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Michael Shacklock has developed a method of

treatment and written a book entitled Clinical
Neurodynamics describing this method. In the text, the
reader is introduced to new diagnostic and treatment
techniques using neurodynamic testing and
movements. The system provides a means by which to
evaluate the ccontributions of the mechanical interface,
the innervated tissue, as well as the neural tissue in
order to create a scheme of treatment. Additionally, he has created a method
of staging the sensitivity of the condition based on physical examination
findings. A progression of treatment is described in a systematic manner.

SomaSimple: Thank you Michael Shacklock for joining us in this program on Somasimple.
We are very pleased and fortunate to have you as our first guest.

In your text, the definition of Clinical Neurodynamics is listed as the following:

clinical application of the mechanics and physiology of the nervous system as they relate
to each other and are integrated with musculoskeletal function.

How did this concept come to be defined?

Michael: Firstly, I'm very honoured to be the first interviewee on Somasimple. I'd like all
your visitors to know that I really appreciate your web site and am so pleased that it
fosters discussion, dissemination and development of this fantastic area.

There are really two parts to the answer to this question.

1. The concept of neurodynamics came to me when I became familiar with the neural
tension approach with David Butler and Helen Slater in the late 1980s and early 1990s
when we were in practice together in Adelaide (acknowledgements to Bob Elvey and Dr
Alf Breig for their earlier pioneering contributions to the area). This was an extremely
stimulating, exciting and formative time for me because the concept of 'neural tension'
was new and growing rapidly with huge interest in regions such as Australia, the UK,
Europe, USA and Canada, to mention only a few. We were developing it with such pace
and intensity that I can only look back on that time with amazement and fond affection.

Anyway, in using the approach on certain conditions, I found that some patients did not
respond well and were sometimes made worse - the acute lumbar nerve root for instance.
I felt that the neural tension approach did not answer a large number of questions that, if
were answered, could really help the approach. So I started reading a subject that I hated
at PT graduate school - physiology. That is when I started reading the basic sciences on
subjects like neurogenic inflammation, neuronal sensitivity (mechanosensitivity),
neuropathy, neuroplasticity, central nervous system mechanisms and finally that four
letter word - PAIN.

So by the end of the 1990s, I had read thousands of scientific and clinical peer-reviewed
papers (I don't read many PT books because I like to get into the detail) and spoken
with authorities in the area such as Professors Patrick Wall, Issy Pilowsky, Ronald
Melzack , Marshall Devor, Marcelo Costa and so forth. Such was the pace and
enthusiasm in our professional environment in Adelaide that, by the mid- 90s, we had
held an international multidisciplinary conference on the subject and produced a book
that has sold almost 10 times the number of copies that was anticipated (Moving in on
Pain, Butterworth Heinemann, 1995). In my inquiries, I learned that mechanics and
physiology of the nervous system are often dynamically interdependent and felt that we
should integrate these aspects in our clinical practice. In 1995, I wrote two papers on
linking the two (Shacklock 1995a, 1995b). That is when I coined the term
'neurodynamics' for physical therapy. It was of course not the first time the term had
been used. It is used ubiquitously in the neurosciences, psychiatry, neuropharmacology
and a wide range of other neural disciplines. But the idea was to encourage therapists to
use many aspects of neural function in their clinical practice in addition to tension, but
only those that were relevant. Neurodynamics became an 'applied science', so to speak.
This naturally meant sliding and compression of nerves, axonal transport, intraneural
blood flow, inflammatory mechanisms and sensitivity of neural tissues.

Fortunately, much of the physical therapy world has adopted the term but more change
is necessary. Still many therapists really only consider the nervous system as a tension
based/mechanical organ with little concern for its movements or physiology. In fact, the
most common search words that land visitors on our web site
(www.neurodynamicsolutions.com) are still 'neural tension'. So there remains much
work to be done for the approach to mature into a fully integrated one.

2. For many therapists, the application of neurodynamics as opposed to neural tension

was a quantum leap. But by the time 2000 had come, I still felt that we needed to make
another jump which was to integrate the nervous system with musculoskeletal function.
This was because still we were mobilising nerves in isolation. Once again, this doesn't
always help, particularly since the mobilisations applied at that time still applied tension
to the nervous system.

