Index

Neural Mobilization ................................................................................................................... 0

Nerve Structure ..................................................................................................................... 3
How Nerves Cause Pain ......................................................................................................... 4
Physiological Principle ............................................................................................................... 5
Fascial Connection ................................................................................................................. 5
Structure ................................................................................................................................ 6
Function ................................................................................................................................. 7
Clinical significance ................................................................................................................ 7
Susceptible sites .................................................................................................................. 10
Indications ............................................................................................................................... 13
{1} Previous Trauma ............................................................................................................ 13
{2} Double Crush Syndrome ................................................................................................ 14
Symptom Profile ...................................................................................................................... 37
Treatment ................................................................................................................................ 37
Neural Tension Test ................................................................................................................. 38
Introduction ......................................................................................................................... 38
Purpose................................................................................................................................ 39
Types.................................................................................................................................... 39
Method to Perform ............................................................................................................. 39
Neural Tension Tests ............................................................................................................... 43
{1} Passive Neck Flexion ...................................................................................................... 43
{2} Straight-Leg Raise........................................................................................................... 44
{3} Prone Knee Bend............................................................................................................ 45
{4} Slump Test...................................................................................................................... 46
Application........................................................................................................................... 47
Self-Mobilization ..................................................................................................................... 48
Precautions .............................................................................................................................. 50
Contraindication ...................................................................................................................... 51
Reference ................................................................................................................................ 53

Neural Mobilization
Neural Mobilization: is a technique that we utilize to
treat nerves that may be adhered, irritated, or
compressed. Many patients that have been unresponsive to
other physical therapy and present with a chronic history of
referred symptoms like pain, numbness, or tingling into the
arms or legs may respond to Neural Mobilization. Every patient
that presents with referred symptoms or pain that has been
unresponsive to localized treatment receives a complete neural
tension evaluation.

Nerve Structure
Nerves are bundled within connective tissue sheaths for
protection from compression and stretch forces. Nerves are
wrapped in a protective connective tissue sheath, or
epineurium. The bundles of conducting fibers in a nerve are
termed fascicles. The fascicles of the nerve are wrapped with
their own connective tissue sheaths with looser connective
tissue between the fascicles. The number of fascicles in a nerve
varies according to the nerve and its location. In areas of
increased mechanical stress, the nerve temporarily divides into
more fascicles with more connective tissue between them in
areas where the nerve is subject to more mechanical force,
such as when it pierces a muscle or crosses a bone.

How Nerves Cause Pain

The nervous system is a continuous organ that runs
throughout the body, like the extensive roots of a tree. It
includes the brain, spinal cord and the nerves that connect
almost every structure of the body to the spinal cord. It is a key
information transmitting organ; whether the information is
instructions to a muscle about when to contract, pain
sensations from the body surface to many other information
functions. It is commonly injured by compression, tension and
friction or chafing on sharp or hard objects outside or inside the
body.

Physiological Principle
Fascial Connection
Like the myofascial system, the neural system is
continuous throughout the body it too is surrounded with
fascia and can be affected by direct and indirect injuries to
fascia and adjacent tissues. The effects of neural injury, like
those of facial injury, can be referred to distant areas. The
referred pain of neural injuries is different from myofascial pain
referral patterns, however.
A fascia: is connective tissue fibers, primarily collagen,
that form sheets or bands beneath the skin to attach, stabilize,
enclose, and separate muscles and other internal organs.
Fasciae are classified according to their distinct layers, their
functions and their anatomical location: superficial fascia, deep
(or muscle) fascia, and visceral (or parietal) fascia.
Like ligaments, aponeuroses, and tendons, fasciae are
dense regular connective tissues, containing closely packed
bundles of collagen fibers oriented in a wavy pattern parallel to
the direction of pull. Fasciae are consequently flexible
structures able to resist great unidirectional tension forces until
the wavy pattern of fibers has been straightened out by the
pulling force. These collagen fibers are produced by the
fibroblasts located within the fascia.
Fasciae are similar to ligaments and tendons as they are
all made of collagen except that ligaments join one bone to
another bone, tendons join muscle to bone and fasciae
surround muscles or other structures.

