Accumulation Of Cerebrospinal Fluid Research Articles

Intracranial hypertension syndrome and hemoglobin level in infants who had suffered cerebral ischemia in neonatal period

Aim. To study the relationship between the clinical and neurosonographic indicators of the hypertensive syndrome and blood hemoglobin level in infants with perinatal disorders of the central nervous system. Methods. A total of 58 children with a diagnosis of «Perinatal hypoxic-ischemic brain damage in the form of hypertensive syndrome» were examined at the age of 12 months and younger. Clinical, neurological examination, neuroimaging, laboratory tests and statistical analysis were performed. Results. The majority of infants who had suffered a hypoxia during labor and had clinical and neurosonographic signs of intracranial hypertension also had different stages of blood hemoglobin level decrease. Comparing the neurosonography data and hemoglobin levels, it was found that children with anemia dominated among children with primary accumulation of cerebrospinal fluid in the interhemispheric fissure. Neurosonography revealed interhemispheric fissure widening in 30 (51.7%) of infants, ventricular system widening - in 28 (48.3%) of infants. The anemia rate was high in infants with interhemispheric fissure widening - in 19 (63.3%) out of 30 infants. Anemia was more frequent in the full-term infants with interhemispheric fissure widening - 4 (87.5%) out of 16 infants, whereas prematurely born infants with interhemispheric fissure widening had relevantly higher rate of normal hemoglobin level - 9 (64.3%) out of 14 infants. In 28 infants with ventriculomegaly 23 (82.1%) had widened anterior horns of the lateral ventricles. In 14 (59.3%) of infants with dilatation of the anterior horns of the lateral ventricles hemoglobin level was within the age-appropriate normal limits. Conclusion. Reduced hemoglobin level aggravates the symptoms of intracranial hypertension, and the continuing anemia leads to tissue edema, which leads to a rapid increase of degenerative changes in the brain, causing mental and physical retardation.

Ethyl pyruvate inhibits HMGB1 phosphorylation and secretion in activated microglia and in the postischemic brain

Ethyl pyruvate (EP) has been shown to have anti-inflammatory effects and confer protective effects in various pathological conditions. For example, EP inhibits secretion of high mobility group box 1 (HMGB1), which is known to be released from activated or dying cells and aggravate inflammatory pathways. In the present study, we investigated whether EP reduces HMGB1 phosphorylation and release in ischemic brain and in cultured microglia. In the postischemic brains (60min middle cerebral artery occlusion (MCAO)), HMGB1 was released extracellularly, generating dual peaks in cerebrospinal fluid (CSF) around 1 and 7 days after ischemic insult, which were probably generated from damaged neurons and activated inflammatory cells, respectively. We showed that treatment with EP 30min post-MCAO (5mg/kg, i.v.), which has been shown to confer a robust neuroprotective effect in the postischemic brain, reduced both peaks. In addition, delayed EP treatment from 4 days post-MCAO reduced HMGB1 accumulation in CSF at 7 day post-MCAO in the absence of accompanying amelioration of ischemic brain damage, indicating that the suppression of HMGB1 release is a direct effect. We also found that EP markedly suppressed the LPS-induced nuclear translocations of protein kinase C alpha and calcium/calmodulin-dependent protein kinase IV, HMGB1 phosphorylation, and subsequent secretion of HMGB1 induced by LPS in BV2 cells and EP-mediated above-mentioned effects were also independent of cell death or survival. These results indicate that EP inhibits HMGB1 phosphorylation and release in activated microglia, which might be responsible for EP-mediated suppression of HMGB1 release in the postischemic brain.

