Syringomyelia Hydrodynamics: An In Vitro Study Based on In Vivo Measurements

Abstract

A simplified in vitro model of the spinal canal, based on in vivo magnetic resonance imaging, was used to examine the hydrodynamics of the human spinal cord and subarachnoid space with syringomyelia. In vivo magnetic resonance imaging (MRI) measurements of subarachnoid (SAS) geometry and cerebrospinal fluid velocity were acquired in a patient with syringomyelia and used to aid in the in vitro model design and experiment. The in vitro model contained a fluid-filled coaxial elastic tube to represent a syrinx. A computer controlled pulsatile pump was used to subject the in vitro model to a CSF flow waveform representative of that measured in vivo. Fluid velocity was measured at three axial locations within the in vitro model using the same MRI scanner as the patient study. Pressure and syrinx wall motion measurements were conducted external to the MR scanner using the same model and flow input. Transducers measured unsteady pressure both in the SAS and intra-syrinx at four axial locations in the model A laser Doppler vibrometer recorded the syrinx wall motion at 18 axial locations and three polar positions. Results indicated that the peak-to-peak amplitude of the SAS flow waveform in vivo was approximately tenfold that of the syrinx and in phase (SAS approximately 5.2 +/- 0.6 ml/s, syrinx approximately 0.5 +/- 0.3 ml/s). The in vitro flow waveform approximated the in vivo peak-to-peak magnitude (SAS approximately 4.6 +/- 0.2 ml/s, syrinx approximately 0.4 +/- 0.3 ml/s). Peak-to-peak in vitro pressure variation in both the SAS and syrinx was approximately 6 mm Hg. Syrinx pressure waveform lead the SAS pressure waveform by approximately 40 ms. Syrinx pressure was found to be less than the SAS for approximately 200 ms during the 860-ms flow cycle. Unsteady pulse wave velocity in the syrinx was computed to be a maximum of approximately 25 m/s. LDV measurements indicated that spinal cord wall motion was nonaxisymmetric with a maximum displacement of approximately 140 microm, which is below the resolution limit of MRI. Agreement between in vivo and in vitro MR measurements demonstrates that the hydrodynamics in the fluid filled coaxial elastic tube system are similar to those present in a single patient with syringomyelia. The presented in vitro study of spinal cord wall motion, and complex unsteady pressure and flow environment within the syrinx and SAS, provides insight into the complex biomechanical forces present in syringomyelia.

Characterization of CSF Hydrodynamics in the Presence and Absence of Tonsillar Ectopia by Means of Computational Flow Analysis

“…Some physical models have been created; an in vitro study of syringomyelia hydrodynamics was performed with a phantom model of the spinal canal created from MR imaging. 17 The main limitation for both numeric simulations and physical models of CSF within the subarachnoid space has been the complexity of the anatomy. For numeric simulations, the high-attenuation mesh required for domain discretization leads to very high computational costs.…”

Effect of the Central Canal in the Spinal Cord on Fluid Movement within the Cord

“…Models for the study of the spinal cord and subarachnoid space include co-axial tube models, where the outer tube represents the dura and the inner tube the spinal cord [8][9][10] , computational fluid-structure interaction models [11][12][13] , and physical models [14][15][16] . The models include the spinal cord with or without a syrinx, but do not consider the inhomogeneous porosity of spinal cord tissue.…”

Management of idiopathic pediatric syringohydromyelia

“…Median clinical follow-up was 20.5 months, and median radiological follow-up was 13 months. The median maximum syrinx diameter was 2 mm (range 0.5-17 mm) and the median number of vertebral levels spanned was 5 (range [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Eighty-one of the patients had a syrinx diameter equal to or greater than 2 mm.…”

“…9 Williams theorized that CSF flow obstructions led to pressure dissociations in which CSF passes through the obstructions during episodes of increased intracranial pressure and, via a ball-valve mechanism, is not able to egress back out even after the pressure has normalized. 8,11,18 This theory was the first to explain etiology, regardless of the presumed underlying pathology, and was the basis for multiple modern theories. 5,6 There remains a paucity of studies on the etiology and natural history of pediatric IS.…”