ChapterPDF Available

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

Authors:

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.
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.
References:
1.
Bednar
DA,
Orr
FW,
Simon
GT
(1995) Observations on the pathomorphology
of
the thoracolumbar
fascia in chronic mechanical back pain: a microscopic study. Spine
20,1161-1164
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Benetazzo
L,
Bizzego
A,
Caro R
De,
et
al.
(2011)
3D reconstruction
of
the crural and thoracolumbar
fasciae. Surg Radio/
Anat
33,
855-862
Corey
SM,
Vizzard MA, Badger
GJ,
et
al.
(2011)
Sensory innervation
of
the
nonspecialized connective
tissues in the
low
back
of
the rat. Cells Tissues Organs 194,
521-530
Dittrich
RJ
(1963)
Lumbodorsal fascia and related structures
as
factors in disability. J Lancet 83,
393-
398.
Gibson
W,
Arendt-Nielsen
L,
Taguchi
T,
et
al.
(2009) Increased pain from muscle fascia following
eccentric exercise: animal and human findings. Exp Brain
Res
194,
299-308
Hirsch C (1963) The anatomical basis for
low
back pain.
Acta
Orthop Scand 33, 1
Hoheisel
U,
Rosner
J,
MenseS
(2015) Innervation changes induced
by
inflammation
of
the rat lumbar
fascia. Neuroscience 300:
351-359
Jensen MC, Brant-Zawadzki MN, Obuchowski
N,
et
al.
(1994) Magnetic resonance imaging
of
the
lumbar spine in people without back pain. N Eng/ J
Med
331,
69-73
Kuslich
SD,
Ulstrom
CO,
Michael
CJ
(1991)
The tissue origin
of
low
back pain and sciatica: a report
of
pain response
to
tissue stimulation during operations on
the
lumbar spine using local anesthesia.
Orthop Clin North
Am
22, 181-187 ·
Langevin HM, Fox
JR,
Koptiuch
C,
et
al.
(2011)
Reduced thoracolumbar fascia shear strain in human
chronic
low
back pain. BMC Musculoskelet Disord
12,
203
Mense 5, Hoheisel U (2016) Evidence
for
the existence
of
nociceptors in rat thoracolumbar fascia. J
Bodyw
Movem Ther, online first: http://dx.doi.org/10.1016/j.jbmt.2016.01.006
Panjabl MM (2006) A hypothesis
of
chronic back pain: ligament subfailure injuries lead
to
muscle
control dysfunction. Eur Spine J
15,
668-676
Progress in Evidence Based Diagnosis and Treatment
9th Interdisciplinary World Congress
on
Low
Back
and
Pelvic Girdle Pain
13.
Pedersen
HE,
Blunck
FJ,
Gardner E (1956) The anatomy
of
lumbosacral posterior rami and meningeal
branches
of
spinal nerves (sinu-vertebral nerves). J Bone Joint Surg Am 38, 377-391
14.
Schleip
R,
Vleeming
A,
Lehmann-Horn
F,
et
al.
(2007) Letter
to
the Editor concerning
'A
hypothesis
of
chronic back pain: ligament subfailure injuries lead
to
muscle control dysfunction'
(M.
Panjabi). Eur
Spine J
16,
1733-1735
15.
Stilwell
DL
(1957) Regional variations
in
the innervation
of
deep fasciae and aponeuroses.
Anat
Rec
127,
635-648
16.
Taguchi
T,
Hoheisel U, Mense S (2008) Dorsal horn neurons having input from low back structures
in
rats. Pain 138, 119-129
17.
Tesarz J, Hoheisel U, Wiedenhofer 8, et
al.
(2011)
Sensory innervation
of
the thoracolumbar fascia
in
rats and humans. Neuroscience 194,
302-308
18.
Yahia
L,
Rhalmi
S,
Newman
N,
et
al.
(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
Progress in Evidence Based Diagnosis and Treatment 133
134
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
ResearchGate has not been able to resolve any citations for this publication.
