Reabsorption Of Cerebrospinal Fluid Research Articles

Arachnoid granulations in idiopathic intracranial hypertension: Do they have an influence?

The aim of this study was to investigate whether the relative narrowing of the dural venous sinuses by arachnoid granulations (AGs) is more pronounced in patients with idiopathic intracranial hypertension (IIH) compared to healthy controls. IIH is characterized by increased intracranial pressure, which is associated with symptoms such as headache and visual disturbances. The role of cerebral venous drainage obstruction in IIH is the subject of ongoing research. In this retrospective case-control study, 3D contrast-enhanced magnetic resonance images of a cohort of 43 patients with IIH were evaluated for (1) the number of AGs per venous sinus and (2) the diameters of the dural venous sinuses at the site of an AG and at standardized measurement points. In addition, the minimum width of the transverse/sigmoid sinus was measured. All data were compared to the same data from a cohort of 43 control participants. Patients with IIH showed less relative sinus narrowing by AG compared to controls (median: 7%, interquartile range [IQR] 10% vs. 11%, IQR 9% in controls; p = 0.009). In patients with IIH, sinus diameter was larger at the site of an AG (70 ± 25 mm2) compared to its diameter at the standardized measurement point (48 ± 23 mm2; p = 0.010). In the superior sagittal sinus (SSS), patients with IIH had smaller AGs (median: 3 mm2, IQR 2 mm2 vs. 5 mm2, IQR 3 mm2 in controls; p = 0.023) while the respective sinus segment was larger (median: 69 mm2; IQR 21 mm2 vs. 52 mm2, IQR 26 mm2 in controls; p = 0.002). The right transverse sinus was narrower in patients with IIH (41 ± 21 mm vs. 57 ± 20 mm in controls; p < 0.001). In contrast to our hypothesis, patients with IIH showed less pronounced relative sinus narrowing by AG compared to controls, especially within the SSS, where AGs were smaller and the corresponding sinus segment wider. Smaller AGs could result in lower cerebrospinal fluid resorption, favoring the development of IIH. Conversely, the smaller AGs could also be a consequence of IIH due to backpressure in the SSS because of the narrower transverse/sigmoid sinus, which widens the SSS and compresses the AG.

Biomechanical instability of the brain-CSF interface in hydrocephalus.

Hydrocephalus, characterized by progressive expansion of the cerebrospinal fluid (CSF)-filled ventricles (ventriculomegaly), is the most common reason for brain surgery. "Communicating" (i.e., non-obstructive) hydrocephalus is classically attributed to a primary derangement in CSF homeostasis, such as choroid plexus-dependent CSF hypersecretion, impaired cilia-mediated CSF flow currents, or decreased CSF reabsorption via the arachnoid granulations or other pathways. Emerging data suggest abnormal biomechanical properties of the brain parenchyma are an underappreciated driver of ventriculomegaly in multiple forms of communicating hydrocephalus across the lifespan. We discuss recent evidence from human and animal studies that suggests impaired neurodevelopment in congenital hydrocephalus, neurodegeneration in elderly normal pressure hydrocephalus, and, in all age groups, inflammation-related neural injury post-infectious and post-hemorrhagic hydrocephalus, can result in loss of stiffness and viscoelasticity of the brain parenchyma. Abnormal brain biomechanics creates barrier alterations at the brain-CSF interface that pathologically facilitates secondary enlargement of the ventricles, even at normal or low intracranial pressures. This "brain-centric" paradigm has implications for the diagnosis, treatment, and study of hydrocephalus from womb to tomb.

Congenital/Primitive Hydrocephalus: Classification, Clinical Aspects, and Rehabilitation Approach

