L14: Biomechanics of Peripheral Nerves
The nerve bed is the interface of the pathway of the nerve and its relationship to surrounding structures.
Peripheral nerve structure
Neurons are composed of a cell body, dendrites, axon and axon terminal. Cell bodies of sensory nerves are located in
the dorsal root ganglion, motor in the ventral horn of the spinal cord and autonomic ones in the lateral horn. Axons are
covered by a myelin sheath (made by Schwann cells) which contain Nodes of Ranvier (small gaps). These speed up the
transmission of signals by insulating the neuron.
Neurons are postmitotic thus cannot divide. If lesioned, they cannot be replaced. As a result, they need to maintain &
renew themselves via O2 and energy (ATP). The cell body synthesizes the components required for structure & function
of the neuron. Neurons have an effective bidirectional system of transport to move molecules along the axon. Axonal
transport going from the cell body to the axon terminal is called anterograde transport. Likewise, transport from the
terminal to the cell body is retrograde transport. This consumes a lot of energy and needs constant sustenance.
Neurons have an endoneurium, perineurium, epineurium and mesoneurium (deep → superficial). Endoneurium
holds bundles of axons+myelin sheaths and is loose connective tissue proper. Perineurium lines the endoneurium
and is a laminar sheath around each fascicle. It’s composed of dense irregular CTP. It contains type I & II collagen fibres,
as well as elastic fibres which are lined in circular, oblique and longitudinal directions. This acts as a biochemical
diffusion barrier. The epineurium is either interfascicular epineurium (holds perineurioma) or episfasciclar (lines
interfascicular epineurium). Lastly, the mesoneurium is perineural tissue that is loose CTP surrounding nerves.
Impulse propagation & axonal transport rely on oxygen and energy. Extrinsic arteries (in mesoneurium) connect to
segmental arteries that connect to the epineurium. This leads to the epineurial arterioles that form an anastomotic
network that provides nerves with the nutrition required. Their diameter can change depending on the nerve’s activity. The
pathway continues to the perineural arterioles and endoneurial capillaries. The latter form the blood-brain barrier.
The relative tortuosity of blood vessels accommodates strain and gliding of the nerve during motion. Lymphatics are
present only in the epineurium, there’s no intrafascicular lymphatic drainage.
The structure of a nerve is constantly changing along its length. There’s a variation in the number of fascicles,
contribution of fascicle & interfascicular epineurium to the total cross-sectional area and endoneurial capillary density
(hence circulation).
Nerve response to loading
Impaired biochemics of nerves can be associated with abnormal nerve function. The response depends on the:
- Type of loading (tension, compression, shear).
- Amount or absence of load, or deformation.
- Rate at which the tissue is loaded.
- Duration of loading (time and repetition).
Elongation of the nerve bed causes simultaneous nerve excursion and strain. Excursion is the displacement or gliding
of the nerve relative to the surrounding nerve bed.
,Excursion of median & ulnar nerves
The direction and magnitude of nerve excursion depends on the anatomical relationship between the nerve and the
axis of rotation in the moving joint. With elongation of the nerve bed, the adjacent segments of the nerve glide
toward the moving joint. With shortening of the nerve bed, the adjacent segments of the nerve realign and glide
away from the moving joint.
Nerve excursion occurs first in the nerve segments immediately adjacent to the moving joint. As limb movement
continues, excursion occurs at nerve segments that are progressively more distant from the moving joint. Similarly, the
magnitude of excursion is greatest in the nerve segments adjacent to the moving joint and is least in the nerve
segments distant from the joint.
For example:
- From 90 - 0 degrees of elbow flexion: median nerve (arm+forearm) moves towards elbow, ulnar nerve glides
away.
- Wrist hyperextension from 0 to 60 degrees: both ulnar & median nerve beds lengthen, so both nerves glide
toward the wrist with a greater amount of movement occurring in the forearm than in the arm.
Strain of ulnar & median nerves
Elongation of the nerve bed will increase strain. The magnitude of strain increase is greatest in the segment closest to
the moving joint. For example:
- Elbow extension from 900 of flexion: Increases tensile strain on median nerve at wrist by 3.7%, decreases
tensile strain on ulnar nerve at wrist & elbow.
- Wrist hyperextension in 00 elbow extension: Increases tensile strain on the median & ulnar nerves at the wrist
and elbow. There’s a greater amount at the moving joint but it still affects the elbow.