Article
Full-text available
Background: The role played by the thoracolumbar fascia in chronic low back pain (LBP) is poorly understood. The thoracolumbar fascia is composed of dense connective tissue layers separated by layers of loose connective tissue that normally allow the dense layers to glide past one another during trunk motion. The goal of this study was to quantify shear plane motion within the thoracolumbar fascia using ultrasound elasticity imaging in human subjects with and without chronic low back pain (LBP). Methods: We tested 121 human subjects, 50 without LBP and 71 with LBP of greater than 12 months duration. In each subject, an ultrasound cine-recording was acquired on the right and left sides of the back during passive trunk flexion using a motorized articulated table with the hinge point of the table at L4-5 and the ultrasound probe located longitudinally 2 cm lateral to the midline at the level of the L2-3 interspace. Tissue displacement within the thoracolumbar fascia was calculated using cross correlation techniques and shear strain was derived from this displacement data. Additional measures included standard range of motion and physical performance evaluations as well as ultrasound measurement of perimuscular connective tissue thickness and echogenicity. Results: Thoracolumbar fascia shear strain was reduced in the LBP group compared with the No-LBP group (56.4% ± 3.1% vs. 70.2% ± 3.6% respectively, p < .01). There was no evidence that this difference was sex-specific (group by sex interaction p = .09), although overall, males had significantly lower shear strain than females (p = .02). Significant correlations were found in male subjects between thoracolumbar fascia shear strain and the following variables: perimuscular connective tissue thickness (r = -0.45, p <.001), echogenicity (r = -0.28, p < .05), trunk flexion range of motion (r = 0.36, p < .01), trunk extension range of motion (r = 0.41, p < .01), repeated forward bend task duration (r = -0.54, p < .0001) and repeated sit-to-stand task duration (r = -0.45, p < .001). Conclusion: Thoracolumbar fascia shear strain was ~20% lower in human subjects with chronic low back pain. This reduction of shear plane motion may be due to abnormal trunk movement patterns and/or intrinsic connective tissue pathology. There appears to be some sex-related differences in thoracolumbar fascia shear strain that may also play a role in altered connective tissue function.
Article
Full-text available
The available data on the innervation of the thoracolumbar fascia (TLF) are inconsistent and partly contradictory. Therefore, the role of the fascia as a potential source of pain in the low back is difficult to assess. In the present study, a quantitative evaluation of calcitonin gene-related peptide (CGRP) and substance P (SP)-containing free nerve endings was performed in the rat TLF. A preliminary non-quantitative evaluation was also performed in specimens of the human TLF. The data show that the TLF is a densely innervated tissue with marked differences in the distribution of the nerve endings over the fascial layers. In the rat, we distinguished three layers: (1) Outer layer (transversely oriented collagen fibers adjacent to the subcutaneous tissue), (2) middle layer (massive collagen fiber bundles oriented obliquely to the animal's long axis), and (3) inner layer (loose connective tissue covering the paraspinal muscles). The subcutaneous tissue and the outer layer showed a particularly dense innervation with sensory fibers. SP-positive free nerve endings-which are assumed to be nociceptive-were exclusively found in these layers. Because of its dense sensory innervation, including presumably nociceptive fibers, the TLF may play an important role in low back pain.
Article
Full-text available
To create computerized three-dimensional models of the crural fascia and of the superficial layer of the thoracolumbar fascia. Serial sections of these two fasciae, stained with Azan-Mallory, van Gieson and anti-S100 antibody stains, were recorded. The resulting images were merged (Image Zone 5.0 software) and aligned (MatLab Image Processing Toolkit). Color thresholding was applied to identify the structures of interest. 3D models were obtained with Tcl/Tk scripts and Paraview 3.2.1 software. From these models, the morphometric features of these fasciae were evaluated with ImageJ. In the crural fascia, collagen fibers represent less than 20% of the total volume, arranged in three distinct sub-layers (mean thickness, 115 μm), separated by a layer of loose connective tissue (mean thickness, 43 μm). Inside a single sub-layer, all the fibers are parallel, whereas the angle between the fibers of adjacent layers is about 78°. Elastic fibers are less than 1%. Nervous fibers are mostly concentrated in the middle layer. The superficial layer of the thoracolumbar fascia is also formed of three thinner sub-layers, but only the superficial one is similar to the crural fascia sub-layers, the intermediate one is similar to a flat tendon, and the deep one is formed of loose connective tissue. Only the superficial sub-layer has rich innervation and a few elastic fibers. Computerized three-dimensional models provide a detailed representation of the fascial structure, for better understanding of the interactions among the different components. This is a fundamental step in understanding the mechanical behavior of the fasciae and their role in pathology.
Article
Full-text available
Mechanisms and structures which are involved in eccentric exercise-induced delayed onset muscle soreness (DOMS) are not yet clarified. Tissue and site specificity may be important considerations in afferent sensitisation following eccentric exercise. This study investigated the nociceptive response to hypertonic sodium solution applied to fascial/epimysium tissue and mechanically sensitised sites in muscle by assessing (1) afferent recordings in animals and (2) psychophysical assessment in humans. Seventeen male rats underwent eccentric contraction of extensor digitorum longus muscle, while 11 rats served as an unexercised naïve group. Two days post-exercise, group IV afferent fibre activity was recorded in response to superfusion of hypertonic Krebs solution on the mechanically sensitised muscle/epimysium site. Mechanical sensitisation was confirmed with significant increases in afferent response and decreases in threshold to mechanical stimulation in the eccentrically exercised rats compared to naïve rats. There was no difference in afferent response magnitude to hypertonic Krebs solution between exercise and naïve groups. In the human study, 13 volunteers participated. After bilateral assessment of pressure pain thresholds (PPT) along the tibialis anterior muscles, eccentric exercise was performed to induce DOMS in m. tibialis anterior of one leg. Site of maximal mechanical sensitivity was identified 24 h later and injected with hypertonic saline at fascial and deep muscle levels. The corresponding site on the opposite unexercised leg served as a control. Fascial injection of the exercised muscle caused significantly higher pain intensity compared to all other injections. Response to deep muscle stimulation was not different between sides. This suggests that fascia rather than muscle tissue is important in DOMS associated sensitisation.
