Hyperaemia in the brain, as elsewhere, is divisible into active and passive. Active hyperaemia occurs generally or locally in consequence of hypertrophy or over-action of the heart, especially when the arteries are atheromatous and unable to control the circulation. It also occurs in inflammations of the brain or meiiinges, and in various conditions of excitement of the brain, as the delirium of fevers, the early stage of general paralysis, the typhoid stage of cholera, in conditions of plethora, or excessive functional activity as over-work or over-strain, or from the action of alcohol and other agents such as nitrite of amyl. In these conditions it may be regarded as an inflammatory phenomenon.

Passive hyperaemia results most directly from thrombosis of the cerebral sinuses (see further on), but is also an occasional consequence of pressure on the jugular veins, or of disease of the heart or lungs leading to general venous engorgement.

The appearances visible after death in both forms are frequently insignificant, especially in active hyperaemia, the existence of which is usually matter of inference rather than of observation. The over-filling of the vessels is most visible in the meninges, but there may be also a deepened colour of the convolutions, and the venous stems in them and in the white substance may be visibly dilated.

Anaemia or Ischaemia results mostly from obstruction of arteries (see below). It may also be a consequence of general anaemia, as from loss of blood, in which case it affects the brain as a whole. It may result from local pressure on the brain produced by tumours, extravasations of blood, or inflammatory exudations. Further, it may result from an unequal distribution of the blood, as in cases of dilatation of certain other vascular areas, as say, when rapid dilatation of the vessels of the abdomen follows the rapid removal of ascitic fluid; stenosis of the aortic orifice is another possible cause, and the condition may also arise from the loss of fluids from the intestine, as in certain cases of protracted diarrhoea in children associated with general malnutrition. Local anaemia in all these cases is liable to result in softening of the brain substance. Post-mortem the brain substance, both grey and white, is pale. The larger veins are full but the smaller vessels of the convexity are empty, and there is an excess of cerebro-spinal fluid present both in the pia and in the ventricles.

(Edema of the brain is also usually but a part of some other lesion. (Edema of the brain substance is a rare and in many cases a hypothetical condition. The more definite oedemas affect the membranes and cavities, and will be considered further on. There is, however, an occasional local oedema of the brain substance in the neighbourhood of haemorrhages, tumours, and veins obstructed by thrombi, and it is also believed to occur at the outset of local inflammations. It may, however, occur in Bright's disease, and according to Franke it is to this that some of the cerebral phenomena of uraemia are due.

The anatomical changes are not unlike those found in anaemia. The brain substance is moist and glistening. The fluid in the ventricles is increased as a rule. The meshes of the pia also contain an excess of fluid, and the whole brain has a sodden aspect.