Paranodal demyelination by gradual nerve stretch can be repaired by elongation of internodes

Abe, Ichiro; Tsujino, Akihito; Hara, Yuki; Ichimura, Harumitsu; Ochiai, Naoyuki

doi:10.1007/s00401-002-0584-y

Cited by 23 publications

(11 citation statements)

References 24 publications

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“…Although diabetes is clearly not the cause of RLN, it is conceivable that a vascular aetiology may be involved. Gradual nerve elongation has been associated with characteristic ischaemic changes in nerves (Abe et al 2002). Differing timing and duration of forces at work in developmental vs. experimental nerve stretch may account for the lack of typical changes in RLN including nodal lengthening, intense paranodal demyelination and abundant intercalating internodes.…”

Section: Discussionmentioning

confidence: 99%

Histological and ultrastructural evidence that recurrent laryngeal neuropathy is a bilateral mononeuropathy limited to recurrent laryngeal nerves

Hahn

Matiasek²,

Dixon

et al. 2008

Equine Veterinary Journal

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Section: Discussionmentioning

confidence: 99%

Histological and ultrastructural evidence that recurrent laryngeal neuropathy is a bilateral mononeuropathy limited to recurrent laryngeal nerves

Hahn

Matiasek²,

Dixon

et al. 2008

Equine Veterinary Journal

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“…When constant forces are applied to the brain, for example during development or in response to tumor growth, the brain adapts gradually over time and displays a time-dependent behavior [35]. In response to body growth or artificial limb lengthening [81], axons can adapt and gradually grow in length [1,68,71]. Nonetheless, time-independent, elastic models have successfully been used to explain prestress in axons and in the brain [24] and to model the effects of high impact loading [5, 58, 74].…”

Section: Introductionmentioning

confidence: 99%

Modeling molecular mechanisms in the axon

2016

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Axons are living systems that display highly dynamic changes in stiffness, viscosity, and internal stress. However, the mechanistic origin of these phenomenological properties remains elusive. Here we establish a computational mechanics model that interprets cellular-level characteristics as emergent properties from molecular-level events. We create an axon model of discrete microtubules, which are connected to neighboring microtubules via discrete crosslinking mechanisms that obey a set of simple rules. We explore two types of mechanisms: passive and active crosslinking. Our passive and active simulations suggest that the stiffness and viscosity of the axon increase linearly with the crosslink density, and that both are highly sensitive to the crosslink detachment and reattachment times. Our model explains how active crosslinking with dynein motors generates internal stresses and actively drives axon elongation. We anticipate that our model will allow us to probe a wide variety of molecular phenomena–both in isolation and in interaction–to explore emergent cellular-level features under physiological and pathological conditions.

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“…Narrowing of axonal diameter after nerve elongation has been reported in nerve elongation, which demonstrates the elasticity of peripheral nerves. 12 Axonal diameter on the shortened side was greater 6 weeks after limb shortening. However, elasticity alone cannot account for this finding.…”

Section: Discussionmentioning

confidence: 91%

“…7-10 Kroeber 11 reported a nerve repair procedure using gradual direct nerve elongation. More rapid nerve elongation, that is, 3 mm/day or more, causes paranodal demyelination, segmental demyelination, and Wallerian degeneration, 12 with higher rates causing more severe injury. 13 On the other hand, nerve shortening has received little attention, because it does not cause nerve injury, but nerve shortening caused by joint contracture and bone resection is well known.…”

mentioning

confidence: 99%

The morphologic characteristics of nerve shortening following traumatic bone loss

Abe¹,

Hara²,

Nishiura³

et al. 2009

Journal Orthopaedic Research

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Little is known about peripheral nerve shortening secondary to joint contracture or traumatic bone loss. We used the rat sciatic nerve as a model to study nerve shortening secondary to leg shortening. Nerve shortening was induced by surgically removing 16 mm of the femur. The histology of the ipsilateral and contralateral (control) sciatic nerves were compared at 1 h, 3 weeks, and 6 weeks. Transverse semithin sections of sciatic nerve were prepared and examined; single fibers also were teased from the nerve for study. The epineurium was shortened about 25% at 6 weeks. Axonal diameter was unchanged at 1 h, but increased over time, and was 0.68 mm larger than controls at 6 weeks (p < 0.05). In teased-fiber preparations, internodal length decreased 2.3% at 6 weeks, but not significantly. Peripheral nerve shortening secondary to leg shortening shortens the epineurium, but does not effect on internodal length. ß

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Paranodal demyelination by gradual nerve stretch can be repaired by elongation of internodes

Cited by 23 publications

References 24 publications

Histological and ultrastructural evidence that recurrent laryngeal neuropathy is a bilateral mononeuropathy limited to recurrent laryngeal nerves

Histological and ultrastructural evidence that recurrent laryngeal neuropathy is a bilateral mononeuropathy limited to recurrent laryngeal nerves

Modeling molecular mechanisms in the axon

The morphologic characteristics of nerve shortening following traumatic bone loss

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