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Original Article

Surgical decompression of the peroneal nerve in the

correction of lower limb deformities: A cadaveric study
Monica Paschoal Nogueira, Arnaldo José Hernandez1, César Augusto Martins Pereira2, Dror Paley3, Anil Bhave4
Department of Orthopedics and Traumatology, State Public Hospital (HSPE), São Paulo, 1Department of Orthopedics and
Traumatology, Institute of Orthopedics and Traumatology, University of São Paulo, 2Institute of Orthopedics and Traumatology,
LIM 4 – Biomechanics Laboratory, University of São Paulo, SP, Brazil, 3The Paley Institute, St. Mary’s Medical Center, West
Palm Beach, Florida, 4Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore, Baltimore, Maryland, USA

Abstract Background: The peroneal nerve is often stretched during limb lengthening and deformity correction.
If the nerve becomes entrapped under the peroneal muscle fascia and/or anterior intermuscular
septum, decompression is indicated to treat nerve compromise.
Purpose: The purpose of this study was to quantify peroneal nerve tension after varus osteotomy
of the proximal tibia and before and after nerve decompression.
Methods: A device, which consisted of a force transducer connected perpendicularly by a hook to
the nerve and integrated to a personal computer, was able to indirectly measure the nerve rigidity
in 14 lower limbs (seven cadaveric specimens). The nerve was neither cut nor disrupted from its
anatomic tract by the rigidity measuring device. We measured the amount of peroneal nerve rigidity
before varus angulation, after varus angulation of a proximal tibial osteotomy, and after peroneal
nerve decompression in the varus angulation position.
Results: Peroneal nerve rigidity increased significantly after limb was angulated into varus (P = 0.0002)
and was reduced significantly after decompression (P = 0.0003). No significant difference was noted
between measurements obtained before varus angulation and measurements obtained after nerve
decompression (P = 0.3664).
Conclusions: Varus osteotomy of the proximal tibia significantly increases peroneal nerve rigidity. Peroneal
nerve rigidity after decompression is not significantly different from nerve rigidity before varus correction.
Clinical Relevance: This study provides biomechanical evidence of the efficacy of nerve
decompression in two specific anatomic sites (peroneus longus muscle fascia and lateral,
intermuscular septum) in relieving the increase in peroneal nerve rigidity that occurs in association
with procedures that stretch the nerve such as limb lengthening and deformity correction.

Key Words: Cadaver, decompression, lower extremity, peroneal nerve, surgical

Address for correspondence:

Prof. Monica Paschoal Nogueira, 426 Maracatins Avenue, Apt. 402, São Paulo 04089‑000, SP, Brazil. E‑mail: monipn@uol.com.br
Received: 19.04.2016, Accepted: 21.07.2016

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How to cite this article: Nogueira MP, Hernandez AJ, Pereira CA, Paley
DOI: D, Bhave A. Surgical decompression of the peroneal nerve in the correction
10.4103/2455-3719.190708 of lower limb deformities: A cadaveric study. J Limb Lengthen Reconstr
2016;2:76-81.

76 © 2016 Journal of Limb Lengthening & Reconstruction | Published by Wolters Kluwer - Medknow
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Nogueira, et al.: Peroneal nerve decompression: Cadaveric study

