Sacroiliac Joint Dysfunction

The sacroiliac joint has now been well established to actually move yet clinicians of my generation and older would certainly be aware of the argument that the sacroiliac joint did not normally move except in pregnancy.  Suffice to say that we have now moved beyond this argument for the normal population and the clinical challenge is diagnosing not only the existence of sacroiliac dysfunction but the mechanism behind the dysfunction.

Radiological imaging does not particularly add to the diagnostic work-up so we are left to rely on clinical assessment.  In the last decade Vleeming and Schneider’s have advanced the concept of both “form and force closure” as the primary mechanisms maintaining sacroiliac stability.

Form & Force Closure

In brief, form closure refers to the configuration of the joint surfaces, the alignment of these surfaces relative to gravity and bodyweight, and the tension in the restraining ligaments associated with normal alignment of the segments.

Force closure refers to the interaction of multiple muscle groups, which act across the joint to enhance compression on the joint surface to assist in joint stability.  This is the so-called oblique sling system, which has been conceptualised to involve the ipsilateral Glueteus Maximus and Tensor Fascia Lata in conjunction with the contra lateral latissimus dorsii.  This is enhanced anteriorly by the oblique abdominal system and the contra-lateral hip adductors.

These two oblique systems effectively form an X  (cross shape) on the anterior and posterior aspects of the pelvis and constitute the dynamic mechanism by which joint integrity is maintained.  These concepts appear to hold some clinical validity and have provided an enhanced framework for us to approach our treatment of the sacroiliac joint.

Lee has integrated this approach with some of the traditional osteopathic models to provide a clinical algorithm for determining sacroiliac dysfunctions. This involves evaluation of:

1)      Lumbar spine

2)      Pelvic landmarks,

3)      Sacral landmarks.

This provides a practical framework where we as clinicians can try to differentiate primary or secondary pelvic dysfunction and therefore target our treatment in the most appropriate way.  Because of the functional interaction of body segments a lumbar scoliosis, for example, can have secondary effects on the sacroiliac joint alignment and conversely sacroiliac mal-alignment may produce secondary scoliosis in the lumbar spine.  This is the classic “chicken and egg” scenario.

So using the above categorisations we can quantify spinal alignment using:

Visual observation

Palpating bony landmarks

Correlating with movement pattern in the lumbar spine.

Looking specifically at the pelvis we can define the position of the bony landmarks on the pelvis using:

ASIS,

PSIS

Ischial tuberosities

as reasonably reliable landmarks to assess the positional orientation of these bones.

The spectrum of pelvic dysfunctions which have been described include:

Anterior innominate rotation

Posterior innominate rotation

Innominate inflare

Innominate outflare

Innominate upslip

Innominate downslip.

Much debate exists regarding the reliability and mechanism of these syndromes so it is largely a clinical diagnosis.

The principle assumption of quantifying bony pelvic orientation is that the pelvic position will determine the position of the sacrum and therefore mal-alignments of the pelvis should be prioritised over sacral mal-alignments when they are observed to co-exist.

Corrective Measures

In general the principles of correction are either to use manipulative thrust procedures, joint mobilisation or muscle energy / myofascial techniques to help to realign the pelvic structures using the leverage of the torso or lower limbs.  This then leaves us in a situation of assessing the sacral position within the corrected pelvic rim and then ascertaining the sacral orientation. A number of sacral dysfunctions have been categorised.

These include:

1)      Nutated sacrum

2)      Counter- nutated sacrum

3)      Oblique axis twist indicating a spinning mechanism where one side of the sacrum lies deep and the other lies more superficial.

Assessing sacral position within the pelvis is challenging clinically, produces more inter-tester variability and is harder to be confident with.  However it is well worthwhile using this clinical algorithm to define  joint mal-alignments clinically and plan treatment strategies.

Crossing the first hurdle of defining the dysfunction the challenge is then to determine why mal-alignments have occurred and whether we can assess breakdowns in functional control (force closure mechanisms) which may be associated with overload- but that’s another day’s work and a discussion for another time

.

Enjoy the clinical challenge.

David

Lumbar spine pain on flexion

Lumbar pain on flexion is one of the commonest symptom reports clinicians hear when treating patients low back pain.  There are a number of clinical reasoning processes, which need to be considered.

Pathology

Much of the literature focuses on the changes in intra-discal pressure associated with spinal flexion implying that spinal flexion pain is associated with increased disc strain reproducing symptoms.  In order to strengthen the hypothesis of disc related flexion pain the clinician needs to establish other components of discogenic characteristics to support the hypothesis.

