International Journal of Osteopathic Medicine 13 (2010) 24–30

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International Journal of Osteopathic Medicine

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Commentary

Composite sacroiliac joint pain provocation tests: A question of clinical

significance
M.C. McGrath*
Department of Anatomy and Structural Biology, Otago School of Medical Sciences, University of Otago, Dunedin, New Zealand

a r t i c l e i n f o a b s t r a c t

Article history: True sacroiliac (SI) joint pain arises for well-established pathological reasons. For example, SI joint
Received 25 March 2009 infection is characterised by non-specific, diffuse and poorly localised pain that makes an initial clinical
Received in revised form diagnosis difficult, even though the condition is a prima facie SI joint lesion. On the other hand, the
18 May 2009
putative sacroiliac joint pain of the ‘sacroiliac joint syndrome’ that is by definition not associated with
Accepted 2 June 2009
morphological and radiological abnormality, is a symptom commonly observed in clinical practice. Such
a presentation possesses a typically well-localisable pain in the region overlying the posterior sacroiliac
joint. The contention is that composite SI joint pain provocation tests, whilst of arguably statistical
Keywords:
Sacroiliac joint ‘significance’, may lack clinical significance particularly in the light of anatomical research that presents
Sacroiliac pain an alternative patho-anatomic basis for localisable sacroiliac pain and may offer a rational basis for
Sacroiliac syndrome diagnosis and treatment.
Long posterior sacroiliac ligament Ó 2009 Published by Elsevier Ltd.
Sacroiliac ligaments
Dorsal sacral rami
Lateral branches
Sacroiliac joint test
Composite tests
Non-specific back pain

1. The sacroiliac joint syndrome, actual SI joint pain and
putative SI joint pain
The International Association for the Study of Pain (IASP) list
four criteria for the ‘SI joint syndrome’.1 One key criterion is
‘ostensibly normal joint morphology without demonstrable path-
ognomic radiographic abnormalities’. This important criterion
occurs in addition to three further criteria namely: pain in the
region of the SI joint, the reproduction of pain by physical tests that
stress the joint and the elimination of the pain by intra-articular
injection. Putative SI joint pain, of the ‘SI joint syndrome’ presents
a number of substantial clinical challenges. First, where is the pain
generator in the absence of discernible pathology? Second, do SI
joint pain provocation tests achieve what they purport to achieve?
Third, do physical tests stress the joint to the exclusion of all other
potential generators? Fourth, are all pain generators in the region
identified? Fifth, is intra-articular injection an effective ‘gold stan-
dard’ for the elimination of putative SI joint pain? The provision of
* Dunedin Osteopathic Clinic Ltd., 483 George Street, Dunedin 9016, New
Zealand. Tel./fax: þ64 3 477 7020.
E-mail address: christopher.mcgrath@anatomy.otago.ac.nz
this commentary is made in order to assist critical thinking about
a controversial clinical subject.
Actual SI joint pain arises from well-identified conditions that
may necessitate medical treatment. These include trauma, infec-
tion, inflammatory conditions, degenerative diseases, metabolic
conditions and tumour as well as pain referred to the SI joint from
other sources.2,3 A diagnosis of SI joint pain requires the estab-
lishment of a treatable cause otherwise it is by default ‘sacroiliac
joint syndrome’, as previously described. Though rare, acute SI joint
infections of septic sacroiliitis,4–7 pneumococcal sacroiliitis8 and
pyogenic sacroiliitis9–11 yield no pathognomic SI joint signs.
Surprisingly, the initial clinical presentation of ‘non-specific’ low
back pain highlights an observation that even with a most
compelling pathological cause, the SI joint resists facile clinical
identification. Moreover, composite SI joint tests seeking to repro-
duce patient symptoms are open to patient reporting bias. The
reproduction of patient symptoms is distinct from the process of
eliciting a clinical sign, with the subsequent observation of an
objective finding. In the case of the SI joint the clinical diagnosis that
identifies the joint as causative is flimsy at best, on account of
a marked paucity of valid clinical signs or pathognomic symptoms
for either SI joint pathology or dysfunction. Therefore, given that
actual SI joint pathology is diagnostically elusive, is it proper to

1746-0689/$ – see front matter Ó 2009 Published by Elsevier Ltd.