AbstractHydrocephalus is a heterogeneous disorder of cerebrospinal fluid (CSF) flow that leads to abnormal enlargement of the brain ventricles. The prevalence of infant hydrocephalus is approximately one case per 1,000 births. Hydrocephalus occurs due to an imbalance between the production and the absorption of CSF. The causes of hydrocephalus secondary to CSF overproduction are papilloma of the choroid plexus and rarely diffuse hyperplasia of the villi. All the other hydrocephalus forms are secondary to obstruction to normal CSF reabsorption and are also known as obstructive hydrocephalus. According to the location of obstruction, obstructive hydrocephalus can be defined as communicating, when caused by extraventricular obstruction of the CSF flow or decreased resorption of CSF distal to the fourth ventricle in the cisterns of the base or in the subarachnoid spaces, or as not communicating, in case of intraventricular obstruction to fluid flow. There is a third category, common in preterm infants, called external hydrocephalus which is secondary to delayed development of arachnoid function. Hydrocephalus leads to an increase in intraventricular pressure because of the lack of the mechanism regulating the homeostasis of the CSF flow. Increased intraventricular pressure is responsible for the clinical symptoms in affected child. Clinical presentation varies with age. In the neonatal period, prolonged or frequent apneic or bradycardic events, increasing head circumference, presence of sunsetting eyes or upward gaze palsy, evidence of full or tense anterior/posterior fontanelle, and splayed cranial sutures are signs of increased intracranial pressure. In infants, the most common signs are progressive macrocephaly, irritability, nausea/vomiting, headache, gait changes, and regression of developmental milestones. The extent of brain damage depends on the cause that led to hydrocephalus, the patient's age, and the rapidity of onset. The surgical treatment modalities consist of endoscopic ventriculostomy of the third ventricle and ventriculoperitoneal or ventriculoatrial CSF shunt.

185 Deuterium MRI for CSF Studies in Normal and Hydrocephalic Rats

INTRODUCTION: The recent characterization of the glymphatic system has revived interest in the interaction of cerebrospinal fluid (CSF) with brain tissue via perivascular spaces. Traditional CSF tracers, such as gadolinium and iohexal, are large molecules that do not cross the blood brain barrier (BBB). The primary component of CSF, however, is water, which is BBB permeable. METHODS: Eight adult male rats underwent cisterna magna catheterization for intrathecal infusion. Brain MR images were obtained in a 7 tesla small-animal MRI system. Temporal T1-weighted images (T1WI) were obtained before, during, and after intrathecal infusion of D2O. Five rats then underwent ventricular kaolin injection for induction of hydrocephalus, after which repeat imaging with intrathecal D2O infusion was performed. RESULTS: Intrathecal deuterium infusion produced consistent changes on MRI imaging. Because conventional MRI does not sense deuterium, the T1WI showed a loss in proton signal with D2O infusion. Rapid D2O uptake of &lt;2.5 minutes was noted in CSF spaces, brain tissue, and saggital and straight venous sinuses. CONCLUSIONS: Use of deuterium as an intrathecal contrast agent provides a physiologically realistic model of CSF behavior. Efforts are ongoing to quantify the relationship between MRI signal loss and deuterium tissue concentration for comparative analysis between healthy and hydrocephalic rats. The loss of MRI signal in the straight sinus after intrathecal infusion implicates the deep venous system in the clearance of CSF, suggesting that CSF is reabsorbed into the venous system via the brain tissue itself. Because traditional CSF tracers do not cross the BBB, the role of the brain tissue in the reabsorption of CSF has been overlooked.

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.

The relationship between myodural bridge, atrophy and hyperplasia of the suboccipital musculature, and cerebrospinal fluid dynamics

The Myodural Bridge (MDB) is a physiological structure that is highly conserved in mammals and many of other tetrapods. It connects the suboccipital muscles to the cervical spinal dura mater (SDM) and transmits the tensile forces generated by the suboccipital muscles to the SDM. Consequently, the MDB has broader physiological potentials than just fixing the SDM. It has been proposed that MDB significantly contributes to the dynamics of cerebrospinal fluid (CSF) movements. Animal models of suboccipital muscle atrophy and hyperplasia were established utilizing local injection of BTX-A and ACE-031. In contrast, animal models with surgical severance of suboccipital muscles, and without any surgical operation were set as two types of negative control groups. CSF secretion and reabsorption rates were then measured for subsequent analysis. Our findings demonstrated a significant increase in CSF secretion rate in rats with the hyperplasia model, while there was a significant decrease in rats with the atrophy and severance groups. We observed an increase in CSF reabsorption rate in both the atrophy and hyperplasia groups, but no significant change was observed in the severance group. Additionally, our immunohistochemistry results revealed no significant change in the protein level of six selected choroid plexus-CSF-related proteins among all these groups. Therefore, it was indicated that alteration of MDB-transmitted tensile force resulted in changes of CSF secretion and reabsorption rates, suggesting the potential role that MDB may play during CSF circulation. This provides a unique research insight into CSF dynamics.

