It is accepted that cerebrovascular dilatation is a constant response during the advanced stage of intracranial hypertension. Severe intracranial hypertension ultimately associates with profound vasodilatation and reduces cerebral blood flow to zero. This irreversible state is called cerebral vasomotor paralysis by Langfitt et al (1965). The rich adrenergic nerve supply of the cerebral vessels suggests that pressor amines possibly affect the cerebral circulation and the cerebral vascular tone. This study is to investigate the reactivity of norepinephrine and phentolamine on intracranial pressure (ICP) in patients with severe intracranial hypertension. The ICP and systemic blood pressure (SBP) monitorings were carried out continuously after the evacuation of intracerebral hematomas due to ruptured intracranial aneurysms. Severe intracranial hypertension due to brain swelling was observed in these patients. Three stages were defined according to the reactivity to norepinephrine and phentolamine on the ICP. In Stage I, norepinephrine caused a transient decrease in the ICP and phentolamine caused a marked rise in the ICP. Stage II was marked by the absence of the ICP response to norepinephrine and phentolamine. During Stage III, the ICP changes synchronously with a variation of the SBP after the administration of norepinephrine and phentolamine. In Stage I patients, the mean ICP level was between 500-1000 mmH2O. Tracing of the ICP in this group showed transient rises called pressure waves and the waves were recurring increases in the ICP to value of 300-500 mmH2O superimposed on an elevated level of the ICP. On the other hand, in Stage II and III patients, the ICP level exceeded 1000 mmH2O. Tracing of the ICP in these groups showed only variations by the arterial pulses. The patients in Stage I had a well prognosis for life if proper treatments such as continuous ventricular drainage were carried out. The patients in Stage II and III had a poor prognosis for life inspite of continuous ventricular drainage. There are varying stages in cerebrovascular dilatation accompanying intracranial hypertension. We have no information on the mechanism of this cerebrovascular dilatation at present. However, we speculate that the pressor amines such as norepinephrine may partly participate in the mechanism responsible for the vasodilation. So, we attempt to grade the degree of this vasodilatation according to the reactivity of norepinephrine and phentolamine on the ICP. It is presumed that cerebrovascular dilatation is slight and reversible in Stage I patients, whereas cerebrovascular dilatation is profund and irreversible in Stage II and III patients. Continuous ICP recording and examination of the reactivity to norepinephrine and phentolamine on the ICP are valuable when considering the prognosis for life in patients with severe intracranial hypertension.