The entrance of the neurosciences into manual and physical therapy was changing the
face of clinical practice. We had gone so far into the neurosciences as a fundamental
subject that therapist were getting bogged down on the complexities and not really
coming away with practical clinical neurodynamic solutions. The subject of pain had
entered the fray, which I believe was a fantastic development of course, but we had
moved so far from the physical that there was a gap in our clinical practice - the Do-It-
Yourself for hands-on neurodynamics.
So I wrote a book and called it 'Clinical Neurodynamics' (Elsevier).

This was to give the clinical therapist a number of things; practical hands-on solutions, a
clinical resource and to take the next step which was test and treat neurodynamics in a
way that the nervous system really moves which is integrated with the musculoskeletal
system. This dealt with the issue of applying tension to the nervous system in isolation
by providing a system for categorising patient problems which needed the compression
and tension to be taken OFF the nervous system as opposed to ON. It also dealt with
the problem confusing sliding dysfunctions of the nerves with tension dysfunctions by
giving diagnostic criteria and systematic treatment progressions from the painful to the
athletic level. Lastly the clinical neurodynamics system now includes techniques on how
to REDUCE tension in the nervous system. Hence, the integration of musculoskeletal
and nervous systems with the term 'Clinical Neurodynamics'.

Shacklock M 1995a Neurodynamics. Physiotherapy 81: 9-16
Shacklock M 1995b Clinical application of neurodynamics. In: Shacklock
M (ed.) Moving in on Pain. Butterworth-Heinemann, Sydney: 123-131

SomaSimple: As you mention, the early neural tension techniques often caused
inconsistent and unpredictable reactions at best, and adverse reactions at worst. This
alone has been an impediment to applying these techniques clinically. As a result, a
common question with neurodynamics has always been, "how much is OK to administer
safely?" As you mentioned above, your framework includes specific diagnoses, staging of
severity, methods of reducing tension, as well as a method of systematic progression of

How does this framework of clinical neurodynamics address the early problems and the
question of safe administration of technique?

Michael: The clinical neurodynamics framework, or system, really helps the important
issue that you raise - provocation of symptoms. The answer I'll give also relates to the
diagnostic categories in my book that are naturally derived from the causal mechanisms.
And overall, there are three key aspects to deciding on the kind and extensiveness of
movements for the patient:

1. diagnostic category,

2. level of the patient, and

3. intended effect of the treatment.

I'll cover two of the common dysfunctions:

1. The diagnostic category helps us decide on the particular movements to use. For
instance, if the patient has a tension dysfunction (remembering that this may not be
adverse neural tension ie. tight nerve, instead it might be hypersensitivity to application
of tension due to ischaemia or inflammation).

In this diagnostic category, symptoms from the neural tissues are evoked (notice I didn't
use the word 'provoke') by application of movements that elongate the neural structure
from both ends (eg. wrist extension and contralateral lateral flexion of the neck in the
MNT1 position, or dorsiflexion and neck flexion with the slump test). In this case the
movements of choice will be either to apply tension to, or relieve tension from, the
nervous system.

2. Level of the patient: Number 1 above is about selecting the KIND of movements and
is based on the actual neurodynamics of the diagnosis (ie. tension dysfunction).

However this second aspect is about selecting the EXTENSIVENESS of movements for
the patient and is influenced by factors such as
the irritability of the patient's symptoms (ease of provocation, severity of
symptoms and how quickly they subside - after Maitland),
neurological status and presence of neurological symptoms (abnormal neurological
symptoms or signs reduce the patient level),
stability of the problem (something that changes greatly from moment to moment
will also lower the patient level),
the presence of pathology in the nervous system or interface (this further lowers
the level),
psychosocial factors (eg. the 'hands-off' patient or someone with a reactive system
who is quite frightened or even aggressive), or
if the therapist is just not sure as to whether the patient will tolerate extensive

These are only some of the features and are decided on by a thorough clinical
examination and sound clinical reasoning.