doi:10.1016/j.ijosm.2009.06.002

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 M.C. McGrath / International Journal of Osteopathic Medicine 13 (2010) 24–30 25

promote clinical confidence in the composite SI joint tests of
a putative ‘SI joint syndrome’ for which, by definition there is no
morphological or radiological abnormality, but in which arguable
statistical utility is shown?
The SI joint tests referred to in this commentary, promoted for
use in a composite manner, are shown in Fig. 1. Five SI joint tests are
shown in this figure: anterior distraction, Fig. 1a; flexed thigh
thrust, Fig. 1b; Gaenslen’s test, Fig. 1c; side-lying iliac compression,
Fig. 1d and prone sacral thrust, Fig. 1e. A further sixth test, ‘the drop
test’ is not shown. This sixth test calls for the patient to stand
upright on one stiffened, straight leg, to raise the heel and then
allow it to suddenly drop, thereby delivering an ipsilateral
mechanical challenge to the pelvis. In utilising composite SI joint
tests, it is said that when either three or more positive test results
occur out of six, or two out of four positive tests (anterior distrac-
tion, side-lying iliac compression, flexed thigh thrust, prone sacral
thrust), the inference is that the pain is likely to arise from the SI
joint on the symptom reported side.12
Whilst it is demonstrated that the asymptomatic SI joint is
capable of pain-generation under experimental conditions of pain
provocation injection mapping,13 this may not reflect clinical
reality. As previously discussed, it is obviously difficult to diagnose
an SI joint infection before it becomes destructive or shows
systemic signs. The SI joint is a large, multisegmental structure of
complex embryology.14 The cartilaginous articular portion of the
joint is deeply located, in contrast to the more superficial inter-
osseous joint region or the periarticular and ligamentous struc-
tures. Deeper somatic structures sharing a common embryonic
somite, generate pain that is characteristically dull, diffuse and
difficult to localise.15–17 Such pain is also described as sclerotomal
pain18 and the non-localisable nature of this pain may offer some
understanding of the persistent difficulty seen in the clinical
identification of the SI joint as a pain generator.
It is the clinical consideration of the character of a putative SI
joint pain that may provide a better diagnostic clue. Deep struc-
tures characteristically produce non-specific, diffuse, sclerotomal
pain that is sometimes described as an ‘ache’ and often indicated by
the patient using the whole hand to indicate a large region. On the
other hand, the localisable pain posterior to the SI joint that clini-
cians attribute to putative joint pain of the ‘SI joint syndrome’ has
an entirely different character. It is localisable, easily indicated and
very well described19–23,2 and it has also been used as a clinical sign,
which relies upon the patient pointing a finger at the localisable site
of pain.24 Anatomically, the location of this painful point is situated
slightly inferior and medial to the posterior superior iliac spine, in
a region that overlies the middle part of the more deeply situated

Fig. 1. (a) Anterior distraction. (b) Flexed thigh thrust. (c) Gaenslen’s test. (d) Side-lying iliac compression. (e) Prone sacral thrust. Composite SI joint tests: reproduced with kind
permission of Elsevier from Laslett L, Aprill CN, McDonald B, Young SB. Diagnosis of sacroiliac joint pain: validity of individual provocation tests and composites of tests. Man Ther
2005;10:207–218.

