scholarly journals Spontaneous spinal cerebrospinal fluid venous-fistula treated with transvenous embolization: A case report

2021 ◽  
Vol 12 ◽  
pp. 492
Author(s):  
Zaid Aljuboori ◽  
Margaret McGrath ◽  
Muhammed Amir Essibayi ◽  
Saif Zaidi ◽  
Danial Hallam ◽  
...  

Background: Spinal cerebrospinal fluid venous fistula (CVF) is a recognized cause of chronic positional headache and spontaneous intracranial hypotension (SIH). It occurs due to an aberrant connection formed between the spinal subarachnoid space and an adjacent spinal epidural vein. The diagnosis of CVF can be difficult to establish but can be documented utilizing advanced imaging techniques (e.g., enhanced MR myelography/digital subtraction myelography). Their treatment involves surgical ligation of the involved nerve root, imaging-guided epidural blood patching, and/or endovascular embolization. Here, we report a 40-year-old male who presented with a symptomatic lumbar CVF successfully treated with transvenous embolization. Case Description: A 40-year-old male presented with several months of positional headaches. The MRI of the brain showed diffuse pachymeningeal enhancement consistent with the diagnosis of SIH. Although the MR of the lumbar spine was unremarkable, the MR myelogram with digital subtraction imaging showed a CVF at the L2 level. Following transvenous embolization (i.e., through the Azygous vein), the patient’s symptoms fully resolved. Conclusion: Spinal CVF are rare and may cause chronic headaches and symptoms/signs of SIH. In this case, an MR myelogram with digital subtraction images demonstrated the anomalous connection between the spinal subarachnoid space and an adjacent spinal epidural vein at the L2 level. Although open surgical ablation of this connection may be feasible, less invasive techniques such as endovascular embolization should become the treatment of choice for the future management of CVF.

2021 ◽  
pp. neurintsurg-2021-018160
Author(s):  
Nicholas Borg ◽  
Soliman Oushy ◽  
Luis Savastano ◽  
Waleed Brinjikji

Cerebrospinal fluid–venous fistula is an increasingly recognized cause of spontaneous intracranial hypotension.1 The site of the leak is between the dural sleeve around a spinal nerve root and the surrounding foraminal veins. In appropriately investigated patients, transvenous embolization of the draining foraminal and paraspinal veins has been shown to be an effective way of treating the disease, with low periprocedural morbidity, improvement in symptoms and radiological appearances.2 Video 1 shows the technique employed in a typical case using Onyx (Medtronic, Minnesota, USA) to embolize a CSF–venous fistula at the right T10 neural foramen.Video 1


1981 ◽  
Vol 2 (9) ◽  
pp. 269-276
Author(s):  
John F. Griffith ◽  
Jimmy C. Brasfield

The infant or child with increasing pressure within the cranial cavity must be identified early and treated promptly in order to prevent serious complications or death. When the pressure elevation is gradual it is frequently well tolerated, and the patient may seem deceptively well. There is a critical point, however, beyond which any further increase in pressure leads to a catastrophic deterioration in the patient's condition.1 When this occurs, the outlook for quality survival is poor despite the best therapy. Unfortunately, this can occur when the underlying process is benign and would have been reversible if recognized and treated promptly. For prompt recognition and treatment, the physician must be familiar with the pathophysiology of raised intracranial pressure. PATHOPHYSIOLOGY The intracranial compartment contains blood vessels, cerebrospinal fluid (CSF), brain, and leptomeninges which include the rigid dural membranes forming the falx and tentorium. Whenever there is an increase in the volume of any one of these intracranial components (brain, CSF, blood) there must be a corresponding reduction in the size of the others in order for the intracranial pressure to remain normal. This type of compensation or buffering capacity is particularly important in the early stages of intracranial disease. As the pressure mounts from any type of mass lesion, the CSF is displaced caudally into the spinal subarachnoid space and there is a corresponding increase in the rate of absorption of CSF.2


2019 ◽  
Vol 216 (11) ◽  
pp. 2492-2502 ◽  
Author(s):  
Qiaoli Ma ◽  
Yann Decker ◽  
Andreas Müller ◽  
Benjamin V. Ineichen ◽  
Steven T. Proulx

The pathways of circulation and clearance of cerebrospinal fluid (CSF) in the spine have yet to be elucidated. We have recently shown with dynamic in vivo imaging that routes of outflow of CSF in mice occur along cranial nerves to extracranial lymphatic vessels. Here, we use near-infrared and magnetic resonance imaging to demonstrate the flow of CSF tracers within the spinal column and reveal the major spinal pathways for outflow to lymphatic vessels in mice. We found that after intraventricular injection, a spread of CSF tracers occurs within both the central canal and the spinal subarachnoid space toward the caudal end of the spine. Outflow of CSF tracers from the spinal subarachnoid space occurred predominantly from intravertebral regions of the sacral spine to lymphatic vessels, leading to sacral and iliac LNs. Clearance of CSF from the spine to lymphatic vessels may have significance for many conditions, including multiple sclerosis and spinal cord injury.