In my book I outline several main levels of patient:

Level 0 - contraindicated

Level 1 - limited physical testing, irritable and sensitive problem or one where there is
pathology to be careful of, restricted movements. This is when a REMOTE sequence of
movements is used. For instance, the painful wrist problem will need contralateral lateral
flexion of the neck, shoulder abduction, elbow flexion to the first onset of symptoms,
then the differentiation between musculoskeletal and neural structures is achieved by
releasing the contralateral lateral flexion. This is so that the build up of forces in the
nerve in the wrist is gradual, well controlled, easily ceased and the differentiating
manoeuvre (lateral flexion) becomes an 'off switch' rather than being an 'on switch' as in
other sequences of movement - MUCH less painful and still gives the neurodynamic

Level 2 - standard neurodynamic tests will be tolerated and are often necessary for many
standard patient problems, non-irritable and neurologically stable or only minor

Level 3 - small problem, difficult to detect which needs an extensive and sensitised
examination for highly specific diagnosis, often an athlete or worker with repetitive
loading with small symptoms

- type 3A - neurodynamically sensitised by performing a standard test but placing more

tension on the nervous system with sensitised movements eg. scapular depression or
contralateral lateral flexion for the MNT1, or localised abduction/pronation of the heel
the medial calcaneal nerve for heel pain.
- type 3B - sensitised by neurodynamic sequencing - this relies on the concept that I
discovered in the late 1980s whereby we may be able load the local nerves more than the
remote nerves in neurodynamic testing. So for a really minor problem you can move the
local nerves first and complete the neurodynamic test from remotes sites eg. for a small
buttock pain the hip can be moved first, then the knee and finally the ankle. Or for a
minorheadache, the upper cervical spine can be flexed, the lower cervical spine, thoracic
spine, then the hips followed by the knees and ankle. This is a great way of sensitising
some examination techniques for the local neural component. This is what I have termed
a LOCAL sequence.
- type 3C - multistructural - this combines musculoskeletal (interface) structures and
neural at the same time. For instance the patient can contract a muscle that pushes on a
nerve during performance of a neurodynamic test eg. the pronator muscle during the
MNT1 for a minor medial elbow pain that spreads down the forearm.
- Type 3D - use of the symptomatic position or movement nominated by the patient.
This is useful in athletic situations or when the patient's symptoms only come with one
particular posture or movement (for more detail, see chapter 6, pp. 105-116).

Clearly, in anyone in whom sufficient information has been gained from testing at level
1 or 2, the level 3 examination is contraindicated. When I look back into the deep past, I
realise that we moved nerves to level 3 because we could rather than because we should!

3. Intended effect of treatment - if the intention is to treat the pathophysiology of the

problem rather than the pathomechanics, the extensiveness and direction of movement
will be modified.

For instance, for a neural tension dysfunction at level 1, the nerves can be placed OUT
OF TENSION and mobilised OUT OF TENSION to work on their sensitivity rather
than placing them in tension and pulling on them.

Later, say at level 3, they can be placed INTO TENSION and mobilised INTO
TENSION but usually this only works when the patient level is judged correctly (by the
way, there are several progressions between these).

That was for the tension dysfunction but the same applies to the sliding dysfunctions.

For the interface dysfunctions, the interface can be opened or closed to either take
pressure off the nervous system or apply pressure to it.

Generally the intention for low level patients is to reduce pressure on and improve blood
flow in the neural tissues but, as the patient improves (say level 2 or 3), the nerves
tolerate forces better and can sometimes benefit from forces such as pressure and a small
degree of tension application.

The key point in relation to the intended effect of treatment is that, at low patient levels,
the therapy is directed at PATHOPHYSIOLOGY of the problem (blood flow,
inflammation, hypersensitivity) whereas, as the patient improves and moves but
produces little force in the nervous system.

At higher levels, the PATHOMECHANICS becomes the focus in which the actual
movements can change to applying force to the nervous system either with movement of
the interfacing structures or the neural tissues themselves (for discussion, see method
treatment pp. chapter 8, 153).

It's quite simple when the therapist integrates all this and, with practice, decisions on the
extensiveness and type of movement/treatment can actually be made in a flash.

SomaSimple: Another aspect of earlier neurodynamic techniques that has remained

vague is the manner in which the movements were to be progressed.

Louis Gifford, a physiotherapist from the UK, advocates treatment based on graded
exposure. It appears as though, in Clinical Neurodynamics, the staging of the level of the
patient not only establishes a level at which treatment will be initiated, but also sets the
stage for progression from one level to the next.

In this system, how have you approached the issue of treatment progression?