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26 M.C. McGrath / International Journal of Osteopathic Medicine 13 (2010) 24–30
long posterior sacroiliac ligament, Fig. 2. The morphological
significance of this location is critical to understanding why local-
isable pain in the region appears unlikely to be SI joint pain and why
clinical tests of the SI joint may be morphologically confounded,
consequent to extraneous and unintended loads applied to the
region.
2. Clinical insight from new clinical histo-anatomical studies
of the sacroiliac region
Clinical anatomy, particularly in osteopathy, is a keystone in the
process of clinical reasoning. The anatomical research of Mixter and
Barr25 revealed the patho-anatomy of the prolapsed intervertebral
disc, thereby removing the overwhelming belief of the time that
a large proportion of low back pain was attributable to the SI joint.
A new understanding of patho-anatomy assisted the development
of a rational clinical approach. Now, 5–30%26–28 of low back pain is
believed to caused by the SI joint. However, a potentially large
proportion of this group is accounted for by the sub-grouping of ‘SI
joint syndrome’, where there is no identified pathology. The
unfortunate lack of knowledge regarding the treatment of SI joint
pain is well-identified29 and is further underpinned by an absence
of knowledge regarding the prevalence of the SI joint as a cause of
acute low back pain.30 Page 70.
Fig. 2. The point of localisable sacroiliac pain at the mid-long posterior sacroiliac
ligament: reproduced with kind permission of Elsevier Masson from McGrath C,
Nicholson H, Hurst P. The long posterior sacroiliac ligament: a histological study of
morphological relations in the posterior sacroiliac region. Joint Bone Spine, 2009
Jan;76(1):57–62. A black asterisk indicates a classically described point of localised
pain. The posterior ilium (I) is shown with the posterior superior iliac spine (PSIS) and
the third sacral lateral tubercle (LT). The long posterior sacroiliac ligament (LPSL) lies
between the PSIS and the LT, creating a region through which the lateral branches of
the dorsal sacral rami (DSR) may pass to the gluteal region. The first to the fourth
dorsal sacral foramen (S1–S4) are shown. The emergent dorsal sacral rami give rise to
medial and lateral branches. The lateral branches form an interconnected form an
interconnected plexus, the posterior sacrococcygeal plexus lying posterior to the
osseous sacrum.
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Of critical relevance to the clinician are recent anatomical and
histological studies31,32 that demonstrate detailed SI joint regional
morphology and offer a clear patho-anatomical rational for the
presence of localised, reproducible pain over the posterior SI joint.
These studies show an intimate relationship between the lateral
and medial neurovascular branches of the dorsal sacral rami
(middle cluneal nerves) and the ligamentous structures of the
posterior SI joint, in particular the long posterior sacroiliac ligament
(LPSL), which is sometimes also referred to as the long dorsal
ligament,33 Fig. 2.
The LPSL arises at the posterior superior iliac spine and, passing
across the posterior SI joint, blends with the sacrum at the largest,
lateral sacral tubercle between the third and fourth sacral dorsal
foramina.20,21,31 Of particular clinical interest is the morphological
observation that the LPSL arises at a confluence of dense fibrous
connective structures, forming a ‘tent’ like ridge over the posterior
sacroiliac joint, Fig. 3.
As a consequence of this morphological arrangement, it appears
likely that the erectors spinae aponeurosis (ESA) medially, the
gluteal aponeurosis laterally and an underlying deep fascial layer
combine at the LPSL, and together serve to isolate the lateral
branches of the dorsal sacral rami. Isolation of the delicate lateral
branches is achieved by the muscle forces of the ESA, gluteus
maximus and medius transmitted as tensile forces in a generally
oblique mediolateral direction through the LPSL, ‘strung and fixed’
between osseous attachment points at PSIS and the lateral sacral
tubercle.
It is important to remember that substantial SI joint counter-
nutational constraint provided by LPSL reaction forces is unsub-
stantiated in the biomechanical or morphological literature34,35
and furthermore, the LPSL is at a lever disadvantage being relatively
distant from the articular SI joint. Instead, SI joint ligamentous
stability is conferred by ligamentous structures with small levers
Fig. 3. The mid-long posterior sacroiliac ligament (LPSL): reproduced with kind
permission of Elsevier Masson from McGrath C, Nicholson H, Hurst P. The long
posterior sacroiliac ligament: histological study of morphological relations in the
posterior sacroiliac region. Joint Bone Spine 2009 Jan;76(1):57–62. A Harris haema-
toxylin & alcoholic eosin stained transverse section of the posterior sacroiliac region
highlights an adipose and loose connective tissue region (Ad) in which the lateral
branches of the dorsal sacral rami course between dorsal sacral foramina (DSF) to the
gluteal aponeurosis (GA) deep to the LPSL. The LPSL was observed to form at
a confluence of dense fibrous connective tissue layers, the deep fascial layer (DFL), the
erectors spinae aponeurosis (ESA) and the gluteal aponeurosis (GA). At the third dorsal
sacral foramen (DSF), the deep fascial layer was fenestrated (black asterisks) and
a vascular structure (V) was observed between the asterisks. The fenestration permits
the passage of the medial neurovascular branch of the dorsal sacral rami. The cauda
equina (CQ), sacral lamina (SL), sacrum (S), ilium (I), interosseous sacroiliac joint (SIJ),
sacral intervertebral canal (IVC) and a spinal nerve (SN), gluteus maximus (GMx),
multifidus (M) were identified. Observe how GMx muscle fibres run nearly parallel to
the gluteal aponeurosis and erectors spinae aponeurosis, where they find attachment.
Muscle forces creating tensile stress in the ESA and GMx may assist in reinforcing the
stiffness of the LPSL and thereby maintaining the patency of the adipose and loose
connective region in which the lateral and medial branches of the dorsal sacral rami
were found.
 M.C. McGrath / International Journal of Osteopathic Medicine 13 (2010) 24–30 27

