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The origin and mechanics of whiplash injury from motor vehicle collisions are poorly understood. Among the proposed injury mechanisms, the inertial loading of the head and neck during whiplash exposures is theorized to produce injurious cerebrospinal fluid pressure (CSFP) transients. To better understand the mechanics and modal behavior of CSFP transients during whiplash exposures, we quantified the time–frequency relationship between input head kinematics and cervical CSFP responses in an in vivo pig model. Wavelet coherence analysis was used to correlate seven head kinematic parameters (including temporal Neck Injury Criterion, NIC) with CSFP during simulated extension and flexion whiplash exposures. Overall, the first and last 50 ms of exposures, and frequency ranges between 30–65 Hz had larger coherences between head kinematics and CSFP, with higher coherences in extension exposures than flexion exposures. NIC did not universally outperform other head kinematic parameters as a correlate of CSFP. These findings highlight the complexity of the dynamics involved in generating CSFP transients in the cervical spine during whiplash exposures.

The principles of cerebrospinal fluid (CSF) production, circulation and outflow and regulation of fluid volumes and pressures in the normal brain are summarised. Abnormalities in these aspects in intracranial hypertension, ventriculomegaly and hydrocephalus are discussed. The brain parenchyma has a cellular framework with interstitial fluid (ISF) in the intervening spaces. Framework stress and interstitial fluid pressure ( ISFP ) combined provide the total stress which, after allowing for gravity, normally equals intracerebral pressure ( ICP ) with gradients of total stress too small to measure. Fluid pressure may differ from ICP in the parenchyma and collapsed subarachnoid spaces when the parenchyma presses against the meninges. Fluid pressure gradients determine fluid movements. In adults, restricting CSF outflow from subarachnoid spaces produces intracranial hypertension which, when CSF volumes change very little, is called idiopathic intracranial hypertension (iIH). Raised ICP in iIH is accompanied by increased venous sinus pressure, though which is cause and which effect is unclear. In infants with growing skulls, restriction in outflow leads to increased head and CSF volumes. In adults, ventriculomegaly can arise due to cerebral atrophy or, in hydrocephalus, to obstructions to intracranial CSF flow. In non-communicating hydrocephalus, flow through or out of the ventricles is somehow obstructed, whereas in communicating hydrocephalus, the obstruction is somewhere between the cisterna magna and cranial sites of outflow. When normal outflow routes are obstructed, continued CSF production in the ventricles may be partially balanced by outflow through the parenchyma via an oedematous periventricular layer and perivascular spaces. In adults, secondary hydrocephalus with raised ICP results from obvious obstructions to flow. By contrast, with the more subtly obstructed flow seen in normal pressure hydrocephalus (NPH), fluid pressure must be reduced elsewhere, e.g. in some subarachnoid spaces. In idiopathic NPH, where ventriculomegaly is accompanied by gait disturbance, dementia and/or urinary incontinence, the functional deficits can sometimes be reversed by shunting or third ventriculostomy. Parenchymal shrinkage is irreversible in late stage hydrocephalus with cellular framework loss but may not occur in early stages, whether by exclusion of fluid or otherwise. Further studies that are needed to explain the development of hydrocephalus are outlined.

