Cerebral Aqueduct

OBJECTIVE: This article describes our experience with two patients who presented with unusual tumors in the cerebellar vermis and cerebral aqueduct. CLINICAL PRESENTATION: Patient 1 was a 42-year-old man who presented with a headache of 1 day's duration and no neurological signs, in whom magnetic resonance imaging disclosed a nonenhancing mass lesion occupying the proximal cerebral aqueduct.  

Brain MRI revealed a markedly re-enlarged and easily enhanced mass at the right anterior horn, which extended into the cerebral aqueduct and resulted in obstructive hydrocephalus.  

In the brainstem, high binding was detected around the cerebral aqueduct of the midbrain and within the dorsal pons, in a volume comprising locus coeruleus.  

To illustrate the value of this type of imaging, the authors present a case of a third ventricular clot that migrated into the cerebral aqueduct exacerbating hydrocephalus..  

MR CSF-flow examination may be performed in the cerebral aqueduct of Sylvius and in the drain of the ventriculo-peritoneal shunt. CONCLUSIONS: MR examination allows the determination of the absence or presence of CSF-flow and its direction and velocity in the cerebral aqueduct of Sylvius and in the drain of the ventriculo-peritoneal shunt.  

The fastest flow was found in the cerebral aqueduct, where a maximum velocity of 11.38 mm/s was observed over five cycles. CSF pressure also varies with geometry with a maximum pressure drop of 1.14 Pa occurring through the cerebral aqueduct.  

By a unilateral transcerebellomedullary fissure approach, it is possible to provide sufficient operative space from cerebral aqueduct to obex without splitting the vermis.  

P2X7 mRNA was expressed in the ependymal cells around the olfactory ventricle, lateral ventricles (LV), third ventricle (3V), cerebral aqueduct (Aq), fourth ventricle (4V), and central canal.  

Several theories have been proposed to explain hydrocephalus in these patients: obstruction of the cerebral aqueduct, impaired absorption of CSF after subarachnoid hemorrhage, passive ex-vacuo mechanism, or thrombosis of an aneurysm.  

Based on a patent cerebral aqueduct and the T2 MR and pathology findings, we postulate that altered brain tissue compliance with impairment of normal pulsatile augmentation of aqueduct CSF flow was the likely cause of obstructive hydrocephalus.  

Magnetic resonance (MR) imaging demonstrated a lobulated cyst arising from the choroid plexus of the left lateral ventricle and herniating through the foramen of Monro into the third ventricle, occluding both the foramen of Monro and the cerebral aqueduct.  

OBJECTIVE: What is known about the cerebral aqueduct is derived mainly from the legacy of classic histology and from the most recent advanced neuroimaging technologies.  

CONCLUSION: cerebral aqueductoplasty is an effective and successful treatment for membranous and/or short-segment stenosis of the sylvian aqueduct.  

The use of the flexible endoscope permitted the neurosurgeon to use the endoscope as a tool to guide the ventricular catheter tip within the third ventricle and through the cerebral aqueduct.  

The authors report on a patient harboring an unruptured cortical arteriovenous malformation (AVM), who had presented with obstructive hydrocephalus due to compression of the cerebral aqueduct by a large venous varix.  

The fitted bulk model parameters provided relative values that correspond approximately to the impedance of arterial capillaries (1.0), cerebral aqueduct ( approximately 0), venous capillaries ( approximately 0), and arteries (0.01) and for the elastic capacitance of the ventricles (4.11), capillaries ( approximately 0), and veins (271).  

The present work was undertaken to reveal the mechanism of cerebral aqueduct agenesis found to result in hydrocephalus following intrauterine exposure to model teratogen, cyclophosphamide, in murine fetuses. Incomplete development and failure of canalization of the cerebral aqueduct were detected when serial sections of brain in coronal and transverse planes were studied under the microscope. Agenesis and non-canalization of the cerebral aqueduct resulted in increased pressure of CSF, which led to rupture of the aqueduct complicated by leakage and accumulation of CSF in brain substance forming a cavity containing CSF parallel and lateral to the unopened part of the cerebral aqueduct. Incomplete development along with non-canalization of the cerebral aqueduct resulted in blockage of CSF flow through the ventricles that manifest as internal hydrocephalus. Cyclophosphamide induced inhibition of mitosis and cell differentiation of ependymal cells reflecting a decreased % viable cell count and cell proliferation assay along with augmentation of apoptosis of brain cells quantified as increased % DNA fragmentation count, which were identified as the contributing factors underlying the agenesis and incomplete development of the cerebral aqueduct. The study also suggests that cell survival, proliferation, migration or differentiation of ependymal cells might have been affected, and we speculate that CSF may have an inducing role in the development and canalization of the cerebral aqueduct..  

