If you look up ‘how-to-do-EBP’ you get a lot of information about appraising the methodology, the bias, the fidelity - but what you don’t EVER get is any discussion on critiquing the actual intervention: taking your clinical experiences and wisdom and critiquing the actual intervention being researched

not how it’s being researched

but how the researchers are applying clinical reasoning to the intervention itself.

Because if we’re going to talk about a body of research related to neuromuscular electrical stimulation, this becomes a critical component of what you are doing.

Why Your Clinical Reasoning is More Important than Your Research Appraisal

Of course it is important to “critically appraise the evidence for validity, fidelity, bias, impact, and applicability - but none of that matters if the clinical reasoning is wrong. Here’s an article that serves as a great example of interesting research missing clinical reasoning. The authors wanted to see if they could reduce stance phase asymmetry in post-stroke gait using a sensor-based multichannel FES system. Unsurprisingly - even though they had the basic idea of using eStim in a functional activity - they were not thinking about motor learning. They used FES to control then knee joint angle - acting essentially like an orthotic over-riding the learning moment rather than facilitating it - but worse - and the patients did the FES gait training with a cane in their unaffected hand (sigh).

Does anyone really wonder why no significant improvement of stance phase asymmetry was found?

When you start to separate research that doesn’t make any clinical sense, from research that does - you start to see a pretty strong case for using neuromuscular electrical stimulation emerging.

Traditional approaches to eStim

Traditional thinking reflects the majority of published research on electrical stimulation. Most researchers are targeting the agonist muscle (e.g., tibialis anterior in swing) or pairing it with the ever-popular Botox to knock out spasticity.

Neither of these approaches is how we should be using eStim.

Clinicians who are up to date with clinical thinking on this matter are just scratching their heads and asking, why are you researching something we know doesn’t work?

So the purpose of this article is to give you the publications that actually look at the way we are currently thinking about eStim, and what their evidence shows. Unfortunately, this is a tiny body of research, precisely because it deviates from the ‘standard practice,’ old-school thinking ( you know that publication-to-clinical-practice gap is bidirectional!), and instead explores the alternative approach: stimulating the antagonist or spastic muscle itself (e.g., the gastrocnemius-soleus complex), either alone or alongside the agonist.

But before I jump into what the evidence actually shows, I want to be clear about why, as clinicians, we have updated our practice away from using Botox to knock out the ‘problematic spastic muscle’ and - along the same line of thinking - why we don’t stimulate the muscle opposing the ‘problematic spastic muscle’

Why Botox-Involved Studies Are Problematic

A number of studies combine electrical stimulation with botulinum toxin A (BTX-A) injection into the spastic muscle. These studies are deliberately excluded from this synthesis for the following reason:

BTX-A works as a temporary chemical denervation, reducing the force-generating capacity of the muscle so spasticity looks like it’s effectively reduced - but instead what it’s done is disconnect the communication line between the brain and the muscle. So the brain may be asking a muscle to do one thing, but the message is not getting through.

Task-specific electrical stimulation (TASES) and functional NMES depend on eliciting an active, functional contraction during a meaningful task, repeated over time, to reinforce a motor pattern through use-dependent motor learning. Motor learning requires a reliable, repeatable response to signals sent from the brain so they can be adapted and adjusted as learning takes place. What might the brain learn from sending out signals to a muscle that is only partially able to respond? Maybe try harder - send more signals? Any wonder there’s a massive rebound of spasticity once the Botox wears off? But I digress…

What does the the literature show: at least one BTX-A + gastrocnemius-stimulation RCT found no additional benefit of adding electrical stimulation to BTX-A alone - a result that is unsurprising if the toxin’s peripheral weakening blunted whatever training effect the stimulation was intended to produce.

Why Agonist-Only Stimulation Studies Are Problematic

A substantial portion of the NMES/FES literature in cerebral palsy stimulates only the agonist muscle (e.g., tibialis anterior) to force a missing movement, such as dorsiflexion to overcome the problematic plantarflexion.

Forcing an agonist to fire against an unaddressed spastic antagonist is analogous to driving a car without ever releasing the accelerator. The vehicle may move forward, but only by fighting the brake. In motor learning terms, this approach does not teach the nervous system to coordinate reciprocal timing between agonist and antagonist, because the spastic muscle’s excessive resistance is still present throughout the movement. What the brain learns instead is that forward progress requires an external driving force to overpower the antagonist, not that the antagonist itself needs to relax, lengthen, or time its release appropriately.

This is consistent with Ho et al.’s (2006) finding that agonist-driven FES changed dynamic gait resources without normalizing the underlying spatiotemporal coordination between muscle groups; and with Mooney & Rose’s (2019) observation that single-channel agonist stimulation improved isolated joint motion but failed to resolve the broader coordination deficits that define spastic gait. In other words, agonist-only protocols force muscles to activate without producing the coordinated, self-regulated muscle timing that functional movement needs.

The word on the ground goes something like this: when you apply FES to tib ant during gait, it works - but only as long as you’ve got the unit on. Clinically, stimulating tibialis anterior never seems to lead to weaning off the stimulator.

Kids on Tib Ant stimulation tend to need the Tib Ant stimulation… indefinitely. Take the device away and the movement goes with it. Kids stimulated through the gastroc-soleus complex, particularly when paired with real task practice, start needing it less. Eventually, some don’t need it at all.

That’s not a small thing to notice. Weaning off is arguably the outcome that matters, because it’s the only one that actually distinguishes

“we made the muscle move” vs “the nervous system learned something.”

You see positive trends in the research, even with functional tests like the GMFM can improve while the device is doing the work. What you don’t see is how these devices are weaned - because they aren’t.

There’s a small cluster of studies to support this clinical experience that’s been done on commercial foot-drop stimulators (WalkAide, NESS L300, and similar TA/peroneal-nerve devices). They’ve specifically tested what happens when you turn the device off after weeks or months of use, and compared that to how the child was walking before treatment started.

And it turns out that the car-and-accelerator metaphor above predicts the answer to.

Here’s what four separate research groups, using three different devices, all found:

• Pool et al. (2016), 32 children, 8 weeks of daily TA-targeted stimulation: muscle volume and strength increased, but selective motor control — the capacity to voluntarily, precisely control the ankle — showed no difference from the untreated control group at any timepoint, including immediately after 8 weeks of daily use.

• Bailes et al. (2016), 11 children, 16 weeks of NESS L300 use: dorsiflexion, walking speed, and endurance all improved — but only while the device was switched on. With the device off at the end of the study, the paper’s own conclusion states plainly that “no carryover effects in ankle dorsiflexion in swing and at initial contact were noted.”

• Segal et al. (2023), 15 children, 5 months of continuous DF-FES use: no significant change in gait kinematics with the device off, comparing month one to month five. Six-Minute Walk distance, if anything, got worse.

• Karunakaran et al. (2019), 7 children, 3 months of WalkAide use: no statistically significant improvement in toe clearance or walking speed with the device off. The authors’ own words: the trend “was not statistically significant and also [was] not observed in all participants.”

Four different labs, four different samples, all stimulating the same muscle target, all landing on the same result: once the device comes off, the underlying movement pattern doesn’t hold up. Not one of these studies found that TA-targeted stimulation taught the nervous system to produce the movement on its own.

So what happens when you stimulate the spastic muscle - in function? Well there’s a small but equally consistent body of research that supports current clinical reasoning in FES / TASES.

Evidence that makes the grade

1. Direct stimulation of the spastic muscle during gait

Comeaux, Patterson, Rubin & Meiner (1997). Pediatric Physical Therapy, 9(3), 103–109. Fourteen children (4–14 years) with hemiplegia or diplegia underwent phased NMES: gastrocnemius alone, then gastrocnemius + tibialis anterior, during gait/functional activity. Heel-strike dorsiflexion improved significantly with both stimulation conditions - notably including gastrocnemius-only stimulation of the spastic muscle.

Ho, Holt, Saltzman & Wagenaar (2006). Physical Therapy, 86(7), 987–1000. FES applied to the gastrocnemius-soleus complex in 13 children with spastic CP (vs. 6 typically developing peers). FES significantly increased speed-normalized dimensionless impulse during walking (10.02 → 16.32).

Gonçalves, Fonseca, Araújo, Souza, Resende & Mancini (2019). Pediatric Physical Therapy, 31(2), 208–215. A single-case A-B design study of four children with spastic unilateral CP combined task-oriented gait training with FES applied directly to the gastrocnemius. All four children improved on impulsive (propulsive) torque and ankle/hip power ratio in the affected leg, and all four improved gross motor function scores; one of the four also improved walking speed. This is one of the closest matches in the literature to the TASES model described in this piece - the spastic muscle stimulated during real task practice rather than in isolation - though the small sample (n=4) and single-case design is acknowledged.