Study design: Prospective vasopressor cross-over interventional study Objectives: To examine how two vasopressors used in acute traumatic spinal cord injury (SCI) affect intrathecal cerebrospinal fluid pressure and the corresponding spinal cord perfusion pressure (SCPP). Setting: Vancouver, British Columbia, Canada. Methods: Acute SCI patients over the age of 17 with cervical or thoracic ASIA Impairment Scale (AIS). A, B or C injuries were enrolled in this study. Two vasopressors, norepinephrine and dopamine, were evaluated in a ‘crossover procedure’ to directly compare their effect on the intrathecal pressure (ITP). The vasopressor cross-over procedures were performed in the intensive care unit where ITP, mean arterial pressure (MAP) and heart rate were being continuously measured. The SCPP was calculated as the difference between MAP and ITP. Results: A total of 11 patients were enrolled and included in our analysis. There were 6 patients with AIS A, 3 with AIS B and 2 with AIS C injuries at baseline. We performed 24 cross-over interventions in these 11 patients. There was no difference in MAP with the use of norepinephrine versus dopamine (84±1 mm Hg for both; P =0.33). Conversely, ITP was significantly lower with the use of norepinephrine than with dopamine (17±1 mm Hg vs 20±1 mm Hg, respectively, P <0.001). This decrease in ITP with norepinephrine resulted in an increased SCPP during the norepinephrine infusion when compared with dopamine (67±1 mm Hg vs 65±1 mm Hg respectively, P =0.0049). Conclusion: Norepinephrine was able to maintain MAP with a lower ITP and a correspondingly higher SCPP as compared with dopamine in this study. These results suggest that norepinephrine may be preferable to dopamine if vasopressor support is required post SCI to maintain elevated MAPs in accordance with published guidelines.

Unprecedented levels of seismicity have been seen in southern Sichuan, China, since the large‐scale exploitation of shale gas. Fluid and pore pressure transported through hydrological channel are thought as pivotal elements in the induction of earthquakes. Our high‐resolution tomography results reveal two inclined seismic anomalies featured by low Vs and high Vp/Vs at different depth range. The deeper anomaly extends 15 km from NE to SE and connects the well g048 from 3 km depth to the vicinity of the Ms 4.7 Gongxian earthquake 5.4 km deep, which is hinted to be a hydrological channel inferred from the high fluid overpressure of 28 Mpa calculated from focal mechanism solution. The injection operation of multiple shale gas wells along the channel may potentially accumulate the pore pressure and cause the fault near the end of the channel to reach critical stress state through various mechanisms. Plain Language Summary Increasing seismicity in southern Sichuan is suspected to be linked to hydraulic fracturing stimulation for shale gas extraction. Induced earthquakes resulting from fracturing operations at nearby wells can be verified using in‐situ fracturing data, while remote‐induced factors are hard to prove. In this study, a seismic anomaly of low Vs and high Vp/Vs inferred to be a long‐distance hydrological channel connecting the 2021 Ms 4.7 Gongxian earthquake to the active shale gas well 15 km away. Our results indicate that pore fluid pressure generated by hydraulic fracturing in multiple wells may continuously accumulated at the end of the channel, ultimately resulting in high pore pressure and triggering the fault rupture. Therefore, it is urgent to plug this channel and prevent the filtration loss. Key Points Two long‐distance hydrological channels were observed in southern Sichuan The injection operation of multiple wells along the channel may increase the pore pressure in the hydrological channel The accumulation of pore pressure at the end of the hydrological channel was confirmed by the occurrence of Ms 4.7 Gongxian earthquake

Previous reports suggest an association between the degree of optic nerve head edema and CSF pressure (CSFp) in idiopathic intracranial hypertension (IIH). We hypothesized that CSFp would be associated with Frisén papilledema grade (FPG) and other clinical features, and that FPG would modify the CSFp response to acetazolamide in participants in the Idiopathic Intracranial Hypertension Treatment Trial (IIHTT). In the IIHTT, eligible patients underwent lumbar puncture (LP) prior to enrollment and were randomly assigned to one of two treatment groups: acetazolamide plus supervised diet or placebo plus supervised diet. Trial eligibility required baseline CSFp ≥250 mm H 2 O or ≥200 mm H 2 O with compelling clinical or imaging IIH findings. Associations between CSFp and FPG and other clinical features were examined at baseline. The effect of acetazolamide on 6-month change in CSFp was examined in those with low FPG (grades I–III) and those with high FPG (grades IV–V) at baseline. All 165 enrolled subjects had a baseline LP and 85 had an LP at 6 months. There was an association between CSFp and FPG at baseline: CSFp was more elevated in subjects with high FPG (378 ± 90 mm H 2 O, n  = 50) than in subjects with low FPG (331 ± 77, n  = 115, p  = 0.002). At 6 months, acetazolamide had a similar effect on CSFp in subjects with high FPG (−79.9 mm H 2 O) and in subjects with low FPG (−50.9 mm H 2 O, p  = 0.50). We found a modest association between CSFp and FPG. Acetazolamide had a beneficial effect on CSFp regardless of baseline FPG.