Michael: The issue of treatment progression is addressed by a number of things that link
the behaviour of the patient's symptoms to neurodynamic mechanisms, clinical
experience and clinical reasoning. When a patient has a pathology that might reduce the
nervous system's ability to tolerate physical forces (eg. disc bulge pushing on a nerve
root), the techniques of choice will often take pressure off the nerve root rather than
apply pressure. Also, if there is evidence of significant pathophysiology in the nervous
system (eg. reduced sensation or motor function), the treatment of choice will once again
be to reduce pressure. This is with the intention of improving physiology in the nervous
system and is localised to the lower levels of patient (particularly the level 1 patient)
described in the answer to the previous question.
When the problem settles and the patient can tolerate movement better, the purpose of
treatment is to slowly change the emphasis from addressing the physiology of the
problem to treat the specific mechanical dysfunction. This tends to be in the form of
closing mobilisations if the dysfunction lies in the mechanical interface and if it is in the
neural tissues (e.g. neural tension dysfunction), the progressions change from moving
out of the direction of the dysfunction to moving into that direction.

So for the neural tension dysfunction at low levels where the key issues are
hypersensitivity of the neural tissue and inflammation, the neural tissues are positioned
out of tension and moved out of tension. Whereas at higher levels, the mobilisation is
progressed to positioning the neural tissues into tension and are moved into tension, as
long as the treatment is safe and produces improvements, of course. This latter technique
will produce more force in the neural tissues which is why it is left to the patient of
higher function. More sensitisation can be performed for the athlete, for instance, with
sensitising movements if the patient needs this.

The neurological evaluation is a key part here because it is possible that patient's pain
can improve at the same time that the neurological status worsens, a change that should
be looked for as a routine part of patient management. One of my concerns is that
therapists do not do neurological testing often enough and miss out on important clues
to the nature of the problem. I believe that, in any patient in whom significant neural
testing or treatment is performed, they should have a neurological evaluation and this
goes right through to the end of the rehabilitation process so we are sure that the
neurological status has improved or at least been maintained. I have seen people's pain
improve when their neurological function has worsened and our priority is to 'do no

Anyway, generally, the purpose of treatment is to, at low levels of function and high pain
levels, move and reduce forces rather than pressure and tension the tissues. At higher
levels this reverses as a way of increasing loading on the tissues. So this is the
progressional system that I have created and takes the patient from low to high levels
when the nervous system is involved and is really a form of 'graded exposure' which, in
my opinion, is what all progressions should do. The key is to match the clinical features
with the neural and musculoskeletal system mechanisms.

This system also addresses the issue of how to select the correct progressions rather than
only using trial and error which was a key modus operandi in the earlier days of neural
tension and neural mobilisation.

Somasimple: You mentioned the gap that had grown between clinical practice and current
neuroscience that contributed to your writing the book. When the theory behind a method
does not hold up in light of current neuroscience the gap is exposed. In the atmosphere of
current evidence based practice, outcome studies have become very important in
justifying treatment methods. However, justifying the theories behind the treatment
method in light of current neuroscience is very important in understanding why what we
do creates positive outcomes.

How does the Clinical Neurodynamics system, while providing useful clinical solutions,
maintain justification in the consideration of current neuroscience?

Michael: In terms of the clinical mechanisms, my belief is that there is so much

neuroscience support for many of the things we do clinically that the notion of clinical
application of the neurosciences in itself presents no philosophical problems for me. But
the challenge is whether the diagnosis and treatment of clinical problems can be made
specific to the mechanisms in question.

I'll answer your question by coming from the angle that the Clinical Neurodynamics
system that I've created integrates or links with current neuroscience in both directions:
from the theory to the application and the application back to the theory; that is, how
both support one another.

Clinical Neurodynamics integrates with the theory of the neurosciences by providing a

set of links on which to base diagnosis and treatment. I facetiously call this set of links
the 'phenomenal chain'. When something is observed to occur, we call it a
'phenomenon'. For any 'phenomenon' to occur there must exist a 'mechanism', for
which there must also exist a 'structure' to provide the mechanism. So we have
'phenomenon',' mechanism' and 'structure' and this goes both ways.

Let's start with a clinical phenomenon, say heel pain with swelling in heel. The pain is
provoked by heel strike and there is tenderness over the medial calcaneal tubercule at the
insertion of the plantar fascia.
The problem (including the swelling) does not respond to NSAIDs. We would often
diagnose plantar fascitis, but this is where the fun starts. The foot is pronated in standing
and walking and palpation of the posterior tibial nerve reproduces the patient's clinical
pain and, if sustained, evokes pins and needles in the medial heel region. This reminds
the patient that they have also been having pins and needles but they didn't tell you
because you didn't ask and they didn't think it was related. Neurological evaluation
reveals reduced sensation over the medial heel area and the tibial neurodynamic test is an
'overt abnormal response'. Static openers for the tarsal tunnel reduce the pins and

Here we have some great neuroscience to link with the point that this problem is related
to a neuropathy, in fact, of the medial calcaneal nerve, which is a branch of the posterior
tibial nerve near the tarsal tunnel. I should say that it is easy to diagnose a neuropathic
problem when there is reduced sensation and pins and needles. But, even in the absence
of these features, a neural problem can be implicated.

