Progressively rising intracranial hypertension reduces cerebral blood flow and cerebral vascular dilatation occurs during the advanced stage of intracranial hypertension. 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.
Simultaneous recording of ICP and systemic blood pressure (SBP) was continuously made in 9 patients after the evacuation of intracerebral hematoma due to a ruptured intracranial aneurysm and hypertensive intracerebral hemorrhage. Severe intracranial hypertension due to brain swelling was observed in these patients. The trace of ICP revealed two patterns. One was that the mean ICP level was between 500-1000 mm H2O and the ICP curve were marked by transient and recurrent fluctuations. This pattern was seen in 5 patients. The other was that the mean ICP level exceeded 1000 mm H2O and the trace of ICP changes only with arterial pulse. This pattern was seen in 4 patients.
Three stages were defined according to the reactivity of norepinephrine and phentolamine on ICP. In stage I, norepinephrine caused a transient decrease in ICP and phentolamine caused a rise in ICP. The trace of ICP in this stage showed transient and recurrent fluctuations. Stage II was marked by the absence of the ICP response to norepinephrine and phentolamine. During stage III, ICP changed depending on the variations of SBP after the administration of norepinephrine and phentolamine. The trace of ICP in stage II and III patients showed monotonous waves synchronous with arterial pulse. In terminal stage, this monotonous arterial pulse wave fell concomitant with SBP.
The patients in stage I had a good chance to live if proper treatment, such as continuous ventricular drainage was carried out. The patients in stage II and III had a poor chance to live in spite of continuous ventricular drainage.
There are varying degrees—in cerebrovascular dilatation accompanying intracranial hypertension. We have no information on the mechanism of this cerebrovascular dilatation at present. We speculate that the pressor amines such as norepinephrine may partly participate in the mechanism responsible for the vasodilatation. So, we attempted to grade the degree of this vasodilatation according to the reactivity to norepinephrine and phentolamine on ICP. It is presumed that cerebrovascular dilatation is slight and reversible in stage I patients, whereas cerebrovascular dilatation is profound and irreversible in stage II and III patients.
