Neurophysiological Model replacing Root's Biomechanical Model

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Up until approximately 2008, I thought in terms of Foot Biomechanics. That postural shifts and resulting chronic musculoskeletal pain were a result of faulty Foot Biomechanics.

The Biomechanical model ascribes postural shifts to gravity. The analogy would be a house built on soft ground. As the foundation shifts, so goes the entire structure (as the foot hyperpronates, so goes the entire postural complex)—a very compelling theory, but unfortunately, not true.

For the past 17 years or so, my research has revolved around the Neurophysiological model as the engine that drives postural shifts:

1 Gravity forces the PreClinical Clubfoot Deformity to roll forward, inward, and downward until the entire plantar surface of the foot rests on the ground.
2 This displaces the CoP patterns medially (See attached diagram, left).
3 This skewed CoP pattern is transmitted to the brain stem (e.g., the Foot's Sensory Feedback).
4 The brain stem has an encoded pattern that it compares to all sensory feedback coming from the feet (See attached diagram, right).
5 If these patterns differ, the brain stem diverts the foot’s sensory feedback to the Cerebellum.
6 The Cerebellum acts on this skewed information and globally distorts the posture on all 3 body planes.

Pretty amazing stuff!

Rothbart BA 2011. Twisting Foot and Musculoskeletal Pain: Root’s Biomechanical Model vs Rothbart’s Neurophysiological Model. Podiatry Review, Issue 186, September.

 

A large percentage of the orthotics commonly manufactured today (Kwemli 2025) distort the posture, resulting in increased musculoskeletal pain.

A formidable statement.

Any refutes?

Kwemli K., 2025. Engineering Smart Orthotics: Improving Mobility and Comfort. IDOSR JOURNAL OF COMPUTER AND APPLIED SCIENCES 10(2):1-7

 

Some believe that the majority of the sensory feedback from the foot, at least in terms of CoP, comes from nerve endings in the intrinsic foot muscles.
Certainly the evidence indicates that a large percentage comes from this source.
Re your insoles ,do you claim they improve sensory feedback from the foot muscles, the cutaneous tissues of the sole of the foot ,both ,or a different set of sensory nerve endings.

 

I believe Viseux (and I) would argue that most of the foot's sensory feedback to the brain stem comes predominantly from the Meissner corpuscules and Merkel's disks, not from the Golgi Tendon Organs, which are embedded in the muscles.

The proprioceptive insoles I use to stabilize posture in patients born with the PreClinical Clubfoot deformity function by shifting the CoP patterns laterally. This unskews the sensory feedback transmitted to the brain stem, resulting in the postural adjustment.

One might refer to this unskewing as improving the foot's sensory feedback.

Viseux FJ 2020. The sensory role of the sole of the foot. Review and update on clinical perspectives. Neurophysiol Clinic, Feb;50(1):55-68.

 

There are a number of textured insoles out there and they do seem to improve standing balance. Any reason your insoles aren't textured?

 

Textured insoles stimulate the Merkel's disks while standing. The insoles I use are textured.

 

You believe that the muscles of the foot have little to do with proprioceptive feedback?

 

Over the past 20 years or so, my research has focused on unraveling the foot's neurophysiological feedback associated with the maintenance of upright posture.

I believe the preponderance of the foot's plantar sensory feedback is generated via the activation of the Meissner Corpuscules (walking) and Merkel's disks (standing). I believe the GTO (Golgi Tendon Organs) play a minor role (at best) in the foot's plantar sensory feedback to the brain stem/cerebellar complex.

Having read many of your contributions on this forum, I appreciate the fact that you may feel differently.

 

So you have studied the intrinsic foot muscles extensively ?

 

I was a Podiatric surgeon for nearly 20 years. So yes, I have studied the intrinsic foot muscles extensively.

 

Brian, at your invitation I read through pieces of your research on ResearchGate and, from memory, there was nothing of any substance on the intrinsic foot muscles.

A paper was recently published on the very subject we are now discussing, whether the intrinsic foot muscles have a significant role to play in proprioception. Have you had a chance to read it yet ? Cutaneous mechanoreceptors in the toes don't seem to have much of a role to play in recording fluctuations in COP but receptors in the muscles do.