Structure
There exists some controversy about what structures are
considered "fascia", and how fascia should be classified. The
two most common systems are:
The one specified in the 1983 edition of Nomina
Anatomica (NA 1983).
The one specified in the 1997 edition of
Terminologia Anatomica (TA 1997).
NA 1983

TA 1997

(not
Superficial considered
fascia
fascia in this
system)

Deep
fascia

Visceral
fascia

Fascia of
muscles

Description

Example

This is found in the subcutis

in most regions of the body,
blending with the reticular
layer of the dermis.

Fascia of
Scarpa

This is the dense fibrous

connective
tissue
that
interpenetrates
and Transversalis
surrounds the muscles,
fascia
bones, nerves and blood
vessels of the body.

This suspends the organs

Visceral
within their cavities and
fascia,
wraps them in layers of Pericardium
parietal fascia connective
tissue
membranes.

Function
Fasciae are normally thought of as passive structures that
transmit mechanical tension generated by muscular activities
or external forces throughout the body.
The function of muscle fasciae is to reduce friction to
minimize the reduction of muscular force. In doing so, fasciae:
1.
2.
3.
4.

Reduces friction between muscles, allowing sliding.

Suspend organs in their cavities.
Transmit movement from muscles to bones.
Provide a supportive and movable wrapping for
nerves and blood vessels as they pass through and
between muscles.

Clinical significance
A Fasciotomy may be used to relieve compartment
syndrome as a result of high pressure within an anatomical
compartment created by fascia.

David Butler, PTDavid Butler is a physiotherapy

graduate of the University of Queensland (1978).
He also has a graduate diploma in advanced
manipulative therapy (1985), a masters degree by
research from the University of South Australia
(1996) and a doctorate in education from Flinders University
(2010). David is a clinician, an international freelance educator
and a senior lecturer at the University of South Australia. His
professional interests focus around the integration of
neurobiology into clinical decision making and public and
professional education in pain, stress and performance
management. David is the author of numerous book chapters
and articles and the texts including, Mobilization of the
Nervous System, The Sensitive Nervous System, and Explain
Pain. David has taught concepts of clinical reasoning, physical
health of the nervous system and pain sciences for many years
and in many countries.
David Butler, PT, has been at the forefront of these
techniques for over 20 years. Although we still do not
completely understand the exact mechanism, he proposes that
NeuroMobilization (what David Butler calls Neurodynamics)
can accelerate nerve healing and quiet down what he calls an
altered impulse generating system (AIGs). These AIGs may
respond to the oscillations of NeuroMobilization by enhancing
circulatory exchange or ion transfer in and around the nerve.
With the publication of this book Butler solves the
problem of scientific imprimatur by adding more references
than you could ever ask for, and these are used with precision
and common sense. Beyond that, he weaves a narrative of
clinical reasoning and management that matches what we
8

know to be true and biologically plausible on a molecular level.

It is difficult to make the connection between what is invisible
to the clinician and how those processes might become
manifest in the patient, but Butler does again and again.

Susceptible sites
Given that the nervous system, like the fascia system, is in
intimate contact with other tissues throughout the body, it
makes sense that when an area suffers an injury, neural tissue
may also be affected. Certain nerves are susceptible to injury
because of their location or pathway Butler (1991) has
identified these five susceptible sites:

[1] In soft tissue or bony tunnels. A good example of this is the

median nerve as it passes through the carpal tunnel at the
wrist.

[2]

Abrupt neural branches, particularly in areas where the

nerves ability to move within the surrounding structures is
limited. For example, the common plantar digital nerve in the
web space between the third and fourth toes has limited
10

movement, is formed from an abrupt junction of the lateral and

medial plantar nerves, and is a common site for Mortons
neuroma.

[3] In areas where the nerves are relatively fixed. The common
peroneal nerve as it traverses around the fibular head is an
example of a relatively fixed nerve with little mobility.

11

[4]

High-friction areas where nerves are close to unyielding

interfaces. Two examples are the nerves passing through the
plantar fascia in the foot and the brachial plexus passing over
the first rib.

[5]

Tension points, such as the tibial nerve in the popliteal

fossa, where abnormal stress can be placed on the nerve.

