Leigh Fortuna

Given the length of time she has had these symptoms, what role do you think sensitization of the nervous system is having on her experience and what findings from the story support your answer?

Given the length of time Ms. PR has been experiencing her symptoms, it is very likely that a component of her symptoms is driven by central nervous system sensitization. Following known timelines for tissue healing, any ongoing symptoms beyond approximately 3 months following an injury cannot be attributed only to tissue. Even in an acute injury less than 3 months old, the nervous system is responsible for producing pain and can immediately respond by increasing sensitivity levels of receptors at tissue level, synapses at spinal cord and in the brain, all in an effort to protect and allow time to heal. Because of the role of the nervous system in producing pain, it is important for health care professionals to spend time educating patients about pain even from early stages of their injuries, so they have an accurate understanding of where their symptoms are coming from. Beyond 3 months or so, while there may be ongoing inputs to the brain from peripheral tissues that may include nociception, these signals are less likely coming from ongoing tissue injury, and more likely from tissue that is unhealthy, compressed, overactive or tight for example. The brain will interpret these signals as either safe or dangerous, and if after it takes into consideration all the other inputs coming into the brain from eyes, ears, past experiences, environment (the list can go on and on!), it determines these signals are dangerous, it will produce pain as an output to continue protecting the body. The brain itself can also be responsible for maintaining ongoing pain, as it can start to interpret signals that are not nociceptive, touch for example, as something that could potentially be dangerous, and thus it produces pain. In Ms. PR’s case, this is happening with her with the sensitivity to touch she has along her pubic bone. Touch should feel like touch! The majority of her symptoms are produced with specific movements, which would suggest they are mechanical in nature, but given the timeframe, even accurate nociceptive input to the brain is likely being “ramped up” by a degree of central sensitization.

Active and passive listening are terms coined by the Barral Institute and integrated into ISM. What do they mean? This will help the reader understand what you mean below when you describe passive listening at the subtalar joints.

Listening techniques are techniques where a therapist uses their hands to feel where vectors of pull are coming from.  In active listening, the patient actively moves through range or into a more optimal alignment to where the first point of resistance is felt, and the therapist uses their hands to note the biomechanics produced and feels where any resistance is coming from.  In passive listening, the therapist passively moves a bone into an alignment that is considered more optimal, and while doing so, feels for any vector of force preventing the bone from being moved.  Then as the bone is released, the therapist feels for which direction that bone is to, and what the quality of that force feels like.

Tell me what the osteokinematic position of the hindfoot, midfoot and forefoot were in sitting compared to the findings in standing. Any changes between position?  Was she sitting on an unlocked SIJ – did changing this i.e. providing control of the pelvis as she sat change any of the findings of her foot.  It’s OK if you didn’t do this – we can have a discussion about possible changes and what they would mean depending on your answer.

In sitting, I did not check if she was in an unlocked SIJ.  I would assume she would have been as I did not hold her foot in a corrected position as she moved into a sitting position.

You are correct.  If she sat through a squat without the left hindfoot correction, it is likely she was sitting with the left SIJ in an unlocked position. What impact would this have on the form closure mechanism of the left SIJ? i.e. what ligaments are less tense and which are more tense?

In an unlocked SIJ the long dorsal ligament is more tense and the sacrotuberous ligament Is less tense.

When in sitting, her left calcaneus was inverted relative to her lower leg. The lateral talar tilt was not present; however, the talus was still plantar flexed relative to the mortise. At the subtalar joint the talus was relatively abducted/dorsiflexed to the calcaneus and the calcaneus was medially rotated relative to the talus (subtalar joint supinated). The navicular remained plantarflexed and externally rotated relative to the talus and the lateral three metatarsals remained splayed (abducted relative to the 2^nd ray).

Describe your hypothesis as to how the calcaneus can appear everted relative to the lower leg in standing and inverted in sitting

In the seated position, when ground reaction forces were eliminated from the left foot, the left talus was no longer tilted in the mortise but was still plantarflexed secondary to the persistent plantarflexion and external rotation of the navicular.  With the lateral tilt eliminated, the left calcaneus was no longer everted relative to the lower leg, but rather was inverted.  The calcaneus remained medially rotated relative to talus (the talus was dorsiflexed and abducted relative to the calcaneus) as it was in standing.

Complex positional findings and very commonly misinterpreted as a pronated hindfoot, it isn’t!

Since it appears it was possible to manually correct the alignment of the talus and calcaneus, what does this tell you about the subtalar joints and which systems are less likely to be impaired.