During a traditional straight leg raise (hip flexion+knee extension), there’s a:
- 0.5-5mm distal excursion (gliding away) of L4, L5 & S1 spinal nerves.
- Transverse excursion toward the pedicle.
- 2-4% increase in strain of tibial nerve (glides away from hip and knee)
During a modified SLR (ankle dorsiflexion, then hip flexion+knee extension)
Ankle DF
- Tibial nerve glides away from ankle by 9.5mm
- Tibial nerve glides away from knee by 3.1mm
- Sciatic nerve barely has any excursion
Hip flexion+knee extension
- Tibial nerve glides towards ankle by 6.4mm
- Tibial nerve glides towards knee by 12.2mm
- Sciatic nerve glides towards hip by 28mm
,Overall, the tibial nerve has a net movement away from the ankle (3.2mm) and towards the knee (9.1mm). The sciatic
nerve glides towards the hip. Dorsiflexion causes tibial nerve to glide away, SLR causes it to glide towards.
So nerves under no movement/strain have undulations of the fascicles within the nerve and the axons within the
fascicles. Initially, there’s a straightening of the fascicles, which increases the elongation of the axons
(straighten+tension). A nerve retains its elastic properties until the perineurium fails, but the rupture of axons precedes
the rupture of the perineurium.
Nerve response to tension
When a nerve is subjected to tensile forces:
1) Nerve straightens.
2) Fascicles straighten, tensioning the perineurium (not axons).
3) Axons straighten & tension.
4) Some axons rupture (4% strain after axons have straightened).
5) Some fascicles rupture.
6) Once a critical number of fascicles rupture, the entire nerve fails with a rapid plastic deformation.
Endoneurial pressure contributes to nerve stiffness. As the fascicles are elongated, the cross sectional area of the
nerve is reduced. This increases the intrafascicular pressure (which resisted further contraction) and compromises
intramuscular microcirculation. Nerves aren’t homologous structures and pressure is greatest in the middle of the
section during compression (transverse contracture). Transverse contracture is a mode of compression that occurs in the
center of the nerve during tension. Their compliance increases when blood vessels are severed.
Nerves are viscoelastic, thus have a non-linear stress strain curve. In the stress-strain curve (assuming slow loading
rate), the elastic limit is ~20%, ultimate failure is ~30%. Their viscoelastic behaviour means that an increase in strain rate
increases the modulus of elasticity, ultimate failure stress and decreases ultimate strain. A suddenly applied load results
in almost double the stress & strain than a gradually applied load.
, Typical stress values for nerves in tension are:
- Maximum tensile stress (of nerve cross-section): 0.5-3 MPa
- Maximum tensile stress (of funicular area): 1.7-6.2 MPa.
The total load is related more to the total funicular cross sectional area rather than the total nerve cross sectional area.
For a given total funicular area, the strength increases as the number of funiculi does. In spinal nerve roots (no
perineurium or funicular plexus), the elastic limit fails at lower stress & strain.
Nerves also undergo stress-relaxation. Most of the relaxation occurs in the first 20 minutes. Repeated strains over small
amplitudes (8-10%) increase nerve compliance (less stress needed for strain). In response to lengthening, nerves
undergo a transverse contracture (middle portions are stretched).
Nerve response to compression
There are 3 modes of compression: transverse contracture and external (cuff and lateral) compression. Cuff is also called
uniform circumferential pressure.
Cuff is akin to squeezing the nerve (pressure all around nerve) and displaces contents transversely & longitudinally.
Contents move towards the center and longitudinally in both directions. The damage is greatest at the edges of the cuff,
meaning demyelination occurs there. This is because the shear forces are greatest towards the edges. Here the diameter
has been altered and endoneurial pressure has increased, decreasing the volume.
Lateral compression occurs when the nerve is compressed between two parallel surfaces (adjacent structures). It
causes a greater change in shape but not volume, as endoneurial pressure has not increased. Because of this, lateral
compression is not as dangerous/injurious. There is still movement of endoneurial components though.
The relative amounts of fascicular & epineurial tissue varies. In general, fascicular contribution to the CSA is from
30-70%. It is more beneficial to have a greater proportion of nerve CSA being contributed from interfascicular epineurium
tissue (such as fat, areolar loose CTP since they provide cushioning and protect the nerve). This increased epineural
tissue acts as a shock absorber. This is because forces are imposed on the main component of the nerve.
For example, the sciatic nerve contributes 20-30% in the gluteal region.