2. Direct stimulation for tone, stiffness, and elasticity

Havuc, Aydeniz & Basaran (2018). Annals of Physical and Rehabilitation Medicine, 61, e324. Electrical stimulation applied directly to the gastrocnemius (50 Hz, 300 ms pulse duration, 5s:5s on:off, 30 min/session) in 18 patients (31 limbs) with diplegic, quadriplegic, and hemiplegic CP. Muscle tone and stiffness decreased significantly; elasticity increased significantly (p < 0.01).

3. Head-to-head comparison against volitional training

Stackhouse, Binder-Macleod, Stackhouse, McCarthy, Prosser & Lee (2007). Neurorehabilitation and Neural Repair, 21(6), 475–485. Eleven children with spastic diplegia compared NMES against volitional isometric strength training, targeting quadriceps and gastroc-soleus. The NMES-trained group showed greater force gains in both muscle groups and improved walking speed - direct evidence that stimulating the spastic muscle can outperform volitional exercise alone, not merely supplement it.

4. Aggregate and scoping-level evidence

Chen, Wang, Liao, Liou, Escorpizo & Chen (2023). Clinical Rehabilitation, 37(1), 3–16. Meta-analysis pooling 421 patients with spastic CP. NMES improved mobility outcomes, particularly GMFM standing, running, and jumping domains.

Greve, Joseph, Berry, Schadl & Rose (2022). Frontiers in Physiology, 13. Scoping review of NMES applications (hip adductors, quadriceps, hamstrings, gastrocnemius, tibialis anterior) across strengthening, gait, and spasticity-reduction uses. Supports NMES-assisted strengthening, NMES-assisted gait, and NMES for spasticity reduction as distinct, evidence-supported applications.

Mooney & Rose (2019). Frontiers in Neurology, 10. Scoping review of gait-specific NMES (tibialis anterior, gastrocnemius, gluteus medius, quadriceps). Single-channel stimulation improved swing-phase ankle motion but was insufficient alone to address more complex gait abnormalities; multi-channel, functionally timed protocols showed broader benefit.

Clinical Synthesis

Task-linked, repeated, functionally timed stimulation produces durable change.

Supporting this pattern:

• Short-term tone/stiffness effects are well supported for direct spastic-muscle stimulation alone (Havuc 2018)

• Strength gains occurred when the spastic muscle was stimulated directly, or alongside its agonist (Stackhouse 2007)

• Functional/gait carryover is strongest when stimulation is timed appropriately during task practice, repeated across many sessions, and paired with a functional goal such as walking (Comeaux 1997)

Practical Takeaways for Therapists

• The evidence does not support any contraindications for direct stimulation of the spastic muscle. Several studies show tone reduction and functional gains when the spastic muscle itself is stimulated actively and repeatedly.

• Embedding stimulation in task practice (walking, functional reach, goal-directed activity) rather than using it as a passive, non-functional dose is a strong predictor of carryover but the eStim should support motor learning, not over-ride motor control (aka act a alternative orthotic)

• Be critical of outcomes in studies that synthesise neuromuscular stimulation techniques without considering motor-learning-based principles.

Note: This is an AI generated conversation taken from transcripts of real conversations with Karen Kangas (Occupational Therapist) as a novel way to make learning fast, fun and easy to listen to. AI has made some errors eg. The basal ganglia are not in the brainstem and the barrier vest is not rigid plastic (sigh) but spotting the errors makes it more fun 😉 and the take-home message is something you need to hear.

Click this link for instructions on making the barrier vest and more about how it works and how to use it > Empowering Movement: Karen Kangas on Transformative Therapies for Children with Complex Disabilities

Rapid Access Summary

Here’s the short summary of the useful stuff covered in this awesome AI conversation…🎙️

If you’ve spent any time in a special education classroom or a pediatric rehab clinic, you’ve likely seen the “90-90-90” rule in action: hips, knees, and ankles all at right angles, strapped in for “symmetry.” But according to veteran occupational therapist Karen Kangas, who has over 50 years of experience, this industry standard might be doing more harm than good.

Kangas, a self-described “badass” in the world of assistive technology (AT), argues that we’ve been treating the bodies of sensate children—those who can feel and respond to their environment—as if they were paralyzed adults. In her recent workshops and interviews, she challenges us to look beyond “postural management” and start looking at postural control.

The Gravity of the Situation

The foundation of Kangas’s philosophy is rooted in sensory integration, specifically the work of Jean Ayres. She emphasizes that human development isn’t “taught” - the body reveals its ability to sit and move when given the right opportunities.

Crucially, the body has two primary processing systems: tactile (resting) and vestibular-proprioceptive (active engagement with gravity). When a child is strapped into a highly contoured, symmetrical chair, their body is forced into tactile processing. They aren’t holding themselves up; the chair is holding them. To find the power to move, use their hands, or focus their eyes, a child must engage with gravity.

“Head control is actually controlled by the pelvis and by gravity,” Kangas explains. When we “jail” a child in a chair with headrests and trunk laterals, we often prevent them from finding the very pelvic stability they need to hold their own head up.

Presuming Intention

One of the most moving parts of Kangas’s work is her insistence on presuming intention. We often interpret a non-verbal child’s “extensor thrust” as a pathological symptom of Cerebral Palsy. Kangas sees it differently: these are often protective reactions.

When a child’s pelvis feels unstable, their body kicks into a “startle” or “opisthotonic reaction”—a surge of extensor tone meant to help them find gravity and protect their organs. If they hit an obstacle, like a rigid headrest or a tray, that tone increases. Kangas’s radical solution? Take the obstacles away. By removing headrests, leg rests, and trays during activity, she has shown that even children labeled as having “no head control” can sit at a regular desk and flip the pages of a book when they are interested in the task.

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The Tools of the Trade: Beyond the Big Red Switch

Kangas also critiques how we approach access to Augmentative and Alternative Communication (AAC). While the industry has moved toward high-tech eye-gaze systems, she reminds us that access must be paired with activity.

She advocates for:

• Electronic Sensors over Mechanical Switches: Mechanical switches require five distinct actions (locate, touch, press, hold, release) which can be impossible for a child with high tone. Electronic “proximity” or fiber-optic switches require zero pressure, making the technology “transparent” so the child can focus on the communication, not the “hit”.

• The Barrier Vest: For children with dystonia who “bridge” or surge when touched on the back, Kangas uses a protective barrier vest. This “barrier” prevents the caregiver’s hands from accidentally triggering a protective reaction at the scapula or sacrum, allowing the child to relax and engage.

  Learn more about the barrier vest

• Feet on the Floor: Weight-bearing is the “calming” signal for the nervous system. Kangas frequently removes footplates to let children feel the actual ground, which she argues is the only way the body truly understands how to orientate support to gravity.

A Shift in Practice

For therapists and parents, the takeaway is a shift from “fixing” to “facilitating.” Kangas suggests the 1-2-3 approach for handling: instead of a sudden “1, 2, 3, lift,” use the count to signal your approach. “I’m coming close, 1, 2, 3, my hand is going to touch your shoulder, 1, 2, 3, ”. This predictability reduces hypervigilance and calms the body’s protective surges.

Ultimately, Kangas reminds us that “relaxation is not life”. A child might be symmetrical and “safe” on the bus, but for them to be a functional human being, they need the freedom to move, to be asymmetrical, and to struggle a little bit with gravity.

As she puts it: “The body knows how to do more by revealing itself... as we give it opportunities”.

Imagine a glitchy Zoom call spanning the entire globe, from the rainy streets of Bradford, UK, to the quiet night in New Zealand. On one side are Tracy, a nurse who has spent 35 years fighting for people with learning disabilities, and Donna, a physiotherapy expert. On the other is Mindy, a researcher ready for bed but eager to hear about a project that is literally saving lives.

Tracy and Donna dropped a truth bomb: in the UK, people with learning disabilities often die 26 to 40 years younger than everyone else, mostly because of lung problems that could have been prevented. They decided they couldn’t just sit back and watch people get sick; they needed a “prequel” to the illness—a way to stop the trouble before it even starts.

They created “Keeping My Chest Healthy” (KMCH), a project so impactful it actually won a national “Oscar” in the healthcare world. It’s not just boring medical paperwork; it’s a co-produced toolkit designed with the very people it helps.

https://keepingmychesthealthy.bdct.nhs.uk/

The KMCH Super-Tools include:

• The Cheat-Sheet Videos: A library of videos under three minutes long that explain things like how to brush your teeth properly or sit right while eating to keep your lungs clear. The best part? A narrator can speak them in 40 different languages, so everyone is included.

• The Risk Checklist: A simple scoring tool that anyone—nurses, families, or even students—can use to spot red flags early. It asks simple questions about things like sleep apnea or past infections to see if someone needs extra help.

• The Traffic Light Care Plan: This is the ultimate “how-to” guide for a person’s health. Green means “I’m feeling great, here’s what I need to stay that way”; Amber means “I’m acting a bit off, let’s fix it now”; and Red means “Emergency—take me to the hospital and don’t forget my specific meds”.

