The Origins of Syringomyelia: Numerical Models of Fluid/Structure Interactions in the Spinal Cord

2005 ◽  
Vol 127 (7) ◽  
pp. 1099-1109 ◽  
Author(s):  
C. D. Bertram ◽  
A. R. Brodbelt ◽  
M. A. Stoodley
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Wave Propagation ◽  
Numerical Models ◽  
Scar Tissue ◽  
Central Canal ◽  
Radial Wave ◽  
Wave Speeds ◽  
Arterial Pulsation ◽  
Elastic Cord

A two-dimensional axi-symmetric numerical model is constructed of the spinal cord, consisting of elastic cord tissue surrounded by aqueous cerebrospinal fluid, in turn surrounded by elastic dura. The geometric and elastic parameters are simplified but of realistic order, compared with existing measurements. A distal reflecting site models scar tissue formed by earlier trauma to the cord, which is commonly associated with syrinx formation. Transients equivalent to both arterial pulsation and percussive coughing are used to excite wave propagation. Propagation is investigated in this model and one with a central canal down the middle of the cord tissue, and in further idealized versions of it, including a model with no cord, one with a rigid cord, one with a rigid dura, and a double-length untapered variant of the rigid-dura model. Analytical predictions for axial and radial wave-speeds in these different situations are compared with, and used to explain, the numerical outcomes. We find that the anatomic circumstances of the spinal cerebrospinal fluid cavity probably do not allow for significant wave steepening phenomena. The results indicate that wave propagation in the real cord is set by the elastic properties of both the cord tissue and the confining dura mater, fat, and bone. The central canal does not influence the wave propagation significantly.

Evaluation of the central canal of the spinal cord in experimentally induced hydrocephalus

1978 ◽  
Vol 48 (6) ◽  
pp. 970-974 ◽  
Author(s):  
A. Everette James ◽  
William J. Flor ◽  
Gary R. Novak ◽  
Ernst-Peter Strecker ◽  
Barry Burns
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Experimental Model ◽  
Alternative Pathway ◽  
Central Canal ◽  
Communicating Hydrocephalus ◽  
Csf Flow ◽  
Content Type ◽  
Histological Appearance ◽  
Fine Print

✓ The central canal of the spinal cord has been proposed as a significant compensatory alternative pathway of cerebrospinal fluid (CSF) flow in hydrocephalus. Ten dogs were made hydrocephalic by a relatively atraumatic experimental model that simulates the human circumstance of chronic communicating hydrocephalus. The central canal was studied by histopathology and compared with 10 normal control dogs. In both groups the central canal of the spinal cord was normal in size, configuration, and histological appearance. In this experimental model dilatation of the canal and increased movement of CSF does not appear to be a compensatory alternative pathway.

scholarly journals Syringohydromyelia associated to therapeutic procedures for severe forms of neurocysticercoses: case report

2004 ◽  
Vol 62 (3b) ◽  
pp. 885-888
Author(s):  
Donizeti Honorato ◽  
Wilson Borges ◽  
Antonio Augusto Roth Vargas ◽  
Ricardo Ramina
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Case Report ◽  
Posterior Fossa ◽  
Central Canal ◽  
Severe Form ◽  
Surgical Decompression ◽  
Therapeutic Procedures ◽  
Surgical Treatments ◽  
Progressive Paraparesis

Syringohydromyelia is defined as a longitudinal dilatation of the central canal of the spinal cord with accumulated cerebrospinal fluid. This condition may cause neurologic deficits when the cavity enlarges and compresses the spinal cord. We present the case of a 33 years-old female with progressive paraparesis caused by syringohydromyelia. This patient underwent previously multiple clinical and surgical treatments for severe form of neurocysticercosis. Surgical decompression of the posterior fossa and syringostomy resolved the neurologic symptoms. The possibility of syringohydromyelia should be considered in the case of patients who have previously undergone surgical and clinical treatment for severe form of neurocysticercosis.

scholarly journals Mechanisms underlying the formation and enlargement of noncommunicating syringomyelia: experimental studies

2000 ◽  
Vol 8 (3) ◽  
pp. 1-7 ◽  
Author(s):  
Marcus A. Stoodley ◽  
Nigel R. Jones ◽  
Liqun Yang ◽  
Christopher J. Brown
Keyword(s):  
Spinal Cord ◽  
Experimental Studies ◽  
Central Canal ◽  
Perivascular Spaces ◽  
Arterial Pulse ◽  
Csf Flow ◽  
Spinal Subarachnoid Space ◽  
Brachiocephalic Trunk ◽  
Rapid Flow ◽  
Arterial Pulsation

