Surely an intracranial hypertension crisis is an emergency that puts the patient’s survival at risk if left untreated. The tools available to the physician in this emergency are undoubtedly few. The only valid method to know these pressure data is invasive: drilling the patient’s skull and inserting a catheter. The problem arises when it is up to the physician to distinguish the patient who deserves this invasive treatment. The Milan consensus conference on traumatic brain injury report and Brain Trauma Foundation guidelines stated that intracranial pressure (ICP) “should be monitored in all salvageable patients with a severe trauma brain injury (3–8 Glasgow Coma Scale) and an abnormal computer tomography (CT) scan.” But from studies that analyze the use of invasive ICP monitoring, what seems to make the difference is the treatment protocol: monitoring alone cannot improve clinical outcome [1]. Considering this, avoiding an invasive procedure burdened by a percentage of complications (hemorrhagic, infectious, and malpositioning) for a patient who is not really at risk of high ICP becomes very important.

In neurocritical care, physicians have always considered the Monro–Kellie doctrine an indispensable dogma. On the other hand, Professor Mascarenhas [2] has devoted many years of study to the observation of variations in the tension of the cranial vault in response to ICP variations. By attaching a strain gauge transducer to an ex vivo skull, the researchers were able to measure the resulting strain signal. Thanks to the insights of Professor Frigeri [2], through collaboration with the company Braincare Corp, a wearable device for humans has been developed. This device is able to interpret the pressure oscillations produced by the transmission of the arterial pressure at the level of the choroid plexus to the cerebrospinal fluid (CSF). The principle is based is the ICP pulse morphology. This morphology analyzes the in vivo CSF waveform (intracranial pressure waveform [ICPW]). ICPWs translate the dynamic balance of intracranial compliance in relation to continuous arterial pulsations, venous outflow, and CSF movements, pointing to the Δvolume/Δpressure. The ICP pressure curve appears to consist of three distinct P waves. The P1 wave, usually characterized by the greatest amplitude, the “percussion wave,” represents the systolic arterial pulsation. The P2 wave, “tidal wave,” represents the intracranial compliance. Finally, the P3 wave represents the aortic valve closure. These three waves sometimes change according to the intracranial pathophysiological conditions. The P2 wave tends to increase in amplitude with increasing ICP. Researchers have identified the relationship between P2 and P1 as a noninvasive “key to interpretation” of ICP, and adding the time-to-peak interval (TTP) has thus generated an indicator. Using this sensor, called Brain4Care (B4C), placed in direct contact with the cranial vault, 3 cm over the anterior third of the orbitomeatal, it is possible to define the ICP without the need to drill the bone. The B4C correlation to invasive ICPW is good (P2/P1 ratio r = 0.72 and TTP r = 0.85), as is its predictive ability of ICP > 20 mm Hg (p < 0.001), with an area under the curve of 0.9. The negative predictive value is 100% for the P2/P1 ratio and 91.7% for TTP to rule out the presence of high ICP, with cutoffs of 1.06 and 0.2, respectively. The application of B4C through a black box algorithm that derives a composite index of intracranial compliance (Intracranial Compliance Scale) from noninvasive ICP waveform surrogates has produced comforting data on small series of patients. However, the method has several limitations. The device is sensitive to patient movements generating artifacts. Another limitation is operator dependence on the recognition of optimal waveform acquisition because an inadequate positioning may alter the results. The B4C system is not currently able to provide an estimate of the actual ICP value. The tool has not been tested on the pediatric population, and finally the B4C data are not yet validated on a healthy adult population (trial in progress) [3].

In addition to the one described in the article by Brasil, there are various other methods for noninvasive ICP assessment. Unfortunately, today, none of these is able to provide us with a progressive number of the ICP. Evensen et al. [4] investigated the correlation between waveforms of systemic blood pressure measured in the radial artery and ICPW. Unfortunately, a very selected series of patients (idiopathic normal pressure hydrocephalus), despite having been provided by the interested parties, was not sufficient to validate the method. Barry Dixon’s [5] group has developed a noninvasive brain pulse monitor that uses light to detect a photoplethysmographic signal arising from the blood vessels on the brain’s cortical surface. While considering the relationship with ICPW and the P2/P1 ratio, the published series is still very small, and the method is not validated. The measurement of the diameter of the optic nerve sheath directly connected to the ventricular chambers through the CSF is a simple method to perform with ultrasonography and is easily repeatable as a bedside follow-up. Unfortunately, a precise cutoff value above which we can be certain of high ICP has not yet been identified; furthermore, in ultrasound, the method is still burdened by an operator-dependent error. Finally, perhaps the most widespread and most promising method is that of the analysis of the velocimetry of the intracranial vessels of the polygon of Willis with transcranial Doppler. After a deep interest in the pulsatility index, many studies have shown that a reduction in the mean velocity and/or in the diastolic velocity of blood flow in the main vessels correlates well with the increase in ICP. Czosnyka’s [6] group has also developed a formula capable of converting these data into the value of noninvasive ICP. Unfortunately, to date, the largest international multicenter study has only been able to validate its negative predictive value [7].

Through all these noninvasive methods, we only can exclude with some certainty which patients do not suffer from high ICP. Together with the indirect neuroradiological signs, the clinical data, and the triggering etiology, we can orient ourselves on the risk of high ICP, and the noninvasive methods can help us increase the aggressiveness of care, choosing an invasive monitoring, which at the moment remains a practice that we still cannot do without.