Could a wedge placed under the big toe advantageously alter afferents from muscles like the abductor hallucis and flexor digitorum brevis, at least in some cases. Quite possibly, IMO.

Firing properties of muscle spindle afferents in the intrinsic foot muscles and tactile afferents from the sole of the foot during upright stance

Thomas P. Knellwolf, Alex Burton, Elie Hamman, Vaughan G. Macefield
First published: 10 April 2025
https://doi.org/10.1113/EP092348

"Conclusion from paper
So, what does this mean? Are cutaneous afferents or muscle spindle afferents more important in postural control? Our observations cannot differentiate between the relative roles of muscle spindles and cutaneous afferents; clearly, both can encode various aspects of upright stance and its perturbation. However, it can be argued that much of the information provided by tactile afferents, with the potential exception of SA II afferents, appears to be incidental (e.g. making and breaking contact with the supporting surface during behavioural or reflex toe movements). It remains to be seen whether stable recordings can be obtained during walking on a treadmill, which is something we are currently embarking on."

 

The location and action of the foot’s intrinsic muscles occupies a great deal of attention, during our 4 years in Podiatric training and especially during our internships and residencies, where we receive most of our surgical training.

I am aware that there is no universal agreement as to which mechanical receptors contribute the preponderance of sensory information to the brain stem and cerebellum in maintaining upright posture. Some researchers hold that it is the muscle spindles, others argue that it is the Meissner corpuscules and Merkel Disks that provide the majority of sensory feedback to the brain stem (this has been the results of my research).

In my research (using pressure plate studies), I have demonstrated, when dealing with the PreClinical Clubfoot deformity, using precision wedges underneath the medial column of the foot, shifts the CoP patterns (the aggregate of Meissner Corpuscules which are FA-I) laterally. This altered CoP pattern is transmitted to the brain stem, then relayed to the cerebellum, where the postural adjustments are made. (Again, this comes from my research, hopefully replication will come quickly. As a side note, it took 20 years for replication/confirmation that the medial column supinatus, aka Rothbarts foot, is found in the adult foot)

Researchers holding that the Golgi Tendon Organs are the primary sensory receptors involved in postural control, have not, to date (I believe), demonstrated how this occurs. I will be very interested in reading their research findings (and extrapolated explanations).

 

Sure, but things have moved on a lot in the last 40 years.

Could we stick to accepted medical terms ?

Likely both cutaneous receptors and muscle spindles play important roles in proprioception in the foot.
Having said that, Knellwolf et al have shown that only a proportion of cutaneous nerve endings faithfully code for COP fluctuations those being "slowly adapting type II endings" ( Ruffini corpusles).
Cutaneous mechanoreceptors

Cutaneous mechanoreceptors respond to mechanical stimuli that result from physical interaction, including pressure and vibration. They are located in the skin, like other cutaneous receptors. They are all innervated by Aβ fibers, except the mechanorecepting free nerve endings, which are innervated by Aδ fibers. Cutaneous mechanoreceptors can be categorized by what kind of sensation they perceive, by the rate of adaptation, and by morphology. Furthermore, each has a different receptive field.[citation needed]

Tactile receptors.
By sensation

• The Slowly Adapting type 1 (SA1) mechanoreceptor, with the Merkel corpuscle end-organ (also known as Merkel discs) detect sustained pressure and underlies the perception of form and roughness on the skin.[1] They have small receptive fields and produce sustained responses to static stimulation.[citation needed]
• The Slowly Adapting type 2 (SA2) mechanoreceptors, with the Ruffini corpuscle end-organ (also known as the bulbous corpuscles), detect tension deep in the skin and fascia and respond to skin stretch, but have not been closely linked to either proprioceptive or mechanoreceptive roles in perception.[2] They also produce sustained responses to static stimulation, but have large receptive fields.[citation needed]
• The Rapidly Adapting (RA) or Meissner corpuscle end-organ mechanoreceptor (also known as the tactile corpuscles) underlies the perception of light touch such as flutter[3] and slip on the skin.[4] It adapts rapidly to changes in texture (vibrations around 50 Hz). They have small receptive fields and produce transient responses to the onset and offset of stimulation.[citation needed]
• The Pacinian corpuscle or Vater-Pacinian corpuscles or Lamellar corpuscles[5] in the skin and fascia detect rapid vibrations of about 200–300 Hz.[3][6] They also produce transient responses, but have large receptive fields.
• Free nerve endings detect touch, pressure, stretching, as well as the tickle and itch sensations. Itch sensations are caused by stimulation of free nerve ending from chemicals.[7]
• Hair follicle receptors called hair root plexuses sense when a hair changes position. Indeed, the most sensitive mechanoreceptors in humans are the hair cells in the cochlea of the inner ear (no relation to the follicular receptors – they are named for the hair-like mechanosensory stereocilia they possess); these receptors transduce sound for the brain.[7]