2018 ◽  
Vol 141 (1) ◽  
Author(s):  
Eleuterio F. Toro ◽  
Ben Thornber ◽  
Qinghui Zhang ◽  
Alessia Scoz ◽  
Christian Contarino

Global models for the dynamics of coupled fluid compartments of the central nervous system (CNS) require simplified representations of the individual components which are both accurate and computationally efficient. This paper presents a one-dimensional model for computing the flow of cerebrospinal fluid (CSF) within the spinal subarachnoid space (SSAS) under the simplifying assumption that it consists of two coaxial tubes representing the spinal cord and the dura. A rigorous analysis of the first-order nonlinear system demonstrates that the system is elliptic-hyperbolic, and hence ill-posed, for some values of parameters, being hyperbolic otherwise. In addition, the system cannot be written in conservation-law form, and thus, an appropriate numerical approach is required, namely the path conservative approach. The designed computational algorithm is shown to be second-order accurate in both space and time, capable of handling strongly nonlinear discontinuities, and a method of coupling it with an unsteady inflow condition is presented. Such an approach is sufficiently rapid to be integrated into a global, closed-loop model for computing the dynamics of coupled fluid compartments of the CNS.


2008 ◽  
Vol 131 (2) ◽  
Author(s):  
Sumeet Gupta ◽  
Michaela Soellinger ◽  
Peter Boesiger ◽  
Dimos Poulikakos ◽  
Vartan Kurtcuoglu

This study aims at investigating three-dimensional subject-specific cerebrospinal fluid (CSF) dynamics in the inferior cranial space, the superior spinal subarachnoid space (SAS), and the fourth cerebral ventricle using a combination of a finite-volume computational fluid dynamics (CFD) approach and magnetic resonance imaging (MRI) experiments. An anatomically accurate 3D model of the entire SAS of a healthy volunteer was reconstructed from high resolution T2 weighted MRI data. Subject-specific pulsatile velocity boundary conditions were imposed at planes in the pontine cistern, cerebellomedullary cistern, and in the spinal subarachnoid space. Velocimetric MRI was used to measure the velocity field at these boundaries. A constant pressure boundary condition was imposed at the interface between the aqueduct of Sylvius and the fourth ventricle. The morphology of the SAS with its complex trabecula structures was taken into account through a novel porous media model with anisotropic permeability. The governing equations were solved using finite-volume CFD. We observed a total pressure variation from −42Pato40Pa within one cardiac cycle in the investigated domain. Maximum CSF velocities of about 15cm∕s occurred in the inferior section of the aqueduct, 14cm∕s in the left foramen of Luschka, and 9cm∕s in the foramen of Magendie. Flow velocities in the right foramen of Luschka were found to be significantly lower than in the left, indicating three-dimensional brain asymmetries. The flow in the cerebellomedullary cistern was found to be relatively diffusive with a peak Reynolds number (Re)=72, while the flow in the pontine cistern was primarily convective with a peak Re=386. The net volumetric flow rate in the spinal canal was found to be negligible despite CSF oscillation with substantial amplitude with a maximum volumetric flow rate of 109ml∕min. The observed transient flow patterns indicate a compliant behavior of the cranial subarachnoid space. Still, the estimated deformations were small owing to the large parenchymal surface. We have integrated anatomic and velocimetric MRI data with computational fluid dynamics incorporating the porous SAS morphology for the subject-specific reconstruction of cerebrospinal fluid flow in the subarachnoid space. This model can be used as a basis for the development of computational tools, e.g., for the optimization of intrathecal drug delivery and computer-aided evaluation of cerebral pathologies such as syrinx development in syringomelia.


1973 ◽  
Vol 39 (4) ◽  
pp. 480-484 ◽  
Author(s):  
Osamu Sato ◽  
Makoto Hara ◽  
Takehiko Asai ◽  
Ryuichi Tsugane ◽  
Naoki Kageyama

✓ The effect of intravenous dexamethasone on cerebrospinal fluid (CSF) production was studied in dogs by a method of caudocephalad perfusion of the spinal subarachnoid space with an inulin-containing buffer. The CSF production rate began to reduce immediately after the injection of 0.15 mg/kg and attained a maximal reduction of 50% in 50 minutes.


2021 ◽  
Vol 14 ◽  
Author(s):  
Steven W. Bothwell ◽  
Daniel Omileke ◽  
Rebecca J. Hood ◽  
Debbie-Gai Pepperall ◽  
Sara Azarpeykan ◽  
...  

Oedema-independent intracranial pressure (ICP) rise peaks 20–22-h post-stroke in rats and may explain early neurological deterioration. Cerebrospinal fluid (CSF) volume changes may be involved. Cranial CSF clearance primarily occurs via the cervical lymphatics and movement into the spinal portion of the cranio-spinal compartment. We explored whether impaired CSF clearance at these sites could explain ICP rise after stroke. We recorded ICP at baseline and 18-h post-stroke, when we expect changes contributing to peak ICP to be present. CSF clearance was assessed in rats receiving photothrombotic stroke or sham surgery by intraventricular tracer infusion. Tracer concentration was quantified in the deep cervical lymph nodes ex vivo and tracer transit to the spinal subarachnoid space was imaged in vivo. ICP rose significantly from baseline to 18-h post-stroke in stroke vs. sham rats [median = 5 mmHg, interquartile range (IQR) = 0.1–9.43, n = 12, vs. −0.3 mmHg, IQR = −1.9–1.7, n = 10], p = 0.03. There was a bimodal distribution of rats with and without ICP rise. Tracer in the deep cervical lymph nodes was significantly lower in stroke with ICP rise (0 μg/mL, IQR = 0–0.11) and without ICP rise (0 μg/mL, IQR = 0–4.47) compared with sham rats (4.17 μg/mL, IQR = 0.74–8.51), p = 0.02. ICP rise was inversely correlated with faster CSF transit to the spinal subarachnoid space (R = −0.59, p = 0.006, Spearman’s correlation). These data suggest that reduced cranial clearance of CSF via cervical lymphatics may contribute to post-stroke ICP rise, partially compensated via increased spinal CSF outflow.


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