Introduction nerve splits in the lateral compartment into superficial and

deep branches. The superficial branch continues unimpeded
Peroneal nerve entrapment and injury are well‑known
through the lateral compartment, whereas the deep branch
complications of acute deformity correction and of limb
has to pass under the intermuscular septum (second tunnel)
lengthening.[1‑12] The primary entrapment described is at
between the lateral and anterior compartments to enter the
the neck of the fibula. Peroneal nerve decompression is a
anterior compartment of the leg. The intermuscular septum
well‑recognized technique for the treatment of peroneal
extends from the anterior fascia covering the anterior and lateral
nerve palsy and entrapment.[7,13] For prophylactic use, the
compartments to the interosseous membrane between the tibia
indication for peroneal nerve compression is a nerve at
and the fibula at its deepest extent.
risk (e.g., acute valgus correction of tibia of more than 5º,
acute valgus correction of the femur of more than 5º). For
Nerve stretch injuries are caused when distraction overcomes
therapeutic decompression, the indication is when there are
the nerve fibers’ elastic and plastic properties. These injuries
signs or symptoms of nerve problems (e.g. referred pain to the
have been the subject of many studies.[4,16‑18] It has been
dorsum of foot, hypersensitivity or hyposensitivity, weakness,
assumed that nerve injury resulting from limb lengthening and
or paralysis of muscles). The potential complications of nerve
from acute valgus to varus deformity correction is a stretch
decompression are nerve injury, infection, and hematoma.
injury. The report of Nogueira et  al.[14] has suggested that
Nogueira et al.[14] found that peroneal nerve decompression is
the problem may be one of the nerve entrapments instead of
efficacious for the treatment of peroneal nerve injury secondary
stretch injury.
to acute and gradual deformity correction and lengthening.
The purpose of this study was to quantify the tension of the
Paley[15] identified two sites of entrapment and described a
peroneal nerve after varus osteotomy of the proximal tibia and
surgical technique to decompress both tunnels [Figure 1a‑e].
before and after nerve decompression. If the entrapment sites
The first entrapment tunnel is located at the fascial arcade
act as tether points to the peroneal nerve when it is placed
of the peroneal muscles over the common peroneal nerve.
under tension, then we would expect to see a reduction of
After passing under the fascial arcade, the common peroneal
tension after decompression of the two sites of entrapment.
This finding would support the rationale of therapeutic and
perhaps prophylactic peroneal nerve decompression when the
nerve is placed under tension by surgery or injury.

Materials and Methods

a b
A preliminary cadaveric study was conducted to develop the
protocol and the device to measure nerve rigidity. Rigidity
c
was used as an indirect measurement of nerve tension. Then,
14 cadaveric lower limbs from seven adult males were studied.