Stenting for Venous Sinus Stenosis in Patients With Idiopathic Intracranial Hypertension: An Updated Systematic Review and Meta-Analysis of the Literature.

Although venous sinus stenting (VSS) improves cerebrospinal fluid reabsorption and decreases intracranial pressure in patients with idiopathic intracranial hypertension (IIH), the underlying pathophysiology of IIH is not well understood. We present a review and meta-analysis of the literature on VSS for IIH treatment, focusing on the rates of restenosis and symptom recurrence. We performed a systematic review of PubMed and Embase databases between January 1, 2011, and December 31, 2021. Articles including ≥5 patients with IIH and venous sinus stenosis treated with VSS and post-treatment rates of restenosis (de novo stenosis at a different anatomic location along the dural sinuses or restenosis within or adjacent to the stent) were selected. Demographic, procedural, and outcomes data were collected and analyzed. Mean values for variables collected were pooled, and a mean value was calculated with a 95% CI. Twenty-four articles were included, comprising 694 patients and 781 VSS cases. The mean age was 33.9 (CI, 31.5-36.2) years. The mean body mass index was 35.3 (CI, 32.9-37.7) kg/m 2 . Before VSS, 98.8% (CI, 96.8%-100.0%) of patients experienced headaches, 87.7% (CI, 80.6%-95.5%) had visual acuity issues, 78.7% (CI, 69.9%-88.5%) had papilledema, 58.3% (CI, 46.0%-73.9%) had tinnitus, and 98.8% (96.4%-100.0%) had symptoms refractory to previous therapies. After VSS, 77.7% (CI, 71.1%-84.95%) experienced symptom improvement and 22.3% (CI, 15.1%-29.0%) had persistent or worsened symptoms. Pooled restenosis rate was 17.7% (CI, 14.9%-20.9%). VSS is effective in alleviating IIH signs and symptoms, but the associated high rates of restenosis and persistent symptoms highlight the need for further investigation of this procedure and other adjunctive treatments for IIH.

CSF-to-blood toxins clearance is modulated by breathing through cranio-spinal CSF oscillation.

Clearance of brain toxins occurs during sleep, although the mechanism remains unknown. Previous studies implied that the intracranial aqueductal cerebrospinal fluid (CSF) oscillations are involved, but no mechanism was suggested. The rationale for focusing on the aqueductal CSF oscillations is unclear. This study focuses on the cranio-spinal CSF oscillation and the factors that modulate this flow. We propose a mechanism where increased cranio-spinal CSF movements enhance CSF-to-blood metabolic waste clearance through the spinal CSF re-absorption sites. A recent study demonstrating that disturbed sleep impairs CSF-to-blood but not brain-to-CSF clearance, supports the fundamentals of our proposed mechanism. Eight healthy subjects underwent phase-contrast magnetic resonance imaging to quantify the effect of respiration on the cranio-spinal CSF oscillations. Maximal CSF volume displaced from the cranium to the spinal canal during each respiration and cardiac cycle were derived as measures of cranio-spinal CSF mixing level. Transition from normal to slow and abdominal breathing resulted in a 56% increase in the maximal displaced CSF volume. Maximal change in the arterial-venous blood volume, which is the driving force of the CSF oscillations, was increased by 41% during slow abdominal breathing. Cranio-spinal CSF oscillations are driven by the momentary difference between arterial inflow and venous outflow. Breathing modulates the CSF oscillation through changes in the venous outflow. The amount of toxins being transferred to the spinal canal during each respiratory cycle is significantly increased during slow and deeper abdominal breathing, which explains enhanced CSF-to-blood toxins clearance during slow-wave sleep and poor clearance during disrupted sleep.