This isn’t just a “nice idea”—it actually works. When they checked the data, they found that people using this pathway had 76% fewer emergency hospital visits. Even more wild, the number of days people spent stuck in hospital beds dropped by 92%.

For Tracy and Donna, this has been a “labor of love” built bit-by-bit without a massive budget. They are now selling licenses to other hospitals to keep the project alive and expanding it so that every doctor’s check-up includes these life-saving lung checks. As the call ended and Mindy headed to bed, the message was clear: prevention is a superpower, and by teaching people simple things like oral care and positioning, we can give everyone a fair shot at a long, healthy life.

Reach out to them if you’re working with children and adults who could benefit from their resources.

Note: This is an AI generated conversation taken from transcripts of real conversations with Dr Penny Butler and Richard Major in discussions with our Optimi Training Track Pod Leaders Group as a novel way to make learning fast, fun and easy to listen to.

Episode Summary

In this episode, we explore a groundbreaking clinical framework that completely inverts conventional wisdom about posture, gravity, and motor control. Drawing from a raw recording of a global summit of physical and occupational therapists, we unpack the SATCo (Segmental Assessment of Trunk Control) and its accompanying Targeted Training protocol — tools developed for treating children with severe cerebral palsy that hold profound insights for everyone’s body.

What We Cover

The Top-Down Paradigm Shift (00:00 – 03:00) Everything you know about posture is probably upside down. Conventional rehab starts from the ground up — feet, pelvis, spine. The S-ATCO protocol does the opposite: postural control must be learned top-down, starting with the head. Why? Because the brain’s spatial map is generated by the visual and vestibular systems (eyes and inner ear). If the head isn’t in neutral vertical alignment, the brain receives “scrambled telemetry” — and no downstream correction can fix corrupted data at the source.

The Fixed Kyphosis Case (03:00 – 04:50) A patient with a rigidly curved upper spine (fixed kyphosis) can’t physically bring their head upright. The elegant clinical workaround: tilt the entire body backward until the C7–T1 vertebrae form a horizontal plane, allowing the head to naturally reach neutral vertical. This artificial platform gives the brain a clean spatial signal — unlocking therapy. Over three months of active top-down neuromuscular engagement, even “fixed” spinal rigidity can begin to yield. Active movement remodels tissue more effectively than passive mechanical force.

The Dizzy Client: Sensory Isolation (04:50 – 06:30) A visually impaired child who has spent their life with a severe forward head posture becomes intensely dizzy and nauseous when placed upright. The vestibular and visual systems are sending conflicting data the nervous system can’t reconcile. The solution: eliminate vision entirely. With eyes closed — or in a darkened room — the brain relies solely on vestibular input. Therapists use pleasant smells or the sound of crinkly paper to guide the head upward without triggering visual conflict. Once head control is established, vision is gradually reintroduced.

The Frog Leg Dilemma (06:30 – 07:30) A child with low muscle tone whose legs chronically flop outward (external rotation) presents a classic challenge. The instinct is to correct the legs first. The S-ATCO protocol says: let them flop. Secure the pelvis independently and ignore the peripheral noise. Trying to manage floppy legs compromises the primary assessment of the trunk. Focus on the anchor point; don’t chase every variable.

Sensory Hacks for Motor Engagement (07:30 – 08:20) A child who refuses to reach for toys — keeping hands tucked in — is coaxed into reaching through clever sensory tricks: a feather duster brushed on the hands, crinkly paper, or direct physical resistance against the back of the hand. The nervous system’s reflexive response to constant pressure is to push back — and that push becomes an active reach. The key: decode what sensory currency each individual nervous system will accept.

The Psychology of Gravity: Fear of Upright (08:20 – 10:00) A child who panics when placed in neutral vertical and fights to return to a slumped posture isn’t being defiant — they are experiencing a genuine neurological fear response. For a nervous system that has never mapped an upright posture, neutral vertical is a terrifying spatial void. The slump is a survival posture: the only state the brain registers as safe. The clinical approach isn’t to force exercise — it’s to provide full support from all angles and then simply wait. Three to four minutes of calm, fully supported stillness gives the hyper-aroused sympathetic nervous system time to realize it is not in free fall.

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The Nudge: Testing Reactive Control (09:40 – 10:40) Once a baseline sense of safety is established, therapists test reactive postural control with what the protocol calls “the nudge.” This is not a slow, gradual push — which gives the nervous system time to anticipate and pre-program a bracing strategy. The nudge must be brisk, sudden, and unanticipated, applied randomly from all four directions, with the clinician standing outside the patient’s visual field. The goal: observe the raw, unfiltered reflex loop — the body catching itself.

The Logistical Reality (10:40 – 12:20) The protocol requires specialized equipment (e.g., Lecky Squiggles TT, R82 Meerkat systems) that’s difficult to source in regions like Australia due to supply chain bottlenecks. The instructor’s advice: organize a “rent-a-mob.” Because algorithms drive supply chains, a clinic of 10 therapists sending one joint request registers as a single data point. Instead, each therapist should submit individual requests on different letterheads and different days to artificially amplify demand signals.

Equally strict: the camera setup for documentation. A true lateral view is essential — even a few degrees off creates parallax distortion that can make non-existent postural control appear present. Physical plumb lines (a weighted string) are hung off posture charts to guarantee the camera axis is perfectly aligned with gravity.

Module 4 Preview: Goodbye, Center of Mass (12:20 – 14:05) The episode ends with a seismic preview of what’s coming next. The traditional concept of “center of mass” — managing a static point over a base of support — is being abandoned entirely as a functional clinical concept. Why? Because it encourages children to freeze and lock down muscle groups to prevent their mass from shifting. True postural control is never static; it is continuous dynamic oscillation. The replacement framework: moments and torques — rotational forces. When a therapist places rigid support just below a specific vertebra, they create a pivot point. Gravity applies torque to the segment above, forcing the nervous system to recruit local muscles to counter it, rather than globally bracing. Segment by segment, the brain learns dynamic control.

The Big Idea

True resilience — physical or psychological — is not rigid bracing. It is adaptable, dynamic control. The same nervous system principles that govern a child learning to sit upright apply to all of us navigating pressure, change, and the forces acting on our lives.

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Closing Thought

Could the segment-by-segment targeted training protocol designed for children with cerebral palsy be the exact protocol needed to rehabilitate astronauts returning from long-term spaceflight? In zero gravity, the vestibular system goes silent and the brain loses its neutral vertical map entirely. Rebuilding motor control from scratch may require precisely the same top-down, sensory-first approach explored in this episode.

Key Terms

SATCo Segmental Assessment of Trunk Control — a clinical assessment tool for postural control

Targeted Training The accompanying intervention protocol developed alongside SATCo

Neutral Vertical The ideal head position where visual and vestibular systems are perpendicular to gravity Fixed Kyphosis Rigid curvature of the upper spine

The Nudge A sudden, unanticipated perturbation used to assess reactive postural control

Moments / Torques Rotational forces used as the new clinical framework in place of “center of mass”

Timestamps

• 00:00 Introduction — the ground-up assumption and why it’s wrong

• 01:00 The S-ATCO and Targeted Training protocol

• 01:50 Top-down control: why therapy starts with the head

• 03:10 The fixed kyphosis case 04:50 The dizzy client: sensory conflict and isolation

• 06:30 The frog leg dilemma

• 07:30 Sensory hacks for eliciting motor engagement

• 08:20 The psychology of gravity: fear of upright

• 09:40 The nudge — testing reactive control

• 10:40 Supply chain advocacy: the “rent-a-mob” strategy

• 11:44 Camera precision and plumb lines

• 12:20 Module 4 preview: replacing center of mass with torque

• 13:49 Closing reflections and the astronaut thought experiment

In this episode, we explore the work of Susan Blum and the principles of Total Motion Release (TMR) — a clinical approach that flips traditional therapy thinking on its head.

Instead of stretching, forcing, and fighting resistance, TMR invites us to listen to the body’s preferred movements and use them to unlock change.

We unpack:

• why traditional “no pain, no gain” therapy can actually increase resistance

• the biomechanics behind shortening vs stretching

• how postural asymmetries block function

• and how small shifts in alignment can create rapid, meaningful changes

Including:

• the story of a child on track for a wheelchair who went on to walk and play soccer

• how “spasticity” can sometimes be a mechanical block, not a permanent neurological limit

• and how parents can become active partners in therapy using simple, everyday positioning

Join Susan Blum For a Live Workshop

Note: This is an AI generated conversation taken from transcripts of real conversations with Susan Blum, founder of TMR Tots n Teens as a novel way to make learning fast, fun and easy to listen to.

🧠 Key ideas from this episode

1. Stop forcing movement — find the block

Instead of asking “what can’t the child do?”
TMR asks “what is stopping them from doing it?”

2. Shortening can release tension

Like a finger trap or a jammed drawer, pushing into the direction of ease can reduce resistance and reset muscle tone.