close to the articular SI joint, such as the interosseous ligaments
and the short posterior sacroiliac ligament. Removal of the anterior
or posterior SI joint ligaments results in an increase of an already
very small SIJ motion34 of approximately 10%, and when both
anterior and posterior ligaments are removed, of 30%.35 In this
study, Wang and Dumas35 did not remove the posterior inteross-
eous ligaments describing them as ‘impossible to tear’. Moreover,
the symphyseal nature of the SI joint36 is a morphological feature
that underpins the functional requirement for a very stable, semi-
rigid, substantial force transmitting structure.37–40
Clearly therefore, the functional role of the SI joint most
consistent with the scientific literature is one that provides
a torsional load attenuation mechanism within the bony ring of the
pelvis that enables a slight ‘yield’ to twisting forces associated with
asymmetric bipedal gait.30 Moreover, it should also be borne in
mind that the term ‘nutation’ is an archaic concept, originating in
the literature in 1851 to describe the observations of Zaglas, an
anatomical assistant in Edinburgh.41 Elegantly depicted by
Kapandji42 in somewhat more recent literature, it nonetheless
remains inconsistent with current scientific knowledge concerning
SI joint morphology and motion.36,34,43
The morphological position of the LPSL is significantly posterior
to the interosseous SI joint and separated from the joint by a layer
of adipose and loose connective tissue in which the lateral
branches of the dorsal sacral rami course, Fig. 4a,b. Beneath the
LPSL and the contributing deep fascial layer, Fig. 3, lies a hitherto,
scarcely recognised region of adipose and loose connective tissue
within which the posterior sacrococcygeal plexus20,31,32,44–47 is
identified. Lateral neurovascular branches of the dorsal sacral rami
(middle cluneal nerves) form this complex and variable plexus,
which lies posterior to the osseous sacrum and SI joint surrounded
by a protective and cushioning layer of adipose and loose
connective tissue, Fig. 4a,b.
The plexus and lateral neurovascular branches are, by virtue of
their location within a confined space, potentially vulnerable to
insult by local pressure, whether of traumatic origin, pregnancy
related peripheral oedema48,49 or indeed from an examining
clinicians hand to name but a few examples. In the case of the latter,
notable localisable pain is observed over the SI joint.22 The lateral or
medial branches of the dorsal sacral rami may in theory be readily
compromised leading to localised pain, an idea consistent with
previous studies that have identified and treated entrapment
neuropathy of the superior cluneal nerves.50 The idea of a localised
entrapment neuropathy of the lateral branches of the dorsal sacral
rami posterior to the SI joint has substantial aetiological appeal and
may well account for a substantial subgroup of putative SI joint
pain sufferers, characterised by localised pain at the posterior SI
joint.
When considering the SI joint tests in the light of this new
knowledge of regional anatomy, it is clear that the posterior sacral
region is vulnerable to the application of a wide variety of
unavoidable, clinician instigated forces and loads. For example,
compressive loads (direct and indirect loads applied by the exam-
ining therapist), or tensile loads (indirect loads remotely applied by
moving an extremity), may both occur in the posterior sacral region
compromising the neurovascular plexus.
SI joint tests may be prone to morphological confounding in the
following ways. In the case of the anterior iliac distraction test, the
uncontrolled application of examining table reaction forces against
the posterior sacrum and SI joint may compress the underlying
neurovascular structures of the posterior sacrococcygeal plexus
deep to the LPSL against the table. A similar case may be made for
thigh flexion thrust, with the addition of tensile forces to the
neurovascular structures applied through tensile loading of the
gluteal muscles, which attach to the LPSL and erectors spinae
aponeurosis. In Gaenslen’s test, similar morphological confounding
conditions exist described for the preceding tests. On the other
hand, the side-lying compression test appears relatively free from
morphological confounding, provided the skin of the thigh is not
drawn anteriorly during the application of the test. In the prone
sacral thrust, compressive load is applied to the sacrum and
morphological confounding appears inevitable. The application of
relatively indiscriminate forces to the region has the effect of
increasing the local pressure surrounding the lateral and medial
neurovascular branches of the dorsal sacral rami. If these neuro-
vascular structures are already in an irritated state, a potential
exists that may elicit an increase in the localisable pain. The ‘drop
test’, like the side-lying compression test, appears free of
morphological confounding in the manner described, with the
exception that the sudden cephalad directed impulse would lead to
sudden compressive loading of the lumbosacral joints and inter-
vertebral disc. Apart from the patient reporting bias already
described, the joints and intervertebral discs of the lumbar and
lumbosacral region would need to be excluded as sources of pain
under similar testing conditions, before the ‘drop test’ could be
considered to have utility.

