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Nerve Conduction Neurobiomechanics
Nerve Conduction Neurobiomechanics
Daniel Robbins
Overview
This presentation is intended to bring together a fuller understanding on nerve conduction and the mechanics that support and influence conduction. It is not intended to be an introduction to nerve conduction, or to replace text book based learning. I aim to summarise the concepts and illustrate areas that I found confusing whilst learning. Hopefully this will aid the learning of others and create some areas for further thought. Initially I will provide a review of the principles of nerve conduction, how the structure of nerves help control conduction and the areas that I found difficult. Next I will cover how mechanical stresses affect nerve conduction, how we measure stresses in nerves and how the structure of nerves deals with these stresses.
Principles of Conduction
Principle of dynamic polarisation.
States that electrical signals within a nerve cell flow only in one direction: from the receiving sites of the neuron (usually dendrites and cell body) to the trigger region at the axon. From there the signal (action positional) is propagated unidirectionally along the length of the axon.
Quantifying Conduction
Conduction/membrane physiology
Action Potential: a) Resting membrane potential (RMP) at -70mV. Na+ on outside and K+ on inside of cell b) As depolarisation reaches threshold of -55mV, the action potential is triggered. Na+ rushes into cell. Membrane potential reaches +30mV on action potential c) Propagation of the action potential
d) Repolarisation occurs with K+ exiting the cell to return to -70mV RMP e) Return of ions (Na+ and K+) to their extracellular and intracellular sites by the sodium/potassium pump
Image taken from https://eapbiofield.wikispaces.com/nervous+system+emily?f=print
Molecular Channels
The transfer of sodium and potassium molecules during nerve conduction occurs via ion channels. The image below explains how these function.
Sodium/Potassium Pump
In addition to ion channels, molecule transfer occurs via sodium/potassium pumps which work in the following manner. Three sodium ions from inside the cell first bind to the transport protein. Then a phosphate group is transferred from ATP to the transport protein causing it to change shape and release the sodium ions outside the cell. Two potassium ions from outside the cell then bind to the transport protein and as the phosphate is removed, the protein assumes its original shape and releases the potassium ions inside the cell.
Confusion???
At this point I always struggled to picture everything in its entirety.
If Molecule transfers provided electrochemical gradients which created the action potentials what constrained them? Intracellular fluids/contents where controlled by membrane physiology but what happens outside of the cell? What controls extracellular fluids? After long, and fairly painful, research I found one article (Nakao et al.1997) which seems to answer the question (at least in rabbit facial nerves anyway). It seems that in addition to intracellular pathways (axoplasmic transport systems), there are also extracellular pathways. To illustrate this we have to go back to nerve structure.
Nakao Y. Tabuchi T.Sakihama N.; Nakajima S. (1997) Extracellular fluid pathway inside the facial nerve fascicles The Annals of otology, rhinology & laryngology 1997, vol. 106, no6, pp. 503-505
Axons Endoneurium (Endo = inner) Intracellular fluid (Intra = inside) Perineurium (Peri = around) Extracellular fluid 1 (Extra = outside) Intrafascicular epineurium (Epi = upon)
Extrafascicular epineurium
Image taken from Topp (2006)
Extracellular fluid 2
Conduction Summary
Neurobiomechanics
At the most basic level tissue stresses can be divided into two areas : type and intensity.
Type is simply: tensile (pulling) or compressive (pressing) Intensity is simply: low, medium, high or excessive.
Mueller and Maluf provided a good overview of the effects of these stresses in their Tissue stress theory.
Stress/Activity Level
Normal High Excessive
rate
Recruitment threshold Activation during MVC
rate
Recruitment
Demyelination
&
threshold Degeneration activation during MVC motor unit synchronization dendritic arborization serotonergic neural activity synaptic transmission
Mueller M, Maluf K. Tissue adaptation to physical stress: a proposed physical stress theory to guide physical therapist practice, education, and research. Phys Ther. 2002;82:383 403.
(A) With elbow extension from 90 of flexion to 0 of flexion, the median nerve bed lengthens and the median nerve glides toward the elbow (converges). With the same joint motion, the ulnar nerve bed shortens and the ulnar nerve glides away from the elbow (diverges).
(B) With wrist extension from 0 of extension to 60 of extension, both nerve beds lengthen; thus, both nerves converge toward the wrist. The magnitude of excursion is greatest closest to the moving joint. Measurements are presented in proximal (P) or distal (D) millimetres
Topp, K.S, Boyed, B.S. Structure and Biomechanics of Peripheral Nerves: Nerve Responses to Physical Stresses and Implications for Physical Therapist Practice. Physical Therapy . Volume 86 . Number 1 . January 2006
Coppietersa,M.W, Butler, D.S. Do sliders slide and tensioners tension? An analysis of neurodynamic techniques and considerations regarding their application. Manual Therapy 13 (2008) 213221
Load Cells
Load cells measure force via a direct attachment, much in the same way the a fisherman will use a strain gauge to measure the weight of a caught fish. The results of the above imposed stretch (displayed as relative strain) are displayed on the next slide, the stretch was imposed for 60 minutes then released. Continuous monitoring of nerve conduction was undertaken simultaneously on both limbs to provide a baseline in addition to effects of stretch on nerve conduction.
Wall E, Massie J, Kwan M, et al. Experimental stretch neuropathy: changes in nerve conduction under tension. J Bone Joint Surg Br. 1992;74:126 129.
Stretch neurobiomechanics
Wall E, Massie J, Kwan M, et al. Experimental stretch neuropathy: changes in nerve conduction under tension. J Bone Joint Surg Br. 1992;74:126 129.
Neurobiomechanics cont.
A similar study by Jou et al. displays the difference in somatosensory evoked potentials (SSEPs ) when stretch is applied to the left limb only.
Jou I, Lai K, Shen C, Yamano Y. Changes in conduction, blood flow, histology, and neurological status following acute nerve-stretch injury induced by femoral lengthening. J Orthop Res. 2000;18:149 155.
The structure of the nerve itself also changes during stretch. The nodes of Ranvier open further as do the Schmidt-Lanterman clefts. Both of these changes affect the levels of local cytoplasm.
Structural defences
Nerve fibres are crimped which helps to provide some defence against stretch induced damage
Nerve Damage
Crimping of fibres is not equal across all fibres. Therefore, when high levels of stretch (or duration) occurs different sections of the nerves structures will be affected before others.
Jou I, Lai K, Shen C, Yamano Y. Changes in conduction, blood flow, histology, and neurological status following acute nerve-stretch injury induced by femoral lengthening. J Orthop Res. 2000;18:149 155.
Questions or feedback???