Ciliogenesis and cerebrospinal fluid flow in the developing Xenopus brain are regulated by foxj1

BackgroundCirculation of cerebrospinal fluid (CSF) through the ventricular system is driven by motile cilia on ependymal cells of the brain. Disturbed ciliary motility induces the formation of hydrocephalus, a pathological accumulation of CSF resulting in ventricle dilatation and increased intracranial pressure. The mechanism by which loss of motile cilia causes hydrocephalus has not been elucidated. The aim of this study was: (1) to provide a detailed account of the development of ciliation in the brain of the African clawed frog Xenopus laevis; and (2) to analyze the relevance of ependymal cilia motility for CSF circulation and brain ventricle morphogenesis in Xenopus.MethodsGene expression analysis of foxj1, the bona fide marker for motile cilia, was used to identify potentially ciliated regions in the developing central nervous system (CNS) of the tadpole. Scanning electron microscopy (SEM) was used to reveal the distribution of mono- and multiciliated cells during successive stages of brain morphogenesis, which was functionally assessed by bead injection and video microscopy of ventricular CSF flow. An antisense morpholino oligonucleotide (MO)-mediated gene knock-down that targeted foxj1 in the CNS was applied to assess the role of motile cilia in the ventricles.ResultsRNA transcripts of foxj1 in the CNS were found from neurula stages onwards. Following neural tube closure, foxj1 expression was seen in distinct ventricular regions such as the zona limitans intrathalamica (ZLI), subcommissural organ (SCO), floor plate, choroid plexus (CP), and rhombomere boundaries. In all areas, expression of foxj1 preceded the outgrowth of monocilia and the subsequent switch to multiciliated ependymal cells. Cilia were absent in foxj1 morphants, causing impaired CSF flow and fourth ventricle hydrocephalus in tadpole-stage embryos.ConclusionsMotile ependymal cilia are important organelles in the Xenopus CNS, as they are essential for the circulation of CSF and maintenance of homeostatic fluid pressure. The Xenopus CNS ventricles might serve as a novel model system for the analysis of human ciliary genes whose deficiency cause hydrocephalus.

Disruption of the mouse Jhy gene causes abnormal ciliary microtubule patterning and juvenile hydrocephalus

Congenital hydrocephalus, the accumulation of excess cerebrospinal fluid (CSF) in the ventricles of the brain, affects one of every 1000 children born today, making it one of the most common human developmental disorders. Genetic causes of hydrocephalus are poorly understood in humans, but animal models suggest a broad genetic program underlying the regulation of CSF balance. In this study, the random integration of a transgene into the mouse genome led to the development of an early onset and rapidly progressive hydrocephalus. Juvenile hydrocephalus transgenic mice (JhylacZ) inherit communicating hydrocephalus in an autosomal recessive fashion with dilation of the lateral ventricles observed as early as postnatal day 1.5. Ventricular dilation increases in severity over time, becoming fatal at 4–8 weeks of age. The ependymal cilia lining the lateral ventricles are morphologically abnormal and reduced in number in JhylacZ/lacZ brains, and ultrastructural analysis revealed disorganization of the expected 9+2 microtubule pattern. Rather, the majority of JhylacZ/lacZ cilia develop axonemes with 9+0 or 8+2 microtubule structures. Disruption of an unstudied gene, 4931429I11Rik (now named Jhy) appears to underlie the hydrocephalus of JhylacZ/lacZ mice, and the Jhy transcript and protein are decreased in JhylacZ/lacZ mice. Partial phenotypic rescue was achieved in JhylacZ/lacZ mice by the introduction of a bacterial artificial chromosome (BAC) carrying 60–70% of the JHY protein coding sequence. Jhy is evolutionarily conserved from humans to basal vertebrates, but the predicted JHY protein lacks identifiable functional domains. Ongoing studies are directed at uncovering the physiological function of JHY and its role in CSF homeostasis.

