An account is given of hypertensive encephalopathy on the basis of neurohistological studies into 54 brains, with additional reference being made to autopsies. Vasculopathy of peripheral arteries and arterioles along with thickening of vascular walls, change of media, and lumen stenosis were primarily recorded by means of optical light and electron microscopy. A difference of more than seven per cent was found to exist between wall thicknesses of arterioles in hypertensive brains, on the one hand, and those in normotensive brains, on the other. Vessels with thickened walls were not rigid but were rather capable of dilation just as under normotensive conditions. Their inner diameters, however, were below normal. Vascular wall fibrosis, to which little attention had been given in the past, was repeatedly recordable from the venous and capillary systems. Impairment of the endothelial barrier function was quite often recorded, with lipid deposits being incorporated in peripheral arterioles and capillaries. No relevance to pathogenesis can be reliably attributed at present to detection of IgG in the arterial system. Microinfarction, micro-haemorrhage as well as disseminated damage to nerve cells are recordable from roughly one third of all hypertensive brains and are primarily located in brain stem ganglia. Demyelinisation and cerebral oedema are quite infrequent. High-protein cerebral oedema was found in some rare cases. Hypertensive encephalopathy should be considered as a nosological entity in which morphological and clinical phenomena are not always correlated to each other.