Abstract

We review our approach for undertaking microelectrode recordings from the posterior tibial nerve at the ankle, which has allowed us to identify, for the first time, the firing properties of muscle spindle endings in the intrinsic muscles of the foot and of cutaneous mechanoreceptors in the sole during unsupported standing. The responsiveness of muscle spindles in the short muscles of the foot to stretch and related joint movements was similar to that of spindles located in the intrinsic muscles of the hand. Only 27% were spontaneously active in the unloaded condition, whereas 50% were active during unsupported free standing. Moreover, in the latter condition firing rates of 67% of the endings were correlated with changes of the centre of pressure (CoP), primarily (88%) along the anteroposterior axis. The firing of cutaneous afferents supplying the sole of the foot in unsupported free standing depended on the receptor type and location of the receptive field: fast-adapting type I and slowly adapting type I afferents responded transiently during contact with the substrate on standing and to spontaneous postural adjustments, whereas the tonic firing of slowly adapting type II endings encoded fluctuations in the CoP. We conclude that muscle spindle endings in the intrinsic muscles of the foot are recruited or increase their spontaneous discharge on standing and can faithfully encode changes in CoP during spontaneous or evoked postural sway, a function shared by slowly adapting type II afferents in the sole. These data emphasize the important contributions of sensory sources in the foot to maintaining and responding to perturbations in upright posture.

 

My Neurophysiological Postural Model (NpPM) is a recent paradigm. I first published on this model in 2011. I acknowledge that currently, NpPM is controversial. But I have a high level of confidence that it will be independently replicated.

Analogously, when I first published on Rothbarts Foot in 2002, characterized by medial column supinatus, and presented my research on this forum in 2006, I felt like I had entered an angry hornet nest! Fast forward nearly 20 years and the existence of medial column supinatus was independently replicated.

This time, I hope NpPM will be independently replicated in less than 20 years.

Regarding sticking to accepted medical terms, the NpPM is a departure from mainstream views, and new concepts sometimes entail new nomenclature. That was the case with Rothbarts Foot, and this is the case with the NpPM.

The abstract you provided above is currently accepted by many researchers. I am not one of them. I believe my research model is correct.

I just recently uploaded a paper on Academia.edu that will be published online in September 2025 (Positive Health Online). This paper presents an up-to-date synopsis of the NpPM. You can preview this paper at:

https://www.academia.edu/143331897/PreClinical_Clubfoot_Deformity_The_Rothbart_Foot_Paradigm


Rothbart BA 2011. Primus Metatarsus Supinatus (Rothbarts Foot): A common cause of musculoskeletal pain – Biomechanical vs Neurophysiological Model. Podiatry Review. 64(4):16-18.

 

A number of papers have been published recently which appear to demonstrate that foot stretching can improve balance in a number of compromised patient groups . For example dynamic foot stretching improves balance in MS suffers as well as stroke victims. Also, the older you get the more you can benefit from maintaining foot strength and flexibility. There is so much that can be improved by simply getting people to maintain their foot health.

With regard to proprioception, the bodies main sources of sensory information are the nerve endings in the muscles, tendons , joints and fascias . The idea that such nerve endings suddenly cease to significant when we come to the foot, which is full of joints and muscles, is frankly ludicrous.

Knellwolf et al was published only a few months ago and teaches towards receptors in the intrinsic muscles making a large contribution to signalling changes in COP but away from the majority of receptors in the cutaneous tissues doing the same.


