Presentation on theme: "Neurobiomechanical Influences on Nerve Conduction Daniel Robbins."— Presentation transcript:
Neurobiomechanical Influences on Nerve Conduction 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. Principle of connectional specificity –States the nerve cells do not connect indiscriminately with one another to form random networks; rather each cell makes specific connections – at particular contact points – with certain postsynaptic target cells but not others.
Nerve Structure and Conduction Dendrites Image taken from a-myelinated-axon-the
Quantifying Conduction Image taken from
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 'Nerve impulse' Produced when 'threshold potential' (- 55mV) reached Sodium channels open –Sodium ions enter –Potential rises to +30mV Potassium channels open –Potassium ions exit –Potential sinks to -70mV The transfer of sodium and potassium molecules during nerve conduction occurs via ion channels. The image below explains how these function. Image taken from
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. Animation taken from
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
Conduction Summary Image taken from potential.jpg Image taken from potential1.jpg
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’.
Tissue Stress Theory Organ SystemStress/Activity Level Low Normal High Excessive Neuromuscular: Max discharge No change Max discharge Axonal rate rate Demyelination Recruitment threshold Recruitment & Activation during threshold Degeneration MVC 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.
Tissue stress theory - Overview of consequences
Neural tension in the upper limb (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. 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 Measurements are presented in proximal (P) or distal (D) millimetres
Linear displacement transducer 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) 213–221 Methods of strain measurement Linear transducers work via mechanical displacement of a sensor which emits an increasing voltage with increased movement. This voltage is externally monitored and used to gauge the distance moved which in turn is related to strain.
Buckle force transducer Kleinrensink G, Stoeckart R, Vleeming A, et al. Mechanical tension in the median nerve: the effects of joint position. Clin Biomech.1995;10:240 –244. Buckle force transducers are more often used on tendons, however sometimes are used on nerves in cadaver studies. They work in a similar principle to that of Golgi tendon organs. A bent ‘E’ shaped clip is placed around the nerve with the limb positioned so the nerve is not in maximum tension. When tension occurs the clip is forced straight. The strain gauge on the clip measures the strain.
Load Cells 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. 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.
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. 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. A similar study by Jou et al. displays the difference in somatosensory evoked potentials (SSEP’s ) when stretch is applied to the left limb only.
Effects of stretch on nerve structure Butler, D. (1991) Mobilisation of the Nervous System, Churchill Livingstone Effects on structure can be split into vascular and functional effects. The major vascular consequence is initially reduced vascular function (especially via oblique blood vessels). Long term vascular issues can also lead to increased pressure via reduced vascular return. 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 Images from Butler (1991) and Topp (2006)
Nerve Damage 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. 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.
Tension at the Brachial Plexus An additional benefit of nerve structure can be observed at a much larger scale (than crimping) in that of the plexus’s. Observe the diagram to the right (the brachial plexus). If force is applied to one of the lower branches in the form of tension, the tension is divided fairly equally amongst the nerve roots. N.B This force is not actually across all nerve roots, for a fuller understanding refer to the paper by Kleinrensink referenced on the buckle transducers slide. Butler, D. (1991) Mobilisation of the Nervous System, Churchill Livingstone
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