Intracranial Pressure

The fine balance between the secretion, composition, volume and turnover of cerebrospinal fluid (CSF) is strictly regulated. However, during certain neurological diseases, this balance can be disrupted. A significant disruption to the normal CSF circulation can be life threatening, leading to increased intracranial pressure (ICP), and is implicated in hydrocephalus, idiopathic intracranial hypertension, brain trauma, brain tumours and stroke. Yet, the exact cellular, molecular and physiological mechanisms that contribute to altered hydrodynamic pathways in these diseases are poorly defined or hotly debated. The traditional views and concepts of CSF secretion, flow and drainage have been challenged, also due to recent findings suggesting more complex mechanisms of brain fluid dynamics than previously proposed. This review evaluates and summarises current hypotheses of CSF dynamics and presents evidence for the role of impaired CSF dynamics in elevated ICP, alongside discussion of the proteins that are potentially involved in altered CSF physiology during neurological disease. Undoubtedly CSF secretion, absorption and drainage are important aspects of brain fluid homeostasis in maintaining a stable ICP. Traditionally, pharmacological interventions or CSF drainage have been used to reduce ICP elevation due to over production of CSF. However, these drugs are used only as a temporary solution due to their undesirable side effects. Emerging evidence suggests that pharmacological targeting of aquaporins, transient receptor potential vanilloid type 4 (TRPV4), and the Na+-K+-2Cl- cotransporter (NKCC1) merit further investigation as potential targets in neurological diseases involving impaired brain fluid dynamics and elevated ICP.

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.

Intracranial pressure (ICP) monitoring is a staple of neurocritical care. The most commonly used current methods of monitoring in the acute setting include fluid-based systems, implantable transducers and Doppler ultrasonography. It is well established that management of elevated ICP is critical for clinical outcomes. However, numerous studies show that current methods of ICP monitoring cannot reliably define the limit of the brain's intrinsic compensatory capacity to manage increases in pressure, which would allow for proactive ICP management. Current work in the field hopes to address this gap by harnessing live-streaming ICP pressure-wave data and a multimodal integration with other physiologic measures. Additionally, there is continued development of non-invasive ICP monitoring methods for use in specific clinical scenarios.

BackgroundLow cerebral perfusion pressure (CPP) has previously been identified as a key prognostic marker after pediatric traumatic brain injury (TBI). Cerebrovascular autoregulation supports stabilization of cerebral blood flow within the autoregulation range. Beyond the upper limit of this range, cerebral blood flow increases with increasing CPP, leading to increased risk of intracranial hypertension and blood-brain barrier disruptions. Based on the hypothesis that children are less sensitive to high CPP, we aimed to characterize the pediatric upper limit of autoregulation and the association between high CPP and outcome.MethodsData acquired as part of the "Studying Trends of Autoregulation in Severe Head Injury in Paediatrics" (STARSHIP) study (a prospective, multicenter, observational study that enrolled 135 children with TBI from July 2018 to March 2023) were explored. The association between different levels of CPP and the autoregulation proxy measure, the pressure reactivity index (PRx), were explored visually. The prognostic value of CPP was assessed by exploring overall averages, overall dose, hourly dose, and percentage time spent above specific thresholds. We employed univariable/multivariable (χ2 tests, logistic regression, sliding dichotomy) and visual (heatmap) methods.ResultsNo clear upper limit of autoregulation could be identified with PRx increasing beyond 0.2 only with CPP values beyond 100 mm Hg. Using iterative χ2 testing and logistic regression analyses, similarly, only hourly dose and percentage time beyond CPP of 90 mm Hg displayed a trend toward worse outcome. Using heatmap analyses, regions of CPP with differing risk stratifications could be identified. No difference in CPP could be identified between patients with and without acute respiratory distress syndrome or secondary hemorrhages.ConclusionsIn contrast to the well-established association between low CPP and poor outcome, our findings suggest that exposure to CPP values above those recommended by the Brain Trauma Foundation guidelines may not be associated with worse outcomes in this cohort. However, given the observational nature of the study and potential confounding factors, these results highlight the need for prospective trials to assess the safety and efficacy of targeting higher CPP in pediatric TBI.