Medicine (Baltimore). 2025 Feb 21;104(8):e41507. doi: 10.1097/MD.0000000000041507
Effects of foot intrinsic muscle dynamic stretching on balance, gait parameters, and dynamic gait index in patients with chronic stroke: A randomized controlled study (CONSORT)
Younghwan Kwag a,b, Donghwan Park b,*

• Author information
• Article notes
• Copyright and License information

PMCID: PMC11857030 PMID: 39993133
Abstract

Background:

Foot intrinsic muscle dynamic stretching intervention can correct balance ability and induce a change in spatiotemporal parameters gait ability. Our objective was to compare the effects of a 4-week program of foot intrinsic muscle dynamic stretching with those of lunge exercise on static balance, dynamic balance, gait parameters (velocity, cadence, step length, and stride length), and the dynamic gait index (DGI) in chronic stroke patients.
Methods:

The participants were randomized to either the foot intrinsic muscle dynamic stretching (n = 10) or standard lunge exercise (n = 10) groups. Both groups performed 3 sets of lunge exercises 5 times per week for 4 weeks. Each set comprised 10 repetitions. Static and dynamic balance, gait parameters, and the DGI were measured after 4 weeks of training.
Results:

After 4 weeks of training, the foot intrinsic muscle dynamic stretching group showed significant improvement in all outcome measures compared with the baseline (P < .05). Furthermore, timed up and go, velocity, step length, stride length, and DGI showed greater improvement in the foot intrinsic muscle dynamic stretching group than in the standard lunge exercise group (P < .05).
Conclusions:

This study demonstrated that foot intrinsic muscle dynamic stretching training improved dynamic balance, velocity, step lengths, stride length, and DGI in patients with chronic stroke.

 

Excellent paper, but not relevant to our present discussion regarding the role that the foot's sensory receptors have on posture (not the role intrinsic foot muscles play in balance and gait in stroke patients).

To reiterate, hopefully to clarify:

My research focused on identifying the etiology of musculoskeletal pain. Primus Metatarsus Supinatus (also known as Rothbarts Foot) and the Preclinical Clubfoot Deformity are the most prevalent causes of abnormal (gravity-driven) foot pronation.

Neurophysiological Postural Paradigm:

• Abnormal pronation alters the Foot's Sensory Feedback to the cerebellum.
• The cerebellum decodes this modified information.
• The result is a distorted posture.
• In time, distorted posture leads to chronic muscle and joint pain.

 

The paper is about improving proprioceptive information from the foot .
From the paper-
"Balance training through foot intrinsic muscle dynamic stretching is thought to improve balance ability as repetitive movements transmit somatosensory sensations from the joints or muscle receptors. Based on our results, we recommend dynamic stretching of foot intrinsic muscle as an effective method to improve balance in patients with chronic stroke."

 

I believe I have already answered you regarding this paper in #16 above. If not, please elaborate.

 

In the figure below, note how closely spindle discharge tracks COP changes (black lines and lighter lines) . The researchers did not find the same close relationship between the majority of cutaneous receptors and COP changes. Intrinsic muscle spindle discharge can clearly inform the brain about changes in COP.

Why would evolution have resulted in the ability of muscle spindles in the intrinsic foot muscles to generate information about COP changes, which are then sent to the brain, if it was not going to be used ?

Although not without a slip or two, Knellwolf is the most up to date and authoritative piece of work on the subject of how afferents are sent to the brain from the foot with regard to COP changes.

Brian, does your "postural paradigm" mention the intrinsic foot muscles at all? If not you might want to reconsider.


Knellwolf et al


FIGURE 6
Open in figure viewerPowerPoint
Spontaneous fluctuations in mean frequency of three muscle spindles (thick lines) superimposed onto corresponding changes in the centre of pressure (thin lines) in the anteroposterior plane. The centre of pressure was smoothed using a Bartlett window of 2 s. (a,b) These recordings correspond to the same recordings shown in Figure 5a,b. (c,d) Data from another two units, recorded from flexor digitorum brevis muscle (c) and flexor hallucis brevis muscle (d), are also shown. Reproduced with permission from Knellwolf et al. (2019).
Finally, although four muscle spindles were not tonically active during free, unsupported standing, they nevertheless responded to transient changes in posture, apparently encoding the resultant changes in muscle length.

