Intracranial Cerebrospinal Fluid Volume Research Articles

Improved Cerebral Glymphatic Flow after Transvenous Embolization of CSF-Venous Fistula.

Spontaneous intracranial hypotension is characterized by symptoms of low intracranial CSF volume due to various mechanisms of CSF leakage. One such mechanism is a CSF-venous fistula, treatable with transvenous embolization resulting in substantial radiographic and clinical improvement. However, the exact mechanisms underlying these improvements, including the potential involvement of the glymphatic system, remain unclear. To noninvasively assess glymphatic clearance in spontaneous intracranial hypotension, we used an advanced MR imaging technique called the DTI along the perivascular spaces in 3 patients with CSF-venous fistula before and after embolization. All 3 patients with spontaneous intracranial hypotension initially had low glymphatic flow, which improved postembolization. Two patients with symptomatic improvement exhibited a more substantial increase in glymphatic flow compared with a patient with minimal improvement. These findings suggest a possible link between cerebral glymphatics in spontaneous intracranial hypotension pathophysiology and symptomatic improvement, warranting larger studies to explore the role of the glymphatic system in spontaneous intracranial hypotension.

Recurrent reflex syncope in idiopathic intracranial hypertension patient resolved after lumbar puncture: pathogenetic implications

BackgroundIdiopathic intracranial hypertension is a disease characterized by increased intracranial cerebrospinal fluid volume and pressure without evidence of other intracranial pathology. Dural sinuses are rigid structures representing a privileged low-pressure intracranial compartment. Rigidity of dural sinus ensures that the large physiologic fluctuations of cerebrospinal fluid pressure associated with postural changes or to Valsalva effect cannot be transmitted to the sinus. An abnormal dural sinus collapsibility, especially when associated with various anatomical sinus narrowing, has been proposed as a key factor in the pathogenesis of idiopathic intracranial hypertension. This pathogenetic model is based on an excessive collapsibility of the dural sinuses that leads to the triggering of a self-limiting venous collapse positive feedback-loop between the cerebrospinal fluid pressure, that compresses the sinus, and the increased dural sinus pressure upstream, that reduces the cerebrospinal fluid reabsorption rate, increasing cerebrospinal fluid volume and pressure at the expense of intracranial compliance and promoting further sinus compression. Intracranial compliance is the ability of the craniospinal space to accept small volumetric increases of one of its compartments without appreciable intracranial pressure rise. In idiopathic intracranial hypertension, a condition associated with a reduced rate of CSF reabsorption leading to its volumetric expansion, a pathologically reduced IC precedes and accompanies the rise of ICP. Syncope is defined as a transient loss of consciousness due to a transient cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery. A transient global cerebral hypoperfusion represents the final mechanism of syncope determined by cardiac output and/or total peripheral resistance decrease. There are many causes determining low cardiac output including reflex bradycardia, arrhythmias, cardiac structural disease, inadequate venous return, and chronotropic and inotropic incompetence. Typically, syncopal transient loss of consciousness is mainly referred to an extracranial mechanism triggering a decrease in cardiac output and/or total peripheral resistance. Conversely, the association of syncope with a deranged control of intracranial compliance related to cerebral venous outflow disorders has been only anecdotally reported.Case PresentationWe report on a 57-year-old woman with daily recurrent orthostatic hypotension syncope and idiopathic intracranial hypertension-related headaches, which resolved after lumbar puncture with cerebrospinal fluid subtraction.ConclusionsA novel mechanism underlying the triggering of orthostatic syncope in the presence of intracranial hypertension-dependent reduced intracranial compliance is discussed.

Fully automated measurement of intracranial CSF and brain parenchyma volumes in pediatric hydrocephalus by segmentation of clinical MRI studies.