Preliminary cadaveric study

d e
Figure 1: Paley’s technique [15]
of two‑tunnel peroneal nerve
decompression are shown. (a) Peroneal nerve passes through two
potential entrapment tunnels: the peroneal fascia and the intermuscular
septum. (b) Short oblique skin incision is made in the same direction
as the nerve (Step 1). (c) Superficial peroneal fascia is divided outside
of the peroneal muscles (Steps 2 and 3), and the common peroneal
nerve is identified. (d) Peroneal muscle fascia is cut. The underlying
peroneal muscles are retracted medially exposing the deep peroneal
muscle fascia, which is then divided (Step 4). (e) Transverse fascial
incision is extended toward the tibia crossing the intermuscular septum
between the anterior and lateral compartments of the leg. The muscle
on either side is retracted, and the septum is transected under direct
vision (Step 5). The deep peroneal nerve passes under this septum,
but it is not visualized (Figure and legend reprinted with permission)
Journal of Limb Lengthening & Reconstruction | Jul-Dec 2016 | Vol 2 | Issue 2 77
In an initial group of 20 cadaveric specimens, the relationship
between the peroneal nerve and its branches to the surrounding
structures was studied, and nerve decompression was
performed. During decompression, the deep peroneal nerve
branch that passes under the anterior intermuscular septum
was identified. These cases were necessary to study the anatomy
and to define the protocol. During this preliminary study, a
device was developed to measure rigidity.
Description of the nerve rigidity device
The device consists of a traction assembly, control unit, signal
conditioner, and an adjustable base. The mobile portion
of the traction assembly contains the electric extensometer
(strain gauge), nylon wire, and connection hook [Figure 2]. The
mobile portion is moved through a screw and nut system that
is connected to a step motor. The motor moves the mobile part
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Nogueira, et al.: Peroneal nerve decompression: Cadaveric study
of the device and pulls the connection hook that is attached
to the nerve.
The force transducer is mounted to an aluminum blade. One
end of the force transducer blade is connected to the mobile
portion of the device, and the other end is connected to the
hook by a 0.32 mm diameter nylon wire. Two 120‑Ω electric
extensometers (strain gauge model EA‑06‑240 LZ‑120;
Measurements Group, Inc., Raleigh, North Carolina) were
glued to the force transducer blade (one on each side of the
blade). The extensometers measure minute deformations caused
by tension. When the hook pulls the nerve, the resulting blade
flexion deformation is read by the signal conditioner (model
P3500, Measurements Group, Inc., Raleigh, North Carolina).
The control unit contains an electronic microprocessor that
controls the step motor and the advancement of the mobile
part with an accuracy of 0.01 mm. The value measured by the
signal conditioner (i.e., microdeformation [µm/m]) is sent to
a computer through a serial port. A computer program was
developed to control the device, to record the data, and to plot
a graph of force versus nerve deformation. The adjustable base
allows the device to be correctly positioned relative to the nerve,
with the connection hook and the nylon wire perpendicular to
the longitudinal axis of the nerve.
Parameters developed during the preliminary study
A preliminary control was performed with twenty cadavers
to determine the maximum elastic range of the nerve before
permanent deformation occurred. The maximum values found
were 0.78 N for force, 20 mm displacement, and 10 mm/min
for velocity of displacement. Based on these findings, these
parameters were not exceeded during the remainder of the study.
The transducer was calibrated with eight standard 10 g
weights that were measured on a digital precision scale with
Figure 2: Illustration shows device for the measurement of
nerve rigidity. Inset, mobile portion of the traction assembly.
A: Connection hook, B: Nylon wire, C: Force transducer blade,
D: Electric extensometer (strain gauge), E: Mobile part, F: Guide rod,
G: Trapezoidal screw, H: Step motor
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an accuracy of 0.1 g (V1200; Acculab, São Paulo, Brazil).
The transducer was calibrated using the standard weights in
10 g increments from 10 g to 80 g. The microdeformation
measured by the transducer was correlated to the mass of the
standard weight that was placed on the device. Based on these
data, we were able to use a computer to calculate the force
needed to cause a certain deformation of the transducer with
an accuracy of 0.2 g.
Cadaveric study
Fourteen lower limbs from seven adult male cadavers were
studied. The cadavers were 34–85 years of age at the time
of death (average age, 56 years) and did not have any known
pathologic abnormalities of the lower limb. The knee was
flexed 60º, as measured with a goniometer, and the lower
limb was fixed to the table with limb holders placed on the
proximal thigh and foot. Care was taken to avoid compressing
the sciatic nerve. An oblique, 5 cm incision was made at the
level of the fibular neck. The superficial fascia was dissected
under the subcutaneous fat, and the common peroneal nerve
was identified just before it entered underneath the peroneal
longus muscle fascia. The nerve was dissected free over a
distance of 1 cm. Two horizontal, 1.5 cm collinear incisions
were made just distal to the tibial tuberosity. A Gigli saw was
passed percutaneously and subperiosteally according to the
technique described by Paley.[9]
A monolateral external fixator was applied on the anteromedial
face of the tibia using two proximal threaded pins placed above
the tibial tuberosity and inclined inferiorly 30°, and two distal
pins placed at the level between the medium and distal thirds of
the limb, perpendicular to the tibia. All the threaded pins were
applied in the same plane and were connected to the fixator.
The two proximal pins were angulated 30° relative to the two
distal ones [Figure 3a].
a b
Figure 3: (a) Leg is shown before varus angulation of the proximal
tibial osteotomy.  (b) Monolateral fixator has been adjusted to position
the leg in varus
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Nogueira, et al.: Peroneal nerve decompression: Cadaveric study