These can range from the overtly obvious…..

gross global movement restriction

spinal shift

radicular pain

positive neuro-provocation tests

neurological signs

to the other end of the spectrum where symptoms are only produced on flexion and only localised in the lumbar spine.  Of course acknowledging that any of the spinal elements may reproduce pain on flexion and this produces a list of potential targets to include:

zygapophyseal joints

supra-spinous ligaments,

intra-spinous ligaments

posterior longitudinal ligament

ligament flavum

local segmental musculature

Symptom Location – clues to aetiology

The ability to localise symptoms can give the clinician some clues as to the possible structures involved, but in cases of centralised pain this does not particularly enhance diagnostic accuracy other than to reduce the likelihood of facet joint involvement.

Treatment

Interestingly typical treatment approaches for flexion related pain is to use extension/McKenzie’s extension protocols, passive accessory intervertebral motion to facilitate extension (Maitland).  Undoubtedly this strategy is helpful for patients when improvements in tolerance for extension related treatments show simultaneous improvement in flexion capacity.  And for those that don’t?…….

What do we do for patients whose flexion does not improve with extension regimes?

The caseload of interest here are the patients who might be categorised as non-specific low back pain who have persistent problems with spinal flexion.  Here is a list of tips for things to evaluate when accessing this function:

1. Spinal segment flexion range.
2. Hamstring flexibility.
3. NeuroDynamic sensitivity.
4. Proximal trunk control.
5. Pelvic rotation on femoral heads.
6. Sacroiliac nutation.
7. Hip extensor muscle function on flexion (eccentric control).
8. Hip extensor muscle function on return to upright (concentric control)
9. Paraspinal / abdominal co-activation on return to upright.
10. Lumbal-pelvic rhythm on flexion.

PS

11. Lumbal-pelvic rhythm on return to upright.

Evaluating each of these components allows the clinician to determine mechanisms of breakdown and plan treatment strategies to facilitate recovery. Exploring these mechanisms is relevant for non-responders to extension regimes.

Enjoy the clinical challenge.
David

LUMBO PELVIC EXTENSION DYSFUNCTION

The basic mechanics of gait and propulsion dictate that the extensor chain mechanism must operate in an integrated way to convert ground reaction force into forward momentum.  From a clinical perspective we are interested in the integrated activity of ankle plantar flexion, hip and knee extension and controlled but stable trunk alignment on the propelling limb.  There are a number of potential mechanisms of breakdown in this region, which can be broadly categorised as:

motion impairment deficiencies

muscle power deficiencies.

Impairment of ankle dorsi flexion range inhibits the ability of the foot to act like a pivot and allow body weight to transfer in front of the axis of the ankle joint in order to facilitate propulsion.

Impairment of knee extension effectively shortens the length of the standing leg and reduces the efficiency of forced transmission through the lower limb.  Typically in association with impaired knee extension is an increased co-activation of the hamstrings and quadriceps with the net result of a stiffening of the limb and reduction in “fluidity” of knee motion.

The next component of the extensor chain is the ability to extend the hip.  In cases where postural alignment tends to be flexed the centre of gravity remains anterior to the axis of the hip joint producing a perpetual flexion moment.  This is perpetuated by sustained hip/flexor muscle activity in conjunction with the anterior abdominal wall.  In order for the hip to function freely there needs to be passive range of hip extension and sufficient power within the prime hip extensors (gluteus maximus) to generate the propulsion.

In clinical practice impairment of this fundamental component of gait is exceedingly common and often  results in a combination of compensatory strategies.  One compensatory strategy for impairment of hip extension is to induce excessive sacroiliac torsion producing increased anterior rotation of the innominate bone.  This may subsequently produce secondary strain through the lumbosacral junction or induce a motion pattern of lumbar hyperextension in order to bring the leg behind the body.  Not only is this movement pattern inefficient but produces a high risk of tissue overload in the zones of compensation.

Clinical Thought

1. How can we detect breakdowns in the extensor chain function?

1. What are the implications of a hyperlordotic strategy for hip extension in relation to trunk stability?

1. What are the implications of anterior innominate rotation as part of the facilitatory mechanism of leg extension?

Share your thoughts and …..

Rise to the clinical challenge.
David

Psychosocial Flags

As one on the frontlines for 20 years the concept of “flags” was useful to provide a strategy for integrating multiple elements into patient management strategies. Unfortunately , much like pain management programs recognition has driven a hands off strategy of patient management on the basis that “manual therapy” is either ineffective or creates dependance in this patient group.

The converse view is that manual therapy and functionally specific rehabilitation can be used directly as a cognitive-behavioural strategy to address specific patient complaints / functional impairments. As physiotherapists we need to recognise that any interactions we have with patients have cognitive / emotive connotations and there is no practical reason why physical means cannot be used to facilitate this approach as an adjunct or an alternative to psychotherapy techniques

Those who attended the “Decade of the Flags” conference in Keel university at the end of 2007 will know that primary care clinicians can now no longer hide behind professional boundaries as an excuse not to challenge patients distorted beliefs or facilitate rehabilitation programs which are tailored to their needs.

This obviously poses clinical challenges but the facts won’t go away by passing the buck.

What do you find the most challenging aspects of of this situation?