Because I was able to move the talus and calcaneus into a neutral position, I can rule out an articular system impairment, as if a joint glide was restricted, it would have been more difficult to move these bones as freely, and a complete correction may not have been possible.  A myofascial system impairment was also less likely given the quality of the resistance felt during the correction (passive listening).

It is not uncommon for the midfoot and forefoot to be compressed/stiff in compensation for hindfoot impairments.  After you released the hindfoot, what was the response of the left mid and forefoot?

The left navicular remained externally rotated and the lateral forefoot remained splayed.  The calcaneus also remained in a slightly medially rotated position relative to the talus (I do not think I released the vector from the soleus fully in this one session, and in subsequent session there was a myofascial vector between talus and calcaneus medially).

Can you briefly describe the principles for motor control training of the foot and how you determine when to progress your program?

Motor control training progresses through stages based on the strength of the muscles being trained.  These principles apply to training any of the foot intrinsics.

Stage 1:  Grade 0-1 strength, flickers of activation but unable to sustain activation through range or under load.  Support the foot in optimal alignment and teach isometric recruitment for the required muscle.  All training done in non-weight bearing. Progress to next stage when able to activate muscle in neutral alignment without extrinsic muscle “cheating”.

Stage 2:  Gr 2 strength.  Use cues trained in stage one but add load, still in non-weight bearing (bands, balls, calf raise when seated and foot on floor).  Progress to next stage when demonstrating good activation, no cheating, maintaining intrinsic activation through range or partial load.

Stage 3: Grade 3 strength.  Progress to weight bearing.  Use cues learned in earlier stages to maintain optimal alignment in double leg standing, toe raises.  Progress to next stage when able to maintain good activation and optimal foot alignment in double leg stance exercises consistently.

Stage 4:  Grade 4 strength.  Progress to single leg stance, step through, single calf raises.  Progress to next stage when maintaining optimal alignment through required tasks at controlled speed.

Stage 5: Grade 5 strength.  Add variability in surface, reaction times, jumps, speed.

These stages of training are from the work of Rachael Corbett, Diane Lee & Associates and differ somewhat from the staging of training presented for the thorax and other body regions. Stages 1 and 2 are the same, Stage 3 has 3 levels (Stage 3/Level 1, Stage 3/Level 2, Stage 3/Level 3) and refer to Rachael’s Stage 3, 4 and 5.

When the 4^th thoracic ring is translated left/rotated right what position is the left rib in osteokinematically and what muscles at this level could restrict or make its correction difficult?

The left rib is anteriorly rotated.

Right rib, posterior rotation.

Inferior vector posterior aspect of rib: iliocostalis thoracis and longissimus thoracis on the right, posterior intercostals on the right.

Left rib, anterior rotation.

Inferior vector on anterior aspect of rib: intercostals anteriorly.

Superior vector on posterior aspect of rib: semispinalis cervicis on the left, iliocostalis cervicis on the left, semispinalis capitus and cervicis on the left.

Left or right rib (variable – in my clinical experience these are sometimes found on the left or the right inducing a ring to rotate and translate)

Vectors between scapula and rib: serratus anterior, pectoralis minor, pectoralis major, rhomboids, middle trapezius.

In your clinical experience, when serratus anterior is the dominant vector what is the resultant position of the impaired thoracic ring and the scapula on that side? How were the short vectors from the left intercostals addressed in treatment?

In my experience I find that when left serratus is the dominant vector it causes an anterior rotation of the rib on that side, inducing an ipsilateral translation/contralateral rotation.  The scapula is often elevated and more protracted and downward rotated. Ring stack and breathe was used in the first session to address the intercostals.

I do too and this often confuses clinicians. It is likely because it is easier to move the mobile scapula than the more resistant rib cage.

Was any home practice given for the 4^th thoracic ring after this first session?

She was given a self-stack/align cue to feel “open” through her axilla.  I did note this was not sufficient to improve the alignment of the ring and she needed further release.  Given the timing of the assessment and what I observed to be great body awareness, I hoped she could start to learn to let go with just the align cue, and further release could be given in future sessions.

Can you be more specific and describe your passive listening technique for analysis of dominant vectors perturbing the alignment of the left hip?

Gentle distraction and posterior glide (to center the femoral head in the acetabulum) was applied to the hip joint, and when the femoral head was released, a short, deep vector was felt pulling straight medially.  This led to palpation externally of the left obturator internus (OI), which was indeed very tender.