A pilot study using residual newborn dried blood spots to assess the potential role of cytomegalovirus and Toxoplasma gondii in the etiology of congenital hydrocephalus

Congenital hydrocephalus is a condition characterized by accumulation of cerebrospinal fluid in the ventricles of the brain. Prenatal infections are risk factors for some birth defects. This pilot study investigated whether residual dried blood spots (DBS) could be used to assess infections as risk factors for birth defects by examining the associations between prenatal infection with Toxoplasma gondii (T. gondii) or cytomegalovirus (CMV) with congenital hydrocephalus. Case-infants with hydrocephalus (N=410) were identified among live-born infants using birth defects surveillance systems in California, North Carolina, and Texas. Control-infants without birth defects were randomly selected from the same geographic areas and time periods as case-infants (N=448). We tested residual DBS from case- and control-infants for T. gondii immunoglobulin M and CMV DNA. When possible, we calculated crude odds ratios (cORs) and confidence intervals (CIs). Evidence for prenatal T. gondii infection was more common among case-infants (1.2%) than control-infants (0%; p=0.11), and evidence for prenatal CMV infection was higher among case-infants (1.5%) than control-infants (0.7%; cOR: 2.3; 95% CI: 0.48, 13.99). Prenatal infections with T. gondii and CMV occurred more often among infants with congenital hydrocephalus than control-infants, although differences were not statistically significant. This pilot study highlighted some challenges in using DBS to examine associations between certain infections and birth defects, particularly related to reduced sensitivity and specimen storage conditions. Further study with increased numbers of specimens and higher quality specimens should be considered to understand better the contribution of these infections to the occurrence of congenital hydrocephalus.

Unilateral cortical hyperexcitability in congenital hydrocephalus: A TMS study

Introduction: Changes in cortical excitability are considered to play an important role in promoting brain plasticity both in healthy people and in neurological diseases. Hydrocephalus is a brain development disorder related to an excessive accumulation of cerebrospinal fluid (CSF) in the ventricular system. The functional relevance of cortical structural changes described in this disease is largely unexplored in human. We investigated cortical excitability using multimodal transcranial magnetic stimulation (TMS) in a case of congenital hydrocephalus with almost no neurological signs. Methods: A caucasian 40 years old, ambidextrous and multilingual woman affected by occult spina bifida and congenital symmetrical hydrocephalous underwent a TMS study. The intracortical and interhemispheric paired pulse paradigms were used, together with the mapping technique. Results: No significant differences were found in the resting motor thresholds between the two hemispheres. Instead, the intracortical excitability curves were statistically different between the two hemispheres (with short intracortical inhibition (SICI) being strongly reduced and intracortical facilitation (ICF) enhanced in the right one), and the interhemispheric curves showed a general hyper-excitability on the right hemisphere (when conditioned by the left one) and a general hypo-excitability in the left hemisphere (when conditioned by the right one). It is noteworthy that an asymmetric right hemisphere (RH) change of excitability was observed by means of mapping technique. Conclusion: We hypothesize that in this ambidextrous subject, the observed RH hyper-excitability could represent a mechanism of plasticity to preserve functionality of specific brain areas possibly devoted to some special skills, such as multilingualism.

α3Na+/K+-ATPase Deficiency Causes Brain Ventricle Dilation and Abrupt Embryonic Motility in Zebrafish

Na(+)/K(+)-ATPases are transmembrane ion pumps that maintain ion gradients across the basolateral plasma membrane in all animal cells to facilitate essential biological functions. Mutations in the Na(+)/K(+)-ATPase α3 subunit gene (ATP1A3) cause rapid-onset dystonia-parkinsonism, a rare movement disorder characterized by sudden onset of dystonic spasms and slow movements. In the brain, ATP1A3 is principally expressed in neurons. In zebrafish, the transcripts of the two ATP1A3 orthologs, Atp1a3a and Atp1a3b, show distinct expression in the brain. Surprisingly, targeted knockdown of either Atp1a3a or Atp1a3b leads to brain ventricle dilation, a likely consequence of ion imbalances across the plasma membrane that cause accumulation of cerebrospinal fluid in the ventricle. The brain ventricle dilation is accompanied by a depolarization of spinal Rohon-Beard neurons in Atp1a3a knockdown embryos, suggesting impaired neuronal excitability. This is further supported by Atp1a3a or Atp1a3b knockdown results where altered responses to tactile stimuli as well as abnormal motility were observed. Finally, proteomic analysis identified several protein candidates highlighting proteome changes associated with the knockdown of Atp1a3a or Atp1a3b. Our data thus strongly support the role of α3Na(+)/K(+)-ATPase in zebrafish motility and brain development, associating for the first time the α3Na(+)/K(+)-ATPase deficiency with brain ventricle dilation.