A fibular osteotomy was performed at the transition between between rigidity measurements obtained before the varus
the middle and distal thirds of the leg. A 3 cm longitudinal angulation (i.e., the initial measurement) and after the nerve
incision was made, and the region between the lateral and decompression (i.e., the final measurement) (P = 0.3664).
posterior compartments of the leg was dissected. The fibula was At least two measurements were always obtained. The time
cut using the multiple drill hole technique and an osteotome; between each measurement varied from 15 to 20 min. The two
the tibia was divided with the Gigli saw. rigidity measurements either remained the same or increased
during this time. A decrease in rigidity was not observed unless
After the monolateral fixator was applied and the osteotomy a decompression was performed.
was performed, the first nerve rigidity test was performed
using the traction assembly [Figure 4]. This measurement
was obtained before moving the leg into varus. The tibia
Discussion
was then angulated 30° into varus and was fixed in that The goal of this study was to quantify the tension of the
position [Figure 3b]. Only the external fixator was adjusted to peroneal nerve after varus osteotomy of the proximal tibia
position the leg in varus. A second nerve rigidity test was then and before and after nerve decompression at two specific
performed. The peroneal nerve was decompressed by releasing
Table 1: Rigidity values
both tunnels [Figure 1a‑e]. A third set of measurements was
Side* Rigidity (N/m)
then obtained. Before varus After varus After nerve
angulation angulation decompression
Statistical methods Specimen 1 L 83.75 150.14 89.63
Each nerve rigidity test was performed twice, and the mean Specimen 1 R 72.67 101.01 109.15
value of the two readings was used for statistical analysis. The Specimen 2 L 94.98 117.68 118.71
Specimen 2 R 91.05 128.81 96.69
average rigidity measurements (obtained before angulating the Specimen 3 L 110.03 116.99 113.90
osteotomy, after varus angulation of the leg, and after the nerve Specimen 3 R 133.13 183.53 121.31
had been decompressed in the varus angulation position) were Specimen 4 L 164.51 201.13 129.50
Specimen 4 R 145.33 185.54 127.68
studied using analysis of variance to repetitive measurement. Specimen 5 L 161.42 184.90 144.50
P < 0.05 was considered statistically significant. Specimen 5 R 112.78 170.19 127.29
Specimen 6 L 174.36 183.14 152.54
Specimen 6 R 128.03 142.78 136.80
Results Specimen 7
Specimen 7
L
R
165.31
136.70
166.27
138.27
114.88
106.60
The average rigidity value before the varus angulation was Mean 126.72 155.03 120.66
126.72 ± 33.28 N/m. The rigidity measurements of the SD 33.28 31.39 17.47
SEM 8.90 8.39 4.67
peroneal nerve increased significantly after varus angulation Minimum value 72.67 101.01 89.63
were performed (average rigidity value, 155.03 ± 31.39 N/m; Maximum value 174.36 201.13 152.54
P = 0.0002) [Figure 5 and Table 1]. After nerve decompression *R: Right, L: Left. SD: Standard deviation, SEM: Standard error of the
mean
was performed, the rigidity measurement decreased
significantly (average rigidity value, 120.66 ± 17.47 N/m;
P  = 0.0003). No statistical difference was observed

Figure 5: Graph shows average rigidity measurements obtained before

Figure 4: Illustration shows the cadaver in a supine position. The nerve
rigidity device is attached to the peroneal nerve. Inset, photograph
shows the connection hook attached to the peroneal nerve
varus angulation, after varus angulation, and after peroneal nerve
decompression. The bars show the confidence intervals. A significant
difference in rigidity was noted between the measurements obtained
before varus angulation and after varus angulation (P = 0.0002) and
between the measurements obtained after varus angulation and
after nerve decompression (P  =  0.0003). No significant difference
in rigidity was observed before varus angulation and after nerve
decompression (P = 0.3664). After the peroneal nerve decompression,
the rigidity returned to normal

