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Research Papers

Spinal Subarachnoid Space Pressure Measurements in an In Vitro Spinal Stenosis Model: Implications on Syringomyelia Theories

[+] Author and Article Information
Bryn A. Martin1

Integrative Bioscience Institute, Laboratory of Hemodynamics and Cardiovascular Technology, École Polytechnique Fédérale de Lausanne, Lausanne 1015, Switzerlandbrynandrew.martin@epfl.ch

Richard Labuda

 Chiari and Syringomyelia Patient Education Foundation, Wexford, PA 15090

Thomas J. Royston

Department of Mechanical and Industrial Engineering, University of Illinois at Chicago, Chicago, IL 60607

John N. Oshinski

Department of Radiology and Biomedical Engineering, Emory University, Atlanta, GA 30322

Bermans Iskandar

Department of Neurological Surgery, University of Wisconsin Medical School, Madison, WI 53792

Francis Loth

Departments of Mechanical and Biomedical Engineering, University of Akron, Akron, OH 44325

1

Corresponding author.

J Biomech Eng 132(11), 111007 (Oct 20, 2010) (11 pages) doi:10.1115/1.4000089 History: Received January 08, 2009; Revised June 12, 2009; Posted September 01, 2009; Published October 20, 2010; Online October 20, 2010

Full explanation for the pathogenesis of syringomyelia (SM), a neuropathology characterized by the formation of a cystic cavity (syrinx) in the spinal cord (SC), has not yet been provided. It has been hypothesized that abnormal cerebrospinal fluid (CSF) pressure, caused by subarachnoid space (SAS) flow blockage (stenosis), is an underlying cause of syrinx formation and subsequent pain in the patient. However, paucity in detailed in vivo pressure data has made theoretical explanations for the syrinx difficult to reconcile. In order to understand the complex pressure environment, four simplified in vitro models were constructed to have anatomical similarities with post-traumatic SM and Chiari malformation related SM. Experimental geometry and properties were based on in vivo data and incorporated pertinent elements such as a realistic CSF flow waveform, spinal stenosis, syrinx, flexible SC, and flexible spinal column. The presence of a spinal stenosis in the SAS caused peak-to-peak cerebrospinal fluid CSF pressure fluctuations to increase rostral to the stenosis. Pressure with both stenosis and syrinx present was complex. Overall, the interaction of the syrinx and stenosis resulted in a diastolic valve mechanism and rostral tensioning of the SC. In all experiments, the blockage was shown to increase and dissociate SAS pressure, while the axial pressure distribution in the syrinx remained uniform. These results highlight the importance of the properties of the SC and spinal SAS, such as compliance and permeability, and provide data for comparison with computational models. Further research examining the influence of stenosis size and location, and the importance of tissue properties, is warranted.

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Copyright © 2010 by American Society of Mechanical Engineers
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Figures

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Figure 1

Schematic diagram for each in vitro experiment indicating the location of the stenosis, syrinx, pressure sensors, spinal cord, flow input (Qin), and flow exit port. (SSE=stenosis and syrinx experiment, SRE=stenosis removed experiment, SAE=stenosis alone experiment, and CSE=Chiari stenosis experiment.)

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Figure 2

The cyclic CSF flow waveform, Q(t), input on the rostral end of each experiment by the computer controlled pulsatile pump

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Figure 3

SAS pressure changes over time measured at distinct axial locations in the stenosis alone experiment (SAE). Legend symbols identify pressure sensor location (sampling frequency was 10 kHz).

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Figure 4

Pressure changes over time measured at distinct axial locations in the SSE. Pressure in the syrinx at 12 cm is also indicated. Legend symbols identify pressure sensor location (sampling frequency was 10 kHz).

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Figure 5

Maximum, average, and minimum pressure in the SAS and syrinx (if present) for each experiment during the CSF pulsation (see SSE for legend). The light gray rectangle denotes location of the syrinx cavity (if present), and the dark gray vertical stripe denotes the location of the SAS stenosis. CSF flow was input at x-axis=0 cm location (skull base, rostral). Note, axis scale is different for each plot. (SSE=stenosis and syrinx experiment, SRE=stenosis removed experiment, SAE=stenosis alone experiment, and CSE=Chiari stenosis experiment).

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Figure 6

Longitudinal pressure dissociation (LPD) (lumbar-cervical) measured in the SAS during the CSF flow pulsation (LPD(t)=PSAS,4 cm(t)−PSAS,32 cm(t)). Sampling frequency for each experiment was 10 kHz. (SSE=stenosis and syrinx experiment, SAE=stenosis alone experiment, and SRE=stenosis removed experiment.)

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Figure 7

TP in the SSE measured at four adjacent sensor locations along the syrinx during the CSF flow pulsation (TP(t)=Psyrinx(t)−PSAS(t)). Positive pressure trace indicates that the pressure in the syrinx is greater than the SAS at adjacent measurement locations. Negative pressure trace indicates that syrinx pressure is less than the SAS. Legend symbols identify pressure sensor location (sampling frequency was 10 kHz).

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Figure 8

Illustration of the diastolic valve mechanism produced by the interaction of the syrinx and stenosis during the CSF pulsation in systole (top-valve open) and diastole (bottom-valve closed) in SSE. Note that valve closure during diastole was not continuous. CSF must return to the rostral end of the SAS to satisfy conservation of mass.

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Figure 9

Images from a video of the SSE at different time points (t1–t6) during the CSF flow pulsation (left). Approximate locations of the syrinx, stenosis, pressure ports, and spinal cord are indicated in the diagram (right). Regions with the greatest spinal cord movement are indicated by white arrows in each video frame. Note that the spinal cord motion is asymmetric, flexing more on the bottom side than on the top. Also, greater spinal cord motion is present rostral to the stenosis than caudal. The outward ballooning of the syrinx is best observed during diastole at t1 and t6 in the region 4 cm rostral to the stenosis. Syrinx contraction can be observed during systole from t3 to t5 (complete video is provided at www.csflab.com/video/20080610_SSE_model.AVI).

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