Intracranial hypertension is one of the most important syndromes in neurology and neurosurgery; raised intracranial pressure is the most common cause of death in neurosurgery. A recent classification of intracranial hypertension is based upon the etiopathogenesis of intracranial hypertension: a) parenchymatous intracranial hypertension, b) vascular intracranial hypertension, c) meningeal intracranial hypertension and d) idiopathic intracranial hypertension. Vascular etiologies can individualize vascular types of intracranial hypertension: (1) cerebral venous thrombosis reduces venous outflow and determines low cerebrospinal fluid drainage and brain edema; (2) hypertensive encephalopathies cause brain swelling, both brain edema and congestive brain swelling with raised Intracranial Pressure (ICP); (3) ischaemic stroke induces an increased capillary permeability with open brain-blood barrier, brain edema and severe ICP increase. The main features of ICP increase are: the speed of ICP increase up to and respectively above, the normal limit of ICP, the pathological value of ICP and the duration that the pathological values of ICP are maintained. These features of ICP increase depend on its etiology: a low speed of ICP increase in cerebral venous thrombosis or a high speed in hypertensive encephalopathies or in ischaemic strokes. Also the periods when ICP stays at high values are different depending on the etiologies of ICH: a long period in cerebral venous thrombosis and a short period in ischaemic strokes.