A method is described for monitoring the relationship between CSF pulse pressure and ICP in clinical patients. Highly significant linear relationships were found during 65 continuous ICP recordings in 58 patients. The slope value of this relationship showed a positive correlation with the elastance coefficient, a volume-pressure parameter assessed by bolus injection. However, the correlation was too weak to allow for a confident prediction of the elastance coefficient on the basis of CSF pulse pressure in the individual patient. This was attributed to the variable magnitude of the volume change underlying the CSF pulse pressure: the pulsatile variation in cerebral blood volume. This quantity was calculated on the basis of a mathematical model from the slope value and the elastance coefficient and was found to vary between 0.36 and 4.38 ml. During plateau waves a disproportionate increase in pulse pressure with the ICP was observed in contrast with a relative decrease in intracranial elastance. This phenomenon was ascribed to an increase in the pulsatile variation in cerebral blood volume. It is concluded that, under certain conditions, the intracranial volume-pressure relationship can be continuously monitored by means of CSF pulse pressure analysis. The findings during plateau waves suggest that the pulse pressure also reflects the state of the cerebral vasomotor tone.

Nociception and loss of awareness during exposure to anaesthetic concentration of nitrous oxide (N2O) were studied in eight male medical students. The cold water nociception test, where a hand is immersed in 0 degree C stirred water, was used for measurement of nociception. At irregular intervals an auditory command was given to oppose two fingers, and this served to monitor consciousness. The selected inspiratory concentration of N2O used per individual was sufficient to induce a loss of consciousness for more than 2.5 min, within 10 min of exposure to N2O. This concentration of N2O varied from 60% to 80%. The experimental exposure to N2O lasted 3 h. In all volunteers significant antinociception was observed within 2 min of exposure to N2O. The maximal analgesic effect was observed between 20 and 30 min of exposure to N2O. The analgesic effect of N2O gradually decreased and was absent in all eight volunteers within 150 min. Two volunteers regained consciousness at 77 and 91 min of exposure, whilst still breathing 60 and 80% N2O. These results show that tolerance to antinociceptive effects of N2O in man rapidly develops and that awareness may occur in some volunteers during prolonged exposure to N2O.

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The cerebrospinal fluid pulse pressure (CSFPP) has found application as a measure of intracranial elastance. However, CSFPP is also dependent on the magnitude of the pulsatile variation in cerebral blood volume (delta Vb). The purpose of the present study was to assess the effect on delta Vb of changes in systemic arterial pressure (SAP) and arterial carbon dioxide tension (PaCO2) as well as elevation of intracranial pressure (ICP). Therefore, delta Vb was computed from the electromagnetically measured flow profile in the vertebral artery of the dog on the assumption of a nonpulsatile cerebral venous outflow. During arterial hypotension, delta Vb was increased due to a shift of flow from diastole to systole, whereas mean flow was not affected. The reverse phenomenon was observed when SAP was raised. Changes in PaCO2 had little effect on pulsatile blood flow. The changes in total blood flow that occurred were evenly distributed over the cardiac cycle. Consequently, delta Vb was not significantly affected, although CSFPP was considerably changed. When ICP was raised, a breakpoint pressure was observed above which cerebral blood flow (CBF) decreased and CSFPP and delta Vb increased. This contradiction was explained by the finding of a decrease in diastolic flow, causing the fall in CBF, whereas systolic flow relative to mean flow was increased, resulting in an increased delta Vb. The underlying mechanisms of the pulsatile flow changes are extensively discussed. It is argued that the arterial inflow profile is largely determined by the compliance of the inflow section of the cerebral vascular bed. Vascular compliance is significantly altered by changes in SAP and ICP because they affect the transmural pressure of the vessels, whereas this is not the case during changes in PaCO2.