Pressure Wave Propagation in Fluid-Filled Co-Axial Elastic Tubes Part 2: Mechanisms for the Pathogenesis of Syringomyelia

2003 ◽  
Vol 125 (6) ◽  
pp. 857-863 ◽  
Author(s):  
P. W. Carpenter ◽  
K. Berkouk ◽  
A. D. Lucey

Our aim in this paper is to use a simple theoretical model of the intraspinal cerebrospinal-fluid system to investigate mechanisms proposed for the pathogenesis of syringomyelia. The model is based on an inviscid theory for the propagation of pressure waves in co-axial, fluid-filled, elastic tubes. According to this model, the leading edge of a pressure pulse tends to steepen and form an elastic jump, as it propagates up the intraspinal cerebrospinal-fluid system. We show that when an elastic jump is incident on a stenosis of the spinal subarachnoid space, it reflects to form a transient, localized region of high pressure within the spinal cord that for a cough-induced pulse is estimated to be 50 to 70 mm Hg or more above the normal level in the spinal subarachnoid space. We propose this as a new mechanism whereby pressure pulses created by coughing or sneezing can generate syrinxes. We also use the same analysis to investigate Williams’ suck mechanism. Our results do not support his concept, nor, in cases where the stenosis is severe, the differential-pressure-propagation mechanism recently proposed by Greitz et al. Our analysis does provide some support for the piston mechanism recently proposed by Oldfield et al. and Heiss et al. For instance, it shows clearly how the spinal cord is compressed by the formation of elastic jumps over part of the cardiac cycle. What appears to be absent for this piston mechanism is any means whereby the elastic jumps can be focused (e.g., by reflecting from a stenosis) to form a transient, localized region of high pressure within the spinal cord. Thus it would seem to offer a mechanism for syrinx progression, but not for its formation.

2009 ◽  
Vol 131 (4) ◽  
Author(s):  
N. S. J. Elliott ◽  
D. A. Lockerby ◽  
A. R. Brodbelt

Syringomyelia is a disease in which fluid-filled cavities, called syrinxes, form in the spinal cord causing progressive loss of sensory and motor functions. Invasive monitoring of pressure waves in the spinal subarachnoid space implicates a hydrodynamic origin. Poor treatment outcomes have led to myriad hypotheses for its pathogenesis, which unfortunately are often based on small numbers of patients due to the relative rarity of the disease. However, only recently have models begun to appear based on the principles of mechanics. One such model is the mathematically rigorous work of Carpenter and colleagues (2003, “Pressure Wave Propagation in Fluid-Filled Co-Axial Elastic Tubes Part 1: Basic Theory,” ASME J. Biomech. Eng., 125(6), pp. 852–856; 2003, “Pressure Wave Propagation in Fluid-Filled Co-Axial Elastic Tubes Part 2: Mechanisms for the Pathogenesis of Syringomyelia,” ASME J. Biomech. Eng., 125(6), pp. 857–863). They suggested that a pressure wave due to a cough or sneeze could form a shocklike elastic jump, which when incident at a stenosis, such as a hindbrain tonsil, would generate a transient region of high pressure within the spinal cord and lead to fluid accumulation. The salient physiological parameters of this model were reviewed from the literature and the assumptions and predictions re-evaluated from a mechanical standpoint. It was found that, while the spinal geometry does allow for elastic jumps to occur, their effects are likely to be weak and subsumed by the small amount of viscous damping present in the subarachnoid space. Furthermore, the polarity of the pressure differential set up by cough-type impulses opposes the tenets of the elastic-jump hypothesis. The analysis presented here does not support the elastic-jump hypothesis or any theory reliant on cough-based pressure impulses as a mechanism for the pathogenesis of syringomyelia.


2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Molly Brady ◽  
Akib Rahman ◽  
Abigail Combs ◽  
Chethana Venkatraman ◽  
R. Tristan Kasper ◽  
...  

