THE POSTERIOR LAYER OF LUMBAR FASCIA AS A POTENTIAL SOURCE OF LOW BACK PAIN

Abstract

The posterior layer of the lumbar fascia is innervated by unmyelinated nerve endings which have a nociceptive capacity. Although indications about tissue injuries in this tissue have been documented, it is not clear to which degree these contribute to the frequent finding of idiopathic low back pain in modern humans. In vivo studies on low back pain patients revealed a reduced shear-motion, which suggests the involvement of an altered fascial architecture in this pathology. In addition, in vivo studies with experimental elicitation of back pain via stimulation of this fascia layer suggest an increased sensitivity of dorsal horn neurons for potential nociceptive stimulation of lumbar fascia. Taken together these findings suggest the posterior layer of the lumbar fascia could possibly be a frequent source of low back pain. However, further studies are needed for a more detailed understanding.

Full text

9th Interdisciplinary World Congress on Low Back
and
Pelvic Girdle Pain
THE POSTERIOR LAYER
OF
LUMBAR FASCIA AS A POTENTIAL
SOURCE
OF
LOW BACK PAIN
Schleip
R.,
Klingler
W.
Fascia Research Group, Division
of
Neurophysiology, Ulm University, Germany
Abstract: The posterior layer
of
the
lumbar fascia
is
innervated
by
unmyelinated nerve endings
which have a nociceptive capacity. Although indications about tissue injuries in this tissue have
been documented, it
is
not
clear
to
which
degree
these contribute
to
the
frequent finding
of
idiopathic
low
back pain in modern humans.
In
vivo studies on
low
back pain patients revealed
a reduced shear-motion, which suggests the involvement
of
an altered fascial architecture in this
pathology.
In
addition,
in
vivo studies with experimental elicitation
of
back pain via stimulation
of
this fascia layer suggest an increased sensitivity
of
dorsal horn neurons
for
potential nociceptive
stimulation
of
lumbar fascia. Taken together these findings suggest
the
posterior layer
of
the
lumbar fascia could possibly be a frequent source
of
low back pain.
However, further studies are needed
for
a more detailed understanding.
Background: It
is
generally accepted
that
disc pathologies account only
for
a minority
of
low back
cases as a causal factor (Jensen
et
al. 1994). The majority
of
low
back pain cases are idiopathic.
Based on this background Panjabi (2006) proposed that microinjuries in lumbar connective tissues
may result in impaired function
of
embedded
proprioceptive mechanoreceptors, which then leads
to
muscle control dysfunction and subsequent biomechanical impairments.
Although this model considered paraspinal connective tissues only, other authors suggested that
posterior layer
of
the
lumbar fascia should also
be
involved as a candidate for similar microinjuries
(Schleip
et
al. 2007; Langevin
et
al.
2011).
Histological Investigations: Dittrich
(1963),
as
well
as
Bednar et
al.
(1995), examined histological
pieces
of
posterior layer
of
lumbar fascia taken from patients with low back pain during lumbar
surgery. They documented frequent signs
of
injury and inflammation (Dittrich, 1963; Bednar et
al.
1995). Several histological examinations documented the presence
of
clearly nociceptive nerve
endings in this tissue layer (Table
1).
These studies, taken together, indicate that the lumbar fascia
may
be
able
to
elicit pain, such as in at least some cases
of
low back pain. None
of
these studies
included a comparison with healthy age-matched patients. It therefore cannot be excluded, that
no difference may exist
in
fascial properties between
low
back patients and healthy patients.
Moreover,
the
above studies cannot confirm whether or not the described tissue dynamics are in
fact a common source
of
low back pain.
Reduced Shear-Motion: More recently, Langevin et
al.
(2011)
conduced a comparison
of
the
posterior layer
of
lumbar fasciae
of
chronic
low
back pain patients with those
of
group
of
age-
matched controls. Using ultrasound cine-recording, this study examined
the
shear-motion within
the posterior layer
of
the
posterior layer
of
the
lumbar fascia during passive lumbar flexion. The
low back pain group was found
to
express a significant reduction
in
shear-strain compared with
their healthy controls. Interestingly,
the
patients
in
this study showed increased thickness
in
this
layer
of
the lumbar fascia. However, this change
in
thickness was found
to
be
significant
in
male
patients only. The reported reduction in shear-strain could
of
course
be
due
to
tissue adhesions
induced
by
previous injury or inflammation. It would then be consistent with
the
proposed etiology
suggested
by
Dittrich
(1963)
and Bednar et al. (1995). However, these findings cannot anwer the
question whether
the
observed tissue changes are cause or effect
of
low
back pain. It is indeed
possible that the tissue alterations are merely
the
result
of
a reduction (immobility) in everyday
lumbar movements
in
low
back pain patients.
In Vivo Studies: Several studies have explored the option
of
stimulating posterior layer
of
lumbar
fascia
for
the
purpose
of
eliciting nociceptive responses in vivo. Pedersen
et
al. (1956) pinched the
corresponing fascia layer
of
decerebrated cats and was able
to
elicit spastic contractions in their
back muscles (mostly ipsilateral), and also in their hamstring and gluteal muscles
of
the
same leg.
Progress in Evidence Based Diagnosis and Treatment
131

