Sixty years have passed since neurosurgeon Nils Lundberg presented his thesis about intracranial pressure (ICP) monitoring, which represents a milestone for its clinical introduction. Monitoring of ICP has since become a clinical routine worldwide, and today represents a cornerstone in surveillance of patients with acute brain injury or disease, and a diagnostic of individuals with chronic neurological disease. There is, however, controversy regarding indications, clinical usefulness and the clinical role of the various ICP scores. In this paper, we critically review limitations and weaknesses with the current ICP measurement approaches for invasive, less invasive and non-invasive ICP monitoring. While risk related to the invasiveness of ICP monitoring is extensively covered in the literature, we highlight other limitations in current ICP measurement technologies, including limited ICP source signal quality control, shifts and drifts in zero pressure reference level, affecting mean ICP scores and mean ICP-derived indices. Control of the quality of the ICP source signal is particularly important for non-invasive and less invasive ICP measurements. We conclude that we need more focus on mitigation of the current limitations of today’s ICP modalities if we are to improve the clinical utility of ICP monitoring.

Time domain analysis of the intracranial pressure (ICP) waveform provides important information about the intracranial pressure-volume reserve capacity. The aim here was to explore whether the tympanic membrane pressure (TMP) waveform can be used to non-invasively estimate the ICP waveform. Simultaneous invasive ICP and non-invasive TMP signals were measured in a total of 28 individuals who underwent invasive ICP measurements as a part of their clinical work up (surveillance after subarachnoid hemorrhage in 9 individuals and diagnostic for CSF circulation disorders in 19 individuals). For each individual, a transfer function estimate between the invasive ICP and non-invasive TMP signals was established in order to explore the potential of the method. To validate the results, ICP waveform parameters including the mean wave amplitude (MWA) were computed in the time domain for both the ICP estimates and the invasively measured ICP. The patient-specific non-invasive ICP signals predicted MWA rather satisfactorily in 4/28 individuals (14%). In these four patients the differences between original and estimated MWA were <1.0 mmHg in more than 50% of observations, and <0.5 mmHg in more than 20% of observations. The study further disclosed that the cochlear aqueduct worked as a physical lowpass filter.

This study explored the hypothesis that the central aortic blood pressure (BP) waveform may be used for non-invasive estimation of the intracranial pressure (ICP) waveform. Simultaneous invasive ICP and radial artery BP waveforms were measured in 29 individuals with idiopathic normal pressure hydrocephalus (iNPH). The central aortic BP waveforms were estimated from the radial artery BP waveforms using the SphygmoCor system. For each individual, a transfer function estimate between the central aortic BP and the invasive ICP waveforms was found (Intra-patient approach). Thereafter, the transfer function estimate that gave the best fit was chosen and applied to the other individuals (Inter-patient approach). To validate the results, ICP waveform parameters were calculated for the estimates and the measured golden standard. For the Intra-patient approach, the mean absolute difference in invasive versus non-invasive mean ICP wave amplitude was 1.9 ± 1.0 mmHg among the 29 individuals. Correspondingly, the Inter-patient approach resulted in a mean absolute difference of 1.6 ± 1.0 mmHg for the 29 individuals. This method gave a fairly good estimate of the wave for about a third of the individuals, but the variability is quite large. This approach is therefore not a reliable method for use in clinical patient management.

Background The dementia subtype idiopathic normal pressure hydrocephalus (iNPH) has unknown etiology, but one characteristic is elevated intracranial pressure (ICP) wave amplitudes in those individuals who respond with clinical improvement following cerebrospinal fluid (CSF) diversion. To explore the mechanisms behind altered ICP wave amplitudes, we correlated central aortic blood pressure (BP) and ICP waveform amplitudes (intracranial aortic amplitude correlation) and examined how this correlation relates to ICP wave amplitude levels and systemic hemodynamic parameters. Methods The study included 29 patients with probable iNPH who underwent continuous multi-hour measurement of ICP, radial artery BP, and systemic hemodynamic parameters. The radial artery BP waveforms were used to estimate central aortic BP waveforms, and the intracranial aortic amplitude correlation was determined over consecutive 4-min periods. Results The average intracranial aortic amplitude correlation was 0.28 ± 0.16 at the group level. In the majority of iNPH patients, the intracranial aortic amplitude correlation was low, while in about 1/5 patients, the correlation was rather high (average Pearson correlation coefficient > 0.4). The degree of correlation was hardly influenced by systemic hemodynamic parameters. Conclusions In about 1/5 iNPH patients of this study, the intracranial aortic amplitude correlation (IAAC AORTIC) was rather high (average Pearson correlation coefficient > 0.4), suggesting that cerebrovascular factors to some extent may affect the ICP wave amplitudes in a subset of patients. However, in 14/19 (74%) iNPH patients with elevated ICP wave amplitudes, the intracranial aortic amplitude correlation was low, indicating that the ICP pulse amplitude in most iNPH patients is independent of central vascular excitation, ergo it is modulated by local cerebrospinal physiology. In support of this assumption, the intracranial aortic amplitude correlation was not related to most systemic hemodynamic variables. An exception was found for a subgroup of the patients with high systemic vascular resistance, where there was a correlation. Keywords ICP wave amplitudes. Central aortic waveforms. Idiopathic normal pressure hydrocephalus. Autoregulation This article is part of the Topical Collection on Neurosurgery general