The pathogenesis of noncommunicating syringomyelia is unknown, and none of the existing theories adequately explains the production of cysts that occur in association with conditions other than Chiari malformation. The authors' hypothesis is that an arterial pulsation–driven perivascular flow of cerebrospinal fluid (CSF) is responsible for syrinx formation and enlargement. They investigated normal CSF flow patterns in 20 rats and five sheep by using the tracer horseradish peroxidase; the effect of reducing arterial pulse pressure was examined in four sheep by partially ligating the brachiocephalic trunk; CSF flow was examined in 78 rats with the intraparenchymal kaolin model of noncommunicating syringomyelia; and extracanalicular cysts were examined using the excitotoxic model in 38 rats. In the normal animals there was a rapid flow of CSF from the spinal subarachnoid space into the spinal cord perivascular spaces and then into the central canal. This flow ceased when arterial pulsations were diminished. In animals with noncommunicating syringomyelia, there was rapid CSF flow into isolated and enlarged segments of central canal, even when these cysts were causing pressure damage to the surrounding spinal cord. Exitotoxic injury of the spinal cord caused the formation of extracanalicular cysts, and larger cysts were produced when this injury was combined with arachnoiditis, which impaired subarachnoid CSF flow. The results of these experiments support the hypothesis that arterial pulsation–driven perivascular fluid flow is responsible for syrinx formation and enlargement.

scholarly journals Rapid, widespread, and longlasting induction of nestin contributes to the generation of glial scar tissue after CNS injury.

1995 ◽  
Vol 131 (2) ◽  
pp. 453-464 ◽  
Author(s):  
J Frisén ◽  
C B Johansson ◽  
C Török ◽  
M Risling ◽  
U Lendahl
Keyword(s):  
Spinal Cord ◽  
Scar Tissue ◽  
Central Canal ◽  
Glial Scar ◽  
Reactive Astrocytes ◽  
Spatiotemporal Pattern ◽  
Cns Injury ◽  
Neuronal Regeneration ◽  
Nestin Expression ◽  
The Central Nervous System

Neuronal regeneration does generally not occur in the central nervous system (CNS) after injury, which has been attributed to the generation of glial scar tissue. In this report we show that the composition of the glial scar after traumatic CNS injury in rat and mouse is more complex than previously assumed: expression of the intermediate filament nestin is induced in reactive astrocytes. Nestin induction occurs within 48 hours in the spinal cord both at the site of lesion and in degenerating tracts and lasts for at least 13 months. Nestin expression is induced with similar kinetics in the crushed optic nerve. In addition to the expression in reactive astrocytes, we also observed nestin induction within 48 hours after injury in cells close to the central canal in the spinal cord, while nestin expressing cells at later timepoints were found progressively further out from the central canal. This dynamic pattern of nestin induction after injury was mimicked by lacZ expressing cells in nestin promoter/lacZ transgenic mice, suggesting that defined nestin regulatory regions mediate the injury response. We discuss the possibility that the spatiotemporal pattern of nestin expression reflects a population of nestin positive cells, which proliferates and migrates from a region close to the central canal to the site of lesion in response to injury.

The morphology and distribution of ‘Kolmer–Agduhr cells’, a class of cerebrospinal-fluid-contacting neurons revealed in the frog embryo spinal cord by GABA immunocytochemistry

1987 ◽  
Vol 232 (1267) ◽  
pp. 193-203 ◽  
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Central Canal ◽  
Ventral Part ◽  
Fixed Tissue ◽  
Frog Embryo ◽  
Axonal Projections ◽  
Embryonic Origin ◽  
Immunocytochemical Method ◽  
Neuron Soma

An immunocytochemical method that localizes GABA in glutaraldehyde- fixed tissue has been applied to the study of the Xenopus embryo spinal cord. This procedure stained an anatomical class of neuron, which had somata forming two more or less continuous rows, one on either side of the central canal, in the ventral part of the spinal cord. The total number of stained neurons in the stage 37–38 embryo spinal cord was about 300. The medial surface of the soma protruded into the central canal and had a brush border which electron microscope studies showed to consist of many microvilli or stereocilia and one or two cilia. The external end of the neuron soma had an ipsilateral ascending axon. The axon of many of these neurons had a growth cone which was also clearly stained. We propose calling these neurons ‘Kolmer–Agduhr cells’ after W. Kolmer and E. Agduhr who described them in the spinal cords of many vertebrate classes. Their early embryonic origin, GABA-like immunoreactivity, axonal projections and distribution as a whole population have not previously been known.