 

Thank you for directing me to Knellwolf et.al. paper published in Experimental Physiology (2025). I enjoyed the read.

The subject regarding the Foot's Sensory Feedback role in postural maintenance is a multifactorial system and thus a somewhat complex subject to discuss. However, having said that, I will endeavor to answer your question (regarding the role GTOs play in postural maintenance) clearly and succinctly as I can. Here goes:

I see the Foot's Sensory Feedback as comprising two separate, but distinct systems:

(1) The Neurophysiological Postural system (NPS), which comprises the cutaneous mechanosensory receptors embedded in the skin.
(2) The Golgi Tendon Organ system (GTOS), which comprises the stretch sensory receptors embedded in the musculotendinous junction.
​

And of particular importance, these two systems function very differently. (My research delineates how the NPS functions).

​

Dysfunction in either system can impact posture, but for different reasons:

• Dysfunction in the GTOS occurs from neurological and systemic diseases, and trauma.
• Dysfunction in the NPS occurs from gravity-driven pronation.

My research focuses on the 2 inherited foot deformations that cause gravity-driven pronation. My research does not deal with trauma or diseases that other researchers have linked to postural distortions (e.g., hemiparesis).

IMO, I do not see the GTOS playing a significant role in postural maintenance in the healthy population.

 

Knellwolf et all is not about Golgi Tendon Organs .

 

~
Read my reply above. I did not say that Knellwolf paper was about the GTO. I simply said that I enjoyed the read.

In your reply #3, you mentioned nerve endings. Both GTO and muscle spindles are classified as sensory nerve endings. But apparently, your interest lies in the latter, not the former. I mistakenly thought otherwise.

However, the comments I made about the GTOS, can also be applied, in large part, to the muscle spindle endings (which is the topic in Knellwolf el.al. paper).

 

Looking at Knellwolf et al , afferents from sensory muscle spindles clearly track COP changes closely . The majority of cutaneous receptors don't. The subjects in the study were healthy .

From Knellwolf
"Moreover, selective anaesthesia of cutaneous afferents of the sole of the foot increases postural sway by only ∼11% (Meyer et al., 2004), whereas increases of ∼40%–60% occur in diabetic neuropathy, in which both muscle and cutaneous afferents are affected (Boucher et al., 1995; Simoneau et al., 1994). Accordingly, it is likely that muscle afferents from the foot contribute more to the control of postural sway than do cutaneous afferents, but in the absence of direct data this is speculation."

 

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All new theories are put to the fire. Mine are no exception.
Posterity were judge whether my Neurophysiological Postural Model is correct or not.

 

After all that was said and done, Knellwolf concluded his paper by saying:

"Our observations cannot differentiate between the relative roles of muscle spindles
and cutaneous afferents." (Knellwolf 2024)

So, the jury is still out. More research is required.

However, I believe my Neurophysiological Postural Model (NPM) will prevail: Meissner and Merkel sensory receptors drive the Foot's Sensory Feedback, not the muscle spindles.

Note: The NPM provides the only explanation, to date, on how exactly the Foot's Sensory Feedback modulates posture.

 

Knellwolf

"5 CONCLUSION

So, what does this mean? Are cutaneous afferents or muscle spindle afferents more important in postural control? Our observations cannot differentiate between the relative roles of muscle spindles and cutaneous afferents; clearly, both can encode various aspects of upright stance and its perturbation. However, it can be argued that much of the information provided by tactile afferents, with the potential exception of SA II afferents, appears to be incidental (e.g. making and breaking contact with the supporting surface during behavioural or reflex toe movements). It remains to be seen whether stable recordings can be obtained during walking on a treadmill, which is something we are currently embarking on."

 

That was very considerate of you to reiterate Knellwolf's total conclusion.

That you for reiterating Knellwolf's entire conclusion. But the bottom line is the same:

Up until the introduction of my Neurophysiological Postural Model there was no explanation as to exactly how the foot’s sensory feedback to the CNS altered posture. That all changed with NPM.