Fig. 4. The lateral branches (LB) of the dorsal sacral rami were observed in situ, posterior to the sacroiliac joint: the deep fascial layer (black asterisk) was dissected from the medial
aspect of the long posterior sacroiliac ligament (LPSL) and reflected superiorly. Lavage of the underlying adipose and loose connective tissue exposed the lateral branches, seen lying
immediately posterior to the osseous sacrum, passing obliquely towards the LPSL. The posterior superior iliac spine (PSIS) and the lateral sacral tubercle (LT) mark the osseous
attachments of the LPSL, with the mid posterior SI joint between them. The main body of the LPSL was sharp dissected away to expose the deepest ligamentous layer. Adipose and
loose connective tissue was observed deep to, and between these ligamentous layers (black arrowheads), within which the lateral branches passed. Acknowledgement is made to
the Department of Anatomy and Structural Biology, University of Otago and to Professor Helen Nicholson. (b) The lateral branches (LB) of the posterior sacrococcygeal plexus at the
posterior sacroiliac joint: a blunt seeker is used to lift the lateral branches deep to the long posterior sacroiliac ligament (LPSL) that was sharp dissected, reflected superiorly and
pinned against the posterior superior iliac spine (PSIS). The osseous attachment sites of the LPSL superiorly at the PSIS and inferiorly, at the third lateral sacral tubercle (LT) were
identified. The second (S2), third (S3) and fourth (S4) dorsal sacral foramina of the sacrum were also identified. Acknowledgement is made to the Department of Anatomy and
Structural Biology, University of Otago and to Professor Helen Nicholson.