Thrombin-induced TGF-β1 pathway: A cause of communicating hydrocephalus post subarachnoid hemorrhage

The mechanism of communicating hydrocephalus after subarachnoid hemorrhage (SAH) remains unclear. Revealing a signaling cascade may provide significant insights into the molecular etiology of the accumulation of cerebrospinal fluid (CSF) in cerebral compartments during SAH. To investigate the mechanism of the communicating hydrocephalus following SAH, we infused CSF with thrombin (TH), resulting in proinflammatory and proliferative responses in rat meninges of SAH. The effect of TH could be completely blocked by a transforming growth factor β1 (TGF-β1) inhibitor, SB-431542, suggesting that TH-stimulated proliferation of meninges is through the TGF-β1 signaling pathway. The cascade of TGF β1-Smad3 was significantly upregulated by TH, which, in turn, stimulated the proliferation of subarachnoid meninges. TH-induced overexpression of TGF-β1 and activation of its downstream factors might be a mechanism of communicating hydrocephalus after SAH.

In-Vitro Evaluation of a Drainage Catheter with Integrated Bioimpedance Electrodes to Determine Ventricular Size

Patients suffering from Hydrocephalus show an increased accumulation of cerebrospinal fluid, which needs to be drained into another body compartment by an im- planted shunt. To prevent from over-drainage, which some- times still occurs despite improvements in shunt technology, a possible future shunt could contain sensors and supervise the ventricular size electrically. This work approaches this and presents the in vitro study of a drainage catheter with integrated bioimpedance evaluation capabilities.

An Assay for Permeability of the Zebrafish Embryonic Neuroepithelium

The brain ventricular system is conserved among vertebrates and is composed of a series of interconnected cavities called brain ventricles, which form during the earliest stages of brain development and are maintained throughout the animal's life. The brain ventricular system is found in vertebrates, and the ventricles develop after neural tube formation, when the central lumen fills with cerebrospinal fluid (CSF) (1,2). CSF is a protein rich fluid that is essential for normal brain development and function(3-6). In zebrafish, brain ventricle inflation begins at approximately 18 hr post fertilization (hpf), after the neural tube is closed. Multiple processes are associated with brain ventricle formation, including formation of a neuroepithelium, tight junction formation that regulates permeability and CSF production. We showed that the Na,K-ATPase is required for brain ventricle inflation, impacting all these processes (7,8), while claudin 5a is necessary for tight junction formation (9). Additionally, we showed that "relaxation" of the embryonic neuroepithelium, via inhibition of myosin, is associated with brain ventricle inflation. To investigate the regulation of permeability during zebrafish brain ventricle inflation, we developed a ventricular dye retention assay. This method uses brain ventricle injection in a living zebrafish embryo, a technique previously developed in our lab(10), to fluorescently label the cerebrospinal fluid. Embryos are then imaged over time as the fluorescent dye moves through the brain ventricles and neuroepithelium. The distance the dye front moves away from the basal (non-luminal) side of the neuroepithelium over time is quantified and is a measure of neuroepithelial permeability (Figure 1). We observe that dyes 70 kDa and smaller will move through the neuroepithelium and can be detected outside the embryonic zebrafish brain at 24 hpf (Figure 2). This dye retention assay can be used to analyze neuroepithelial permeability in a variety of different genetic backgrounds, at different times during development, and after environmental perturbations. It may also be useful in examining pathological accumulation of CSF. Overall, this technique allows investigators to analyze the role and regulation of permeability during development and disease.