E32 Intra cranial hypertension in juvenile neurolupus

Abstract Introduction Neurolupus is one of the two key prognostic parameters of lupus. Its manifestation can be central or peripheral, revealing the disease or occurring during the course of evolution. It’s important to not consider all neurological manifestations during SLE as related to lupus, ruling out Central nervous system (CNS) infection and anti-phospholipid syndrome (APS) is primordial. Objectives To share 3 rare observations of neurolupus with intracranial hypertension syndrome and discuss their therapeutic modalities. To highlight the lack of evidence in the treatment of such cases. Method A retrospective analysis of data from medical records. Results We report three observations of Intracranial hypertension syndrome involving three girls, ranging from 9 to 14 years. Clinical symptomatology was dominated by headache, vomiting and visual disturbances. Examination found papillary oedema stage 3 in all the three patients, convergent strabismus in two patients and elevated intracranial pressure measurement in all the three girls ranged from 95 mm to 57 mm of H2O. Brain MRI performed in all three-patients was normal. Data from laboratory tests showed, thrombocytopenia in one patient, pancytopenia in one patient, positive antinuclear antibodies in all patients, positive anti-DNA antibody in one patient, C3, C4 consumption in two patients, positive proteinuria in two patients and positive anti phospholipid antibodies in one patient. All patients had active SLE at the time of admission with a Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) at least at 17. Symptomatic treatment with carbonic anhydrase inhibitor was initiated, followed by methylprednisolone pulse therapy then oral corticosteroids and hydroxychloroquine in all the three patients. Immunosuppressive therapy with Rituximab 1 g at two-week intervals was administrated in two patients, the third one did not receive any suppressive treatment in addition to corticosteroids due to the favorable outcome. The course was favorable in all patients with regression of clinical symptoms of intracranial hypertension and papillary oedema immediately after cerebro spinal fluid (CSF) subtraction. Discussion and Conclusion Neurolupus presents with heterogeneous symptoms that make its diagnosis difficult. Intracranial hypertension syndrome is a rare manifestation resulting from a disorder of CSF resorption, its pathogenesis is poorly understood with an inflammatory hypothesis based on immune deposits. There are no therapeutic recommendations to date. This isolated syndrome without other neurological signs of severity responds very well to symptomatic treatment with carbonic anhydrase inhibitors and to CSF withdrawal, as was the case in our patients. The use of immunosuppressive therapy (rituximab in our patients) was indicated due to the severity of the clinical picture with severe renal involvement. In addition, other immunosuppressive drugs can be an alternative option therapy. Ethics The study was performed according to the principles of the Declaration of Helsinki.

Protocolo diagnóstico de la hidrocefalia

Hydrocephalus is the pathological increase in the size of the cerebral ventricles due to an increase in cerebrospinal fluid (CSF), mainly due to a defect in the circulation or reabsorption of CSF and exceptionally due to an increase in production (such as choroid plexus papilloma). The causes of hydrocephalus are numerous, both in children and in adults. They may produce symptoms of intracranial hypertension (ICHT), with the diagnostic approach being different in each case. One type of hydrocephalus in adults is normal pressure hydrocephalus (NPH) and its Hakim-Adams triad. Ventriculoperitoneal shunting is the treatment of choice.

Abstract Number ‐ 12: First‐In‐Human Endovascular Treatment of Idiopathic Intracranial Hypertension Using a Miniature Biomimetic Transdural Shunt.

Introduction Successful percutaneous transvenous deployment of a miniature valved biomimetic transdural endovascular shunt (CereVasc eShunt, Auburndale, MA, USA) via an inferior petrosal sinus approach was recently described for treatment of post‐subarachnoid hemorrhage communicating hydrocephalus.The endovascular shunt replicates the function of the arachnoid granulation by draining cerebrospinal fluid (CSF) from the cerebello‐pontine angle cistern to the ipsilateral internal jugular vein. Idiopathic intracranial hypertension (IIH), usually resulting from venous transverse sinus stenosis, can be treated with pharmacological inhibition of CSF production, surgical ventriculoperitoneal shunting, or using venous stent angioplasty. In IIH, elevated CSF pressure can act to exacerbate venous sinus stenosis, resulting in worsening CSF reabsorption, thereby perpetuating a vicious cycle. The authors sought to evaluate the role of the minimally invasive eShunt approach in IIH management. Methods A 50‐year‐old male patient with history of dyslipidemia and IIH initially presented 6 years ago with diplopia initially treated with poorly tolerated acetazolamide and periodic lumbar punctures with subsequent symptom improvement. The patient was admitted following rapid evolution of sudden onset horizontal diplopia and headache. Brain magnetic resonance revealed flattening of the posterior sclera, partially empty Sella Turcica, enhancement of the prelaminar optic nerves and enlarged Meckel´s cave. Lumbar puncture was performed with opening pressure of 28 cmH2O. Cerebral angiography with 3D venography confirmed bilateral transverse sinus stenosis, though without a significant pressure gradient. Results The patient declined surgical ventriculoperitoneal shunting and was approved for compassionate use of eShunt by regulatory and bioethics committees.He underwent successful endovascular transdural deployment of the eShunt, which he tolerated well and was discharged at 48 hours post‐procedure with rapid symptomatic headache relief. Upon 30‐day follow‐up repeat brain MRI showed improvement of the prominent subarachnoid space around both optic nerves and sustained improvement of his pre‐procedural headache and diplopia.A repeat lumbar puncture revealed a lowed opening pressure of 20 cmH2O and MRI cisternography confirmed maintained patency of the biomimetic valve with accumulation of Gadolinium‐enhanced CSF drainage through the eShunt into the jugular bulb. Conclusions The current report describes the first‐in‐human use of the eShunt device for treatment of IIH resulting in sustained symptomatic relief along with decrease in CSF pressure and pre‐laminar optic nerve edema. The current results, which require confirmation in a larger cohort with longer follow‐up, are encouraging and suggest a possible role for minimally invasive endovascular transdural eshunt placement in the management of IIH.