3. Release → Organise → Activate

TMR follows a clear clinical sequence:

• Release the restriction (position of ease)

• Organise the new alignment (proprioceptive input)

• Activate the new movement (use it immediately)

4. The body works as a whole

A twisted neck may be driven by a pelvic or trunk asymmetry.
Treating the whole system often resolves local problems.

5. Not all “spasticity” is neurological

Some children appear to have high tone, but are actually mechanically stuck in asymmetrical patterns.

6. Parents can be powerful change agents

TMR can be integrated into daily routines:

• cuddling

• carrying

• play

• rest positions

No force. No pain. Just positioning into ease.

💡 Why this matters

Many children (and parents) experience therapy as effortful, stressful, and sometimes painful.

TMR offers a different path:

• less force

• more listening

• more collaboration

• more ease

And in some cases, faster and more meaningful progress.

🎟️ Want to learn more?

We’re hosting a live Q&A session with Susan Blum where we go deeper into:

• applying TMR in clinical practice

• identifying blocks in real cases

• integrating this approach into your current therapy model

👉 https://www.wiredondevelopment.com/ama-with-susan-blum

🔔 Final thought

Sometimes progress doesn’t come from pushing harder.

Sometimes it comes from noticing where the body already feels easy…
and starting there.

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‘Where’s the evidence?’

I have a tendency to break out in hives - but before you stop reading, I'm not about to tear down foundational science in pediatric therapy and re/habilitation, let me be unequivocally clear:

We absolutely need evidence!

I didn’t spend 4 years of my life getting a PhD because I thought research was a waste of time. But in those 4 years I did learn a lot about how research is done, how it is shared and how it is misused by those who wish to elevate their message by massaging the facts - which is probably where my allergy developed.

But I’ve pulled myself back from the brink and am working through how to navigate Evidence-Based Practice in a context that values all 3 of the orginal tennents (sometimes referred to as the three legs of the evidence-based practice stool)

1. Lived Experinece

2. Clinical Judgement

3. Evidence

1. The Problem With Lived Experience

You’ll be aware of the endless discussion of hot topics that circulate on social media - hot topics because everyone’s got an opinion, and no one has a definitive answer. There’s a long list from developmental milestones like tummy time and crawling, to treatment modalities like NDT and Hyperbaric Oxygen Therapy. But no doubt if yo’ve been on Facebook you’ve seen a post asking "Is W-sitting good or bad?"

And like clockwork, the responses flood in:

"It's terrible! It damages the hips!"
"There's no evidence it's harmful!"
"I don't believe it's good to W-sit. I'm 28, I'm already having pain, and my kids W-sit. I'm going to train them out of it."
"I was a W-sitter. I never had any problems and played college basketball."

Round and round we go. These discussions happen on repeat because we don't actually have definitive evidence on the long-term impacts of W-sitting. If it truly is helpful or harmful, or if it’s neither.

So we're left with anecdotal evidence, lived experiences, educated guesses and no resolution. We cannot solve this question definitively without robust and long-term research - so yes - we need research.

2. The Problem with Clinical Judgement

Back in the early 2000s as a young clinician, I was working with a six-year-old girl who'd had a near-drowning accident, let’s call her Sarah. If you've worked with near-drowning cases, you know how devastating this brain injury can be.

Sarah was so spastic that doctors were considering removing her teeth to avoid her biting off her tongue. Her feet were so plantar-flexed we weren’t even sure surgery would help - and she was unresponsive to vision, auditory or tactile cues - only occasionally responding to pain or discomfort with crying.

At that time, there was huge excitement about hyperbaric oxygen therapy. Parents were literally mortgaging their houses to pay for these treatments (some still are). This particular family desperately wanted it but couldn't scrape together the funding.

So they didn't get it.

Fast forward 18 months, and Sarah was doing brilliantly - exceeding all expectations. She was walking independently, talking (albeit with the typical slow speech of a brain injury), normal vision and heading back to school. She had fallen into the pool in winter - had the hypothermia had a protective effect? We can only guess. But here’s the thing: IF she had received hyperbaric oxygen therapy, you would not have been able to convince me that it didn't work.

My clinical experience would have cemented a belief that hyperbaric oxygen was the magic bullet. I would have been recommending parents mortgage their houses for sure because "it's so worth it."

But Sarah never had hyperbaric oxygen therapy - she had standard therapy - and her recovery was a miracle that had absolutely nothing to do with her medical treatment or her therapy rehabilitation - because none of these were remarkable or different to the many other kids I’ve sadly seen with near-drowning brain injuries who didn’t show the same progress.

This is the cold reality of clinical experience – every child is your n-of-1, every single time. And that is not enough.

So yes, we need evidence.

The evidence-based practice pyramid was created in 1992 by Dr. David Sackett with the noble aspiration to bridge the gap between scientific research and clinical decision-making. Randomized controlled trials sat at the top, with meta-analyses and systematic reviews forming the "gold standard".

But in the 30+ years since, we find ourselves in the position of no-less significant variability and uncertainty

We now have a mind-blowingly extensive list of validated outcome measures across the ICF spectrum to measure intervention effects. The academic world has been pushing hard to make research more clinically relevant so that we don’t conclude nearly

every

single

meta-analysis

with the sentence - ‘needs more research’.

This recognition of needing to push the clinical relevance of EBP has led to a new the EBP pyramid with Clinical Practice Guidelines at the pinacle for us busy clinicians who don’t have the time or access to research and really just need to be told what to do. The pyramidnow looks something like this:

It looks solid, doesn't it? Like a structure you can trust.

But here's my favorite movie reference – and yes, I'm going to quote My Cousin Vinny at you:

"The DA's got to build a case. Building a case is like building a house. Each piece of evidence is just another building block... But there's one thing he's not gonna show you. When you look at the bricks at the right angle, they're as thin as this playing card. His whole case is an illusion, a magic trick."

Practice Guidelines are built on systematic reviews and meta-analysis of RCTs and in paediatric rehabilitation, when you look at these RCTs and meta-analyses of RCTs at just the right angle they’re as flimsy as a playing card - but everybody just goes around pretending that they’re real bricks.

3. The Problem with Evidence: A House of Cards

You’ve no doubt seen Iona Novak’s traffic light papers - these evidence based interventions that are held up as the rule book on what we should and should not be doing for children with cerebral palsy. Pretty much every talk on EBP in paediatric physiotherapy starts with sharing some version of the traffic lights as an enlightened version of how we should be practicing.

This talk by Diane Damiano at a European Academy of Childhood and Development Conference was a particularly interesting example for me. She starts off this talking saying, “ We now have evidence based practice,”

Two minutes into the talk she’s talking about Novak’s traffic lights,

“So when we look at the 2 goal areas of improving motor activities or improving function in self care, I drew a circle around all the physical and occupational strategies that actually can do those things, and we have very good evidence for, as well as drawing the circle around the physical and the occupational therapy techniques at the bottom that we should not be doing”

She presents these ‘ bricks’ just so - so they seem solid - along with the thinly veiled criticism of the ‘active resistance’ they run into with those of us 🙋‍♀️ who think these bricks are really just gigantic, very impressive playing cards

Because Dr Damiano then spends the rest of her talk explaining how the research is not quite meeting the challenges of our very diverse and complex field. The research that she is referring to of course, is much of the research that substantiates her house of cards.

Here’s a few snippets from the talk

• Trials are not long enough or intensive enough to reflect real-life requirements for changes in body structure, function and participation

• “in our research studies, we try to minimize the amount of time we keep people in the studies, but they're very short periods. And, obviously, in the clinic you would you would persist with these things. So we have to really think, do we stop our studies too soon?”

• “60 hours at least was needed to have a clinically significant effect. And that for that effect to persist really needed to be more than 90 hours…what we found there is that the doses in those trials range from 10 to 20 hours at most”

• RCTs require us to analyse data at the group level that disguises the large variability in responses of trial participants

• “they have some really high responders, they have that middle group that kinda changes that pushes the mean positive. However about 25% of the kids in their trials (strength, CIMT and more) actually [get] worse …we’re starting to realize that this is really happening in all our trials.

• I’ll just say that again

25% of children actually getting worse with treatments like constraint-induced movement therapy that sit in our "green light" category.

In one breath she’s telling us we have the evidence, and in the next she’s telling us the evidence is flawed - and in the next she’s saying if you don’t swallow what the flawed evidence is saying then you are unethical and resisting progress!

Just turn those brick sideways and you can’t not see that house of cards.

When researchers are being academically honest (always appreciated) they’ll tell you that confidence in systematic reviews is low - critically low.

A 2021 study looked at the quality of systematic reviews of interventions for children with cerebral palsy found critically low confidence in the conclusions of 88% of systematic reviews.

Let me repeat that:

The study concluded that "current recommendations for treating children with CP based on these flawed systematic reviews need re-evaluation."