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28 M.C. McGrath / International Journal of Osteopathic Medicine 13 (2010) 24–30
The lateral branches of the dorsal sacral rami, which form the
resulting delicate posterior sacrococcygeal plexus that intercon-
nects the fifth lumbar and each subsequent sacral dorsal rami over
the posterior sacrum, lie encased within a thin cushioning layer of
loose connective and adipose tissue in a protective ligamentous
‘sandwich’ immediately posterior to the sacrum. The fascinating
conclusion is that this morphological arrangement appears to
provide a safe egress of the lateral branches of the dorsal sacral
rami from the axial region of the sacrum, over the posterior
sacroiliac joint to the appendicular gluteal region, without
compromise from substantial, adjacent force transmitting muscle.
As previously stated the LPSL, formed at a confluence of the erectors
spinae aponeurosis, a deep ligamentous layer and the gluteal
aponeurosis, resembles the ridge of a tent strung between the PSIS
and the third lateral sacral tubercle. It is therefore the morpho-
logical key in this functional arrangement. This sophisticated
morphological arrangement appears to utilise the high levels of
transmitted muscle forces between the axial structures (erectors
spinae aponeurosis and spine) and the gluteal region (gluteal
aponeurosis, gluteus maximus, gluteus medius). Such functional
muscle forces maintain stiffness in the LPSL and thereby ensure the
functional integrity of the sub-ligamentous region, in which the
lateral branches of the dorsal sacral rami course.
3. Composite SI joint tests: statistical significance is not
necessarily clinical significance
A composite of SI joint tests are advocated for the clinical testing
of the intra-articular SI joint.12,51 Statistically, if the SI joint tests are
combined their discriminative utility improves51 and it is said that
this is a method of ‘cross-referencing’. A comparison is made with
various tests undertaken for the clinical diagnosis of a herniated
lumbar disc.12 However, it is important to point out that the clinical
tests undertaken to assess potential sensory and motor changes
associated with a intervertebral disc prolapse provide an intersec-
tion of objective information that is derived from objective signs
such as reflex response, limb power and dermatome mapping.
Corroboration may also be sought by suitable imaging. In contrast,
the composite tests for putative SI joint pain in the ‘SI joint
syndrome’ are all pain provocation, alleged joint stress tests, which
merely seek to reproduce a symptom. They cannot therefore
represent a true composite of ‘cross-referencing’ tests that bring
objective information in the form of clinical signs from different
sources, and which together assist the construction of a robust
diagnosis.
The application of SI joint stress ‘tests’ clearly do not have the
ability to exclude all structures except the SI joint. Either singly or
applied in different ways, the SI joint tests remain morphologically
non-specific. They stress a variety of other pain generating struc-
tures local and distant to the SI joint such as the posterior sacro-
coccygeal neurovascular plexus, muscles of the thigh and low back
and ligaments in the region.
Whilst it is claimed that SI joint stress tests are a ‘composite’
method of testing,51 they are in fact only repetitions of a non-
specific mechanical challenge, and instead of eliciting objective
clinical signs they simply provoke a reported symptom. Such SI
joint tests do not achieve what they purport to achieve, which is the
accurate identification of a painful SI joint52,53 because they engage
a wide range of pain generating structures other than the SI joint
and are open to patient reporting bias. Not possessing morpho-
logical selectivity, they are confounded, particularly by the dense
neurovascular elements of the posterior SI region.31,32 It is clear that
the entire posterior SI region is susceptible to indiscriminate load
with the patient lying supine, whether or not the clinician applies
a testing force. The same may be said for the clinician applying
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a direct force to the region, or by the indirect and remote applica-
tion of tensile stress through the region by lower limb placement.
All loads of this nature readily compress the posterior sacroiliac
region in a manner that potentially elicits pain from other pain
generating structures such as the lateral branches of the dorsal
sacral rami and posterior sacrococcygeal plexus.
4. Clinical anatomy informs practice
Clearly morphologically complex, the SI joint defies more
urbane anatomical descriptions as a synovial articulation or dia-
throsis.54 High resolution, magnetic resonance (MR) study corre-
lates imaging with histology, of the normal SI joint36 and indicates
that the SI joint may better be classified as a symphysis. Whilst the
SI joint is considered in ‘synovial’ terms it bears scant resemblance
to a true diarthrodial joint. The debate over SI joint classification is
not new and may be traced back to the early literature. For example,
Sashin (1930) cites Meckel (1854) as the first author to classify the
SI joint as a symphysis, and von Luschka (1854) as one of the
earliest authors to have described the presence of a synovial
membrane in the cartilaginous part of the joint.55 What SI joint
movement exists is minute and unpredictable and lacks clinical
utility.43 Observations of the minute SI joint motion between
individuals56–59 mirror what is already long established both
anatomically and radiologically.46 The joint possesses variably
interdigitating contours and convoluted folds in three-dimensions
that do not permit meaningful and predictable joint motion, or
