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TECHNICAL PAPERS

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

[+] Author and Article Information
P. W. Carpenter, K. Berkouk, A. D. Lucey

Fluid Dynamics Research Center, University of Warwick, Coventry CV4 7AL, UK

J Biomech Eng 125(6), 857-863 (Jan 09, 2004) (7 pages) doi:10.1115/1.1634281 History: Received November 01, 2002; Revised May 03, 2003; Online January 09, 2004
Copyright © 2003 by ASME
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References

Storer,  K. P., Toh,  J., Stoodley,  M. A., and Jones,  N. R., 1998, “The Central Canal of the Human Spinal Cord: A Computerized 3-D Study,” J. Anat., 192, 565–572.
Williams,  B., 1969, “The Distending Force in Production of Communicating Syringomyelia,” Lancet, 2, pp. 189–193.
Williams,  B., 1974, “A Demonstration Analogue for Ventricular and Intraspinal Dynamics (DAVID),” J. Neurol. Sci., 23, 445–461.
Lockey,  P., Poots,  G., and Williams,  B., 1975, “Theoretical Aspects of the Attenuation of Pressure Pulses within Cerebrospinal Fluid Pathways,” Med. Biol. Eng., 13, pp. 861–869.
Williams,  B., 1976, “Cerebrospinal Fluid Pressure Changes in Response to Coughing,” Brain, 99, pp. 331–346.
Williams,  B., 1986, “Progress in Syringomyelia,” Neurol. Res., 8, pp. 129–144.
Williams,  B., 1990, “Syringomyelia,” Neurosurg. Clin. N. Am., 1, 653–685.
Oldfield,  E. H., Murasko,  K., Shawker,  T. H. , 1994, “Pathophysiology of Syringomyelia Associated with Chiari I Malformation of the Cerebellar Tonsils. Implications for Diagnosis and Treatment,” J. Neurosurg., 80, pp. 3–15.
Heiss,  J. D., Patronas,  N., DeVroom,  H. L., , 1999, “Elucidating the Pathophysiology of Syringomyelia,” J. Neurosurg., 91, pp. 553–562.
Greitz,  D., Ericson,  K., and Flodmark,  O., 1999, “Pathogenesis and Mechanics of Spinal Cord Cysts. A New Hypothesis Based on Magnetic Resonance Studies of Cerebrospinal Fluid Dynamics,” Int. J. Neurorad., 5, pp. 61–78.
Milhorat,  T. H., Capocelli,  A. L., Kotzen,  R. M., , 1997, “Intramedullary Pressure in Syringomyelia: Clinical and Pathophysiological Correlates of Syrinx Distortion,” Neurosurgery, 41, 1102–1110.
Stoodley,  M. A., Jones,  N. R., Yang,  L., and Brown,  C. J., 2000, “Mechanisms Underlying the Formation and Enlargement of Noncommunicating Syringomyelia: Experimental Studies,” Neurosurg Focus, 8(3), Article 2.
Fischbein,  N. J., Dillon,  W. P., Cobbs,  C., and Weinstein,  P. R., 1999, “The “Presyrinx” State: A Reversible Myelopathic Condition That May Precede Syringomyelia,” Am. J. Neuroradiol., 20, 7–20.
Milhorat,  T. H., Johnson,  R. W., Milhorat,  R. H., , 1995, “Clinicopathological Correlations in Syringomyelia Using Axial Magnetic Resonance Imaging,” Neurosurgery, 37, 206–213.
Gardner,  W. J., and Goodall,  R. J., 1950, “The Surgical Treatment of Arnold-Chiari Malformation in Adults: An Explanation of Its Mechanism and Importance of Encephalography in Diagnosis,” J. Neurosurg., 7, 199–206.
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Berkouk, K., 1999, “Theoretical and Physical Models of Pressure Pulse Propagation in the Spinal System,” Ph.D. thesis, University of Warwick, U.K.
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Figures

Grahic Jump Location
A schematic sketch of the human spinal cord and associated CSF system. Key: 1, cerebellum; 2, pons; 3, medulla; 4, brain stem; 5, fourth ventricle; 6, cisterna magna; 7, pontine cistern; 8, spinal cord (SC); 9, central canal (CC); 10, nerve roots; 11, arachnoid; 12, pia mater; 13, spinal subarachnoid space (SSS); 14, choroid plexus; 15, terminal ventricle.
Grahic Jump Location
A schematic sketch of a case of noncommunicating syringomyelia, showing the hind-brain tonsil that is a feature of Arnold-Chiari malformation. The black arrow indicates the direction of tonsil displacement during systole; it moves in the opposite direction during the diastolic phase of the cardiac cycle.
Grahic Jump Location
A schematic illustration showing the propagation of a pressure pulse along the co-axial flexible tube system. On the right the pulse is incident on a blockage to the tube A representing a stenosis of the spinal subarachnoid space. (a) A wave diagram showing that the leading edge of the pulse steepens with time to form an elastic jump. The dotted line denotes the initial deformation of the tube wall. The transient, localized region of high pressure generated, as the elastic jump reflects from the blockage, is denoted by HP. The forms of the tube-wall displacement at times t=t1 and t=t2 are shown in (b) and (c) respectively.
Grahic Jump Location
A schematic sketch showing the control volume for determining the relationships between flow quantities ahead and behind an elastic jump propagating away from a blockage after reflecting from it
Grahic Jump Location
A schematic sketch showing the theoretical model for the head as the end condition to the co-axial-tube model of the intraspinal CSF system
Grahic Jump Location
A wave diagram and instantaneous tube wall displacements for the case where the end condition is an oscillating piston for channel A and a complete blockage for B: (a) the wave diagram showing the periodic formation of elastic jumps (the broken line on the right indicates the position of the piston); (b) and (c) respectively show instantaneous displacement profiles of the tube wall at time t=t1 when the piston is moving to the left and at time t=t2 when it is moving to the right.

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