Mulligan Concept MWM's: A critical review of basic principles

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The Mulligan Concept is one of the commonly used manual therapy techniques in management of musculoskeletal conditions. Pioneered by Brian Mulligan in the 1970's, it is based on Kaltenborn's concept of restoring the accessory component of physiological joint movement. Its been over 12 years since I underwent training in Mulligan Concept. In this article, I first review the basic principles of the concept and then later look at some of the literature around the effectiveness of Mulligan Concept. 

Mulligan concept is based on the positional fault hypothesis and use of passive accessory joint mobilisations in combination with active, pain free movements - hence called mobilisations with movement (MWM). 

The Positional Fault Hypothesis

  • Mulligan proposed that injuries or sprains might result in a minor "positional fault" to a joint causing restrictions in physiological movement.  Injury can theoretically result in a positional fault that alters joint kinematics of the spine and peripheral joints.
  • The techniques have been developed to overcome joint `tracking' problems or `positional faults', i.e. joints with subtle biomechanical changes.
  • Normal joints have been designed in such a way that the shape of the articular surfaces, the thickness of the cartilage, the orientation of the fibres of ligaments and capsule, the direction of pull of muscles and tendons, facilitate free but controlled movement while simultaneously minimizing the compressive forces generated by that movement.
  • Normal proprioceptive feedback maintains this balance. Alteration in any or all of the above factors would alter the joint position or tracking during movement and would provoke symptoms of pain, stiffness or weakness in the patient. It is common sense then that a therapist would attempt to re-align the joint surfaces in the least provocative way. The positional fault can be responsible for pain and decreased range of motion, which should be resolved when the positional fault is corrected.

Principles of treatment

  1. During assessment the therapist will identify one or more comparable signs as described by Maitland. These signs may be a loss of joint movement, pain associated with movement, or pain associated with specific functional activities (i.e., lateral elbow pain with resisted wrist extension, adverse neural tension).
  2. A passive accessory joint mobilisation is applied following the principles of Kaltenborn (i.e., parallel or perpendicular to the joint plane). This accessory glide must itself be pain free.  The direction of the applied force (translation or rotation) is typically perpendicular to the plane of movement or impaired action and in some instances it is parallel to the treatment plane. 
  3. The therapist must continuously monitor the patient’s reaction to ensure no pain is recreated. Utilising his/her knowledge of joint arthrology, a well-developed sense of tissue tension and clinical reasoning, the therapist investigates various combinations of parallel or perpendicular glides to find the correct treatment plane and grade of movement.
  4. While sustaining the accessory glide, the patient is requested to perform the comparable sign. The comparable sign should now be significantly improved (i.e., increased range of motion, and a significantly decreased or better yet, absence of the original pain).
  5. Failure to improve the comparable sign would indicate that the therapist has not found the correct contact point, treatment plane, grade or direction of mobilisation, spinal segment or that the technique is not indicated.
  6. The previously restricted and/or painful motion or activity is repeated by the patient while the therapist continues to maintain the appropriate accessory glide. Further gains are expected with repetition during a treatment session typically involving three sets of ten repetitions.
  7. Further gains may be realised through the application of passive overpressure at the end of available range. It is expected that this overpressure is again, pain-free.

The acronym PILL guide the administration of MWM's. The "PILL" acronym refers to Pain-free mobilizations that produce Immediate effects, and achieve Long Lasting results. If PILL response is not elicited, then it is considered that MWM is not indicated and alternative management strategies should be utilised. Sustained improvements are necessary to justify ongoing intervention. The improvement is often enhanced and maintained following several repetitions (e.g. 2–3 sets of 6–10 repetitions) of therapist delivered treatment and over a course of several weeks by patient-delivered self-mobilization exercises.

While there are several studies which have highlighted the positive, significant impact of Mulligan's MWM's on pain and range of motion in several musculoskeletal conditions e.g. painful stiff shoulder, tennis elbow, ankle, knee, hip as well as cervical and lumbar conditions, 

But the question is do positional faults really occur? Is there any evidence for it? 


Ankle is one of the most commonly studied joint in terms of identifying and proving the existence of positional faults. Here I summarise some of the most cited studies. 

In one of the first studies to explore this issue, Hsieh et al. 2002 used pre- and post intervention MRI scans to identify the existence and correction of positional fault.  the authors employed MRI scans to study the positions of the phalanx and metacarpal bones and the effects of MWM on these bony positions. A small positional fault was found in the axial plane of the MPJ of the thumb, which appeared consistent with the mode of injury described by the patient. Interestingly, the MWM, which was chosen purely on a clinical reasoning basis (i.e. pain alleviation and improved range of motion), addressed this positional fault during its application. There was an immediate change in bony position during application of the MWM, as seen on repeat MRI scans. However, while the patient experienced significant improvement in pain and function, follow-up MRI scans taken after the completion of the treatment program showed no long term change from the positional fault seen on the pre-treatment MRI scans. 

Another example of a positional fault is mechanical instability of the ankle following a lateral ankle sprain. A plantar flexion and inversion mechanism of injury is likely to result in a sprain of the anterior talofibular ligament and possibly the calcaneofibular ligament as well. Mulligan suggested that mechanical instability and limited function may be caused by a primary injury (e.g., ligament pathology) or a secondary tissue response (e.g., edema) that induces a positional fault. The theory that positional faults occur in the ankle following injury has been supported by comparison of the position of the fibula to that of the tibia with an external measurement device, fluoroscopic examination, and magnetic resonance imaging (MRI) (Kavanagh et al 1999, Hetherington et al 2008, Mavi et al 2002). 

Kavanagh (1999) measured change in bone position with application of the anteroposterior glide MWM of the inferior tibio-fibular joint. The foot to be tested was placed in standardized position with the posterior heel supported on a wooden block and the posterior surface of each of the malleoli resting on potentiometers. The posterior displacement that occurred at the distal fibula during the MWM was recorded and plotted against the applied force. The author claimed that the data supported the proposal of anterior-caudal positional fault of the inferior tibio-fibular joint in ankle sprain patients. The author argued that the data from 2 of the 6 acute ankle sprains that demonstrated greater posterior movement (displacement) per unit force was sufficient to support the positional fault hypothesis.

Hubbard et al 2006 assessed the position of the distal fibula in individuals with chronic ankle instability (CAI) in thirty subjects with unilateral CAI and 30 subjects with no previous history of ankle injury. Through comparison of fluroscopic lateral images for both ankles, they reported statistically significant differences in fibular position for the subjects with unilateral CAI compared to their non-injured limb as well as the control group, suggesting an anterior positional fault was present in those with unilateral CAI. 

Landrum et al 2008 found that after a single application of Grade III anterior-to-posterior talocrural joint mobilization, dorsiflexion ROM and posterior ankle joint stiffness were significantly increased.  There was also a trend toward less posterior talar translation immediately after immobilization. The authors attributed the findings to correction of a positional fault at the talocrural joint. Residual loss of the posterior glide may be representative of an anterior positional fault of the talus on the tibia and may result in an abnormal axis of talocrural rotation.  Through an acute mechanism of injury, such as ankle sprain, the talus may anteriorly subluxate and become stuck, thus resulting in restricted posterior glide and compromised ankle function.  It is possible that the patients in our study who were immobilized for a prolonged period of time also developed positional faults of the talus and that these positional faults were corrected via either the joint mobilizations and/or the arthrometer testing. 

These papers have been extensively cited in manual therapy literature related to chronic ankle instabilty. However, what must be recognised is that all these are small, clinical studies with limited external validity and there is no substantive evidence for the positional fault theory. 

So if not positional fault, what else could it be?

To be continued. 

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