Background Although widely used in the evaluation of the diseased, normal intracranial pressure and lumbar cerebrospinal fluid pressure remain sparsely documented. Intracranial pressure is different from lumbar cerebrospinal fluid pressure. In addition, intracranial pressure differs considerably according to the body position of the patient. Despite this, the current reference values do not distinguish between intracranial and lumbar cerebrospinal fluid pressures, and body position-dependent reference values do not exist. In this study, we aim to establish these reference values. Method A systematic search was conducted in MEDLINE, EMBASE, CENTRAL, and Web of Sciences. Methodological quality was assessed using an amended version of the Joanna Briggs Quality Appraisal Checklist. Intracranial pressure and lumbar cerebrospinal fluid pressure were independently evaluated and subdivided into body positions. Quantitative data were presented with mean ± SD, and 90% reference intervals. Results Thirty-six studies were included. Nine studies reported values for intracranial pressure, while 27 reported values for the lumbar cerebrospinal fluid pressure. Reference values for intracranial pressure were −  5.9 to 8.3 mmHg in the upright position and 0.9 to 16.3 mmHg in the supine position. Reference values for lumbar cerebrospinal fluid pressure were 7.2 to 16.8 mmHg and 5.7 to 15.5 mmHg in the lateral recumbent position and supine position, respectively. Conclusions This systematic review is the first to provide position-dependent reference values for intracranial pressure and lumbar cerebrospinal fluid pressure. Clinically applicable reference values for normal lumbar cerebrospinal fluid pressure were established, and are in accordance with previously used reference values. For intracranial pressure, this study strongly emphasizes the scarcity of normal pressure measures, and highlights the need for further research on the matter.

Induced seismicity represents a negative drawback during subsurface exploitation for geothermal energy production. Understanding the triggering mechanisms of induced earthquakes can help implement effective seismic hazard mitigation actions. Among the triggering mechanisms, the pore fluid pressure is of primary importance. Here we provide a static picture of the excess pore fluid pressure at the hypocenters of a seismic sequence induced at the deep geothermal field in St. Gallen, Switzerland, in July 2013. We find that in addition to the Coulomb static stress change, fluids play a key role in promoting the sequence. The estimated excess pore fluid pressure for approximately half of the earthquakes is higher than the injection pressure necessary during the well control phase to fight the unexpected gas kick, that accidently occurred during field operations when a trap of overpressured gas was broken. Plain Language Summary In July 2013, a sequence of more than 340 earthquakes was induced during the exploitation of the subsurface for energy production in St. Gallen geothermal field (Switzerland). To understand the mechanisms underlying the evolution of the sequence, we investigated the role of fluids and elastic stress transfer. The excess pore fluid pressure measurements suggest that the main triggering mechanism is related to high‐pressure fluids. The high values of the pore fluid pressure may be due to an already existing in situ overpressure condition from which a documented unexpected gas kick occurred. Key Points The main earthquake triggering mechanism is the effect of high‐pressure fluids The high pore fluid pressure values may be due to an already existing in situ overpressure condition

The morphology of fault zones formed by slow faulting is markedly different from that of brittle faulting. In this study, we quantify the three‐dimensional (3D) pore distribution and permeability structures of two rock samples that have been deformed to failure by slow and brittle faulting, respectively. Our results show that the permeability structure of fault zones varies greatly depending on the faulting mechanism. Fault cores formed by slow faulting exhibit much higher porosity and permeability compared to the surrounding damage zone and wall rocks, unlike those formed through brittle faulting. Since slow slip events associated with high pore fluid pressures are common in active tectonic regions, we propose that slow slip events can serve as a mechanism to maintain the permeable pathways beneath the seismogenic zone, facilitating the movement of mantle‐derived fluids from deep reservoirs toward the surface.

