Pathological changes of isolated spinal cord axons in response to mechanical stretch

Shi, Riyi; Pryor, John H.

doi:10.1016/s0306-4522(01)00596-6

Cited by 117 publications

(101 citation statements)

References 30 publications

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“…Following anesthesia the spinal cord was extracted as previously described (Shi and Blight, 1996;Shi and Borgens, 2000;Shi and Pryor, 2002), and was then incubated in oxygenated Krebs' solution (124 mM NaCl, 2 mM KCl, 1.2 mM KH 2 PO 4 , 1.3 mM MgSO 4 , 2 mM CaCl 2 , 10 mM dextrose, 26 mM NaHCO 3 , and 10 mM sodium ascorbate).…”

Section: Animalsmentioning

confidence: 99%

“…However, it is also possible, although less studied, that acute and persistent myelin damage may also contribute to overall functional loss in SCI. Myelin sheath disruption is a known cause for the loss of axonal conduction seen in mechanical injury (Blight, 1983a;Blight and Decrescito, 1986;Shi and Blight, 1996;Shi and Pryor, 2002). Thus understanding the mechanism of demyelination and the subsequent conduction failure of the surviving, but functionally silent, axons is important not only to ascertain the role of demyelination in functional loss, but also to provide helpful clues for the purpose of eventually establishing potential treatments to restore function after SCI.…”

Section: Introductionmentioning

confidence: 99%

“…However, the mechanism of secondary myelin damage in such a traumatic injury model has not been studied. The stretch of spinal cord axons is a significant component of compression injury, and stretch injury itself is an important central nervous system (CNS) injury (Blight and DeCrestcito, 1986;Shi and Pryor, 2002). However, paranodal myelin damage has not been studied in detail in stretch injury.…”

Section: Introductionmentioning

confidence: 99%

“…The present study aims to investigate the mechanism of acute myelin damage following ex vivo stretch injury, especially focusing on the paranodal region. Using an ex vivo controlled guinea pig spinal cord stretch injury model ( Jensen and Shi, 2003;McBride et al, 2006;Shi and Pryor, 2002), we aimed to determine the differential contribution of primary and secondary injury in myelin disruption during the acute period (0-2 h) post-SCI. With multi-modal imaging techniques we demonstrated immediate paranodal myelin damage and nodal region lengthening following stretch injury.…”

Section: Introductionmentioning

confidence: 99%

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Paranodal Myelin Damage after Acute Stretch in Guinea Pig Spinal Cord

Sun

Shi

et al. 2012

Journal of Neurotrauma

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Mechanical injury causes myelin disruption and subsequent axonal conduction failure in the mammalian spinal cord. However, the underlying mechanism is not well understood. In mammalian myelinated axons, proper paranodal myelin structure is crucial for the generation and propagation of action potentials. The exposure of potassium channels at the juxtaparanodal region due to myelin disruption is thought to induce outward potassium currents and inhibit the genesis of the action potential, leading to conduction failure. Using multimodal imaging techniques, we provided anatomical evidence demonstrating paranodal myelin disruption and consequent exposure and redistribution of potassium channels following mechanical insult in the guinea pig spinal cord. Decompaction of paranodal myelin was also observed. It was shown that paranodal demyelination can result from both an initial physical impact and secondary biochemical reactions that are calcium dependent. 4-Aminopyridine (4-AP), a known potassium channel blocker, can partially restore axonal conduction, which further implicates the role of potassium channels in conduction failure. We provide important evidence of paranodal myelin damage, the role of potassium channels in conduction loss, and the therapeutic value of potassium blockade as an effective intervention to restore function following spinal cord trauma.

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Section: Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Paranodal Myelin Damage after Acute Stretch in Guinea Pig Spinal Cord

Sun

Shi

et al. 2012

Journal of Neurotrauma

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“…Assuming that positive elongation strain, that is stretching, of CNS neurons is the essential cause of closed head injury, one can investigate the underlying pathophysiology using isolated neurons, optic nerves, or spinal cord subjected to sudden stretching [44][45][46]49 . Such preparations can be studied in terms of their function (nerve transmission) histopathology, membrane permeability, and responses to drugs.…”

Section: Implications For Researchmentioning

confidence: 99%

Brain Motion and Deformation During Closed Head Injury in the Presence of Cerebrospinal Fluid

Babbs

2005

J. Mech. Med. Biol.

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This paper presents a new analysis of the physics of closed head injury following brief, intense acceleration of the head. It focuses upon the buoyancy of the brain in cerebrospinal fluid, which protects against damage, the propagation of strain waves through the brain substance, which causes damage, and the concentration of strain in critical anatomic regions, which magnifies damage. Numerical methods are used to create animations or "movies" of brain motion and deformation. Initially a 1 cm gap filled with cerebrospinal fluid (CSF) separates the brain from the skull. Whole head acceleration induces artificial gravity within the skull. The brain accelerates because its density differs slightly from that of CSF, strikes the inner aspect of the skull, and undergoes viscoelastic deformation. The computed pattern of brain motion correlates well with published high-speed photographic studies. The sites of greatest deformation correlate with sites of greatest pathological damage. This fresh biomechanical analysis allows one to visualize events within the skull during closed head injury and may inspire new approaches to prevention and treatment.

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Diffusion tensor magnetic resonance imaging in spinal cord injury

Ellingson¹,

Schmit²,

Ulmer³

et al. 2008

Concepts Magnetic Resonance

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Noninvasive assessment of spinal cord integrity following injury is critical for precise diagnosis, prognosis, and surgical intervention strategies. Diffusion weighted imaging and diffusion tensor imaging are more sensitive to the underlying spinal cord microstructure than traditional imaging techniques. As a result, diffusion imaging is emerging as the clinical technique for imaging the spinal cord after trauma, surgery or during progressive degenerative diseases. This review describes the basic physics of diffusion imaging using magnetic resonance, techniques used to visualize diffusion measurements, and expected changes in diffusion measurements following spinal cord injury.

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Pathological changes of isolated spinal cord axons in response to mechanical stretch

Cited by 117 publications

References 30 publications

Paranodal Myelin Damage after Acute Stretch in Guinea Pig Spinal Cord

Paranodal Myelin Damage after Acute Stretch in Guinea Pig Spinal Cord

Brain Motion and Deformation During Closed Head Injury in the Presence of Cerebrospinal Fluid

Diffusion tensor magnetic resonance imaging in spinal cord injury

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