12

Indications
{1} Previous Trauma
Previous trauma can predispose an area to neural
symptoms later. Like all other tissue nervous tissue is
surrounded by layers of fascia that serve to support and supply
nutrients to the nerves. If a nerve is injured, it undergoes the
healing process discussed in chapter 2. Scar tissue can be
produced by the nerve, its surrounding fascia, and the other
structures involved in the injury the result can be binding of the
nerve that can affect its neurobiomechanics and
neurophysiology.
Even an injury not directly involving neural tissue can
affect the nervous system. Locally damaged blood vessels and
ensuing edema can cause neural changes. The nervous system
is very dependent on a continuous blood flow for survival and
for functioning. Although the nervous system constitutes only
2% of the bodys mass, it uses 20% of the circulating bloods
oxygen supply (Dommisse 1975). Because nerve tossie has no
means of storing reserves, if the blood supply is interrupted,
damage to the nerve tissue can result from a lack of adequate
oxygen and nutrients.
Nerve tissue damage secondary to either edema or
vascular insufficiency results in fibrosis. A tethering effect on
the nerve by the restriction of the scar tissue can reduce the
flexibility and mobility of the neural tissue. Ultimately,
symptoms of abnormal neural tension can occur in locations
along the nervous system other than the site of injury.
According to Butler (1991), this transpires because the
13

mechanical alterations in one nerve location can alter tissue

tension throughout the nervous system, impaired neural
stimulation at one site can affect the entire neuron, mechanical
changes from an injury are accompanied by vascular changes,
and an abnormal nerve impulse can cause abnormal neural
firing elsewhere in the nervous system.

{2} Double Crush Syndrome

The term double crush syndrome originates from work

published by Upton and McComas (1973) and as such it would
follow established practice if their original statement of the
hypothesis were to become the working definition of 'double
crush'. The abstract of their paper read as follows:
"A comprehensive electromyographic study has been
made of 115 patients with carpal-tunnel syndromes or lesions
of the ulnar nerve at the elbow. In 81 cases there was
14

electrophysiological evidence, often supported by clinical

symptoms, of associated neural lesions in the neck. This
association is not thought to be fortuitous, but rather the result
of serial constraints of axoplasmic flow in nerve fibres."
However, I have since had discussions with Dr. Upton in
which he has extended the overall concept to include situations
which cannot result from serial constraints of axoplasmic flow
in nerve fibres because he would now like to include within the
syndrome cases in which the two lesions actually affect
different nerve fibres. Nevertheless the original hypothesis may
be stated as:Local damage to a nerve at one site along its course may
sufficiently impair the overall functioning of the nerve cells that
they become more susceptible than would normally be the
case to trauma at other sites. It is worth noting however, that
for sensory nerve cells, this implies that the proximal
component of the double crush needs to be between the dorsal
root ganglion (which lies outside the spine) and the carpal
tunnel, not between the spinal cord and the dorsal root
ganglion, which is where most entrapment from degenerative
disease of the cervical spine occurs.
Upton and McComas further suggested that a high
proportion (75%) of patients with one peripheral nerve lesion
did in fact have a second lesion elsewhere and they implied
that both lesions were contributing to the symptoms.
The idea that patients may have more than one lesion,
and even the concept that both may be contributing to the
symptoms is, and was not in 1973, anything new. The new
elements of Upton and McComas's paper were the idea that
15

one lesion could PREDISPOSE to the other, and the very high
percentage of patients in whom they found evidence of two
lesions. The element of predisposition by a mechanical lesion
remains unproven 38 years later, and in the absence of definite
proof on this, the term 'double crush' has widened somewhat
to include symptoms which result from a combination of two
separate, local lesions at different anatomical sites in the same
nerve, whether or not one actually contributes to the causation
of the other.
I feel that attempts to widen the definition still further
(see my comment about recent discussions with Dr. Upton)
should be resisted unless there is VERY good reason. Provided
we keep more or less to the original proposition the essential
elements are then:1) This is a neurological problem (i.e. involving nerve only
and not a combination of a nerve lesion with
pathology in another body system joint, tendon etc.).
2) There are two physically separate lesions of the same
nerve.
3) Symptoms are present.
Anyone using the term 'double crush syndrome' for cases
which do not meet these three criteria is misusing the term. It
is not strictly a diagnosis but rather, all cases of double crush
syndrome should be describable in terms of two other
diagnoses.
There have been some attempts to test the hypothesis in
animal experiments (Nemoto 1987, Dellon 1991, Seiler 1983,
Shimpo 1987) but in general these have only been able to show
that two lesions, unsurprisingly, produce a greater overall
16