132
9th Interdisciplinary World Congress
on
Low
Back
and
Pelvic Girdle Pain
The observed responses were much stronger in response
to
pinching
the
fascia than pinching
the
underlying muscle tissues. This finding was contrasted
to
the
findings
of
an extensive investigation
done
by
Kuslich
et
al.
(1991)
that used progressive local anesthesia in
low
back pain patients during
disc surgery. While mechanical stimulation
of
the
nerve root induced strong and often radiating
back pain symptoms,
the
same stimulation on
the
posterior layer
of
lumbar fascia failed
to
elicit
similar responses
in
the majority
of
patients. A more recent examination by Taguchi
et
al.
(2008),
on the other hand demonstrated that pinching the posterior layer
of
lumbar fascia
of
rats as well as
applying hypertonic saline
to
it with a cotton ball induced clear responses in a significant number
of
neurons
of
the dorsal horn
of
their spinal cord. Since application
of
hypertonic saline is known
to
be
the
most effective stimulus for type
VI
afferents,
the
authors interpreted their findings as
evidence for a nociceptive functional capacity
of
the
lumbar fascia.
Interestingly,
the
same study demonstrated that inducing a chronic inflammation in
the
local
musculature lead
to
a threefold increase in
the
number
of
dorsal horn neurons that are responsive
to
stimulation
of
the posterior layer
of
lumbar fascia. Their finding is reminiscent
of
the
study
of
Gibson et
al.
(2009), which reported that hypertonic saline strongly increased pain when injected
into
the
investing fascia
of
a muscle exposed
to
delayed onset soreness after eccentric exercise,
although no comparable response was observed when
the
substance was injected into
the
actual
muscle itself or into
the
non-exercised muscle in
the
contralateral leg.
Conclusion: The innervation
of
posterior layer
of
lumbar fascia clearly supports a nociceptive
capacity. The nociceptive capacity suggests at least three different mechanisms for fascia-based
low
back pain sensation:
1)
microinjuries and resulting irritation
of
nociceptive nerve endings in
the posterior layer
of
lumbar fascia may directly induce back pain;
2)
tissue deformations due
to
injury, immobility or excessive may impair proprioceptive signaling, which
by
itself could induce
an augmentation in pain sensitivity via
an
activity-dependent sensitization
of
wide dynamic range
neurons; and finally,
3)
irritation in other tissues innervated
by
the same spinal segment could
elicit an increased sensitivity in
the
posterior layer
of
lumbar fascia, which would then respond
with nociceptive signaling, even
to
gentle stimulation. The question whether or
not
each
of
these
scenarios (or various combinations
of
them) manifest in
low
back pain patients, or
how
often
they
occur, provides an important but also challenging background for future investigation. Clarification
of
these questions promises
to
offer valuable contributions
for
the treatment and prevention
of
back pain.
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Bednar
DA,
Orr
FW,
Simon
GT
(1995) Observations on the pathomorphology
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the thoracolumbar
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GJ,
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Dittrich
RJ
(1963)
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Hirsch C (1963) The anatomical basis for
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Progress in Evidence Based Diagnosis and Treatment