Article
Recently, the existence of nociceptive fibers in fascia tissue has attracted much interest. Fascia can be a source of pain in several disorders such as fasciitis and non-specific low back pain. However, little is known about the properties of fascia nociceptors and possible changes of the fascia innervation by nociceptors under pathological circumstances. In this histologic study, the density of presumably nociceptive fibers and free nerve endings was determined in the three layers of the rat TLF: inner layer (IL, covering the multifidus muscle), middle layer (ML) and outer layer (OL). As markers for nociceptive fibers, antibodies to the neuropeptides CGRP and SP as well as to the transient receptor potential vanilloid 1 (TRPV1) were used. As a pathological state, inflammation of the TLF was induced with injection of complete Freund's adjuvant. The density of CGRP- and SP-positive fibers was significantly increased in the inner and outer layer of the inflamed fascia. In the thick middle layer, no inflammation-induced change occurred. In additional experiments, a neurogenic inflammation was induced in the fascia by electrical stimulation of dorsal roots. In these experiments, plasma extravasation was visible in the TLF, which is clear functional evidence for the existence of fascia nociceptors. The presence of nociceptors in the TLF and the increased density of presumably nociceptive fibers under chronic painful circumstances may explain the pain from a pathologically altered fascia. The fascia nociceptors probably contribute also to the pain in non-specific low back pain.
Article
Recently, the fascia innervation has become an important issue, particularly the existence of nociceptive fibers. Fascia can be a source of pain in several disorders such as fasciitis and non-specific low back pain. However, nothing is known about possible changes of the fascia innervation under pathological circumstances. This question is important, because theoretically pain from the fascia cannot only be due to increased nociceptor discharges, but also to a denser innervation of the fascia by nociceptive endings. In this histological study, an inflammation was induced in the thoracolumbar fascia (TLF) of rats and the innervation by various fiber types compared between the inflamed and intact TLF. Although the TLF is generally considered to have proprioceptive functions, no corpuscular proprioceptors (Pacini and Ruffini corpuscles) were found. To obtain quantitative data, the length of fibers and free nerve endings were determined in the three layers of the rat TLF: inner layer (IL, adjacent to the multifidus muscle), middle layer (ML) and outer layer (OL). The main results were that the overall innervation density showed little change; however, there were significant changes in some of the layers. The innervation density was significantly decreased in the OL, but this change was partly compensated for by an increase in the IL. The density of SP-positive - presumably nociceptive - fibers was significantly increased. In contrast, the postganglionic sympathetic fibers were significantly decreased In conclusion, the inflamed TLF showed an increase of presumably nociceptive fibers, which may explain the pain from a pathologically altered fascia. The meaning of the decreased innervation by sympathetic fibers is obscure at present. The lack of proprioceptive corpuscular receptors within the TLF does not preclude its role as a proprioceptive structure, because some of the free nerve endings may function as proprioceptors. Copyright © 2015. Published by Elsevier Ltd.
Article
Chronic musculoskeletal pain, including low back pain, is a worldwide debilitating condition; however, the mechanisms that underlie its development remain poorly understood. Pathological neuroplastic changes in the sensory innervation of connective tissue may contribute to the development of nonspecific chronic low back pain. Progress in understanding such potentially important abnormalities is hampered by limited knowledge of connective tissue's normal sensory innervation. The goal of this study was to evaluate and quantify the sensory nerve fibers terminating within the nonspecialized connective tissues in the low back of the rat. With 3-dimensional reconstructions of thick (30-80 μm) tissue sections we have for the first time conclusively identified sensory nerve fiber terminations within the collagen matrix of connective tissue in the low back. Using dye labeling techniques with Fast Blue, presumptive dorsal root ganglia cells that innervate the low back were identified. Of the Fast Blue-labeled cells, 60-88% also expressed calcitonin gene-related peptide (CGRP) immunoreactivity. Based on the immunolabeling with CGRP and the approximate size of these nerve fibers (≤2 μm) we hypothesize that they are Aδ or C fibers and thus may play a role in the development of chronic pain.