Hydrocephalic Ro1 mice displayed enlarged ventricles, partial denudation of the ependymal cell layer, altered subcommissural organ morphology, and obliteration of the cerebral aqueduct.  

Intraventricular processes leading to membrane formation play an important role in occlusion of the cerebral aqueduct orifices and final isolation of the fourth ventricle in postinflammatory hydrocephalus..  

Approximately 2 months later, she developed acute obstructive hydrocephalus and was found to have small cystic lesions in the left ambient cistern, fourth ventricle and cerebral aqueduct, which had probably caused the previous ischemic symptoms due to emboli/ thrombi.  

The trapped fourth ventricle is caused by occlusion of outlets of fourth ventricle, including cerebral aqueduct and foramina of Luschka and Magendie.  

OBJECTIVE: To evaluate clinical usefulness of cerebrospinal fluid stroke volume (SV) assessed in the cerebral aqueduct, via cine phase-contrast magnetic resonance imaging, for predicting outcome after shunt surgery in suspected normal pressure hydrocephalus. CONCLUSION: The data from this study show no evidence that cine phase-contrast magnetic resonance imaging measurements of SV in the cerebral aqueduct are useful for selecting patients with normal pressure hydrocephalus symptoms to shunt surgery..  

RESULTS: Flow quantification in these 5 patients, representative of the diseases mainly concerned by cerebral hydrodynamics, is useful to guide the indication for ventricular shunting in patients with hydrocephalus, to demonstrate obstruction of the cerebral aqueduct, to demonstrate recirculation of ventricular CSF after ventriculostomy and to characterize the dynamic features of CSF inside a spinal cavity.  

In this study, dimensions of the HF have been standardized and they revealed normal distributions for each side and each sex: the width of the hippocampal head at the level of the amygdala was 16.42 +/- 1.9 mm, and its height 7.93 +/- 1.4 mm; the width of the tail at the level of the cerebral aqueduct was 8.54 +/- 1.2 mm, and the height 5.74 +/- 0.4 mm.  

CSF oscillations were recorded at the cerebral aqueduct and C2-C3 subarachnoid space (SAS), where a vascular sequence was also performed to quantify artery blood flow.  

Significant differences in the CSF flow (width of systolic flow peak and diastolic flow volume, both P<0.01) through the cerebral aqueduct were observed for the group of treatment-resistant patients when compared to age matched controls.  

OBJECTIVE: We report a case of a choroid plexus vascular malformation of the cerebral aqueduct, third, and fourth ventricles of an adolescent female that was resected with endoscopic assistance. Subsequent magnetic resonance imaging scans with and without contrast revealed an enhancing mass originating in the third ventricle, traversing the cerebral aqueduct, and terminating in the fourth ventricle.  

The assessment of the flow-void in the cerebral aqueduct of patients with post-traumatic hydrocephalus on magnetic resonance imaging (MRI) evaluation could concur the right diagnosis and have a prognostic value. In head-injured patients, fast flow-void in the cerebral aqueduct is diagnostic for post-traumatic hydrocephalus and its reduction after ventriculo-peritoneal shunt is correlated with a neurological improvement.  

The assessment of the flow-void in the cerebral aqueduct of patients with post-traumatic hydrocephalus on magnetic resonance imaging (MRI) evaluation could concur the right diagnosis and have a prognostic value. In head-injured patients, fast flow-void in the cerebral aqueduct is diagnostic for post-traumatic hydrocephalus and its reduction after ventriculo-peritoneal shunt is correlated with a neurological improvement.  

Sometimes the increasing intracranial pressure due to obstruction of the cerebral aqueduct (ball-valve mechanism) is intermittent, producing relapsing/remitting symptoms; this life-threatening phenomenon is called "Bruns syndrome." METHODS: Between 1996 and 2004, among a group of 285 patients with neurocysticercosis and Bruns syndrome caused by cysticercal cysts of the third ventricle was diagnosed in seven patients by using magnetic resonance imaging.  

Magnetic resonance (MR) imaging was performed, and the images were used to classify patients into three groups: those with hypertrophy of the tectum in whom isointensity appeared on T1-weighted images (Group 1); those with a tectal tumor occupying the cerebral aqueduct in whom decreased signal intensity appeared on T1-weighted images, as well as no enhancement after gadolinium administration (Group 2); and those with a tectal tumor in whom mixed signal intensity appeared on T1-weighted images and conspicuous evidence of contrast enhancement (Group 3).  

cerebral aqueduct stenosis was the commonest congenital anomaly encountered and was found in 24% of case.  

METHODS: Seven children with symptomatic IFV and membranous aqueductal stenosis underwent endoscopic aqueductoplasty alone or combined with placement of a stent in the cerebral aqueduct.  