Symptom: Runny Nose Six Years After Acoustic Neuroma Surgery

Symptom: Runny Nose Six Years After Acoustic Neuroma Surgery

Elevated Intracranial Pressure in Cryptococcal Meningoencephalitis: Examining Old, New, and Promising Drug Therapies.

Despite the availability of effective antifungal therapy, cryptococcal meningoencephalitis (CM) remains associated with elevated mortality. The spectrum of symptoms associated with the central nervous system (CNS) cryptococcosis is directly caused by the high fungal burden in the subarachnoid space and the peri-endothelial space of the CNS vasculature, which results in intracranial hypertension (ICH). Management of intracranial pressure (ICP) through aggressive drainage of cerebrospinal fluid by lumbar puncture is associated with increased survival. Unfortunately, these procedures are invasive and require specialized skills and supplies that are not readily available in resource-limited settings that carry the highest burden of CM. The institution of pharmacologic therapies to reduce the production or increase the resorption of cerebrospinal fluid would likely improve clinical outcomes associated with ICH in patients with CM. Here, we discuss the potential role of multiple pharmacologic drug classes such as diuretics, corticosteroids, and antiepileptic agents used to decrease ICP in various neurological conditions as potential future therapies for CM.

Regulation of Ncbe in the Choroid Plexus of Mice after Hemorrhage‐Induced Hydrocephalus

The choroid plexus (CP) is a small tissue located inside brain ventricles. It is responsible for the production of most of the cerebrospinal fluid (CSF); approximately 500 mL of CSF per day in the adult human [1, 2]. CSF production occurs as a net result of transcellular movement of salt and water, carried out by various cellular transporters.Ncbe is a sodium‐coupled bicarbonate transporter located in the basolateral membrane of the choroid plexus epithelial (CPE) cells. It transports Na+ and HCO3‐ into the cell in exchange for Cl‐. Ncbe is the main sodium loader of the cell and CSF production is probably dependent on this transporter [3].Posthemorrhagic hydrocephalus (PHH) is a pathological state, caused by an accumulation of CSF in the ventricular system following intraventricular hemorrhage. CSF buildup is caused by a disproportion in CSF production and reabsorption. This leads to an expansion of the brain ventricles. Intraventricular hemorrhage (IVH) is known to cause inflammation in the CP, which is coupled to an over‐production of CSF [4‐6].Initially we hypothesized that IVH would stimulate Ncbe in the CPE through increased protein abundance as well as transporter activity. This would lead to increased CSF formation, similar to the response found after treatment with e.g. the cyclic‐AMP agonist forskolin [7]. Our preliminary data, however, suggest that Ncbe abundance is reduced by 24% (n=4, p=0.0329) in mice in the initial stages of PHH and then normalizes.The aim of this study is to investigate which role Ncbe plays in PHH and how Ncbe knock down affects CSF production in both healthy mice and a disease model.An adeno‐associated virus (AAV) shRNA knockdown vector system has been developed to knock down Ncbe gene expression by intracerebroventricular injections. Our preliminary data shows that the CPE cells incorporate the vector when tagged with GFP.We have established an IVH model and recording of CSF secretion rates in mice. Increased CSF formation rate was validated with ventriculo‐cisternal perfusion (data shown in figure). The resulting changes in ventricular volume will be investigated using magnetic resonance imaging (MRI).We propose that Ncbe knock down inhibits CSF production and could potentially target inflammation‐dependent hypersecretion by reducing the availability of the sodium supplying the apical transporters in the CP.