Clinical studies implicate low cerebrospinal fluid pressure (CSFP) or a high translaminar pressure difference in the pathogenesis of primary open angle glaucoma (POAG) and normal tension glaucoma (NTG). This study was performed to examine the effect of age, sex, race and body mass index (BMI) on CSFP. Electronic medical records from all patients who had a lumbar puncture (LP) performed at the Mayo Clinic from 1996-2009 were reviewed. Information including age, sex, race, height and weight, ocular and medical diagnoses, intraocular pressure (IOP) and LP opening pressure was obtained. Patients using medications or with medical diagnoses known to affect CSFP, and those who underwent neurosurgical procedures or where more than one LP was performed were excluded from analysis. Electronic medical records of 33,922 patients with a history of having an LP during a 13-year period (1996-2009) were extracted. Of these, 12,118 patients met all entry criteria. Relative to mean CSFP at age group 20-49 (mean 11.5±2.8 mmHg), mean CSFP declined steadily after age 50, with percent reduction of 2.5% for the 50-54 age group (mean 11.2±2.7 mmHg, p<0.002) to 26.9% for the 90-95 group (mean 8.4±2.4 mmHg, p<0.001). Females had lower CSFP than males throughout all age groups. BMI was positively and independently associated with CSFP within all age groups. There is a sustained and significant reduction of CSFP with age that begins in the 6(th) decade. CSFP is consistently lower in females. BMI is positively and independently associated with CSFP in all age groups. The age where CSFP begins to decline coincides with the age where the prevalence of POAG increases. These data support the hypothesis that reduced CSFP may be a risk factor for POAG and may provide an explanation for the mechanism that underlies the age-related increase in the prevalence of POAG and NTG.

Dilatant hardening is one proposed mechanism that causes slow earthquakes along faults. Previous experiments and models show that dilatant hardening can stabilize fault rupture and slip in several lithologies. However, few studies have systematically measured the mechanical behavior across the transition from dynamic to slow rupture or considered how the associated damage varies. To constrain the processes and scales of dilatant hardening, we conducted triaxial compression experiments on cores of Crab Orchard sandstone and structural analyses using micro‐computed tomography imaging and petrographic analysis. Experiments were conducted at an effective confining pressure of ∼10 MPa, while varying confining pressure (10–130 MPa) and pore fluid pressure (1–120 MPa). Above 15 MPa pore fluid pressure, dilatant hardening slows the rate of fault rupture and slip and deformation becomes more distributed amongst multiple faults as microfracturing increases. The resulting increase in fracture energy has the potential to control fault slip behavior. Plain Language Summary When rocks are breaking, the pore spaces and developing fractures dilate, resulting in a decrease in pore fluid pressures. This decrease can strengthen the rock from ongoing deformation in a process known as dilatant hardening. We conducted experiments to better understand how this strengthening effect works, in particular looking at the ratio of pore fluid pressure to the external confining pressure (simulating rocks buried at depth), and also analyzed how the fractures that develop can vary from dilatant hardening. We found a threshold pressure at which the strengthening peaked, and increasing pore fluid pressure did not change how strong the rocks got from continuing deformation. We also observed a drastic increase in how damage was distributed due to this hardening effect at both a large (visible to the naked eye) and small scale (only visible in a high‐magnification microscope). These results indicate that dilatant hardening can increase how much energy must be expended to break the rock and to cause faults to slip when pore fluid pressures are high enough, and likely plays a role in stabilizing fault slip, causing earthquakes to slow down and be less dynamic. Key Points We measured the transition between dynamic and stable rupture as a result of dilatant hardening We observed differences in microstructural development tied to the shift in rupture style We developed a model of fracture nucleation and propagation at different pore fluid pressures