So back-tracking, the 'phenomenon' is heel pain, the 'mechanism' is inflammation but I

will argue that this is provided by neurogenic inflammation (which has neuroscience
basis) and the 'structures' are the heel tissues, medical calcaneal/tibial nerve and tarsal
Features that link to the neurosciences in this case:

- numbness usually means reduced nerve function

- pins and needles may implicate ischaemia of the nerve, among other mechanisms.
Studies show that nerve ischaemia produces ectopic impulse generation and reversal of
this can correct the pins and needles.
- the nerve can release neuropeptides (substance P and calcitonin gene related peptide
(CGRP)) into the tissues innervated by the medial calcaneal nerve (medial heel, plantar
fascia and medial tubercule of the calcaneum), especially when the neuropathy is one of
hypersensitivity and mechanosensitivity. The distal (efferent) actions of the C fibres in
the nerve produce this release outward from the site of sensitivity toward the periphery.
These effects may be triggered by mechanical stimulation of the area of nerve
sensitivity/compression/irritation in the tarsal tunnel. Research in humans shows that
neuropathies can produce altered inflammation in the innervated tissues such that these
tissues can become a looking glass for the neuropathy. Better inflammation-better nerve,
worse inflammation-worse nerve.
- NSAIDs don't influence histologically-evaluated inflammatory changes so this could be
one reason that the problem does not respond to NSAIDs. The inflammation is likely to
be maintained by the sensitized activity in the nerve, particularly with the pronated foot
because pronation has been shown in cadavers to produce increased strain and
compression in the nerve.
- manual opener techniques for the tarsal tunnel relieving the pain and pins and needles
suggests that the pressure and tension are coming off the nerve and improve the blood
flow (therefore ischaemia) of the nerve (we have shown this opening effect with real-time
imaging of the nerves in the tarsal tunnel on the CD in my book). With the reduction in
pressure on the nerve with the openers, there could also be a reduction in the mechanical
stimulation of the nerve therefore less triggering of inflammation in the heel from the
neuropathy site.
- numerous studies show that levels of SP and CGRP in inflamed tissues are elevated (eg.
in osteo- and rheumatoid arthritis). Remembering that SP and CGRP trigger
inflammation in the musculoskeletal tissues and are manufactured in the nervous system
and not the innervated (musculoskeletal) tissues. Therefore elevated levels of these
substances in the musculoskeletal tissues means there has been up-regulation and
increased release from the innervating nerve into the musculoskeletal tissues. The key
point here is that inflammation is actually regulated by the nervous system. When faulty,
the inflammatory mechanisms in the musculoskeletal tissues can go wrong, a point
which is often omitted in clinical reasoning.

In the above patient, treatment in the form of openers and sliders for the nerve produced
a reduction in the inflammation (ie. swelling) and tenderness over the heel and the
patient made a full recovery, although the neurological loss did not return to normal as
quickly. Actually this is a true case history.

The above is an illustration of the 'phenomenal chain' that supports two-way interaction
between the neurosciences and Clinical Neurodynamics. The key is to make the
diagnosis and treatment match the mechanisms which ultimately leads to linking the
'phenomenon' to the 'mechanism' to the 'structure'. Treatment then works on the
'structure' which works on the 'mechanism' which then works on the 'phenomenon'.
This is a perfect link between the neurosciences and Clinical Neurodynamics, both of
which support the other.

By me saying that there had emerged a gap between the complexity of the neurosciences
and their clinical application, my brain was overflowing with 'data' but not much
'information'. I was troubled by this for two reasons. First, I found it irritating because I
prefer simplicity and directness. Second I was disillusioned at not being able to make the
system more useable for therapists and patients alike. So my book was a form of therapy
for me - to try and make some sense of neurodynamics. I'm so pleased and fortunate that
it is a great success and is actually helping someone. By the way, it is now being
translated into five languages and more likely on the way.

I'd like to take this opportunity to thank all those at Somasimple for doing such a great
job on this fantastic web site and inviting me to contribute. Your work is noticed widely
and deserves every possible success.