deficit in nerve function than one. More studies have been

devoted to trying to assess the incidence and clinical relevance
of the syndrome. In their original paper Upton and McComas
claimed that 75% of their patients with CTS or ulnar nerve
lesions had evidence of a second proximal lesion. Other studies
have come up with the following:
1000 hands in 888 patients 11 felt to have double crush
(1%) (Carroll 1982).
100 clinically diagnosed CTS patients 6% thought to
have double crush (Kuntzer 1994).
Double crush in 0.7% of 12736 patients (Morgan 1998).
40 of 271 patients with thoracic outlet syndrome felt to
have CTS too (Narakas 1990).
37 of 1183 patients with CTS found to have cervical
radiculopathy (3.1%) (Wilbourn 1986).
74 of 165 cases of thoracic outlet syndrome found to have
a peripheral entrapment neuropathy (44%) (Wood 1990).
Evidence of double crush found in 74 limbs out of 758 in
681 patients with thoracic outlet syndrome (9.76%) (Abe
1999).
Of 525 patients with CTS 105 (20%) had other
entrapments in the same limb (Yu 1979).
In general the incidence of double crush in patients with
definite CTS has tended to be lower than that suggested by
Upton and McComas though there have been claims that it
exists in as many as 83% of CTS cases and it is often invoked as
a reason for failed carpal tunnel surgery. It does seem however
that the rates of CTS in patients with thoracic outlet syndrome
may be higher than those of thoracic outlet syndrome in
patients with CTS.
17

How can supposedly scientific data vary so much?

Much of the evidence in these papers is derived from
EMG (Electromyography) and nerve conduction studies. To
understand the variations one has to understand a good deal
about the nature of the tests and the way in which tests in
general are used in medicine. One also has to appreciate
something of the relationship between disease and symptom
prevalence in the population.
EMG and nerve conduction studies are not 'all or nothing'
tests producing a logical YES/NO answer as to whether a
problem is present or not. With nerve conduction studies, at
least the results are numerical measurements and different
investigators can agree about what the limits of normal are, but
even here there is some overlap between patient groups some patients with no symptoms will have results that fall in
the 'abnormal' range (false positives) and some patients with
disease which is causing symptoms will nevertheless have
results which are normal (false negatives). There is therefore no
absolute dividing line in the test results which will reliably place
all patients correctly into the two groups 'Disease' and 'Normal'
and one has to set an arbitrary cut-off point as 'normal'. This
can be set so as to minimize the number of false positive
18

results or to minimize the number of false negatives. If the

consequences of a false negative are catastrophic - for example
in other circumstances, missing a potentially treatable
malignancy - one tends to bias the cut-off point towards
minimizing the false negatives at the expense of having rather
more false positives and vice versa. One can therefore see that
there is no absolute 'RIGHT' answer.
With EMG, the situation is further complicated by the fact
that the 'result' is largely a subjective judgment by the
examiner rather than a quantifiable number. This is far more
difficult to standardize between laboratories and is open to
wide interpretative variations, further compounding the
difficulties outlined above for nerve conduction studies.
Now what about the relationship of disease to
symptoms? The concept of asymptomatic disease is easy
enough to comprehend and everyone is now familiar with the
idea of screening tests to detect such. Not so familiar however
is the fact that some tests, and in this I would include postmortem studies of accident victims and the like, produce
positive results in surprisingly high proportions of the normal
population, for example up to 40% of people may show
pathological evidence of carpal tunnel syndrome at postmortem. The physician can thus frequently be presented with
the difficult problem of determining whether the symptoms of
which his/her patient is complaining are actually due to the
disease which he has been able to demonstrate by examination
or investigation. In doing this, he or she is forced to fall back on
knowledge of what symptom pattern is typically associated
with each disease and has to make a judgment as to how

19

closely the patients symptoms match - and by implication, how

likely it therefore is that the disease in question is responsible.
How does this apply to RSI, Carpal Tunnel Syndrome (CTS)
and Double Crush? Well, two types of pathology are known to
be very common in the population at large and therefore
present the problems outlined in the last paragraph - these are
CTS and the group of conditions which, for want of a better
term, I will call 'root/plexus problems'. This last includes
arthritic degeneration of the cervical spine producing nerve
root compression, thoracic outlet syndromes (cervical ribs) and
perhaps entities such as adverse mechanical tension. Now,
EMG and/or nerve conduction studies may be used to look for
evidence of both of these. The mainstay of examination for CTS
is nerve conduction studies, whereas examination for root and
plexus problems relies much more heavily on EMG with its
attendant difficulties. The end result is that neurophysiological
tests for CTS produce a much more reliable (though not
perfect) differentiation of 'DISEASED' from 'NORMAL' than
neurophysiological tests for root and plexus problems where
there is a much greater overlap between the test results of the
symptomatic and asymptomatic populations. Given the
situation that I have described above, it is not difficult to see
that one investigator can inadvertently bias his/her findings
towards finding evidence of second lesions in the
neck/shoulder and another investigator can do the opposite.