Brain parenchyma (BP) and intracranial cerebrospinal fluid (iCSF) volumes measured by fully automated segmentation of clinical brain MRI studies may be useful for the diagnosis and follow-up of pediatric hydrocephalus. However, previously published segmentation techniques either rely on dedicated sequences, not routinely used in clinical practice, or on spatial normalization, which has limited accuracy when severe brain distortions, such as in hydrocephalic patients, are present. We developed a fully automated method to measure BP and iCSF volumes from clinical brain MRI studies of pediatric hydrocephalus patients, exploiting the complementary information contained in T2- and T1-weighted images commonly used in clinical practice. The proposed procedure, following skull-stripping of the combined volumes, performed using a multiparametric method to obtain a reliable definition of the inner skull profile, maximizes the CSF-to-parenchyma contrast by dividing the T2w- by the T1w- volume after full-scale dynamic rescaling, thus allowing separation of iCSF and BP through a simple thresholding routine. Validation against manual tracing on 23 studies (four controls and 19 hydrocephalic patients) showed excellent concordance (ICC>0.98) and spatial overlap (Dice coefficients ranging from 77.2% for iCSF to 96.8% for intracranial volume). Accuracy was comparable to the intra-operator reproducibility of manual segmentation, as measured in 14 studies processed twice by the same experienced neuroradiologist. Results of the application of the algorithm to a dataset of 63 controls and 57 hydrocephalic patients (19 with parenchymal damage), measuring volumes' changes with normal development and in hydrocephalic patients, are also reported for demonstration purposes. The proposed approach allows fully automated segmentation of BP and iCSF in clinical studies, also in severely distorted brains, enabling to assess age- and disease-related changes in intracranial tissue volume with an accuracy comparable to expert manual segmentation.

Cerebrospinal Fluid Production and Absorption and Ventricular Enlargement Mechanisms in Hydrocephalus.

Cerebrospinal fluid (CSF) production and absorption concept significantly changed in the early 2010s from "third circulation theory" and "classical bulk flow theory" to a whole new one as follows: First, CSF is mainly produced from interstitial fluid excreted from the brain parenchyma, and CSF produced from the choroid plexus plays an important role in maintaining brain homeostasis. Second, CSF is not absorbed in the venous sinus via the arachnoid granules, but mainly in the dural lymphatic vessels. Finally, the ventricles and subarachnoid spaces have several compensatory direct CSF pathways at the borders attached to the choroid plexus, e.g., the inferior choroidal point of the choroidal fissure, other than the foramina of Luschka and Magendie. In idiopathic normal pressure hydrocephalus (iNPH), the lateral ventricles and basal cistern are enlarged simultaneously due to the compensatory direct CSF pathways. The average total intracranial CSF volume increased from about 150 mL at 20 years to about 350 mL at 70 years due to the decrease in brain volume with aging and further increased above 400 mL in patients with iNPH. CSF movements are composed of a steady microflow produced by the rhythmic wavy movement of motile cilia on the ventricular surface and dynamic pulsatile flow produced by the brain and cerebral artery pulsation, respiration, and head movement. Pulsatile CSF movements might totally decrease with aging, but it in the ventricles might increase at the foramina of Magendie and Luschka dilation. Aging CSF dynamics are strongly associated with ventricular dilatation in iNPH.

Aging-related volume changes in the brain and cerebrospinal fluid using artificial intelligence-automated segmentation

ObjectivesTo verify the reliability of the volumes automatically segmented using a new artificial intelligence (AI)-based application and evaluate changes in the brain and CSF volume with healthy aging.MethodsThe intracranial spaces were automatically segmented in the 21 brain subregions and 5 CSF subregions using the AI-based application on the 3D T1-weighted images in healthy volunteers aged > 20 years. Additionally, the automatically segmented volumes of the total ventricles and subarachnoid spaces were compared with the manually segmented volumes of those extracted from 3D T2-weighted images using the intra-class correlation and Bland–Altman analysis.ResultsIn this study, 133 healthy volunteers aged 21–92 years were included. The mean intra-class correlations between the automatically and manually segmented volumes of the total ventricles and subarachnoid spaces were 0.986 and 0.882, respectively. The increase in the CSF volume was estimated to be approximately 30 mL (2%) per decade from 265 mL (18.7%) in the 20s to 488 mL (33.7%) in ages above 80 years; however, the increase in the volume of total ventricles was approximately 20 mL (< 2%) until the 60s and increased in ages above 60 years.ConclusionsThis study confirmed the reliability of the CSF volumes using the AI-based auto-segmentation application. The intracranial CSF volume increased linearly because of the brain volume reduction with aging; however, the ventricular volume did not change until the age of 60 years and above and then gradually increased. This finding could help elucidate the pathogenesis of chronic hydrocephalus in adults.Key Points• The brain and CSF spaces were automatically segmented using an artificial intelligence-based application.• The total subarachnoid spaces increased linearly with aging, whereas the total ventricle volume was around 20 mL (< 2%) until the 60s and increased in ages above 60 years.• The cortical gray matter gradually decreases with aging, whereas the subcortical gray matter maintains its volume, and the cerebral white matter increases slightly until the 40s and begins to decrease from the 50s.