The nerve bed is the interface of the pathway of the nerve and its relationship to surrounding structures.
Peripheral nerve structure
Neurons are composed of a cell body, dendrites, axon and axon terminal. Cell bodies of sensory nerves are located in
the dorsal root ganglion, motor in the ventral horn of the spinal cord and autonomic ones in the lateral horn. Axons are
covered by a myelin sheath (made by Schwann cells) which contain Nodes of Ranvier (small gaps). These speed up the
transmission of signals by insulating the neuron.
Neurons are postmitotic thus cannot divide. If lesioned, they cannot be replaced. As a result, they need to maintain &
renew themselves via O2 and energy (ATP). The cell body synthesizes the components required for structure & function
of the neuron. Neurons have an effective bidirectional system of transport to move molecules along the axon. Axonal
transport going from the cell body to the axon terminal is called anterograde transport. Likewise, transport from the
terminal to the cell body is retrograde transport. This consumes a lot of energy and needs constant sustenance.
Neurons have an endoneurium, perineurium, epineurium and mesoneurium (deep → superficial). Endoneurium
holds bundles of axons+myelin sheaths and is loose connective tissue proper. Perineurium lines the endoneurium
and is a laminar sheath around each fascicle. It’s composed of dense irregular CTP. It contains type I & II collagen fibres,
as well as elastic fibres which are lined in circular, oblique and longitudinal directions. This acts as a biochemical
diffusion barrier. The epineurium is either interfascicular epineurium (holds perineurioma) or episfasciclar (lines
interfascicular epineurium). Lastly, the mesoneurium is perineural tissue that is loose CTP surrounding nerves.
Impulse propagation & axonal transport rely on oxygen and energy. Extrinsic arteries (in mesoneurium) connect to
segmental arteries that connect to the epineurium. This leads to the epineurial arterioles that form an anastomotic
network that provides nerves with the nutrition required. Their diameter can change depending on the nerve’s activity. The
pathway continues to the perineural arterioles and endoneurial capillaries. The latter form the blood-brain barrier.
The relative tortuosity of blood vessels accommodates strain and gliding of the nerve during motion. Lymphatics are
present only in the epineurium, there’s no intrafascicular lymphatic drainage.
The structure of a nerve is constantly changing along its length. There’s a variation in the number of fascicles,
contribution of fascicle & interfascicular epineurium to the total cross-sectional area and endoneurial capillary density
(hence circulation).
Nerve response to loading
Impaired biochemics of nerves can be associated with abnormal nerve function. The response depends on the:
- Type of loading (tension, compression, shear).
- Amount or absence of load, or deformation.
- Rate at which the tissue is loaded.
- Duration of loading (time and repetition).
Elongation of the nerve bed causes simultaneous nerve excursion and strain. Excursion is the displacement or gliding
of the nerve relative to the surrounding nerve bed.
,Excursion of median & ulnar nerves
The direction and magnitude of nerve excursion depends on the anatomical relationship between the nerve and the
axis of rotation in the moving joint. With elongation of the nerve bed, the adjacent segments of the nerve glide
toward the moving joint. With shortening of the nerve bed, the adjacent segments of the nerve realign and glide
away from the moving joint.
Nerve excursion occurs first in the nerve segments immediately adjacent to the moving joint. As limb movement
continues, excursion occurs at nerve segments that are progressively more distant from the moving joint. Similarly, the
magnitude of excursion is greatest in the nerve segments adjacent to the moving joint and is least in the nerve
segments distant from the joint.
For example:
- From 90 - 0 degrees of elbow flexion: median nerve (arm+forearm) moves towards elbow, ulnar nerve glides
away.
- Wrist hyperextension from 0 to 60 degrees: both ulnar & median nerve beds lengthen, so both nerves glide
toward the wrist with a greater amount of movement occurring in the forearm than in the arm.
Strain of ulnar & median nerves
Elongation of the nerve bed will increase strain. The magnitude of strain increase is greatest in the segment closest to
the moving joint. For example:
- Elbow extension from 900 of flexion: Increases tensile strain on median nerve at wrist by 3.7%, decreases
tensile strain on ulnar nerve at wrist & elbow.
- Wrist hyperextension in 00 elbow extension: Increases tensile strain on the median & ulnar nerves at the wrist
and elbow. There’s a greater amount at the moving joint but it still affects the elbow.