Abstract Background Continuous circulation and drainage of cerebrospinal fluid (CSF) are essential for the elimination of CSF-borne metabolic products and neuronal function. While multiple CSF drainage pathways have been identified, the significance of each to normal drainage and whether there are differential changes at CSF outflow regions in the aging brain are unclear. Methods Dynamic in vivo imaging of near infrared fluorescently-labeled albumin was used to simultaneously visualize the flow of CSF at outflow regions on the dorsal side (transcranial and -spinal) of the central nervous system. This was followed by kinetic analysis, which included the elimination rate constants for these regions. In addition, tracer distribution in ex vivo tissues were assessed, including the nasal/cribriform region, dorsal and ventral surfaces of the brain, spinal cord, cranial dura, skull base, optic and trigeminal nerves and cervical lymph nodes. Results Based on the in vivo data, there was evidence of CSF elimination, as determined by the rate of clearance, from the nasal route across the cribriform plate and spinal subarachnoid space, but not from the dorsal dural regions. Using ex vivo tissue samples, the presence of tracer was confirmed in the cribriform area and olfactory regions, around pial blood vessels, spinal subarachnoid space, spinal cord and cervical lymph nodes but not for the dorsal dura, skull base or the other cranial nerves. Also, ex vivo tissues showed retention of tracer along brain fissures and regions associated with cisterns on the brain surfaces, but not in the brain parenchyma. Aging reduced CSF elimination across the cribriform plate but not that from the spinal SAS nor retention on the brain surfaces. Conclusions Collectively, these data show that the main CSF outflow sites were the nasal region across the cribriform plate and from the spinal regions in mice. In young adult mice, the contribution of the nasal and cribriform route to outflow was much higher than from the spinal regions. In older mice, the contribution of the nasal route to CSF outflow was reduced significantly but not for the spinal routes. This kinetic approach may have significance in determining early changes in CSF drainage in neurological disorder, age-related cognitive decline and brain diseases.


Author(s):  
Bryn Martin ◽  
Philippe Reymond ◽  
Olivier Balédent ◽  
Jan Novy ◽  
Nikos Stergiopulos

A preliminary coupled 1-D model of the systemic arterial tree and cerebrospinal fluid (CSF) system was constructed. The systemic tree model includes arteries greater than 2 mm in diameter and a simplified spinal cord vasculature. Coupling of the arterial tree and CSF system is accomplished by a transfer function based on in vivo cerebral blood flow (CBF) and CSF pulsation measurements in 17 young healthy adults. A 1-D tube model of the CSF in the spinal subarachnoid space (SSS) is formed based on in vivo measurements and used to determine flow and pressure along the SSS. The pressure and flow results in the CSF and systemic arterial tree are qualitatively and quantitatively similar to in vivo measurements in healthy subjects. The relative arrival time of blood pulsations in the spinal cord and CSF in the SSS is impacted by CSF system compliance and geometry. With low CSF system compliance the CSF pulsations arrive around the spinal cord before arterial pulsations and vice versa. Overall, the preliminary results support that geometric and mechanical properties of the CSF and cardiovascular system have an important impact on the flow and pressure environment and accent the importance to obtain in vivo measurements to improve modeling capabilities.


Injury ◽  
2015 ◽  
Vol 46 (4) ◽  
pp. 634-637 ◽  
Author(s):  
Rebecca E. Franco-Bourland ◽  
Horacio J. Reyes-Alva ◽  
Alejandra Quintana-Armenta ◽  
Angelina Martinez-Cruz ◽  
Ignacio Madrazo ◽  
...  

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.


1974 ◽  
Vol 41 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Howard M. Eisenberg ◽  
James E. McLennan ◽  
Keasley Welch

✓ Cats were made hydrocephalic by cisternal instillation of kaolin. Three to 8 weeks later it was found by perfusion between the ventricular system and the spinal subarachnoid space that communication had been reestablished through a demonstrably dilated central canal of the spinal cord. Absorption of fluid from the ventricular system, measured both by ventriculospinal perfusion and, after ligation of the spinal cord, by perfusion between the lateral ventricles, was found to be indistinguishable from zero over a wide range of ventricular pressure.


Sign in / Sign up

Export Citation Format

Share Document