Jen Cardew

This opening paragraph suggests that her complaints are mainly cognitive (concerned about ‘her back’, concerned about a spondylolisthesis at L5-S1).  Can you explain more in this paragraph exactly what her concerns were (i.e. sensorial (pain limiting function), cognitive (beliefs about what a spondylolisthesis is) and what specifically the ‘daily issue’ was?

Ms. A was primarily concerned about pain when walking. She had put on weight over recent years as her activity levels had dropped. She wanted to lose weight, but was nervous of making her back pain worse. Often exercise would increase the pain to the point that she was unable to undertake activities of daily living unaided.  She had not been able to find any form of pain-free exercise at the time and/or afterwards, which was very bothersome. Her cognitive beliefs were that she had a mechanical weakness in her lumbar spine that would only get worse the more she pushed her activity levels. She had not been able to find any treatment or self-correction that improved her pain sufficiently to increase her activity levels. She was worried that if her Lumbar spine was ‘unstable’ that she may suffer further neurological symptoms and that she may even suffer irreversible damage to her spinal cord. Her long-term goal was to be able to run/jog, but she felt that she needed to be able to walk without pain first, so, in that sense her goals were realistic. Her daily issue was right-sided lower lumbar pain (that was ‘fairly’ diffuse) at constant low level, increasing with activity, and right groin pain that increased variably, but generally after a few minutes of walking her dog. She had numerous other aches and pains, but first she wished to focus on her low back pain experienced whilst walking and running.

Given the length of time Ms. A has been experiencing pain, do you suspect any of her pain to be centrally mediated or mediated by her cognitive beliefs?  What features from her story guide your clinical reasoning process?

Ms. A has had low back pain for many years and the information that we have from pain science would suggest a strong likelihood of central sensitisation. Central sensitisation can occur when the nervous system misinterprets normal stimuli as a threat. The sympathetic nervous system (fight/flight mechanism) can become more dominant and stress-hormone levels rise. Sleep can be affected which in turn will lessen the body’s ability to heal. Ms. A has reported PTSD and fibromyalgia in her past medical history which suggests a change in the way that her body is managing and coping with stress. One hypothesis is that if the nervous system is already altered due to stress it is more likely to have a difficulty with regulating pain information. Fear avoidance can also impact how the nervous system perceives pain and a chronic cycle may then become embedded.

How can you address these realistic hormonal and nervous system changes with the ISM approach?

The ISM approach was developed to help clinicians to organise their knowledge and personal scope of practice to quickly and effectively treat the ‘whole person’, together focusing on the patient’s functional goal. The model incorporates the definition of ‘health’ as being a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity’ (WHO Constitution, The Pelvic Girdle 4th ED). The ‘whole person’ approach includes input to the ‘body-self neuromatrix’ (Melzack, 2001, 2005, The Pelvic Girdle 4th Ed.) and related outputs. The inputs include, for example: cognitive-related brain areas (memories, past experiences); sensory signaling systems (musculoskeletal, cutaneous); emotion-related brain areas (Limbic system, hypothalamic-pituitary-adrenal axis). The outputs to brain areas producing, for example: pain perception, such as action programs (involuntary and voluntary action patterns) and stress regulation programs (hormonal). By understanding that a balance is required for all the aforementioned systems, the clinician can incorporate the knowledge that they have to maximise the effectiveness of their treatment ensuring that each system has been addressed.

Once a ‘driver’ has been identified and a ‘likely and lovely’ hypothesis created, the therapist can discuss with the patient how their impairment may have occurred. At this point past fears or concerns can be more easily alleviated, as an alternative theory has been offered. The hypothesis is reinforced through the patient experiencing how it ‘feels’ to move in the most optimal way. Commonly we describe this as a ‘wow’ moment, a catalyst for change. Having the patient ‘on board’ is one of the most fundamentally important parts of the treatment program. We know that to retrain a new movement pattern or strategy, we need to optimise neuroplasticity. The most effective way of doing so is to have focused attention and awareness; to make the task/exercise specific to the functional goal and to have a high level of repetition (quality over quantity). Positive feedback (reward) is also considered to be of importance as is sensory input (tactile cuing). By disproving unnecessary fears (“I may be paralysed”), creating a safe and goal-specific treatment program, and the patient experiencing the change within their own body (with positive and tactile reinforcement) they can begin to retrain optimal movement strategies, that in turn will change the input and output of the neuromatrix.

This term ‘listening’ comes from the Barral Institute osteopathic visceral approach and can be passive or active.  Can you please define the difference between ‘active listening’ and ‘passive listening’ and which one you used to determine the noted visceral thoracic vector.

Active listening is a technique that involves using your hands to determine a vector type. For example, you would correct the thoracic ring to the point of first resistance (R1), and as you are correcting you are bringing your awareness to any resistance that you feel. As you gently and slowly let go of the correction you would focus your attention, through your hands, to the ‘feel’ and direction of the pull, thus ‘passively’ listening. This can help you to establish, for example, if the vector of pull is short or long. This is used to identify the first vector that is acting on a region that needs to be released (as you only perform vector analysis on the driver).