The number of systematic reviews has increased over five years, but the methodological quality has not improved. In simple terms, that means

the researchers are pumping out meta-analyses of systematic reviews of RCTs where 88% are considered unreliable!

Another study looked at infant neurodevelopmental trials and found that 72% of studies had null findings

No benefits for early intervention were seen in 72% of studies.

Even the much touted GAME intervention (Goals-Activity-Motor Enrichment in infants with cerebral palsy) by Kathy Morgan found no significant improvement in gross and fine motor skills in the intervention group at age two years of age.

Now, we all know that early intervention matters, right? So when the research doesn’t show what we see clinically we look for reasons for the mismatch.

Much of the arguments in this article explaining the null findings are an echo of arguments used for decades by NDT therapists to explain the null findings in NDT research. These very same authors dismissed these argument then as "just excuses."

You know… Resistance to change, unethical, all that

I do have to say here that I am slightly amused by the change in tune - it’s kind of like parenting: things you’ll never do when you’re a mom… until you’re a mom!

But the truth is, this kind of reporting is brave and should be celebrated. There's honesty here - which is rare. More often than not, what we get is something far more insidious - we get publication-based practice masquerading as evidence-based practice, and we don’t see it because we are too busy to read past the headlines.

What’s the Evidence?

My allergy for evidence based practice started with this question:

What’s the evidence for this approach?

It seems like a reasonable question - until you consider that when it comes to paediatric practice - the truthful answer more ofen than not is - there is none.

I’ll give you a perfect example from school-based therapy research. In 2014, Effgen and Kaminker rightly said that ideas around ideal practice for therapy in schools were based on IDEA policies and theory in the absence of strong empirical research."

No empirical research.

aka ‘there is none’.

Got it.

Then in 2021, Ciarello, Effgen, and Pallisano (all big names in the field) published another paper looking at therapy in schools. They examined the goals and subsequent service delivery and outcomes of 109 very experienced school based therapists.

They looked at participation vs non-participation based goals and found that regardless of the goals there was no difference in outcomes for the students.

And just in case you’re wondering - non-participation goals included things like quality of skill performance whereas participation goals might include things like sitting and transfers.

So the authors’ obvious conclusion was…

Therapists should do more participation based goals.

Because although their research couldn’t prove it, they had found some evidence in other research showing, "service delivery in alignment with professional and stated guidelines has been found to be more effective [than traditional therapy]"

This ‘evidence’ was a study from 1995 that somehow they hadn't managed to dig up in their previous 2014 article (see above 👆).

Curious, I went back to look at this 1995 study that proved more traditional therapy in schools was ineffective.

Three children.

The entire evidence base for recommending against tradional therapy was a study of three children. That’s not much better than our n-of-one clinical experience is it?

But it was enough to publish a bold statement of effectiveness, accepted in a peer reviewed paper - and requoted countless times until it becomes a ‘known fact’.

Three children.

This 1995 study referenced only one other study from 1989, which was also used to support the message that tradional therapy was less effective than more ideological ideas of therapy in the classroom. The evidenc however, when you actually read the study, showed a preference for in-class therapy by the TEACHERS because therapists could assist them. In other words, therapists could be really helpful teacher aides! Great!

This, my friends, is publication-based practice. Taking publications – of any quality – and using them to support what you want others to believe.

A cure to my alergy

I finally found relief from my “allergy” when I realized what I was truly reacting to: not evidence-based practice itself, but publication-based practice masquerading as evidence. Evidence-based practice, at its core, is a solid foundation for our profession—but only if we approach it honestly and without self-deception.

• Lived experience is unreliable.

• Clinical experience is unreliable.

• Research is unreliable.

Each of these foundational 'legs' is flawed on its own, yet when woven together, they create something far more solid, a three-legged stool strong enough to support reflective, ethical clinical work. We have no choice but to stand on this uneven support, patching gaps with thoughtful inquiry and humility.

Evidence-based practice is essential for our collective progress, allowing us to move forward step by careful step. But we must always keep sight of the limitations:

The greatest danger isn't skepticism, resistance to change or even outdated treatement approaches. It’s publication-based practice dressed up as evidence-based knowledge - the wolf in sheep’s clothing.

True critique is dismissed, valid doubts are silenced, and we risk turning our field into a parody of intellectual rigor.

So I’ll keep challenging both practitioners and academics, valuing lived experience and clinical wisdom just as much as the latest publication.

I’ll call out the hypocrisy every time publication-based practice tries to pass itself off as true evidence-based care.

And I’ll challenge our colleagues to be more rigorous in gathering the long-term outcomes, and using newer research tools like SCEDS that support clinical research behind the approaches they are teaching.

Because none of it stands on it’s own and our kids deserve a solid foundation.

Come join me on this allergy free journey to knowing better and doing better.

And the responses were stacking up - from thoughtful questions, ‘what does this infant look like on the floor?’ to practical ideas, and possible culprits like reflux. Social Media shines when speedy brainstorming and shared ideas are what you’re looking for. Sometimes, that quick-fire exchange is exactly what’s needed. But here’s what nagged at me: the response that racked up the most likes was, “What’s the HINE score?”

The HINE (Hammersmith Infant Neurological Examination) is described as

a simple and scorable standardized neurological examination that can be used to help identify infants between 3 and 24 months of age who have a high probability of all types of CP. It includes 26 items assessing cranial nerves, posture, movements, tone and reflexes (ref)

And it is a fantastic tool. It gives us standardized data, helps sidestep subjectivity, and can flag high-risk infants early. But you know what it can’t do? Tell you WHY this baby is arching, and what needs to be done about it.

To figure that out requires so much more than a tick box assessement - and if we’re not thinking about the WHY - then we’re not just fumbling. We’re risking falling into burnout, lost between what’s expected and what we actually know. Sometimes it gets dressed up and we call it “burnout.” In truth, it’s deeper:

So much of pediatric neurodisability education now is about WHAT to do - How to score, when to refer, which guideline to follow. Rarely do we get to dig into the WHY. Why is this child choosing extension? What’s happening with their breathing, their eye-gaze, their posture, their sensory world? The true magic (and the hard work) lives here: in clinical analysis, in curiosity, in connecting the dots that a checklist can’t see.

You don’t learn them from a clinical guideline or a publication or a meta-analysis of a bunch of RCTs.

You learn them from attending courses that teach you to observe, to connect dots, to be curious and to do it all from a solid foundation of understanding components of movement, system interaction and typical development.

Where are therapists getting that kind of learning these days?

I know back in the day that was my Bobath/NDT training - but the relentless traffic light campaign has all but killed that route - So I’m honestly asking: Where are therapists today getting this kind of learning? Who’s teaching new-to-peadiatric therapists to merge evidence with insight and bring clinical reasoning to life?

And there is unquestionably a mountain of research showing Botox is effective in decreasing spasticity and increasing range of movement in children with cerebral pasly… in the short term.

And there’s the catch!

Despite being ‘mainstream’ for more than two decades, there is deafening silence on the long-term benefits and harms of this poison that we are so willing to inject into developing muscles of 18 month old children, 3 year old toddlers and anyone else who has the label ‘cerebral palsy’.

I was a huge fan of Botox in the early years, but around 2010, I started to feel a little uneasy about what I was seeing. With each subsequent injection, children seemed stiffer, the Botox seemed less effective, and I was left wondering if what I was seeing was jus the natural sequalie of cerebral palsy, or that each subsequent injection was giving us diminishing returns.

And then I saw some research to support this, and a trickle of other ‘nay-sayers’ some pointing to significant changes in muscle morphology. And I’ve now reached a point where I am no longer a fan.

If you push aside the overhwhelmingly positive research regarding short term efficacy studies, there is a growing number of stuides discussing potential long-term harms and very few studies to support long-term benefits. Quantity and mass consensus is not a replacement for quality and truth when it comes to research (or anything else of value)

So here are a few studies and thoughts that have moved me from super fan to non-believer.

[Brought to you by me and my co-writer, Perplexity]

Does Botox improve Therapy Outcomes?

1. BTX-A + Physiotherapy vs. Physiotherapy Alone

• Study: Intramuscular botulinum toxin prior to comprehensive rehabilitation has no added value for improving motor impairments, gait kinematics and goal attainment in walking children with spastic cerebral palsy (2018)

• GMFCS I-III, multi-center comparitive study (65 children)

• Design: Intensive therapy with and without Botox.

  • Functional leg muscle strength, passive range of motion, angle of catch, cerebral palsy-related pain, walking speed, kinematic gait parameters, goal attainment, and proxy-reported general functioning were assessed at baseline, primary end-point (12 weeks) and 24-week follow-up.

• Findings: no statistically significant differences in treatment effects between the groups.