Obturator internus is an external rotator therefore I would have expected a short ER vector of pull on the femoral head prior to the medial pull.  If it was straight medial, I would have gone to iliococcygeus (IC) first.

Yes- this makes sense I see this clearly now– but even as a reactor, OI would be perturbing the femoral head- yes?  A combination of the 2 forces may be medial?  For IC to be perturbing the hip, the force would need to be through fascia through OI would it not? I’m uncertain how you could confidently distinguish between the two.

By the presence, or lack, of any rotation of the femoral head.

Sorry I am still stuck on this.  If the iliococcygeus is the dominant vector, the force would go through the fascia to the OI, and then via the OI to the hip.  There is no connection from the iliococcygeus and the hip otherwise is there?  A fascial connection other than through OI?  Because of the anatomical connection between the iliococcygeus and OI with OI being the go-between, I still don’t see how one could externally rotate the hip and the other not.  If IC is dominant it will pull through the OI and would this not be the same as if the OI was dominant? (May be similar confusion about scapular/upper ring vectors – the anatomy just doesn’t seem to jive with what you are saying you observe clinically.  This is where clinical experience is important I guess!).

I wasn’t clear enough in my answer.  If OI is the dominant vector, the first ‘listening’ you feel is external rotation followed by a medial vector of force that goes beyond the obturator foramen.  If IC is the dominant vector, you are right that the force is conveyed through the OI fascia but since OI is not contracting (or at least is not dominant) then there is no initial external rotation of the femoral head and an immediate vector of pull medial past the obturator foramen.

The vector you felt on passive listening of the left hip (no rotation) actually supports this assessment first rather than one of obturator internus.

Yes – but also to confirm/deny her cognitive belief, and she had been told by a gynecologist years prior to strengthen her pelvic floor and do lots of Kegels!

Absolutely!

What about her left foot?  Correcting her left hindfoot in standing improved her pelvic control and left hip position.  This highly suggests that the foot is responsible for the change in motor control strategy.  It is likely, since you didn’t mention it, that you didn’t do it, which is OK we can hypothesize relationships and mechanisms for this on the next go around.

No I didn’t do it for a couple reasons – I know that the left foot correction improved the hip and the thorax, so I used reverse reasoning and corrected the hip and the thorax instead of the foot so I could reach and palpate at same time.  Also – I didn’t check so I don’t know – if a foot is corrected in NWB, is the impact the same as in WB with ground reaction forces?

No, gravity and ground reaction forces are different, which is why testing a primary foot driver’s impact on the pelvic floor recruitment pattern should be done in a screening task more related to the meaningful task, i.e. standing in this case.

It’s a really important feature of this case report – foot driven pelvic floor BUT you didn’t actually test the foot correction on the pelvic floor behaviour! At least I don’t see it being tested either with ultrasound or palpation.  In a perfect world, your pelvic floor assessment would have been done next in standing, ultrasound (US) probe held by patient suprapubically and then the foot position changed with ground reaction forces to witness the change in resting tone of puborectalis and OI.

OK so we haven’t gotten far into her mid and forefoot and with the bunion surgery I think this is important – how was her ROM of the 1^st MTP?

I didn’t measure but it was mobile, not 45 degrees though from what I remember. A lack of 1^st MTP extension could have driven more “pronation” through her mid and hind foot to advance during gait, leading to changes up the chain. This is likely the reason why her foot posture was the way it was, and no foot rehab ever pre or post-surgery, likely contributed to her significant lack of intrinsic strength)

This is biologically plausible because if the OI was causing the hip malalignment and the left foot was adapting to this what position would the left hindfoot be in?

Her subtalar joint would remain with her calcaneus medially rotated relative to the talus, but I would not expect her talus to be laterally tilted as it was.  If it were adapting, the talus would be neutral in the mortise with the calcaneus medially rotated, or the talus would be medially tilted.

This again fits that the OI was NOT the initial vector on vector analysis of the hip – you felt a straight medial pull which is not OI. The tender point you noted was likely because it is a reactor.  Releasing this would not have been effective.

Yes — I see this point for sure.  I even called it a reactor above!! In looking back at my notes carefully, after our first session she did note her bladder was more irritated but she thought it was because of things she was doing with naturopath. I thought it was because release/align of foot didn’t hold and thus OI came back on, which was part of it, but releasing OI also likely caused it to revolt and become more irritable.  Later on I gave her more general release cues and perineal ball release- which likely got more vectors and more muscles, and between a more general release to pelvic floor and the foot starting to come, hip and bladder started to improve.