A Fluid Structure Interaction Simulation of the Cerebrospinal Fluid, Spinal Cord, and Spinal Stenosis Present in Syringomyelia

2010 ◽  
Author(s):  
Yifei Liu ◽  
Bryn A. Martin ◽  
Thomas J. Royston ◽  
Francis Loth
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Wave Propagation ◽  
In Silico ◽  
Fluid Structure Interaction ◽  
Csf Flow ◽  
Fluid Structure ◽  
Structure Interaction ◽  
Csf Pressure

Syringomyelia (SM) is a neurological disease in which a fluid-filled cystic cavity, or syrinx, forms in the spinal cord (SC) resulting in progressive loss of sensory, motor functions, and/or pain in the patient. It has been hypothesized that abnormal cerebrospinal fluid (CSF) pressure distribution and absorption in the subarachnoid space (SAS), resulting from a CSF flow blockage (stenosis), could be a key etiological factor for syrinx pathogenesis. In particular, the magnitude of the abrupt SAS pressure waves produced during coughing has been correlated with headache and pain in the patient. To better understand the influence of coughing on the spinal SAS, four axisymmetric fluid-structure interaction (FSI) in silico models representative of various conditions associated with SM were constructed. Each of the models was subjected to a cough-like CSF pressure pulse. The CSF flow stenosis was shown to attenuate and decelerate the CSF wave propagation in the SAS. The spinal SAS distensibility was also shown to have significant influence on the wave propagation. The in silico pressure results were found to be in agreement with a set of similar in vitro experiments [1].

scholarly journals Cerebrospinal Fluid Drop Metastases of Canine Glioma: Magnetic Resonance Imaging Classification

2021 ◽  
Vol 8 ◽  
Author(s):  
R. Timothy Bentley ◽  
Amy B. Yanke ◽  
Margaret A. Miller ◽  
Hock Gan Heng ◽  
Aaron Cohen-Gadol ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Magnetic Resonance ◽  
Central Canal ◽  
Resonance Imaging ◽  
Primary Tumors ◽  
Stereotactic Radiation ◽  
Primary Mass ◽  
Drop Metastasis

Dissemination of glioma in humans can occur as leptomeningeal nodules, diffuse leptomeningeal lesions, or ependymal lesions. Cerebrospinal fluid (CSF) drop metastasis of glioma is not well-recognized in dogs. Ten dogs with at least two anatomically distinct and histologically confirmed foci of glioma were included in this study. The 10 dogs underwent 28 magnetic resonance imaging (MRI) examinations, with distant CSF drop metastasis revealed in 13 MRIs. The CSF drop metastases appeared as leptomeningeal nodules in four dogs, diffuse leptomeningeal lesions in six dogs, and ependymal lesions in seven dogs; six dogs had a combination of lesion types. Primary tumors were generally T2-heterogeneous and contrast-enhancing. Many metastases were T2-homogeneous and non-enhancing. Diffuse leptomeningeal lesions were seen as widespread extra-axial contrast-enhancement, again very dissimilar to the intra-axial primary mass. Primary masses were rostrotentorial, whereas metastases generally occurred in the direction of CSF flow, in ventricles, CSF cisterns, and the central canal or leptomeninges of the cervical or thoracolumbar spinal cord. Seven of the dogs had received therapy limited to the primary mass, such as surgery or stereotactic radiation, then developed metastasis in the following months. CSF drop metastasis of glioma may take a very different appearance on MRI to the primary mass, including periventricular lesions that are more homogeneous and less contrast-enhancing, rostral horn signal changes, or leptomeningeal enhancement ventral to the brainstem or encircling the spinal cord.

scholarly journals Graded calcium spikes differentially signal neurotransmitter input in cerebrospinal fluid contacting neurons of mouse spinal cord

2020 ◽  
Author(s):  
Emily Johnson ◽  
Marilyn Clark ◽  
Claudia MacLean ◽  
Jim Deuchars ◽  
Susan A. Deuchars ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Action Potential ◽  
Central Canal ◽  
Mouse Spinal Cord ◽  
Voltage Gated ◽  
Neural Communication ◽  
Lower Amplitude ◽  
Nav Channels ◽  
Rapid Kinetics

AbstractThe action potential and its all-or-none nature is fundamental to neural communication. Canonically the action potential is initiated once voltage-gated Na+ (NaV) channels are activated and their rapid kinetics of activation and inactivation give rise to the all-or-none nature. Here we show that cerebrospinal fluid contacting neurons (CSFcNs) surrounding the central canal of the mouse spinal cord employ a different strategy. Rather than using Nav channels to generate binary spikes, CSFcNs use two different types of voltage-gated Ca2+ channel, enabling spikes of different amplitude. T-type Ca2+ channels are required for spontaneous spiking and generate lower amplitude spikes, whereas large amplitude spikes require high voltage activated Cd2+ sensitive Ca2+ channels. We show that these different amplitude spikes signal input from different transmitter systems; purinergic inputs evoke smaller T-type dependent spikes while cholinergic inputs evoke large T-type independent spikes. Different synaptic inputs to CSFcNs can therefore be signalled by the spike amplitude.

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