2. BTX-A + Casting vs. Casting Alone

• Study: The Effects of Botulinum Toxin and Casting in Spastic Children With Cerebral Palsy: A Systematic Review and Meta-Analysis (2023)

• Design: five publications with a total of 190 cerebral palsy patients were included in this systematic review and meta-analysis

• Findings: no significant difference between BTX-A and casting alone for spasticity management

2. BTX-A in the lower limb vs. PhysiotherapyAlone

• Study: The efficacy of botulinum toxin A lower limb injections in addition to physiotherapy approaches in children with cerebral palsy: A systematic review (2019)

• Design: The population represented by this systematic refview were age between 11 month to 15 years. Overall there were 153 children all diagnosed with CP

• Findings: The question of whether the treatment of BTX-A plus physiotherapy has a greater improvement on functional capacity, such as gross motor function or gait parameter than only physiotherapy treatments, was inconclusive.

3. BTX-A + Therapy vs. Therapy Alone (Post-Stroke)

• Study: Efficacy of physical therapy associated with botulinum toxin type A on functional performance in post-stroke spasticity: A randomized, double-blinded, placebo-controlled trial (2018)

• Design: Patients with post stroke spasticity were enrolled either to BTx-A injections and a pre-defined program of physical therapy or saline injections plus physical therapy. Primary endpoint was functional performance evaluated through time up and go test, six minutes walking test and Fugl-Meyer scale for upper limb. Secondary endpoint was spasticity improvement.

• Findings: there was no difference regarding functional performance after 9 months of treatment. When analyzing gait speed and performance, both groups showed a significant improvement in the third month of treatment

CIMT/Bimanual Therapy

• Study: Effects of botulinum toxin A and/or bimanual task-oriented therapy on upper extremity activities in unilateral Cerebral Palsy: a clinical trial (2015)

• Design: 4 groups: BoNT-A-only (n = 5), bimanual task-oriented therapy (BITT) -only (n = 11), BoNT-A + BITT (n = 13), and control (n = 6).

• Findings: BoNT-A showed a significant negative effect at 12 and 24 weeks in the most important goal. BITT, more than BoNT-A + BITT, showed positive effects on the GAS score at 12 (significant), 18 and 24 weeks.

• Study: Botulinum toxin A as an adjunct to treatment in the management of the upper limb in children with spastic cerebral palsy (2004)

• Design: Cochrane Review: To assess the effectiveness of intramuscular BtA injections as an adjunct to managing the upper limb in children with spastic CP.

• Findings: This systematic review has not found sufficient evidence to support or refute the use of intramuscular injections of BtA as an adjunct to managing the upper limb in children with spastic cerebral palsy.

Why This Matters

• Botox is expensive and emerging evidence points to structural and functional changes in muscle tissue, with negative implications for long-term neuromuscular integrity.

• If our mandate is first do no harm, and the benefits of Botox are highly questionable, whilst the side effects are increasingly seeming to be harmful - why would you be injecting this poison into young, developing muscles without robust research to show these changes are not negatively impacting our vulnerable young children?

  Below is a synthesis of key physiological alterations and their clinical correlations:

Physiological Changes

Fibrosis and Extracellular Matrix Changes

• Collagen Deposition: BTX-A triggers increased intramuscular collagen content, particularly in spastic muscles like the gastrocnemius, leading to elevated passive stiffness. This fibrosis is linked to reduced muscle lengthening capacity and contributes to fixed contractures despite transient spasticity relief.

• Inflammatory Response: Histological studies show post-injection inflammatory infiltrates and vascular changes, exacerbating fibrotic remodeling. For example, fibrous tissue proliferation was observed in masseter muscles 4 weeks post-BTX-A

Loss of Muscle Fibrils and Atrophy

• Sarcomere Disorganization: High-dose BTX-A causes microstructural damage, including shortened sarcomeres, mitochondrial swelling, and glycogen accumulation. Synchrotron imaging reveals blurred muscle fiber edges and reduced anisotropy, indicating loss of linear fibrillar organization.

• Muscle Fiber Atrophy: BTX-A induces type-specific atrophy, with fast-twitch fibers disproportionately affected. Animal studies demonstrate 20–40% reductions in muscle mass and cross-sectional area, linked to acetylcholine blockade and prolonged disuse.

Cellular Damage and Regeneration

• Apoptotic Pathways: BTX-A activates endoplasmic reticulum stress and unfolded protein responses, leading to heterochromatic nuclei (indicating apoptosis) and autophagic vacuole formation. These changes are dose-dependent and ONLY partially reversible within 3–6 months.

• Regenerative Attempts: Centralized nuclei in muscle fibers—a hallmark of regeneration—are observed post-injection, but repeated doses impair complete structural recovery.

• Medial Gastrocnemius Muscle Properties of Children With Cerebral Palsy After Different Tone Treatments

  • This study looked at the muscles of 3 kids with a biopsy from gastrocs taken during TAL surgery

    Child 1 - minimal tone treatment

    Child 2 - Frequent Botox

    Child 3 - Previous SDR

    Please note: ALL children had plantarflexor contractures, weakness, and impaired motor control before the biopsy. ie. Neither Botox nor SDR had prevented contractures in these 3 children.

    Results

    The most pronounced difference was the abundance of centrally located nuclei in the botulinum toxin A participant (52%) compared with the others (3–5%).

    What does this mean? Not really sure but the presence of centrally located nuclei in a muscle biopsy is a significant pathological finding. It is a hallmark feature of muscular dystrophy and other muscle disorders. It's a sign that the muscle is trying to regenerate and repair.

The child who had had frequent Botox had muscles that looked like they had a degeneative muscle disease (52% vs 3-5% in children that were Botox naive).

Neuromuscular Integrity Compromise

• Neuromuscular Junction (NMJ) Remodeling: BTX-A initially causes NMJ sprouting and increased density, but chronic use leads to motor endplate degeneration and reduced desmin expression, destabilizing the cytoskeleton

• ‼Hyper-Reflexia: Paradoxically, BTX-A induces compensatory neuroplasticity in spinal circuits, increasing stretch reflex gain by 150–200% in rat models. This negates intended antispastic effects and exacerbates stiffness.

Clinical Correlations and Sequelae

1. Contracture Development
   Fibrosis and passive stiffness increases (up to 300% in rat TA muscles) directly correlate with loss of joint range of motion, particularly in non-ambulatory CP patients.

2. Functional Impairments

   • Weakened Force Production: Active force range narrows by 25–35% in injected muscles due to fibril disorganization. (Let’s keep in mind that spastic muscles are already weak and we want to strengthen them!)

3. Gait Abnormalities: Microstructural damage from high-dose BTX-A impairs locomotor coordination, as shown in rodent gait analysis.

4. Adjacent Muscle Spread
   BTX-A diffuses up to 45 mm, causing weakness in non-targeted muscles (e.g., dysphagia after neck injections) and altering compartmental biomechanics.

In 2019, Multani et. al. concluded: In this review we found that studies in human volunteers and in experimental animals show muscle atrophy after an injection of BoNT-A for at least 12 months. Muscle atrophy was accompanied by loss of contractile elements in muscle and replacement with fat and connective tissue. It is not currently known if these changes, mediated at a molecular level, are reversible. We conclude that there is a need to revise clinical protocols by using BoNT-A more thoughtfully, less frequently and with greatly enhanced monitoring of the effects on injected muscle for both short-term and long-term benefits and harms.

And lastly - no research to show this, but clinical reasoning suggests that constantly changing the muscle properties on a system that is already struggling with motor learning may not actually help motor learning - here’s a good conversation if you want to dive into this explanation in more detail > A Conversation with Dr Susan Hastings

Conclusion

BTX-A’s antispastic benefits are counterbalanced by dose- and time-dependent structural degradation. Fibrosis and fibril loss create a biomechanical "double bind" where reduced spasticity coexists with increased passive stiffness and contracture risk.

Is weakness, fibrosis, degradation and hyper-refelxia what we’re hoping to provide with our therapy and rehabilitation for kids growing up with cerebral palsy?

Additional references:

Injection of high dose botulinum-toxin A leads to impaired skeletal muscle function and damage of the fibrilar and non-fibrilar structures

Long-Term Effects With Potential Clinical Importance of Botulinum Toxin Type-A on Mechanics of Muscles Exposed

Botulinum toxin injection causes hyper-reflexia and increased muscle stiffness of the triceps surae muscle in the rat

Effect of botulinum toxin type A on masticatory function and musculoskeletal structure in rabbits

Long-Term Effects of Different Number of Botulinum Toxin Injections Into the Gastrocnemius Muscle on Function and Muscle Morphology in Children With Cerebral Palsy

Sarcopenia, Cerebral Palsy, and Botulinum Toxin Type A

Botulinum Toxin in the Management of Children with Cerebral Palsy :

Join the Biz Accelerator

Let’s be honest—none of us became pediatric therapists because we dreamed of wrestling with payroll, chasing down insurance claims, or designing the perfect Instagram post. We chose this path because we’re wired to care, and energized by the possibility of helping kids reach their potential.

Or at least that’s why I became a peadiatric physio (or pedi PT if you prefer).