Voxel-based morphometric magnetic resonance imaging evaluation of small head fetus: A comparative study with normal developmental fetus.

To explore the application value of voxel-based morphometric (VBM) in prenatal diagnosis of microcephaly. A retrospective study of magnetic resonance imaging of fetuses with microcephaly was performed using a single-shot fast spin echo sequence; semiautomatic segmentation of grey matter (GM), white matter (WM), and cerebrospinal fluid (CSF); calculation of their volumes; and VBM analysis of their GM. Two independent samples t-test was used to statistically analyse the fetal GM volume in the microcephaly and normal control groups. Total intracranial volume (TIV), GM volume, WM volume, and CSF volume were linearly regressed against gestational age and compared between the two groups. In the fetus with microcephaly, GM volume of frontal lobe, temporal lobe, cuneus, anterior central gyrus, and posterior central gyrus decreased significantly (P < 0.001, corrected by family-wise error at mass level). The GM volume of microcephaly was significantly lower than that of the control group (except for 28 weeks of gestation) (P < 0.05). TIV, GM volume, WM volume, and CSF volume were all positively correlated with gestational age, and the curves in the microcephaly group were all lower than those in the control group. Compared with the normal control group, the GM volume of microcephaly fetuses decreased, and there were significant differences in many brain regions through VBM analysis.

[Mechanisms of Cerebrospinal Fluid Production and Absorption and Ventricular Dilatation in Hydrocephalus].

The concept of cerebrospinal fluid(CSF)production and absorption changed significantly in the early 2010s from "third circulation theory" and "classical bulk flow theory" as follows. First, CSF is mainly produced from the interstitial fluid excreted from the brain; CSF produced by the choroid plexus is important in maintaining homeostasis of the brain. Next, CSF is not absorbed in the venous sinus via the arachnoid granules, but rather in the dural lymphatic vessels. Finally, the ventricles and subarachnoid spaces have several compensatory direct CSF pathways around the attachment of the choroid plexus other than the foramina of Luschka and Magendie. Because of the compensatory direct CSF pathways, the lateral ventricles and the basal cistern are enlarged simultaneously in idiopathic normal pressure hydrocephalus(iNPH). Due to the decrease in brain volume with aging, the average total intracranial CSF volume increases from approximately 150 mL at 20 years to approximately 350 mL at 70 years, and further increases by approximately 50-100 mL to above 400 mL in patients with iNPH. CSF movement is composed of a steady flow produced by the rhythmic wavy movement of motile cilia on the ventricular surface and the dynamic pulsatile flow produced by the pulsation of the cerebral arteries or brain, respiration, and head movement. In general, this pulsatile CSF flow decreases with aging but increases at the opening of the foramen of Magendie and causes the ventricles to expand in iNPH.

Fully Automated Measurement of Intracranial CSF and Brain Parenchyma Volumes in Pediatric Hydrocephalus by Segmentation of Clinical MRI Studies

Fully Automated Measurement of Intracranial CSF and Brain Parenchyma Volumes in Pediatric Hydrocephalus by Segmentation of Clinical MRI Studies

Intracranial compartment volumes and their distribution among clinically diagnosed patients with normal pressure hydrocephalus and brain atrophy in a Nigerian population

