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Chronic Response of the Rat Sciatic Nerve to the Flat Interface Nerve Electrode

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Abstract

The chronic effects of a reshaping nerve electrode, the flat interface nerve electrode (FINE), on sciatic nerve physiology, histology, and blood–nerve barrier (BNB) are presented. The FINE electrode applies a small force to a nerve to reshape the nerve and fascicles into elongated ovals. This increases the interface between the nerve and electrode for selective stimulation and recording of peripheral nerve activity. The hypothesis of this study is that a small force applied noncircumferentially to a nerve can chronically reshape the nerve without effecting nerve physiology, histology, or the blood–nerve barrier permeability. Three FINE electrode designs were implanted on rat sciatic nerves to examine the nerve's response to small, moderate, and high reshaping forces. The chronic reshaping, physiology, and histology of the nerve were examined at 1, 7, and 28 days postimplant. All FINEs significantly reshape both the nerve and the fascicles compared to controls. FINEs that applied high forces caused a neurapraxia type injury characterized by changes in the animal's footprint, nerve histology, and the BNB permeability. The physiological changes were greatest at 7 days and fully recover to normal by 14 days postimplant. The moderate force FINE did not result in changes in the footprint or BNB permeability. Only a minor decrease in axon density without accompanying evidence of axon demyelination or regeneration was observe for the moderate force. The small force FINE does not cause any change in nerve physiology, histology, or BNB permeability compared to the sham treatment. An electrode that applies a small force that results in an estimated intrafascicular pressure of less than 30 mm Hg can reshape the nerve without significant changes in the nerve physiology or histology. These results support the conclusion that a small force chronically applied to the nerve reshapes the nerve without injury. © 2003 Biomedical Engineering Society.

PAC2003: 8717Nn, 8719Nn, 8780Xa, 8719Uv

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References

  1. Dahlin, L. B.Aspects on pathophysiology of nerve entrapments and nerve compression injuries. Neurosurg. Clin. N. Am.2:21–29, 1991.

    Google Scholar 

  2. Delfiner, J. S.Dynamics and pathophysiology of nerve compression in the upper extremity. Orthop. Clin. North Am.27:219–226, 1996.

    Google Scholar 

  3. Dellon, E. S., and A. L. Dellon. Functional assessment of neurologic impairment: Track analysis in diabetic and compression neuropathies. Plast. Reconstr. Surg.88:686–694, 1991.

    Google Scholar 

  4. Gelberman, R., R. Eaton, and J. Urbaniak. Peripheral nerve compression. J. Bone Jt. Surg., Am. Vol.75:1854–1878, 1993.

    Google Scholar 

  5. Gelberman, R. H., et al. The carpal tunnel syndrome. A study of carpal canal pressures. J. Bone Jt. Surg., Am. Vol.63:380–383, 1981.

    Google Scholar 

  6. Larsen, J. O.et al. Degeneration and regeneration in rabbit peripheral nerve with long-term nerve cuff electrode implant: A stereological study of myelinated and unmyelinated axons. Acta Neuropathol. (Berlin)96:365–378, 1998.

    Google Scholar 

  7. Lundborg, G., and L. B. Dahlin. Anatomy, function, and pathophysiology of peripheral nerves and nerve compression. Hand Clin.12:185–193, 1996.

    Google Scholar 

  8. Lundborg, G.et al. The effect of ischemia on the permeability of the perineurium to protein tracers in rabbit tibial nerve. Acta Neurol. Scand.49:287–294, 1973.

    Google Scholar 

  9. Lundborg, G., R. Myers, and H. Powell. Nerve compression injury and increased endoneurial fluid pressure: A “miniature compartment syndrome.”J. Neurol., Neurosurg. Psychiatry46:1119–1124, 1983.

    Google Scholar 

  10. Munger, B. L., G. J. Bennett, and K. C. Kajander. An experimental painful peripheral neuropathy due to nerve constriction. I. Axonal pathology in the sciatic nerve. Exp. Neurol.118:204–214, 1992.

    Google Scholar 

  11. Myers, R. R.et al. The role of focal nerve ischemia and Wallerian degeneration in peripheral nerve injury producing hyperesthesia. Anesthesiology78:308–316, 1993.

    Google Scholar 

  12. Nitz, A. J., J. J. Dobner, and D. H. Matulionis. Pneumatic tourniquet application and nerve integrity: Motor function and electrophysiology. Exp. Neurol.94:264–279, 1986.

    Google Scholar 

  13. Nitz, A. J., and D. H. Matulionis. Ultrastructural changes in rat peripheral nerve following pneumatic tourniquet compression. J. Neurosurg.57:660–666, 1982.

    Google Scholar 

  14. Olsson, Y. Studies on vascular permeability in peripheral nerves. I. Distribution of circulating fluorescent serum albumin in normal, crushed and sectioned rat sciatic nerve. Acta Neuropathol. (Berlin)7:1–15, 1966.

    Google Scholar 

  15. Powell, H. C., and R. R. Myers. Pathology of experimental nerve compression. Lab. Invest.55:91–100, 1986.

    Google Scholar 

  16. Rydevik, B., M. D. Brown, and G. Lundborg. Pathoanatomy and pathophysiology of nerve root compression. Spine9:7–15, 1984.

    Google Scholar 

  17. Rydevik, B., and G. Lundborg. Permeability of intraneural microvessels and perineurium following acute, graded experimental nerve compression. Scand. J. Plast. Reconstr Surg.11:179–187, 1977.

    Google Scholar 

  18. Rydevik, B., G. Lundborg, and U. Bagge. Effects of graded compression on intraneural blood blow. An study on rabbit tibial nerve. J. Hand Surg. [Am]6:3–12, 1981.

    Google Scholar 

  19. Rydevik, B., G. Lundborg, and C. Nordborg. Intraneural tissue reactions induced by internal neurolysis. An experimental study on the blood–nerve barrier, connective tissues and nerve fibers of rabbit tibial nerve. Scand. J. Plast. Reconstr. Surg.10:3–8, 1976.

    Google Scholar 

  20. Steinwall, O., and I. Klatzo. Selective vulnerability of the blood–brain barrier in chemically induced lesions. J. Neuropathol. Exp. Neurol.25:542–559, 1966.

    Google Scholar 

  21. Takahashi, K.et al. Double-level cauda equina compression: An experimental study with continuous monitoring of intraneural blood flow in the porcine cauda equina. J. Orthop. Res.11:104–109, 1993.

    Google Scholar 

  22. Tyler, D. J., and D. M. Durand. A slowly penetrating interfascicular nerve electrode for selective activation of peripheral nerves. IEEE Trans. Rehabil. Eng.5:51–61, 1997.

    Google Scholar 

  23. Zochodne, D. W., and P. A. Low. Adrenergic control of nerve blood flow. Exp. Neurol.109:300–307, 1990.

    Google Scholar 

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Authors and Affiliations

  1. Applied Neural Control Laboratory, Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH

    Dustin J. Tyler & Dominique M. Durand

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  1. Dustin J. Tyler
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  2. Dominique M. Durand
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Tyler, D.J., Durand, D.M. Chronic Response of the Rat Sciatic Nerve to the Flat Interface Nerve Electrode. Annals of Biomedical Engineering 31, 633–642 (2003). https://doi.org/10.1114/1.1569263

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