As pediatric therapists we are uniquely wired for compassion. Which means we naturally pour our hearts into helping children and families, and when the systems we find ourselves working in don’t align with that, many of us dream about starting our own clinics where we get to make the rules.

And when we do, it’s amazing…

Until it’s not.

When therapists step into business ownership, that same deep empathy that makes us excellent clinicians, can make it challenging to set boundaries, prioritize sustainability, and keep our clinics financially healthy.

How do we find the balance between doing what we love - all the heart, warmth and compassion - with being a succesful business owner - assertive, analytical, competitive?

This is exactly what Kelsey Baas and I get into in this interview. And I have to say, I had a few good chuckles when Kelsey was telling me her story, because it could have been my story. Bending over backwards to accomodate everyones schedules, saying “yes” even when it meant stealing time from your own family - not to mention the pro bono kids (you know what I’m talking about).

Kelsey’s runs Compleo, a thriving pediatric clinic in Texas employing 20 clinicians across multiple disciplines (PT, OT, mental health, lactation, dietetics, etc.). Her story is not one of overnight success. It’s about a lot of grit and missteps, sustained by a vision for a clinic that not only provided compelete care, serving the whole family (that’s where the name comes from), but also attracted and retained exeptional clinicians.

And she’s doing it!

In this interview we dig into how Kelsey grew from taking on too many free clients and not paying herself, to running a financially stable clinic with amazing staff and a flexible work schedule that still gives her time to be a mom.

It was such a great conversation and I highly recommend you listen to the whole thing, but my favorite advice was a counterintuitive gem!

This isn’t just a productivity hack; it’s a mindset shift that frees you to focus on your strengths and passions - which is why you wanted to start your own clinic in the first place right? You’ll move further, faster by investing in support for your weak spots and doubling down on the areas that light you up.

I love this!

(side note: think TMR - practice the easy stuff first 😉)

Here’s some other great strategies Kelsey shared:

• Set and honor your boundaries—for your time, your staff, and your services.

  • Map out your ideal week

  • Time block

  • Delegate scheduling

• Track your finances closely—know your break-even point, your cost per patient (not what you bill per patient), and what you need to thrive. When you do this, you can make decisions that allow you to give generously—without risking your clinic’s future.

  • Understand the difference between revenue and profit

  • Track your expenses obssesively

  • Put your own oxygen mask on first - if your clinic is not making money, you’re not going to be able to sustain the pro-bono work you want to offer.

• Seek mentorship and support early—you can’t be an expert at everything. Invest in help where you need it, so you can focus on what you do best.

If you’re nodding along, but still feeling like you’d just love someone to just take your hand and lead you gently through the steps to starting or growing your clinic into a thriving business that is as sustainable as it is compassionate, then I get you! You’re definitely going to want to come hang out with me and a bunch of other clinic owners in June as we work through implementing this stuff in real time, but in the meantime here’s some take-aways from Kelsey’s interview that you can action today:

1. Invest in yourself first

   Kelsey’s biggest regret was not hiring a business coach earlier, but she also gives some great advice about courses you can take to make sure you’ve got the basics under control. For example, practical courses or downloadable checklists on legal setup, documentation systems, and taxes

2. Track One Metric This Month
   Revenue, cost per patient, no-shows—pick one. Building knowledg around your financial metrics, and the true cost of treating each patient makes every other decison easier and is the key to long term sustainability.

3. Build Your Village

   Being the boss can be lonely. No matter how much you love your staff, and they love you, they are no longer your peers. You are the one carrying the weight of your clinic, navigating challenges and making the hard decisions. Having other pediatric clinic owners to bounce ideas off isn’t just a nice-to-have; it’s the secret sauce that fuels creativity, resilience, and growth. Don’t go it alone - invest in your peer-to-peer relationships.

4. Embrace your compassion, it’s is your secret weapon

   Compassion is what naturally drives you to invest in your families and your staff’s well-being so you see better outcomes and higher satisfaction. Just make sure to share some of that compassion with yourself!

If integrating compassion with clear financial strategies and boundaries (so that your care for others doesn’t come at the expense of your own sustainability) is something you want to get better at, then you might want to join Kelsey and I for a 7-week Biz Accelerator starting in June, packed with practical business skills, mentorship, and the kind of community support that will energize you.

We’re going to walk you through

• Setting boundaries without guilt

• Hiring clinicians who share your vision

• Building systems so your clinic runs without you

This isn’t about becoming a CEO. It’s about creating a practice that fuels your passion and pays the bills.

Sign up HERE if you want to join us.

Mindy Silva (Believer in messy, joyful collaboration.)

Join the Biz Accelerator

If we only focus on muscles and milestones, we’re missing the real, messy, life-changing work our kids desperately need.

AND WE’RE NEVER GOING TO SEE THE RESULTS WE’RE HOPING FOR.

It’s taken me a few (many) years to get here, but I truly believe that ignoring the gut is harming our kids, and it’s time to shout to the world about it.

Why Now?

Because first and foremost, the kids and families struggling continence and constipation are seriously impacted (excuse the pun) and although it’s true that we should have helped them get it sorted years ago - NOW is the next best time.

And the best person to help us do that is Dawn Sandalcidi, PT, RCMT, BCB-PMD

Dawn is a pioneer in this work and I have been so privileged to be able to work with her as one of our Clinical Excellence Online (CEO) experts.

I could make a long list of the things she has helped me see - that were honestly hiding in plain site, but the first thing I had to learn from her (and she’s so great at teaching it) is to not feel weird talking about pee and poop to families and colleagues.

So now, totally reformed and comfortable in this space, here’s 5 stories that should make you uncomfortable. Not because we’re talking about pee and poop, but because we’ve all had kids like this and it’s uncomfortable to think that we may have missed some huge opportunities to help them, simply by reaching out to Dawn and other therapists experienced in this area of work.

Uncomfortable is good!

Most times we need to get pushed out of our comfort zone to make changes for the better, and these stories will make you feel uncomfortable about not taking action. They are inspiring, motivating, mind blowing and life changing (and I’m not exaggerating).

Tell me if it doesn’t give you that loving nudge to reach out to Dawn to pick her brain and absorb some of her wisdom!

You can do just that! Just Click HERE to join us

1. The Persistent Wetting Mystery: “They Poop Every Day-So What?”

This 7-year-old was seen by every specialist under the sun and still struggling with wetting accidents. Mom (a nurse!) and the therapist were convinced constipation wasn’t the issue. After this child was pooping daily, no pain, no smearing.

But value of years and years of clinical experience meant that Dawn saw something nuanced in the case history and suspected otherwise.

Sure enough, scans confirmed her suspicions.

Dawn goes on and on about this and this story really brings it home » daily poops don’t mean a child isn’t constipated, especially when other symptoms persist.

Have a listen to see how they addressed this and the fabulous outcomes they saw

2. The Spinning Top Urethra: When “Try Harder” Isn’t the Answer

A 9-year-old with seven outfit changes a day.

Think about how this impacts quality of life.

Even though the family and medical team doubled down on constipation treatment, the wetting was getting worse and the team was stumped.

Dawn cut through the noise and called a rare diagnosis-spinning top urethra - none of the specialists had picked this up but when mom had the info she needed to take to the team from Dawn - the diagnosis was confirmed.

It’s such a win for the family and reminder of the value of clinical wisdom. We are the one that spend the time understanding the whole picture for the family, and when we team up with an expert who spends ALL her clinical time on this topic - it’s not really surprising that it’s the therapists who figure it out!

3. The Night Wetting Breakthrough: “Almost” Fixed Isn’t Fixed

A 13-year-old with endless night wetting, even after textbook-perfect therapy and GI protocols. The specialists had discharged and recommended behavioral interventions - but the therapist was not ready to give up?

One CEO session with Dawn and the missing puzzle piece surfaced. One tweak to the program and for the first time this child was having success with being dry.

Sometimes being satisfied with “almost there,” is not good enough. Real change by real expert collaboration changes lives.

4. Avoiding Surgery: The 4-Year-Old Who Didn’t Need a Colostomy

This story is so important to pay attention to.

A 4-year-old lined up for a colostomy!!

Such invasive surgery because the team had not been able to manage significant chronic constipation and where reaching for last resorts. Working with the therapist, guided by Dawn, this child is out of nappies, off laxative and did not need surgery!

Life changing is an understatement…

5. A Wake-Up Call: “I Didn’t Know What I Didn’t Know”

When an uber experienced therapist says she didn’t know, it gives us all permission to be a little kinder to ourselves - but also to step up and take note.

You can’t know that you’re missing a big piece of the puzzle when you don’t even have the right puzzle in front of you.

Working with Dawn was a transformative experience for this six-year-old with severe dyskinetic cerebral palsy experiencing unexplained pain and distressing episodes.

Addressing chronic, severe constipation that had been present for decades produced unexpected wins.

Huge wins!

Decreased tone, better sleep, better regulation!