Normal pressure hydrocephalus is a form of non-obstructive hydrocephalus characterized by the triad of symptoms. These symptoms are typical or atypical. Because of its potential reversibility, researchers have paid attention to its diagnosis and in differentiating it with other forms of dementia such as brain atrophy. To determine the intracranial compartment volumes and their differences among patients with NPH and Brain Atrophy (BA). This was a cross-sectional study involving consenting patients diagnosed with NPH and BA who were referred for routine brain CT. Medical conditions known to influence intracranial volume were excluded. Age -matched normal control were clinically and radiologically confirmednormal and were also recruited. Intracranial volumes and CSF distribution determination was based on Cavalieri test point computation principle. Test point summation was on a locally developed software for this purpose. Overall, the values of BA recorded higher mean values for most of the intracranial compartment volumes. Intraventricular volume was consistently higher in NPH groups. Statistical difference exists among intraventricular and total intracranial CSF volume across patients with BA, NPH and control. A post hoc test revealed control-NPH comparison across these variables. Control-BA comparison was evident in total intracranial CSF volume only. Higher mean values of intracranialcompartment volumes were observed in patients with BA than among patients with NPH and their control. Anthropometric indices did not show any difference between patients with BA, NPH and their control. These indices can be used as basis in objectively differentiating NPH from BA.

Spontaneous Intracranial Hypotension Without CSF Leakage-Concept of a Pathological Cranial to Spinal Fluid Shift.

Objective: Spontaneous intracranial hypotension (SIH) is typically caused by CSF leakage from a spinal dural tear, a meningeal diverticulum, or a CSF venous fistula. However, some patients present with classic orthostatic symptoms and typical intracranial imaging findings without evidence of CSF leakage despite repeated diagnostic work-up. This article aims to elaborate a hypothesis that would explain a pathologically increased orthostatic shift of CSF from the cranial to the spinal compartment in the absence of a CSF leak.Medical Hypothesis: The symptoms of SIH are caused by a decrease in intracranial CSF volume, intracranial hypotension, and downward displacement of intracranial structures. A combination of pathologically increased spinal compliance, decreased intracranial CSF volume, low CSF outflow resistance, and decreased venous pressure might result in a pathological orthostatic cranial-to-spinal CSF shift. Thus, in rare cases, intracranial hypotension may occur in the absence of CSF leakage from the dural sac.Conclusion: We propose a pathophysiological concept for the subgroup of SIH patients with typical cranial imaging findings and no evidence of CSF leakage. In these patients, reducing the compliance or the volume of the spinal compartment seems to be the appropriate therapeutic strategy.

Intracranial Cerebrospinal Fluid Volume Evaluation in Healthy People and Hydrocephalus Patients using SPACE Sequence.

IntroductionCerebrospinal Fluid (CSF) is produced mainly by the choroid plexus but with a substantial influence by the ependymal lining of the ventricles in the brain. Hydrocephalus occurs as a result of discrepancy in the production as well as circulation of CSF as a result of congenital and acquired conditions. Nevertheless, studies on the differences between CSF dynamics according to age and gender are still insufficient. Thus, this study evaluated the volume of intracranial CSF in healthy people and hydrocephalus patients taking into account the differences between CSF dynamics according to age and gender using Sampling Perfection with Application optimised Contrast using different flip-angle Evolution (SPACE) sequence.Methods120 healthy volunteers and 60 patients with hydrocephalus were included in this study. SPACE sequence was used to evaluate intracranial CSF with a 3.0T magnetic resonance machine. The total volume of intracranial CSF and the amount of CSF in the ventricle were obtained using a software, and the volume ratio of CSF in the subarachnoid space, the ventricle and the subarachnoid space were calculated.ResultsThe mean volume of intracranial CSF, ventricular CSF, and subarachnoid CSF of male volunteers were (206.9±47.7) cm3, (33.0±10.7) cm3, (173.9±37.9) cm3 respectively. The average volume of intracranial CSF, ventricular CSF, and subarachnoid CSF of female volunteers were (199.7±44.9) cm3, (30.8±9.4) cm3, and (168.9±37.0) cm3, respectively. Thus, no significant statistically (P>0.05) difference between males and females was found. (3) The mean values ​​of intracranial CSF, ventricle CSF and subarachnoid CSF, ventricle and subarachnoid CSF volume ratio in patients with hydrocephalus were significantly greater than health volunteers. Thus, the difference between the two groups was statistically significant (P<0.05).ConclusionSPACE sequence can quantitatively determine the content of CSF. The change of CSF volume has nothing to do with gender but with age. It is feasible to use SPACE sequence to evaluate the spatial distribution and volume of intracranial CSF.

Intracranial Volume After Cranial Vault Remodeling: To What Degree Does Intracranial Composition Change After Surgery?