Does Long-Duration Exposure to Microgravity Lead to Dysregulation of the Brain and Ocular Glymphatic Systems?

Spaceflight-associated neuro-ocular syndrome (SANS) has been well documented in astronauts both during and after long-duration spaceflight and is characterized by the development of optic disc edema, globe flattening, choroidal folds, and hyperopic refractive error shifts. The exact mechanisms underlying these ophthalmic abnormalities remain unclear. New findings regarding spaceflight-associated alterations in cerebrospinal fluid spaces, specifically perivascular spaces, may shed more light on the pathophysiology of SANS. The preliminary results of a recent brain magnetic resonance imaging study show that perivascular spaces enlarge under prolonged microgravity conditions, and that the amount of fluid in perivascular spaces is linked to SANS. The exact pathophysiological mechanisms underlying enlargement of perivascular spaces in space crews are currently unclear. Here, we speculate that the dilation of perivascular spaces observed in long-duration space travelers may result from impaired cerebral venous outflow and compromised cerebrospinal fluid resorption, leading to obstruction of glymphatic perivenous outflow and increased periarterial cerebrospinal fluid inflow, respectively. Further, we provide a possible explanation for how dilated perivascular spaces can be associated with SANS. Given that enlarged perivascular spaces in space crews may be a marker of altered venous hemodynamics and reduced cerebrospinal fluid outflow, at the level of the optic nerve and eye, these disturbances may contribute to SANS. If confirmed by further studies, brain glymphatic dysfunction in space crews could potentially be considered a risk factor for the development of neurodegenerative diseases, such as Alzheimer’s disease. Furthermore, long-duration exposure to microgravity might contribute to SANS through dysregulation of the ocular glymphatic system. If prolonged spaceflight exposure causes disruption of the glymphatic systems, this might affect the ability to conduct future exploration missions, for example, to Mars. The considerations outlined in the present paper further stress the crucial need to develop effective long-term countermeasures to mitigate SANS-related physiologic changes during long-duration spaceflight.

Bumetanide lowers acute hydrocephalus in a rat model of subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) can lead to acute hydrocephalus (AH). AH pathophysiology is classically attributed to an obstruction of the arachnoid granulations by blood. Recent findings in rodents suggest that after intraventricular hemorrhage, AH is related to cerebrospinal fluid (CSF) hypersecretion by the choroid plexus (CP), as it can be reduced by intracerebroventricular (ICV) injection of bumetanide. Here, we investigated if and how CSF hypersecretion and/or CSF outflow disorders contribute to post-SAH hydrocephalus. Ninety-four Wistar rats were used. SAH was induced by the endovascular perforation technique. The presence of AH was confirmed by magnetic resonance imaging (MRI), and rats with AH were randomly assigned to 4 groups: control group, superior sagittal sinus (SSS) thrombosis to block CSF reabsorption, ICV injection of saline, and ICV injection of bumetanide to decrease CSF secretion. Clinical outcome was evaluated with a neuroscore. A second MRI was performed 24h later to evaluate the ventricular volume. Fifty percent of rats that survived SAH induction had AH. Their ventricular volume correlated well to the functional outcome after 24h (r = 0.803). In rats with AH, 24h later, ventricular volume remained equally increased in the absence of any further procedure. Similarly, ICV injection of saline or SSS thrombosis had no impact on the ventricular volume. However, ICV injection of bumetanide reduced AH by 35.9% (p = 0.002). In rodents, post-SAH hydrocephalus is may be due to hypersecretion of CSF by the CP, as it is limited by ICV injection of bumetanide. However, we cannot exclude other mechanisms involved in post-SAH acute hydrocephalus.

