurysm and hypoplasia, dolichoectatic basilar artery, embolism, or vasospasms are known to block the orifices of penetrating branch arteries and cause an infarct in the territory of the obstructed branches. An association between basilar artery branch disease and isolated pontine infarction exists; moreover, the enlargement of pontine lesion seems to be associated with neurologic worsening and fluctuating symptoms, but we know little about stroke mechanisms in patients with fluctuating symptoms and about the role of branch atherosclerotic disease. The treatment remains controversial, even in acute cases. Implementation of new neuroimaging techniques, such as high-resolution MRI, could be helpful in identifying pathogenetic mechanisms of isolated pontine infarction, thus improving therapeutic strategy and secondary prevention.