Case Series: Long segment extra-arachnoid fluid collections: Role of dynamic CT myelography in diagnosis and treatment planning

We report five patients in whom spinal MRI revealed extra-arachnoid fluid collections. These spinal fluid collections most likely resulted from accumulation of cerebrospinal fluid (CSF) from a dural leak. The patients presented with either compressive myelopathy due to the cyst or superficial siderosis (SS). All of these fluid collections were long segment, and MRI demonstrated the fluid collections but not the exact site of leak. Dynamic CT myelogram demonstrated the site of leak and helped in the management of these complicated cases. Moreover, we also found that the epicenter of the fluid collection on MRI was different from the location of the leak on a dynamic CT myelogram. Knowledge of these associations can be helpful when selecting the imaging studies to facilitate diagnosis and treatment.

Delayed superior forniceal CSF accumulation and conjunctival prolapse after superior orbital wall fracture

Dear Editor, Posttraumatic cerebrospinal fluid (CSF) leakage is one of the well-documented sequelae of skull base fracture. Typically, it is presented as rhinorrhea, and less frequently, headache, otorrhea, dysgeusia, facial numbness, and discharge through orbit [1]. To the best of our knowledge, conjunctival prolapse due to CSF leakage has not been previously reported. Herein, we report a patient who experienced delayed severe conjunctival prolapse after skull fracture. A 3-year-old girl visited the emergency room for a fallingdown injury. Brain computed tomography (CT) showed multiple comminuted skull fractures, including both frontal bones and left orbital roof (Fig. 1a). Periorbital tissue swelling was severe, and no other abnormal finding was noted in the anterior segment and fundus. She was admitted for close observation. After a few days, her eyelid swelling became more severe, and left superior forniceal conjunctiva became prolapsed (Fig. 1b). Orbit CT showed brain parenchymal herniation through the left orbital roof, implying injury of dura mater. She underwent open reduction of orbital roof and frontal bone with repair of dura mater. Five days after the operation, conjunctival prolapse got worse and a yellow fluid level was seen in the prolapsed conjunctiva. Spontaneous regression couldn’t be expected, and we decided to perform reductive surgery. Under general anesthesia, prolapsed conjunctiva was incised, and fluid was drained, collected, and sent to lab for analysis. The shrunken tissues were securely anchored to the superior fornix by fullthickness eyelid sutures through silicone 240 retinal band (MIRA, USA) lying in the superior fornix (Fig. 1c). Laboratory analysis of the drained fluid revealed that red blood cell (RBC) density was 27,648/mm, and white blood cell (WBC) density was 6/mm. There were no cells other than RBC or WBC. Glucose level was 98 mg/dl. Reference ranges in CSF are 50–80 mg/dl of glucose, negative for RBCs, and 0–3 WBCs [2]. We could rule out the possibility of blood and conjunctival fluid, because their cell densities are 4–5 million/mm and about half a million/mm respectively. This fluid was diagnosed as CSF based on the cell density and glucose level [2–4]. Two months after the surgery, superior fornix was well-formed and maintained without recurrent conjunctival prolapse (Fig. 1d). Skull base fracture can cause CSF leaks and more than 60% of patients with CSF leaks present with CSF rhinorrhea [5]; however, orbital CSF accumulation can also develop if skull base fracture is accompanied with superior orbital wall J. Lee :N. Kim :H.-K. Choung : S. I. Khwarg Department of Ophthalmology, College of Medicine, Seoul National University, Seoul, Korea

Taponamiento cardíaco como complicación de derivación ventrículo atrial

Cardiac tamponade is an uncommon disorder in pediatric patients. We report a case of cardiac tamponade secondary to accumulation of cerebrospinal fluid due to ventriculo-atrial derivation (VAD) disfunction. An 11-month-old girl was assisted because of respiratory distress and tachycardia, without fever. She had a ventriculoatrial derivation, because of hydro-cephalus since two month earlier. The echocardiogram showed a pericardial effusion and the distal VAD located inside the right cardiac ventricle. The distal VAD was retired and replaced between superior cava vein and right atrium. The patient recovered ad integrum without pericardial effusion. In cases of patients with VAD presenting a clinical disorder, it should be ruled out VAD dysfunction or inappropriate placement.