BACKGROUND: The intracranial cavity is composed of brain tissue as well as cerebrospinal fluid (CSF), blood, and air. These fluid components allow volume to be shunted out of the intracranial region in the setting of skull-based compression to minimize the effect of compression on the brain. The degree of change to the intracranial compartment in the setting of craniosynostosis and the speed at which they occur and resolve after surgery are not fully understood. This study sought to rigorously analyze the intracranial volume compositions of patients with craniosynostosis prior to and after CVR. METHODS: The authors compared volume measurements for age-matched patients with unicoronal (n = 4), metopic (n = 4), and sagittal (n = 4) craniosynostosis. Intracranial segmentation and analysis were performed on Materialize Medical 21.0 (Materialise; Leuven, Belgium) using the following segmentation thresholds: bone 226-3066 HU, CSF -281-18 HU, and air 19-225 HU, and then manually edited utilizing typical segmentation techniques. On expert consultation, brain segmentation volumes were determined to be less reliable measurements than intracranial, CSF, and air volumes and were thus calculated by subtracting the other volumes from ICV. Paired t tests, one-way analysis of variance, and multiple regression analyses were performed on STATA 15.1 (StataCorp, College Station, TX). RESULTS: The average age at surgical repair was 8.7 ± 0.83 months. All postoperative imaging was performed between 3 and 5 days postoperatively aside from one patient with imaging at 19 days postoperatively. There was a significant increase in total ICV (913772.5 ± 102480.5 mm3 versus 1068165 ± 95752.5 mm3; P < 0.001) and intracranial air volume (18608.8 ± 9639.1 versus 53230.2 ± 32607.4; P = 0.001) after CVR. On subgroup analysis by affected suture, there was a significant increase in ICV (851748.9 ± 87438.1 versus 1043117 ± 149763; P = 0.009) and brain volume (737312.3 ± 80166.5 versus 829060.9 ± 61405.6; P = 0.021) in the metopic cohort and a significant increase in ICV (1006379 ± 31359.5 versus 1133497 ± 45574.1; P = 0.013) and intracranial air volume (18056.21± 5397.634 versus 53230.16± 32607; P = 0.001) in the sagittal cohort. The metopic cohort had the largest percent change in intracranial volume (18% ± 3.4%) and CSF volume (28% ± 24%). There were dramatic postoperative increases in intracranial air volumes in all cohorts (percent change: unicoronal 46% ± 16%; sagittal 58% ± 36%, metopic 58% ± 23%) at this postoperative time period. On multiple regression analysis with affected suture, type of CVR, age at repair and time from surgery to postoperative imaging as independent variables, age at repair was the only significant predictor of percent change in ICV (coef, −5.35; 95% CI, −10.2 to −0.51; P= 0.04) at the 0.05 significance level. CONCLUSION: The ICV increase created by CVR allows subsequent increases in brain, CSF, and air volumes in the early postoperative time period. Significant brain tissue volume increases were seen in the metopic cohort with significant intracranial air volume increases in the sagittal cohort. We hope to perform additional analysis with follow-up data to determine if some of the noted air volume increase is redistributed to brain tissue or CSF at a later time.

Impact of brain volume and intracranial cerebrospinal fluid volume on the clinical outcome in endovascularly treated stroke patients

PurposePreviously, brain volume (BV) and intracranial cerebrospinal fluid volume (CSFV) have been investigated regarding clinical outcomes of subgroups of ischemic stroke patients. This study aimed to examine if the preexisting, preischemic BV and CSFV have an impact on good functional outcome and mortality in acute ischemic stroke (AIS) patients treated with mechanical thrombectomy (MT). MethodsPreischemic BV, CSFV, and CSFV/Total intracranial volume (TICV)-ratio were calculated with a fully automated segmentation platform. Univariate and multivariate analyses were used to study associations. ResultsIn this retrospective study 107 subsequent AIS patients of a prospective database were included. The segmentation results of the fully automated algorithm based on non-contrast computerized tomography scans (NCCT) correlated significantly with the segmentation results obtained from 3D T1 weighted magnetic resonance images (P < 0.001). In the univariate analysis a preexisting BV (P < 0.001), preexisting CSFV (P = 0.009), and the ratio CSFV/total intracranial volume (P < 0.001) each significantly correlated with good functional outcome and mortality. However, in the multivariate regression analysis, also correcting for patient age, none of these volumes remained to correlate with these outcome parameters. ConclusionIn summary, an association of BV, CSFV, and the CSFV/TICV-ratio with good functional outcome and mortality in AIS treated with MT could not be established. A fully automated segmentation algorithm based on NCCT was successfully developed in-house for calculating the volumes of interest.