The treatment of patients with posthemorrhagic hydrocephalus

The article discusses the possible causes of polycystic posthemorrhagic ventriculomegaly in infants, as well as predictors of this pathological process. When choosing a treatment method the doctor shall take into account not only the etiology of the disease, but also age parameters, concomitant pathology. An important aspect in the approach to the treatment of polycystic posthemorrhagic multilevel hydrocephalus includes the determination of the biomechanical properties of the craniospinal system, especially the compliance of the brain and resorption of cerebrospinal fluid. Particular attention is paid to the timely correction of complications, including the analysis of inflammatory changes markers in the craniospinal system, which serve as predictors of the outcome of cerebrospinal fluid resorption. The authors also noted that the violation of the cerebrospinal fluid outflow from the cranial cavity in children may depend on a large number of «extracerebral» factors. They consider the stages of neurosurgical care to patients in this group on a clinical example. This example and literature data demonstrate that children with age develop changes not only in the craniospinal segment, which is responsible for the transformation of free fluid, but also in the extracranial cavities. Thus, we are able to recommend an integrated approach for the management of newborns with intracranial hemorrhage, complicated by posthemorrhagic hyporesorbent and occlusive hydrocephalus, with the justification of the optimal neurosurgical tactics for managing drainage-dependent patients, the course of the disease in which is accompanied by a multicomponent inflammatory syndrome.

Renal Pelvis Opacification on Postmyelography Computed Tomography as an Indicator for Cerebrospinal Fluid Loss in Spontaneous Intracranial Hypotension

PurposeTo assess early renal pelvis opacification on postmyelography computed tomography (CT) as a marker for cerebrospinal fluid (CSF) loss in patients with spontaneous intracranial hypotension (SIH).MethodsThe SIH patients referred to our hospital between January 2012 and May 2018 were retrospectively reviewed and divided into 2 groups based on the presence of spinal longitudinal extrathecal CSF collection (SLEC): (1) SLEC(+) with, and (2) SLEC(−) without proof of SLEC on multimodal imaging. Non-SIH patients (n = 20) undergoing CT myelography served as controls. The renal pelvis density on postmyelography CT was measured in all patients. Mean difference in renal pelvis density between the groups was calculated.ResultsIn total, 111 SIH patients (mean age 48 ± 13 years; 60% female) were included, 71 (64%) SLEC(+) and 40 (36%) SLEC(−). The adjusted renal pelvis density in the SLEC(+), SLEC(−), and the non-SIH group was 108 Hounsfield unit (HU), 83 HU, and 32 HU, respectively, resulting in a significant difference between SLEC(+) vs. control group 1 (75 HU, p < 0.001), SLEC(−) vs. control group 1 (50 HU, p < 0.001), and a tendency for higher density in SLEC(+) than SLEC(−) (25 HU, p = 0.16).ConclusionIncreased renal pelvis opacification on postmyelography CT was observed in SIH patients, even in the absence of a CSF leak or a CSF venous fistula, when compared to non-SIH patients. Although the provenance of early renal opacification in SLEC (−) SIH patients remains unclear, our results suggest that it may be a surrogate for increased spinal CSF resorption via spinal arachnoid granulations and along spinal nerve sheaths occult to direct imaging.

Communicating chronic hydrocephalus: A review

Formerly called normal pressure hydrocephalus, communicating chronic hydrocephalus (CCH) is a condition affecting 0.1 to 0.5% of patients over 60years of age. The pathophysiology of this disease is poorly understood, but a defect in cerebrospinal fluid (CSF) resorption appears to be commonly defined as the cause of the neurological disorders. The last important discovery is the description of the glymphatic system and its implication in CCH and CSF resorption. Comorbidities (Alzheimer's disease, microangiopathy, parkinsonism) are very frequent, and involve a diagnostic challenge. The clinical presentation is based on the Hakim and Adams triad, comprising gait disorders, mainly impairing walking, cognitive disorders, affecting executive functions, episodic memory, visuospatial cognition, and sphincter disorders as urinary incontinence (detrusor hyperactivity). The diagnosis is suspected through a set of arguments, combining the clinical presentation, the radiological data of the magnetic resonance imaging (MRI) showing a ventriculomegaly associated with signs of transependymomous resorption of the CSF and disappearance of the cortical sulci, and the clinical response to the depletion of CSF. In the presence of all these elements, or a strong clinical suspicion, the standard treatment will be of a permanent CSF shunt, using a ventriculoatrial or ventriculoperitoneal shunt. The effectiveness of this treatment defines the diagnosis. The clinical improvement is better when treatment occurs early after the onset of the disorders, reaching 75 to 90% of motor improvement.

Letter: Cranioplasty Reverses Dysfunction of the Solutes Distribution in the Brain Parenchyma After Decompressive Craniectomy

Letter: Cranioplasty Reverses Dysfunction of the Solutes Distribution in the Brain Parenchyma After Decompressive Craniectomy