Prevalence of congenital hydrocephalus in the Hashemite kingdom of Jordan: A hospital-based study

Background: Congenital hydrocephalus, an important cause of neurologic morbidity and mortality in children, is a medical condition characterized by an abnormal accumulation of cerebrospinal fluid in the brain. It can be caused by abnormal brain development, obstruction of the cerebral aqueduct flow, Chiari malformations, and Dandy-Walker malformation. The prevalence of congenital hydrocephalus is 2.2 to 18 per 10,000 live births. Objectives: To determine the prevalence of congenital hydrocephalus among livebirths in the Hashemite Kingdom of Jordan (HKJ). Methods: Clinical data were collected from medical records of all livebirths with congenital hydrocephalus born at Al Bashir Hospital, Amman/The Hashemite Kingdom of Jordan in 2004-2005 and 2008-2011. Descriptive analysis was carried out using the Statistical Package for the Social Science (SPSS 20). Results: The prevalence of hydrocephalus was 0.092% with a relative predominance among males. Conclusion: The study concluded that the prevalence of congenital hydrocephalus is comparable to that of developed countries. The efforts made by the Ministry of Health seem to have paid off. More research on stillbirths is recommended.

Increased CSF osmolarity reversibly induces hydrocephalus in the normal rat brain.

BackgroundHydrocephalus is a central nervous system (CNS) disorder characterized by the abnormal accumulation of cerebrospinal fluid (CSF) in cerebral ventricles, resulting in their dilatation and associated brain tissue injury. The pathogenesis of hydrocephalus remains unclear; however, recent reports suggest the possible involvement of abnormal osmotic gradients. Here we explore the kinetics associated with manipulating CSF osmolarity on ventricle volume (VV) in the normal rat brain.MethodsCSF was made hyper-osmotic by introducing 10KD dextran into the lateral ventricle, either by acute injection at different concentrations or by chronic infusion at a single concentration. The induction and withdrawal kinetics of dextran infusion on VV were explored in both contexts.ResultsAcute intraventricular injection of dextran caused a rapid increase in VV which completely reversed within 24 hours. These kinetics are seemingly independent of CSF osmolarity across a range spanning an order of magnitude; however, the magnitude of the transient increase in VV was proportional to CSF osmolarity. By contrast, continuous intraventricular infusion of dextran at a relatively low concentration caused a more gradual increase in VV which was very slow to reverse when infusion was suspended after five days.ConclusionWe conclude that hyperosmolar CSF is sufficient to produce a proportional degree of hydrocephalus in the normal rat brain, and that this phenomenon exhibits hysteresis if CSF hyperosmolarity is persistent. Thus pathologically-induced increases in CSF osmolarity may be similarly associated with certain forms of clinical hydrocephalus. An improved understanding of this phenomenon and its kinetics may facilitate the development of novel therapies for the treatment of clinical hydrocephalus.

Congenital Hydrocephalus in Genetically Engineered Mice

There is evidence that genetic factors play a role in the complex multifactorial pathogenesis of hydrocephalus. Identification of the genes involved in the development of this neurologic disorder in animal models may elucidate factors responsible for the excessive accumulation of cerebrospinal fluid in hydrocephalic humans. The authors report here a brief summary of findings from 12 lines of genetically engineered mice that presented with autosomal recessive congenital hydrocephalus. This study illustrates the value of knockout mice in identifying genetic factors involved in the development of congenital hydrocephalus. Findings suggest that dysfunctional motile cilia represent the underlying pathogenetic mechanism in 8 of the 12 lines (Ulk4, Nme5, Nme7, Kif27, Stk36, Dpcd, Ak7, and Ak8). The likely underlying cause in the remaining 4 lines (RIKEN 4930444A02, Celsr2, Mboat7, and transgenic FZD3) was not determined, but it is possible that some of these could also have ciliary defects. For example, the cerebellar malformations observed in RIKEN 4930444A02 knockout mice show similarities to a number of developmental disorders, such as Joubert, Meckel-Gruber, and Bardet-Biedl syndromes, which involve mutations in cilia-related genes. Even though the direct relevance of mouse models to hydrocephalus in humans remains uncertain, the high prevalence of familial patterns of inheritance for congenital hydrocephalus in humans suggests that identification of genes responsible for development of hydrocephalus in mice may lead to the identification of homologous modifier genes and susceptibility alleles in humans. Also, characterization of mouse models can enhance understanding of important cell signaling and developmental pathways involved in the pathogenesis of hydrocephalus.