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Nogueira, et al.: Peroneal nerve decompression: Cadaveric study
sites: Peroneus longus muscle fascia and lateral, intermuscular
septum. Peroneal nerve injury is a well‑recognized complication
that is associated with acute angular correction and with
limb lengthening. Mont et  al.[7] reported that correction
of deformities of more than 15° of valgus put the nerve at
risk when performing total knee arthroplasty and achieving
correction in varus. When nerve decompression was performed
on patients undergoing limb lengthening, intraoperative
findings included hemorrhage, nerve flattening, narrowing
of the nerve at the entrance of the fascial tunnel, and
reduction of the  paraneural vascularization  at the site of
compression. These findings are typical of nerve entrapment
and not of stretch injury. Paley and Herzenberg[14] used
peroneal nerve decompression both prophylactically and
therapeutically when performing acute valgus to varus
deformity corrections about the knee. Intraoperative potential
nerve monitoring was used in some cases, and a sudden loss
of nerve potentials was observed minutes after acute valgus
to varus correction. Immediate decompression of the nerve
leads to restoration of normal potentials.[14]
Nogueira et  al.[14] documented that when peroneal nerve
injuries are caused by limb lengthening, acute deformity
correction, or gradual deformity correction, the timing of
decompression affected the rate of nerve recovery. Performing
an early decompression resulted in patients experiencing an
early recovery, and performing a late decompression resulted in
patients experiencing a late recovery. However, this study failed
to find a relationship between nerve injury and the amount or
percent of lengthening, suggesting again that entrapment and
not stretch injury is the cause.
Nerve entrapment might also be a factor when stretch or
compression injury occurs. Injury leads to inflammation. The
peroneal tunnels are normally very tight, leaving little space to
accommodate additional swelling. Consequently, a secondary
injury might follow the original stretch injury when the
nerve swells against the nonexpandable walls of the peroneal
tunnels. For this reason, early decompression is warranted
while the initial injury is recoverable; the secondary injury
might make the situation irrecoverable. This is suggested by
the observation that the longer the interval between the injury
and the decompression, the longer the interval until recovery
of the nerve.[14] Therapeutic decompression is the standard of
care for the median nerve of the hand. The carpal tunnel is
much more capacious than the peroneal tunnels. Prophylactic
or therapeutic nerve decompression within 24 hr should also
become the standard of care for the peroneal nerve.
If tension can precipitate entrapment, then decompression
should be able to reduce the tension on the peroneal nerve. We
tested this hypothesis by creating a cadaver model of acute 30°
80 Journal of Limb Lengthening & Reconstruction | Jul-Dec 2016 | Vol 2 | Issue 2
lateral opening wedge varus osteotomy. This clinical situation
is known to precipitate peroneal nerve injury. As expected, the
rigidity (our indirect measurement used to estimate tension)
of the peroneal nerve increased significantly after the varus
angulation and showed no sign of decreasing with time if no
decompression was performed. After the decompression, the
rigidity of the peroneal nerve decreased and even returned to
the prevarus angulation level [Figure 5]. This is direct evidence
that the fascia of the peroneal tunnels tethers the peroneal nerve
and that this tether can be surgically relieved.
Previous studies measured tension by removing the nerve and
obtaining measurements.[17,19‑21] We wanted to measure the
tension of the peroneal nerve while it was in its anatomic
tract. To measure tension, sensors would have to be applied in
a standard fashion. It is difficult to create a standard protocol
and to maintain consistency across all cadaveric specimens that
are a limitation of this study. Therefore, the measurement of
tension was obtained indirectly. The rigidity was calculated by a
major or minor resistance of the nerve to perpendicular traction.
The biomechanical findings of this study were complementary
to the clinical findings of Nogueira et  al.[14] and reinforced
that it is not necessary to discontinue lengthening or undo an
angular correction if the nerve is decompressed promptly. In
this study, both peroneal tunnels were decompressed to achieve
the final rigidity measurement. We did not separately measure
the rigidity change after decompressing only the first tunnel
versus decompressing both tunnels. This would be a worthwhile
follow‑up study.
Conclusion
Performing an acute 30° proximal tibial varus angulation
causes an increase of peroneal nerve rigidity. Decompressing
the peroneal nerve reduces the rigidity to the initial level. This
study supports the efficacy of peroneal nerve decompression
both prophylactically and therapeutically when a corrective
varus osteotomy of the proximal tibia is performed. The results
of this study suggest that the mechanism of nerve injury might
be nerve entrapment rather than stretch injury.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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