The physiological effect of posture on intracranial pressure (ICP) is not well described. This study defined and evaluated three mathematical models describing the postural effects on ICP, designed to predict ICP at different head-up tilt angles from the supine ICP value. Model I was based on a hydrostatic indifference point for the cerebrospinal fluid (CSF) system, i.e., the existence of a point in the system where pressure is independent of body position. Models II and III were based on Davson's equation for CSF absorption, which relates ICP to venous pressure, and postulated that gravitational effects within the venous system are transferred to the CSF system. Model II assumed a fully communicating venous system, and model III assumed that collapse of the jugular veins at higher tilt angles creates two separate hydrostatic compartments. Evaluation of the models was based on ICP measurements at seven tilt angles (0-71°) in 27 normal pressure hydrocephalus patients. ICP decreased with tilt angle (ANOVA: P < 0.01). The reduction was well predicted by model III (ANOVA lack-of-fit: P = 0.65), which showed excellent fit against measured ICP. Neither model I nor II adequately described the reduction in ICP (ANOVA lack-of-fit: P < 0.01). Postural changes in ICP could not be predicted based on the currently accepted theory of a hydrostatic indifference point for the CSF system, but a new model combining Davson's equation for CSF absorption and hydrostatic gradients in a collapsible venous system performed well and can be useful in future research on gravity and CSF physiology.

Objective: The discovery of a posture-dependent effect on the difference between intraocular pressure (IOP) and intracranial pressure (ICP) at the level of lamina cribrosa could have important implications for understanding glaucoma and idiopathic intracranial hypertension and could help explain visual impairments in astronauts exposed to microgravity. The aim of this study was to determine the postural influence on the difference between simultaneously measured ICP and IOP.Methods: Eleven healthy adult volunteers (age 46±10 years) were investigated with simultaneous ICP, assessed through lumbar puncture, and IOP measurements when supine, sitting, and in 9° head down tilt (HDT). The trans-lamina cribrosa pressure difference (TLCPD) was calculated as the difference between the IOP and ICP. To estimate the pressures at the lamina cribrosa, geometrical distances were estimated from MRI and were used to adjust for hydrostatic effects. Results:The TLCPD (mm Hg) between IOP and ICP was 12.3±2.2 for supine, 19.8±4.6 for sitting and 6.6±2.5 for HDT. The expected 24-hour average TLCPD on earthassuming 8 h supine and 16 h upright-was estimated to be 17.3 mm Hg. By removing the hydrostatic effects on pressure, a corresponding 24 h-average TLCPD in microgravity environment was simulated to be 6.7 mmHg. Interpretation:We provide a possible physiological explanation for how microgravity can cause symptoms similar to those seen in patients with elevated ICP. The observed posture dependency of TLCPD also implies that assessment of the difference between IOP and ICP in upright may offer new understanding of the pathophysiology of idiopathic intracranial hypertension and glaucoma.

Recent interest in intracranial pressure (ICP) in the upright posture has revealed that the mechanisms regulating postural changes in ICP are not fully understood. We have suggested an explanatory model where the postural changes in ICP depend on well-established hydrostatic effects in the venous system and where these effects are interrupted by collapse of the internal jugular veins (IJVs) in more upright positions. The aim of this study was to investigate this relationship by simultaneous invasive measurements of ICP, venous pressure, and IJV collapse in healthy volunteers. ICP (monitored via the lumbar route), central venous pressure (peripherally inserted central catheter line), and IJV cross-sectional area (ultrasound) were measured in 11 healthy volunteers (47 ± 10 yr, mean ± SD) in 7 positions, from supine to sitting (0-69°). Venous pressure and anatomical distances were used to predict ICP in accordance with the explanatory model, and IJV area was used to assess IJV collapse. The hypothesis was tested by comparing measured ICP with predicted ICP. Our model accurately described the general behavior of the observed postural ICP changes (mean difference, -0.03 ± 2.7 mmHg). No difference was found between predicted and measured ICP for any tilt angle ( P values, 0.65-0.94). The results support the hypothesis that postural ICP changes are governed by hydrostatic effects in the venous system and IJV collapse. This improved understanding of postural ICP regulation may have important implications for the development of better treatments for neurological and neurosurgical conditions affecting ICP.

There was no evidence of reduced ICP in NTG patients as compared with healthy controls, either in supine or in upright position. Consequently, the hypothesis that NTG is caused by an elevated TLCPD from low ICP was not supported.