Fluid accumulation in the fetal extracerebral spaces: External hydrocephalus or subdural hygromas?

External hydrocephalus is defined as enlargement of the subarachnoidal space with accumulation of cerebrospinal fluid (CSF). In adults, there are several reasons for external hydrocephalus, such as disruption of CSF resorption or meningeal inflammations. During fetal development the occurrence of external hydrocephalus is a very rare event and pathogenetic mechanism as well as neuropathological classification considerably differs from that of adults. Here we report on a 25th gestational week fetus with the ultrasonic diagnosis of an external hydrocephalus with macrocephalus and microencephaly. Neuropathological examination revealed extensive subdural hygroma, associated with chronic subdural haemorrhages. The central nervous system (CNS) showed a distinct microencephaly with pronounced neocortical migration defects and various stages of neuronal maturation. Due to our findings we were able to exclude the diagnosis of an external hydrocephalus. Instead, we suggest, that the atrophic hemispheres lead to a chronic stretch of the bridging veins with drainage of fluid into the subdural space.

Normal pressure subdural hygroma with mass effect as a complication of decompressive craniectomy

Background:Subdural posttraumatic collections are called usually Traumatic Subdural Hygroma (TSH). TSH is an accumulation of cerebrospinal fluid (CSF) in the subdural space after head injury. These collections have also been called Traumatic Subdural Effusion (TSE) or External Hydrocephalous (EHP) according to liquid composition, or image features. There is no agreement about the pathogenesis of these entities, how to define them or if they are even different phenomena at all.Case Description:We present a case of a complex posttraumatic subdural collection, the role of cranioplasty as definite solution and review the literature related to this complication.Conclusion:Patients who undergo decompressive craniectomy (DC) have a risk of suffering a subdural collection of 21-50%. Few of these collections will become symptomatic and will need evacuation. When this happens, cranioplasty might be the definitive solution.

C-Shaped Incision for Lateral Suboccipital Approach: Anatomical Study and Clinical Correlation

Objectives: The standard incision for lateral suboccipital approaches has been the classic “reverse hockey stick.” Although that incision provides ample exposure, concern has been raised that excessive muscle dissection and skin elevation might lead to accumulation of cerebrospinal fluid (CSF) under the flap with increased risk of CSF leak. Using the C-shape incision for lateral suboccipital approaches can minimize the amount of muscle dissection and still provide optimal exposure and surgical outcomes. Describing the real advantages and safety of this technique and generalizing the use of it can provide the general neurosurgeon with a more familiar incision and less morbid approach for lesions in this area.

Cerebral water transport using multiple-network poroelastic theory: application to normal pressure hydrocephalus

The twenty-first century is bearing witness to a drastic change in population demographics and diseases of old age, such as dementia, are placing an unprecedented burden on the global healthcare system. Normal pressure hydrocephalus may be the only curable form of dementia, yet its pathophysiology is paradoxical and a consistent treatment currently remains elusive. A novel application of multiple-network poroelastic theory (MPET) is proposed to investigate water transport in the cerebral environment. Specifically, MPET is modified to allow a detailed investigation of spatio-temporal transport of fluid between the cerebral blood, cerebrospinal fluid (CSF) and brain parenchyma across scales. This framework thus allows an exploration of hypotheses defining the initiation and progression of both acute and chronic hydrocephalus. Results show that a breakdown in the transport mechanisms between the arterial vascular network and interstitial space within the parenchyma may be a cause of accumulation of CSF in the ventricles. Specifically, there must be an increase in the compliance of the arteriole/capillary network, which may combine with a breakdown in the blood–CSF barrier to allow an increased flow from the arteriole/capillary blood to the CSF. The results of this study should prove useful to guide experimental exploration in areas that warrant further investigation and validation.