Abstract WP74: Automated Measurement of Cerebral Atrophy and Outcome in Endovascular Thrombectomy

Background and Purpose: Methods of identifying ischemic stroke patients with a greater probability of poor outcome following endovascular thrombectomy (EVT) might improve shared treatment decision-making between patients, families and physicians. Visually-graded cerebral atrophy is associated with worse functional outcome following EVT. We used an objective, automated method to measure cerebral atrophy and investigated whether this was associated with functional outcome in EVT patients. Methods: Consecutive EVT patients from a single-center registry were studied. CT brain scans were segmented with a combination of a validated U-Net and Hounsfield unit thresholding. Intracranial cerebrospinal fluid (CSF) volume was used as a marker of cerebral atrophy and calculated as a proportion of total intracranial volume. The primary outcome was functional independence, defined as a 3-month modified Rankin Scale (mRS) score of 0-2. Results: 360 EVT patients were included. Functional independence was achieved in 204 (56.7%) patients. The mean±SD CSF volume was 9.0±4.7% of total intracranial volume. Multivariable regression demonstrated that increasing CSF volume was associated with reduced functional independence (OR=0.65 per 5% increase in CSF volume; 95% CI, 0.48- 0.89; P=0.007) and higher 3-month mRS scores (common OR=1.59 per 5% increase in CSF volume; 95% CI, 1.05-2.41; P=0.03). Conclusions: Cerebral atrophy determined by automated measurement of intracranial CSF volume is associated with functional outcome in patients undergoing EVT. If validated in future studies, this simple, objective, and automated imaging marker could potentially be incorporated into decision-support tools in order to improve shared treatment decision making.

Abstract 58: Prediction of Malignant Edema Formation After Endovascular Treatment for Middle Cerebral Artery Infarction: The Added Value of Intracranial Cerebrospinal Fluid Volume

Introduction: Prediction models may guide decisions in the management of patients at risk for malignant middle cerebral artery infarction. The ratio of intracranial cerebrospinal fluid (CSF) volume to intracranial volume (ICV) has been identified as a predictor of malignant edema in ischemic stroke patients treated with intravenous thrombolysis. The added predictive value in stroke patients who received endovascular treatment is unknown. Methods: Patients with available thin-slice non-contrast CT data on admission were selected from the MR CLEAN Registry, which is a prospective national multicenter registry of patients with large vessel occlusion who were treated with endovascular treatment between 2014 and 2017. Baseline characteristics and CT imaging data were collected. The CSF/ICV ratio was automatically measured on baseline thin-slice non-contrast CT. The primary outcome was the formation of malignant edema based on clinical and imaging features on follow-up. A previously built logistic regression model was fitted and included the following baseline predictors: age, National Institutes of Health Stroke Scale, Alberta Stroke Program Early CT score, poor collateral filling and reperfusion. An extended model with the CSF/ICV ratio was compared to the previous model by using the likelihood ratio test. Odds ratios (OR), areas under the receiver operating characteristic curve (AUROC) and 95% confidence intervals (CI) were reported. Results: Of the included 683 patients 40 (6%) developed malignant edema. The CSF/ICV ratio of the group with malignant edema (mean 9±5%) was lower than the group without malignant edema (mean 14±6%, P&lt;0.001). In the extended model, the CSF/ICV ratio was associated with the formation of malignant edema (per one percent decrease OR 1.2, 95% CI 1.1-1.3, P&lt;0.001). In addition, the discriminative performance of the model with the CSF/ICV ratio (AUROC 0.87, 95% CI 0.82-0.91) was higher than that of the model without the CSF/ICV ratio (AUROC 0.84, 0.78-0.89, P&lt;0.001). Conclusions: The CSF/ICV ratio improves the prediction of malignant edema formation in ischemic stroke patients who received endovascular treatment.