To discover candidate genes in the pathogenesis of congenital hydrocephalus, gene arrays were utilized to analyze transcripts from the midbrain region of 5-day-old H-Tx rats; these animals develop hydrocephalus due to closure of their cerebral aqueduct between embryonic day 18 and post-natal day 5. This is the first experiment of its kind to identify changes in gene expression in a congenital model of rodent hydrocephalus that are occurring locally in the area surrounding the cerebral aqueduct.  

During the first postnatal day, GLUT1 is strongly induced in the upper region of the third ventricle and in the ventral area of the rostral cerebral aqueduct.  

cerebral aqueductoplasty has gained popularity as an effective treatment for membranous and short-segment stenoses of the sylvian aqueduct. METHODS: A retrospective chart review was performed to document the success of cerebral aqueductoplasty procedures via the foramen magnum trans-fourth ventricle approach in patients who had membranous or short-segment stenosis of the cerebral aqueduct. Nine patients underwent 11 cerebral aqueductoplasty procedures. CONCLUSIONS: The authors state that in their experience, performing cerebral aqueductoplasty via the foramen magnum trans-fourth ventricle approach is both effective and safe. They advocate the use of this technique, if performed by an experienced neuroendoscopist, for select cases involving membranous or short-segment stenosis of the cerebral aqueduct, a trapped fourth ventricle, or aqueductal stent placement..  

Sections through the walls of the cerebral aqueduct and lateral ventricles were processed for lectin binding and immunocytochemistry using antibodies against ependyma, astroglia, neuroblasts, and macrophages markers.  

MRI showed a left medial thalamic infarction extending to a rostral part of the midbrain anterolateral to the cerebral aqueduct at the superior colliculi level.  

To control for this, we occluded the cerebral aqueduct to restrict CSF flow between the forebrain and CBS ventricles and tested all combinations (same and cross ventricle) of ghrelin (150 pmol/1 microl) and NPY receptor antagonist delivery.  

The lateral ventricles, the third ventricle, the cerebral aqueduct, the fourth ventricle, and the subarachnoid basal cisterns are among the most non-accessible regions of the central nervous system.  

The periaqueductal gray matter (PAG), the midbrain region made up of neuronal columns encircling the cerebral aqueduct, plays a key role in nociception.  

Ventricular dilatation is associated with abnormalities in the cerebral aqueduct and subcommissural organ.  

Here, we show that ependymal cilia generate a laminar flow of cerebrospinal fluid through the cerebral aqueduct, which we term as 'ependymal flow'.  

The results demonstrated: 1) in the fetus and young infant with Chiari II malformations, congenital aqueductal stenosis, and hydromyelia, vimentin is focally upregulated in the ependyma only in areas of dysgenesis and not in the ependyma throughout the ventricular system; 2) GFAP and S-100beta protein are not coexpressed, indicating that the selective upregulation of vimentin is not simple maturational delay; 3) vimentin upregulation also is seen in the ependymal remnants of the congenital atretic cerebral aqueduct, not associated with Chiari malformation; 4) in the older child and adult with Chiari II malformation, vimentin overexpression in the ependyma becomes more generalized in the lateral ventricles as well, hence evolves into a nonspecific upregulation.  

OBJECTIVE: To evaluate whether the results of cerebrospinal fluid (CSF) flow quantification differ according to the anatomical location of the cerebral aqueduct that is used and the background baseline region that is selected. Velocity maps were acquired perpendicular to the cerebral aqueduct at three different anatomical levels: the inlet, ampulla and pars posterior. However, no other differences were observed among the mean flows according to the location of the cerebral aqueduct or the baseline ROI. CONCLUSION: We obtained a set of reference data of the CSF peak velocity and mean flow through the cerebral aqueduct in young healthy volunteers. Although the peak systolic velocity and mean flow of the CSF differed somewhat according to the level of the cerebral aqueduct at which the measurement was made, this difference was not statistically significant..  

Forebrain contribution was addressed by delivery of the GLP-1-R antagonist to the third ventricle with the caudal flow of cerebrospinal fluid blocked by occlusion of the cerebral aqueduct.  

The most important features of homozygous mutants that we observed were the absence or malformation of the posterior commissure (PC) and of the subcommissural organ (SCO), the collapse of the cerebral aqueduct, and the development of hydrocephalus.  

The H-Tx rat has fetal-onset hydrocephalus associated with closure of the cerebral aqueduct and a reduction in the secretory cells of the subcommissural organ (SCO), a circumventricular organ situated in the dorsal wall of the cerebral aqueduct.  

During the first postnatal week the cerebral aqueduct becomes obliterated and a severe hydrocephalus develops.  

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