We have reviewed the most relevant data regarding ABPM and brain damage, with specific reference to first and recurrent stroke, silent structural brain lesions such as lacunar infarcts and white matter lesions, and cognitive impairment. Only two large studies have evaluated the usefulness of ABPM in relation to antihypertensive treatment in primary stroke prevention. In the Syst-Eur trial, drug treatment reduced ABPM and office BP more than placebo in patients with sustained isolated systolic hypertension (ISH). In contrast, in those patients with white-coat hypertension (WCH) changes in ABPM between the treatment groups were not significantly different. Patients with WCH had a lower incidence of stroke (p < 0.05) during follow-up than patients with sustained ISH, suggesting that WCH is a benign condition. In the HYVET trial 50 % of the very elderly patients included with office systolic BP > 160 mmHg had WCH. However, a significant 30 % stroke reduction was observed in treated patients including those with WCH, indicating that WCH may not be a benign condition in the elderly. In the acute stroke setting, where treatment of hypertension is not routinely recommended due to the lack of evidence and the differing results of the very few available trials, ABPM data shows that sustained high BP during the first 24 h after acute stroke is related to the formation of cerebral edema and a poorer functional status. On the other hand, even when nondipping status was initially related to a poorer prognosis, data indicate that patients with very-large nocturnal dipping, the so-called "extreme dippers", are those with the worse outcomes after stroke. The association between different ABPM parameters (circadian pattern, short-term variability) and poorer performance scores in cognitive function tests have been reported, especially in elderly hypertensives. Unfortunately most of these studies were cross-sectional and the associations do not establish causality.