During a traditional straight leg raise (hip flexion+knee extension), there’s a:
- 0.5-5mm distal excursion (gliding away) of L4, L5 & S1 spinal nerves.
- Transverse excursion toward the pedicle.
- 2-4% increase in strain of tibial nerve (glides away from hip and knee)
During a modified SLR (ankle dorsiflexion, then hip flexion+knee extension)
Ankle DF
- Tibial nerve glides away from ankle by 9.5mm
- Tibial nerve glides away from knee by 3.1mm
- Sciatic nerve barely has any excursion
Hip flexion+knee extension
- Tibial nerve glides towards ankle by 6.4mm
- Tibial nerve glides towards knee by 12.2mm
- Sciatic nerve glides towards hip by 28mm
,Overall, the tibial nerve has a net movement away from the ankle (3.2mm) and towards the knee (9.1mm). The sciatic
nerve glides towards the hip. Dorsiflexion causes tibial nerve to glide away, SLR causes it to glide towards.
So nerves under no movement/strain have undulations of the fascicles within the nerve and the axons within the
fascicles. Initially, there’s a straightening of the fascicles, which increases the elongation of the axons
(straighten+tension). A nerve retains its elastic properties until the perineurium fails, but the rupture of axons precedes
the rupture of the perineurium.
Nerve response to tension
When a nerve is subjected to tensile forces:
1) Nerve straightens.
2) Fascicles straighten, tensioning the perineurium (not axons).
3) Axons straighten & tension.
4) Some axons rupture (4% strain after axons have straightened).
5) Some fascicles rupture.
6) Once a critical number of fascicles rupture, the entire nerve fails with a rapid plastic deformation.
Endoneurial pressure contributes to nerve stiffness. As the fascicles are elongated, the cross sectional area of the
nerve is reduced. This increases the intrafascicular pressure (which resisted further contraction) and compromises
intramuscular microcirculation. Nerves aren’t homologous structures and pressure is greatest in the middle of the
section during compression (transverse contracture). Transverse contracture is a mode of compression that occurs in the
center of the nerve during tension. Their compliance increases when blood vessels are severed.
Nerves are viscoelastic, thus have a non-linear stress strain curve. In the stress-strain curve (assuming slow loading
rate), the elastic limit is ~20%, ultimate failure is ~30%. Their viscoelastic behaviour means that an increase in strain rate
increases the modulus of elasticity, ultimate failure stress and decreases ultimate strain. A suddenly applied load results
in almost double the stress & strain than a gradually applied load.
, Typical stress values for nerves in tension are:
- Maximum tensile stress (of nerve cross-section): 0.5-3 MPa
- Maximum tensile stress (of funicular area): 1.7-6.2 MPa.
The total load is related more to the total funicular cross sectional area rather than the total nerve cross sectional area.
For a given total funicular area, the strength increases as the number of funiculi does. In spinal nerve roots (no
perineurium or funicular plexus), the elastic limit fails at lower stress & strain.
Nerves also undergo stress-relaxation. Most of the relaxation occurs in the first 20 minutes. Repeated strains over small
amplitudes (8-10%) increase nerve compliance (less stress needed for strain). In response to lengthening, nerves
undergo a transverse contracture (middle portions are stretched).
Nerve response to compression
There are 3 modes of compression: transverse contracture and external (cuff and lateral) compression. Cuff is also called
uniform circumferential pressure.
Cuff is akin to squeezing the nerve (pressure all around nerve) and displaces contents transversely & longitudinally.
Contents move towards the center and longitudinally in both directions. The damage is greatest at the edges of the cuff,
meaning demyelination occurs there. This is because the shear forces are greatest towards the edges. Here the diameter
has been altered and endoneurial pressure has increased, decreasing the volume.
Lateral compression occurs when the nerve is compressed between two parallel surfaces (adjacent structures). It
causes a greater change in shape but not volume, as endoneurial pressure has not increased. Because of this, lateral
compression is not as dangerous/injurious. There is still movement of endoneurial components though.
The relative amounts of fascicular & epineurial tissue varies. In general, fascicular contribution to the CSA is from
30-70%. It is more beneficial to have a greater proportion of nerve CSA being contributed from interfascicular epineurium
tissue (such as fat, areolar loose CTP since they provide cushioning and protect the nerve). This increased epineural
tissue acts as a shock absorber. This is because forces are imposed on the main component of the nerve.
For example, the sciatic nerve contributes 20-30% in the gluteal region.