uniform intra-articular loading. Instead, the minute amounts of
unpredictable motion that do occur are said to attenuate torsional
forces in the ring of the pelvis associated with bipedal gait.30
page 27 The established absence of articular uniformity in a joint
with some characteristics of a symphysis, is another substantial
barrier to meaningful SI joint testing, even more the case when the
application of the SI joint tests are required to be highly stand-
ardised.51 The ‘highly’ standardised application of a test procedure
to a ‘non-standard’ variable joint is unlikely to result in predictable
intra-articular joint loading, aside from any other cause of
morphological confounding. This is another reason why the clinical
significance of such SI joint ‘tests’ remains highly questionable.
5. Incomplete abolition of sacroiliac joint pain: there is no
‘gold standard’
The lack of a comparative ‘gold standard’ for pain relief in the
case of the SI joint is well recognised. The general effectiveness of
local blockade depends upon three premises: first, that nociception
from peripheral afferent nerve endings must come from a specific
source by a unique and consistent nerve root. Second, injection of
local anaesthetic should completely abolish sensory function of
a desired nerve and should not affect other nerves. Third, the relief
of pain is attributed solely to the blockade of afferent neural
pathways.60 As the sacroiliac joint possesses a variable pattern of
multisegmental innervation derived from ventral (L3–S2) and
dorsal lumbosacral sources (L4–S4) and the pelvic portion of the
sympathetic outflow, the hypogastric plexus,46,61–64 satisfying
criteria for effective joint blockade is most unlikely. It is also unclear
whether intra-articular spread of local anaesthetic injectate is
necessary to achieve efficacy.60 These facts, together with the high
false positive rate of induced pain provocation by image guided
joint injection12,52 means that studies which deem SIJ double
blockade as an ‘acceptable’ comparative reference standard need to
be treated with caution.53 ‘Acceptable’ is not a ‘gold’ standard and
a judgement of ‘acceptability’ or ‘satisfactory’ is not robust
‘evidence’. In the case of the SI joint, the use of image guided double
blockade as a ‘gold’ standard, let alone the adoption of any
 M.C. McGrath / International Journal of Osteopathic Medicine 13 (2010) 24–30
‘acceptable’ or ‘satisfactory’ standard continues to remain
suspect.60,65–69 Moreover, the three-dimensional and convoluted
nature of SI joint morphology raises further questions concerning
the use of contrast arthrography, used in SI investigation and
double blockade procedures. Fluoroscopic images that purport to
show infiltration of contrast medium into the joint space70 tend to
highlight periarticular spread and are not well confirmed by the
evidential publication of images acquired in three axis of imaging
planes. This would be necessary to properly image the three-
dimensional contour of the SI joint and to demonstrate complete
articular spread through the cartilaginous portion of the joint.
Indeed, sometimes no corroborating images are shown.71 Recent
reviews of the evidence regarding the validity of SI joint tests
further highlight the lack of a ‘gold standard’ and state specifically
that such ‘intra-articular anaesthetic block procedures neglect pain
arising from the ligamentous apparatus surrounding the joint, i.e.
the long dorsal ligament and the SI joint interosseous ligaments
and other dorsally located ligaments of the joint, which are prob-
ably an important source of pain’.33
6. Rational clinical practice
A rational step is the identification of a localised pain generator
in the region within the context of a morphological basis. New
morphological studies have suggested a possible patho-anatomic
basis for localised posterior SI joint pain.31,32 The continued search
for an elusive ‘SI joint syndrome’ with putative SI joint pain of
indeterminate cause may well remain an exercise of statistical
persuasion rather than one with any compelling clinical rationale.
As has been seen historically, clinical anatomy informs clinical
reasoning and provides a basis for new insight and aetiology. A
morphologically based rational as proposed here, also offers the
possibility of removing a large subset of putative sacroiliac joint
pain sufferers from SI joint classification, by virtue of defining the
patho-anatomic basis of sacral dorsal rami lateral branch (middle
cluneal nerves) entrapment neuropathy that accounts for localised
pain over the posterior sacroiliac joint. Moreover, of current rele-
vance is the use of radiofrequency neurotomy of both the lateral
and medial branches of the dorsal sacral rami. This procedure is
gaining increasing attention for its ability to treat putative SI joint
pain.45,72–77,29 The relationship of the posterior sacrococcygeal
plexus together with its comparatively ‘superficial’ and predictable
location offers, in principle, at least a greater accessibility to the
interventions available at the hands of the clinician. The functional
implications engendered by muscle attachment (ESA, gluteus
medius and gluteus maximus) to the LPSL provide not only
a interventional basis for therapeutic exercise regimens but one
which may also bring morphological justification to a regional
finding of somatic dysfunction and therefore, manual intervention.
Statement of competing interests
The author declares no competing interests.
Acknowledgements
Gratitude is extended to the Department of Anatomy and
Structural Biology, University of Otago School of Medical Sciences,
Dunedin, New Zealand and in particular to Professor HD Nicholson,
Dr PR Hurst and Dr M Zhang.
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