Almost!  Active listening is when the patient is ‘moving actively’ and the therapist feels (listens) to what is happening.  Are the biomechanics consistent with the task? do you feel any ‘resistance’ to the movement? Passive listening is when the therapist passively moves the patient and feels for resistance during this correction of either alignment, biomechanics and/or control.  Passive listening is also when the therapist lets go of this passive correction and feels for the location, quality (direction, strength, length) of the vector of pull. So, vector listening informs us of the primary side, direction, length and possibly the system of the underlying impairment.

You mention that you monitor the opposite rib of the ring being corrected as well as the one above and below.  What are you monitoring for?  What are the possible things that could happen and what do those possibilities suggest?

When correcting a thoracic ring the first part of the correction requires space to be created between the rings to allow for the corrected movement to take place. It is possible for the rings to become compressed together making the correction difficult as the rings feel like one unit and are difficult to separate. Compressed rings are commonly found when the patient has a habitual long term change in their posture, such as Mums that carry babies on their hips and actively compress one side of their thorax to help to stabilise themselves as the baby gets heavier. Often the compression is caused by the intercostal muscles locally to the ring in question. Another possibility is that two rings are ‘glued together’. In this instance if you start to correct one ring by posteriorly rotating one side of the ring, the ring above or below that it is glued to will rotate more on the opposite side (worsen). With a glued ring you need to slightly correct both rings together to gain the best correction, and prevent worsening of the other ring.  Glued rings often occur as the body tries to automatically correct a segment that is not being controlled well, for example after an injury that isn’t rehabilitated properly. This was the finding with Ms Abbot. Her TR3 and 4 were ‘glued’ together.

Two rings rotated in opposite directions can be compressed or glued. Compression is usually caused by long vectors that don’t glue the rings together such that when you correct one of the rings, the other automatically corrects.  A glued ring is one that cannot move independently of one either above or below and is usually caused by vectors between them – the intercostals is one example of a neuromuscular vector that can cause two rings to be unable to move independently.

What would the difference in ‘personality’ of the vector be if it was originating in:

1. Iliocostalis (and for this to be the primary vector which way should the ring be translated – to the same or opposite side of the iliocostalis incriminated by vector analysis)
2. Pectoralis minor
3. Intercostals between thoracic rings 3 and 4

1. If iliocostalis was the primary vector it would be felt posteriorly and the pull would be longer. The translation of the ring would be to the opposite side as iliocostalis pulls the posterior segment of the ring caudally therefore posteriorly rotating the same side of the ring which in turn creates a translation to the opposite side of the thorax.
2. Pectoralis minor would prevent posterior rotation and would be felt quickly but not as immediately as an articular fibrosis or an intercostal muscle.
3. Intercostals appear immediately on palpation, they can prevent separation of the rings initially as you start to correct and have a compressive nature.

To avoid confusion, I would suggest reserving the use of the word compression or compressive to reflect those rings that can move independently and glueing for those that can’t. Intercostals most often glue, not compress, rings in my experience. How does a pectoralis minor vector prevent posterior rotation of a rib given its attachment to the coracoid process?

If Pectoralis Minor was the vector the rib would already be held in posterior rotation (preventing any further posterior rotation) and therefore resisting anterior rotation of the rib on that side. It would create a contralateral shift on the opposite side of the ring. The direction of pull would be superior in nature.

Pec Minor is interesting in that it can posteriorly rotate the rib OR the rib can be anteriorly rotated – it really depends on what the scapular stabilizers do in response to the ring shift so be prepared to find both!

When there is a loss of SIJ control it is often assumed that there is an underlying motor control deficit of the postural pelvic stabilizers (TrA, pelvic floor and/or deep multifidus at the sacral level).  In this case, why is it not necessary to assess the motor recruitment strategy for pelvic control?

In this instance, the correction of the driver ‘automatically’ restored optimal motor control for the pelvic stabilisers. When TR3/4 were corrected the SIJ remained stable. If this was not the case, if the driver was in this region, or if the control was poor, it would then be important to specifically re-train the motor control.

Not an unexpected response given the home program given. Why? How could you have ensured that she had enough posterior tibial nerve mobility and sacrococcygeal mobility to handle the home exercise program you gave her to avoid this over-dose?

Firstly, I should have tested passive sacroiliac joint (SIJ) mobility. In crook-lying one hand monitors for response posteriorly over the SIJ and using the other hand to distract the joint along the three parts/poles of the joint. If ischiococcygeus was over-active it would compress the inferior part of the joint, preventing a parallel glide between the innominate and the sacrum. Secondly, I should have tested the dynamic mobility of the posterior tibial nerve. One way of testing for compression or tethering is to have the patient in supine and perform a passive straight leg raise (PSLR) with a bias of pronation at the foot. I could also have given the home-practice of a ‘Tai-Chi Kick’ which should help with balance re-training, SIJ control and neural mobility as we progress towards running.

More to come in Dublin – August 2017!  Long dural/neural vectors can create incongruent rotations from the cranium all the way to the subtalar joint.  With a story such as this, it is critical to ensure that the nervous system can tolerate the elongation that you are creating with the release of the skeleton.  Often, when the dural/neural system is the underlying system impairment, multiple sites of FLT are merely because the skeleton is trying to shorten itself to give the nervous system more mobility.  It may have been another reason for the inability to completely correct TR4.

Awesome Jen!  If you see this patient again, and if she is still undergoing the dental work, it would be good to understand the relationship between the sphenoid, ICT and coccyx to further clarify the role of adverse neural tension here and then down to the lower extremities/feet.