9th Interdisciplinary World Congress
on
Low
Back
and
Pelvic Girdle Pain
13.
Pedersen
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Blunck
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Gardner E (1956) The anatomy
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DL
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16.
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T,
Hoheisel U, Mense S (2008) Dorsal horn neurons having input from low back structures
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Tesarz J, Hoheisel U, Wiedenhofer 8, et
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(2011)
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of
the thoracolumbar fascia
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302-308
18.
Yahia
L,
Rhalmi
S,
Newman
N,
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(1992) Sensory innervation
of
human thoracolumbar fascia. An
immunohistochemical study.
Acta
Orthop Scand 63, 195-197
Study
Tissue
source
Method
Nerve
endings
Remarks
fnunrl~
Stilwell1957 Macaca mulatta Methylene blue. Rich supply
by
Study included
(n=17),
FNE.
Groups
of
human tissues
rabbit
(n=4)
large Pacinian too. However, no
corpuscles at nerve type analysis
penetration
was performed on
points
of
dorsal those.
rami through
the
fascia. Also
small Pacinian-
like and Golgi-
Mazzon
i
rnrnooc::rl<>c:: *
Hirsch
et
al
Human
(n=?)
Methylene blue
FNE,
Number
of
donors
1963 "complex
not
mentioned.
unencapsulated
Also found:
endings"·
unmyelinated
nerve fiber network
associated with
hloorl
VPC::C::PIC::
Yahia
et
al. Human
(n=7)
IH:
Neurofilament
FNE,
Ruffini,
1992 protein and
S-1
00
Pacini.*
nrntoin
Bednar
et
al
Human
(12),
IH:
neuron-specif-
No
terminal Study performed
1995 ic enolase nerves found. * with CLBP patients
only.
Found: small
peripheral nerve
bundles at the
margins and
in
association with
.:;mAll \/oc::c::olc::
Corey et al.
Rats
(5)
3-D reconstruc-
CGRP
positive Also found: Some
2011
tions
of
thick
FNE.
non-terminating
(30-80J..1m)
tissue
CGRP-Iabeled
sections. fibers along blood
vessels,
IH:
PGP9.5,
CGRP,
f:oc::t
hlooo
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9th Interdisciplinary World Congress on Low Back
and
Pelvic Girdle Pain
Tesarz
et
al.
2011
Benetazzo
et
al.
2011
Hoheisel
et
al.
2015
Mense
et
al.
2016
Rat
(n-8)
Human
(n=3)
Human
(2)
Rats
(10)
Rats
(5)
IH:
PGP
9.5,
CGRP,
SP
Rich innervation
TH, with presumable
nociceptive
nerve edings
(PG,
CGRP).
3D reconstruction
of
serial sections. Study did not
investigate
n e r v e
terminations.
IH:
S100
IH:
PGP
9.5,
TH,
CGRP,
SP
IH:
PGP
9.5,
TH,
CGRP,
SP,
TRPV1
Rich innervation
with presumable
nociceptive
nerve edings
(PG,
CGRP).
Rich
innervation
with presumable
nociceptive
nerve edings
(PG,
CGRP,
TRPV1\
Most nerve fibers
located
in
the outer
layer
of
the lumbar
fascia and
in
the
subcutaneous
'tio:;o:;u~-
Small nerves
(mean diameter
15
iJm)
found, flowing
from the superficial
sub-layer into
the adjacent
subcutaneous
loose connective
tissue. No
nerves visible in
intermediate and
deep sub-layers.
lnflamation
of
the
fascia induced
an
increase
of
presumably
nociceptive fibers.
lnflamation
of
the
fascia induced
an
increase
of
presumably
nociceptive fibers
Table
1:
Histological studies exploring
the
superficial layer
of
the
PLF.
IH:
immunohistochemical analysis.
FNE:
free nerve endings. *Method
of
identification
of
termination
of
small nerves
not
mentioned. Not included in this table are studies on supraspinous, interspinsous
or
iliolumbar ligaments.
Progress in Evidence Based Diagnosis and Treatment
From: Vleeming A et al.:
9th Interdisciplinary World Congress on Low Back & Pelvic Pain.
Progress in Evidence Based Diagnosis and Treatment.
Singapore, October 31- November 4, 2016
Worldcongress LBP Foundation, Netherlands, 2013
ISBN/EAN 978-90-816016-2-7