This overactivity was contributing to her lower urinary tract symptoms.

Reflection is the key to all learning!

ISM can be very helpful to know when specific muscle training is required for pelvic control.  What finding from your assessment tells you that specific motor control individual muscle training for the core muscles of the pelvis is NOT required here.

When her hip was centered and alignment and biomechanics improved, control of her left SI joint was restored through the range that squat was tested.  As such, it was thought motor control training for her core was not required at that time and for that given task.  However, the control of the right SI joint was not reassessed, and this becomes relevant later on.

Above you hypothesize that “The obturator internus is an external rotator of the hip, and overactivity in this muscle may have been present as a reactor to the internal rotation force from her excessive foot pronation.”  If the obturator internus is truly a reactor to some other primary vector, what would you expect the response to releasing this muscle be?

Her bladder became more irritable!  I initially thought this was because the release of OI could not be maintained because her foot was still not well controlled, which is what was happening, but the OI should not have been released in the first place because her OI was reacting to her foot and not likely the primary vector perturbing her hip.  Releasing it caused a reaction where the muscle became more overactive, and she reported increased bladder irritability.  We initially thought the bladder irritability was because of some changes with her naturopath combined with needing more foot treatment to make the release of OI be maintained, which was true.  In hindsight, the bladder irritability was at least in part due to the fact that the OI was a reactor that was released.

Tell me more about the shape of the foot or findings that told you FHB, AH, TP and ADDHal were weak? Could she recruit them? What grade of strength were they – what stage of training did you prescribe that relates to the grade of strength and why?

The most obvious finding was minimal intrinsic muscle bulk throughout her left foot.  On the medial side of the first metatarsal, the metatarsal could easily be palpated with minimal muscle bulk felt between the skin and the bone.  More proximally, this would be abductor hallucis, and more distally towards the 1^st MTP this would be flexor hallucis brevis.  She was unable to actively abduct her 1^st toe or attempt to shorten her medial longitudinal arch, and dominant extensor hallucis was observed when this was attempted.  Gr. 1 abductor hallucis strength.  Similarly, trying to plantarflex the first metatarsal was difficult without recruitment of flexor hallucis longus and extensor digitorum longus.   Gr. 2- flexor hallucis brevis strength as some activation of the muscle was palpated but not sufficient to move through range out of gravity.  Adductor hallucis was determined to be weak by the shape of her transverse arch, which was flattened with lateral 3 metatarsals splayed, but this muscle was not specifically strength tested.  The focus initially was on the flexor hallucis brevis and abductor hallucis as these muscles would have a bigger impact on supporting the medial longitudinal arch.  Tibialis posterior was also not specifically tested for strength but given the posture of her hind and mid-foot, was assumed to be lengthened and not active to the degree it should be.    When she was given cues to ground through both first and fifth MTP joints as well as calcaneus and imagine a lift through her arch, she was able to do this briefly but could not hold it under any load (this was not specific to tibialis posterior), and it was inferred that there was decreased strength in tibialis posterior. For a thorough foot assessment this muscle should have been more specifically tested.

Excellent!

What findings from your ISM assessment support your hypothesis “with her foot more supported her 4^th thoracic ring and left hip would start to improve”

It had been determined that correcting alignment of her left foot partially improved her left hip and 4^th thoracic ring; these regions were following her foot.  While there was treatment to be done to both the hip and 4^th thoracic ring, it would be less and easier to maintain when her foot was not continually causing these areas to adapt on these regions.

Interesting that she didn’t need the orthotics for an improvement to be noticeable even in Yoga where she wouldn’t be able to wear her orthotics anyway!

Yes!  I think this was in part due to cueing to ground through her 5^th MTP and be mindful of not letting her foot collapse fully.  Given the timing of her coming for treatment and impending move, as well as her plan to get her old orthotics replaced, we moved quicker than I would have ideally moved into getting them fitted – I wanted the pedorthotist in our clinic to look at her feet, and glad I did as prior orthotic support was insufficient. I also wondered given the degree of change of the alignment of her foot and prior surgery how much she would be able to get back and how quickly – and the orthotics gave her a huge buy in to her foot being a primary player in her hip pain.  Also, her hindfoot was released, and this was likely making it easier for her to try maintain somewhat better alignment.   As well, she had been releasing her hip and thoracic ring, which was all part of the picture.