Better motor function!!

Dawn’s expert guidance on fluid intake, bowel clean-out, and collaborative care led to dramatic improvements. Bowel health was a crucial gap in treatment for this child but like so many of us do - we just assume that difficulties managing bowel and bladder are just part of the CP picture.

Ie we’re not asking the questions that need to be asked - and its so within our wheelhouse to support families with these simple bowel and bladder strategies- or look for more expert answers when we need to.

Kids can’t thrive if their basic body functions aren’t working-and neither can their families.

You don’t have to be an expert to make a difference. Start by asking the right questions. Get curious. Partner with specialists when you need to. And never underestimate the power of looking beyond what you’ve always done.

We owe it to our kids to see the whole picture-not just the muscles, not just the milestones, but the messy, real-life stuff that makes or breaks their quality of life.

If you’re a therapists who isn’t afraid to ask, “Could this be a bowel or bladder issue?”

Then come join our live Zoom workshop » An Ask-Me-Anything with the amazing Dawn Sandalcidi

You’re not alone in this. I’ll be there asking questions too.

And honestly? The changes you might make from the things that you learn are bigger than you think.

Ready to talk about the stuff nobody else wants to? Good. That’s where the real change starts.

Click HERE to join us

Listen to Dawn’s WiredOn Development Interview HERE

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You got my attention

I’ve been wanting to start a Substack for a few months now, and a recent post by a parent asking questions about NeuroCytonix ramped up my motivation to have a place where we could share long-form thoughts and ideas about things that impact us as pediatric therapists, and impact the children and families we work with.

So welcome to my musings, let’s jump in…

Why This, Why Now?

Recently, a new intervention called NeuroCytonix has been making waves, promising “quantum magnetic resonance therapy” to stimulate brain repair and functional gains. The slick marketing and heartwarming testimonials are guarenteed to get parent’s attention, but the promise of a randomised clinical trial that has legitimatly been registred at clinicaltrials.gov takes things to a whole other level in terms of legitimacy and hope. So I spent a few hours exploring this approach and here’s what I found…

What Is NeuroCytonix?

NeuroCytonix is based on technology originally developed for cancer treatment, using non-invasive radio frequencies to “stimulate neurogenesis and repair.” The therapy’s creator, Dr. J. Roberto Trujillo, is a physician-scientist with a background in infectious diseases and cancer, not neurodevelopmental disorders. The company claims their device can improve motor function, reduce spasticity, and even enhance brain connectivity in children with CP.

The Clinical Trial: What’s Actually Been Studied?

In 2018, Dr. Trujillo’s team registered a randomized, two-arm, double-blind, placebo-controlled trial in Mexico (NCT03743623), enrolling 52 children with CP. The trial reportedly finished in 2021, but as of this writing, no results have been published in peer-reviewed journals, nor have any conference presentations or protocol papers been made public. This is highly unusual for a study of this size and scope.

Let’s break it down:

First to get clear on the terminology (it sounds very fancy)

1. Randomized - this usually means that participants were randomly select to receive either the actual treatment or a sham treatment. In the study description registered on clinicaltrials.gov it is unclear if patients are paying for treatments if they are part of the study.

   1. On social media, parent’s note that it is an exceptionally expensive treatment and this raises an initial concern.

2. Double-blind - Neither the participants or the researchers / practitioners were aware if the treatment was sham or real

3. Two-arm just means there were two treatments - the sham and the actual treatment.

4. Placebo-controlled just means their was a treatment group who got the actual treatment and a control group that didn’t

Key Concerns with the Study Design

1. There is no research available at all for the Neurocytoron. Parent’s have been told that it takes a long time for research to be published. However, typically researchers will start building up to a clinical trial by doing literature reviews and publishing articles related to the topic BEFORE they jump into a randomized controlled trial (RCT). One would expect articles discussing the theoretical background and how they came to develop the novel intervention. In addition, it is typical (and expected) for RCTs to have a protocol paper published describing the RCT and it’s rationale before the trial starts. Considering this study was initially registered in 2018.

   1. Dr Trujillo is a Harvard trained and published scientist. He is not a clinician with limited experience in research and academics. It is not unreasonable to expect to see a protocol or related theoretical publication by now.

   2. Note: Registering a trial with clinicaltrials.gov is not equivalent to publishing a protocol paper. Anyone can register a trial. It is not peer-reviewed.

2. Dr Trujillo has no publications on Cerebral Palsy (CP) or neurodisability. His work has predominantly been related to cancer, HIV and other infectious disease. This would not be an issue, however he has not partnered with any specialists in the area of neurodisability and CP for his clinical trial. The lead investigator listed for this RCT on clincaltrials.gov is Lorenzo R Morales Mancías.

   1. I found only ONE publication by Lorenzo R Morales Mancías and this was unrelated to CP, neuromotor disability, neuroplasticity or other areas that may be relevant to the clinical trial

3. Dr Trujillo cites Dr Kumar and his development of the Cytotron as the foundation for his Neurocytonix work. From what I can see, Dr Kumar appears to be involved in work around Quantum Magnetic Resonance Therapy for which there is a small number of studies, and only one by anyone with a surname of Kumar. This study is related to cancer. For someone who has developed a novel treatment, one could again expect more publications.

4. The outcome measures described in the clinicaltrials.gov for this RCT are concerning.

1. Primary outcome measure

   1. Pediatric Evaluation of Disability Intervention (PEDI) and Pediatric Quality of Life Inventory (PedsQL) Scales

      1. Both these measures are subjective and useful as a secondary outcome measures - but not a primary measure

   2. Ashworth Scale from Baseline and Gross Motor Scale

      1. The Ashworth scale is subjective, does not differentiate spasticity from fascial restrictions and muscle tightness and does not measure the dynamic nature of spasticity or deficits in motor control which is the primary difficulty in CP

      2. Gross Motor Scale? I’m not even sure what this is - The GMFCS maybe? This is a diagnostic reference, not an outcome measure.

2. Secondary Outcome measures

   1. Reduction in Use of Baseline Drug Treatment [Time Frame: 28 Days] compared to Placebo Group

      1. I am assuming this is in relation to anti-epileptics or drugs like Baclofen or similar tone reducing medications. It’s unclear in the description, however 28 days is insufficient to judge the effect of decreasing these meds.

   2. Decreases in Use of Orthoses [Time Frame: 28 Days] compared to Placebo Group

      1. Considering no one on the study seems to have any neurodevelopmental expertise - how will they judge if decreasing orthoses is appropriate in terms of gait kinematics and biomechanics. This then becomes a subjective measure with no objective data.

   3. Reductions in Number of Seizures or Epileptic Crisis [Time Frame: 28 Days] compared to Placebo Group

      1. This time frame is not long enough to judge outcomes in epilepsy

   4. Changes in functional activity and brain anatomy [Time Frame: 28 Days] Using functional Magnetic Resonance Imaging (fMRI), Diffusion Tensor Imaging (DTI) and Electroencephalography (EEG)

      1. Why are these objective measures (the only objective measures that might be meaningful) listed as a secondary outcomes?

3. Finally - no results are posted despite finishing the study in 2021, no references or links are provided and families are still being told, “it takes time to publish”. They recently updated their clincaltrials.gov submission to show the study is current. What was the update? A change of address and an increase in the study participants from 52 (in 2021) to 53 in Feb 2025.

   

   Marketing vs. Medicine

Perhaps most concerning is the marketing approach. All information is heavily directed at families with very slick marketing and emotive language. The ‘case studies’ are fluffy with no substantive data to back them up.

• They show images of MRI’s superimposed with pretty graphics to represent increasing brain connectivity, but no actual data against which these claims can be checked or verified.

• They show snapshots of kids but no progression videos or data to back their claims.

• There are no references to conference presentations,

• There are no backup of results from other experts not associated with the company

• There is no transparency about treatment costs.

What Does This Mean for Therapists and Families?

Evidence can take time to gather and publish, but the scientific underpinnings of an approach should be verifiable.

In addition, innovation is essential if we are going to seek better outcomes for the children we work with but extraordinary claims require extraordinary evidence.

At this time, I could not find any published data to support NeuroCytonix’s claims. Nothing that would typically be expected from a Harvad trained and published scientist.

Bottom Line

• No published evidence supports NeuroCytonix for cerebral palsy as of May 2025.

• Study design concerns and lack of transparency raise significant red flags.

• Marketing is outpacing science-be skeptical of emotive testimonials without data.

Dr Trujillo may be an accomplished physician and scientist who believes in his work, but there are too many red flags and nothing of substance to balance these for me to buy into this ‘novel approach’.

Bottom line: Don’t feel guilty for not mortgaging your house for this one.

Resources & Further Reading:

• ClinicalTrials.gov: NCT03743623

• NeuroCytonix Official Site

• LinkedIn: Dr. J. Roberto Trujillo

Feel free to correct my thinking on this topic or share any relevent research or evidence.

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