Automated Measurement of Cerebral Atrophy and Outcome in Endovascular Thrombectomy

Background and Purpose- Methods of identifying ischemic stroke patients with a greater probability of poor outcome following endovascular thrombectomy (EVT) might improve shared treatment decision-making between patients, families, and physicians. We used an objective, automated method to measure cerebral atrophy and investigated whether this was associated with outcome in EVT patients. Methods- Consecutive EVT patients from a single-center registry were studied. CT brain scans were segmented with a combination of a validated U-Net and Hounsfield unit thresholding. Intracranial cerebrospinal fluid (CSF) volume was used as a marker of cerebral atrophy and calculated as a proportion of total intracranial volume. The primary outcome was functional independence, defined as a 3-month modified Rankin Scale score of 0 to 2. Results- Three-hundred sixty EVT patients were included. Functional independence was achieved in 204 (56.7%) patients. The mean±SD CSF volume was 9.0±4.7% of total intracranial volume. Multivariable regression demonstrated that increasing CSF volume was associated with reduced functional independence (OR=0.65 per 5% increase in CSF volume; 95% CI, 0.48-0.89; P=0.007) and higher 3-month modified Rankin Scale scores (common OR, 1.59 per 5% increase in CSF volume; 95% CI, 1.05-2.41; P=0.03). Conclusions- Cerebral atrophy determined by automated measurement of intracranial CSF volume is associated with functional outcome in patients undergoing EVT. If validated in future studies, this simple, objective, and automated imaging marker could potentially be incorporated into decision-support tools to improve shared treatment decision-making.

Choroid plexus perfusion and intracranial cerebrospinal fluid changes after angiogenesis

Recent studies have provided evidence that cortical brain ischemia may influence choroid plexus function, and such communication may be mediated by either traditional CSF circulation pathways and/or a possible glymphatic pathway. Here we investigated the hypothesis that improvements in arterial health following neoangiogenesis alter (i) intracranial CSF volume and (ii) choroid plexus perfusion in humans. CSF and tissue volume measurements were obtained from T1-weighted MRI, and cortical and choroid plexus perfusion were obtained from perfusion-weighted arterial spin labeling MRI, in patients with non-atherosclerotic intracranial stenosis (e.g. Moyamoya). Measurements were repeated after indirect surgical revascularization, which elicits cortical neoangiogenesis near the revascularization site (n = 23; age = 41.8 ± 13.4 years), or in a cohort of participants at two time points without interval surgeries (n = 10; age = 41.7 ± 10.7 years). Regression analyses were used to evaluate dependence of perfusion and volume on state (time 1 vs. 2). Post-surgery, neither CSF nor tissue volumes changed significantly. In surgical patients, cortical perfusion increased and choroid plexus perfusion decreased after surgery; in participants without surgeries, cortical perfusion reduced and choroid plexus perfusion increased between time points. Findings are discussed in the context of a homeostatic mechanism, whereby arterial health, paravascular flow, and/or ischemia can affect choroid plexus perfusion.

Intracranial Cerebrospinal Fluid Volume as a Predictor of Malignant Middle Cerebral Artery Infarction.

Background and Purpose- Predicting malignant middle cerebral artery (MCA) infarction can help to identify patients who may benefit from preventive decompressive surgery. We aimed to investigate the association between the ratio of intracranial cerebrospinal fluid (CSF) volume to intracranial volume (ICV) and malignant MCA infarction. Methods- Patients with an occlusion proximal to the M3 segment of the MCA were selected from the DUST (Dutch Acute Stroke Study). Admission imaging included noncontrast computed tomography (CT), CT perfusion, and CT angiography. Patient characteristics and CT findings were collected. The ratio of intracranial CSF volume to ICV (CSF/ICV) was quantified on admission thin-slice noncontrast CT. Malignant MCA infarction was defined as a midline shift of >5 mm on follow-up noncontrast CT, which was performed 3 days after the stroke or in case of clinical deterioration. To test the association between CSF/ICV and malignant MCA infarction, odds ratios and 95% CIs were calculated for 3 multivariable models by using binary logistic regression. Model performances were compared by using the likelihood ratio test. Results- Of the 286 included patients, 35 (12%) developed malignant MCA infarction. CSF/ICV was independently associated with malignant MCA infarction in 3 multivariable models: (1) with age and admission National Institutes of Health Stroke Scale (odds ratio, 3.3; 95% CI, 1.1-11.1), (2) with admission National Institutes of Health Stroke Scale and poor collateral score (odds ratio, 7.0; 95% CI, 2.6-21.3), and (3) with terminal internal carotid artery or proximal M1 occlusion and poor collateral score (odds ratio, 7.7; 95% CI, 2.8-23.9). The performance of model 1 (areas under the receiver operating characteristic curves, 0.795 versus 0.824; P=0.033), model 2 (areas under the receiver operating characteristic curves, 0.813 versus 0.850; P<0.001), and model 3 (areas under the receiver operating characteristic curves, 0.811 versus 0.856; P<0.001) improved significantly after adding CSF/ICV. Conclusions- The CSF/ICV ratio is associated with malignant MCA infarction and has added value to clinical and imaging prediction models in limited numbers of patients.

Neurological Symptoms of Intracranial Hypotension

Intracranial hypotension usually arises in the context of known or suspected leak of cerebrospinal fluid (CSF). This leakage leads to a fall in intracranial CSF pressure and CSF volume. The most common clinical manifestation of intracranial hypotension is orthostatic headache. Post-dural puncture headache and CSF fistula headache are classified along with headache attributed to spontaneous intracranial hypotension as headache attributed to low CSF pressure by the International Classification of Headache Disorders. Headache attributed to low CSF pressure is usually but not always orthostatic. The orthostatic features at its onset can become less prominent over time. Other manifestations of intracranial hypotension are nausea, spine pain, neck stiffness, photophobia, hearing abnormalities, tinnitus, dizziness, gait unsteadiness, cognitive and mental status changes, movement disorders and upper extremity radicular symptoms. There are two presumed pathophysiologic mechanisms behind the development of various manifestations of intracranial hypotension. Firstly, CSF loss leads to downward shift of the brain causing traction on the anchoring and supporting structures of the brain. Secondly, CSF loss results in compensatory meningeal venodilation. Headaches presenting acutely after an intervention or trauma that is known to cause CSF leakage are easy to diagnose. However, a high degree of suspicion is required to make the diagnosis of spontaneous intracranial hypotension and understanding various neurological symptoms of intracranial hypotension may help clinicians. Key Words: Intracranial hypotension, Cerebrospinal fluid leak, Headache, Post-dural puncture headache, Ventriculoperitoneal shunt

Osmotic Shifts, Cerebral Edema, and Neurologic Deterioration in Severe Hepatic Encephalopathy.

We sought to determine the effect of acute electrolyte and osmolar shifts on brain volume and neurologic function in patients with liver failure and severe hepatic encephalopathy. Retrospective analysis of brain CT scans and clinical data. Tertiary care hospital ICUs. Patients with acute or acute-on-chronic liver failure and severe hepatic encephalopathy. Clinically indicated CT scans and serum laboratory studies. Change in intracranial cerebrospinal fluid volume between sequential CT scans was measured as a biomarker of acute brain volume change. Corresponding changes in serum osmolality, chemistry measurements, and Glasgow Coma Scale were determined. Associations with cerebrospinal fluid volume change and Glasgow Coma Scale change for initial volume change assessments were identified by Spearman's correlations (rs) and regression models. Consistency of associations with repeated assessments was evaluated using generalized estimating equations. Forty patients were included. Median baseline osmolality was elevated (310 mOsm/Kg [296-321 mOsm/Kg]) whereas sodium was normal (137 mEq/L [134-142 mEq/L]). Median initial osmolality change was 9 mOsm/kg (5-17 mOsm/kg). Neuroimaging consistent with increased brain volume occurred in 27 initial assessments (68%). Cerebrospinal fluid volume change was more strongly correlated with osmolality (r = 0.70; p = 4 × 10) than sodium (r = 0.28; p = 0.08) change. Osmolality change was independently associated with Glasgow Coma Scale change (p = 1 × 10) and cerebrospinal fluid volume change (p = 2.7 × 10) in initial assessments and in generalized estimating equations using all 103 available assessments. Acute decline in osmolality was associated with brain swelling and neurologic deterioration in severe hepatic encephalopathy. Minimizing osmolality decline may avoid neurologic deterioration.