Does double crush explain much misdiagnosis of

CTS?
It is sometimes suggested that the failure of symptoms to
respond to treatment for CTS, often surgery, is a result of
20

misdiagnosis of double crush syndrome as CTS. The implication

is often that many patients who have double crush syndrome
are mistakenly treated as having CTS when they don't have it
as though the two conditions are entirely separate. Most of the
patients we are talking about will have CTS as one part of their
'double crush' as CTS is far more common than other
entrapment neuropathies in the arm. For practical purposes, a
double crush consisting of CTS combined with a root/plexus
lesion probably accounts for 95% of all double crush
syndromes. It may help at this point to enumerate the possible
scenarios for an RSI patient:
1) The patient has CTS and a plexus/root lesion both
contributing symptoms independently.
2) The patient has CTS causing symptoms and an
asymptomatic root/plexus lesion which is completely
unconnected.
3) The patient has symptomatic root/plexus disease and an
irrelevant and asymptomatic CTS.
4) The patient has CTS which would normally cause few or
no symptoms alone but the presence of a root/plexus
lesion is somehow enhancing the symptoms and making
the CTS a problem. In another version of this scenario
the patient has raised pressure in the carpal tunnel
which would not normally be enough to damage an
otherwise unimpaired nerve but because the median
nerve is in trouble proximally it is unable to cope with
the situation at the wrist and develops a lesion there
too. In both versions the symptoms are only those of the
CTS otherwise this would be case 1).

21

5) The patient has a root/plexus lesion which would

normally cause few or no symptoms but the presence of
a CTS is somehow enhancing the symptoms and making
the root/plexus lesion a problem. Rather less plausibly,
the same alternative scenario could be invoked in
reverse as for. In this case the symptoms are only those
of a root/plexus lesion.
6) The patient has only a CTS.
7) The patient has only a root/plexus lesion.
8) The patient has neither CTS nor root/plexus problems
nor the symptoms have another cause entirely.
9) The patient has CTS and/or root/plexus problems but
both are innocent bystanders and another disease is
actually causing the symptoms.

Note that these scenarios represent the underlying

'truth'. When we superimpose the uncertainties of diagnosis
and testing, some patients will be miscategorised in the
simplest example, a patient with tenosynovitis may turn up test
results which show EMG evidence of a root/plexus problem
which simply does not exist - i.e. a simple false positive. Such a
patient is in danger of being miscategorised as 7 rather than 8 if
the physician is not alert to all the possibilities. Overall, I would
22

expect an experienced clinician dealing with such cases to

correctly identify and categories in the above groups about 90%
of all patients who have symptoms suggestive of either CTS or
plexus/root problems.
Given the correct categorization, patients in groups 2, and
6 will respond well to treatment of CTS. Patients in group 1 will
gain relief of some of their symptoms. Patients in groups 4 and
5 may benefit from CTS treatment. Conversely, patients in
groups 3, and 7 should respond well to treatment of the
neck/shoulder (though this is therapeutically more difficult
than treating CTS). Again patients in groups 4 and 5 may benefit
from treatment directed at the shoulder too. To look at it the
other way around: the groups that should NOT be treated as
CTS are 3, 7, 8 and 9. The reader is left to draw his or her own
conclusions as to the answer to the question at the head of this
section. Groups 1, 4 and 5 could all be regarded as double
crush but group 1 are a special case because both lesions are
independently causing symptoms and thus, though some of
their symptoms may respond to treatment of either lesion they
will gain most benefit from having BOTH treated. Such cases
are probably the ones which account for failure of correctly
performed carpal tunnel decompression to relieve the
symptoms of a correctly diagnosed CTS in studies of failed
carpal tunnel decompression. In the other cases in which
'double crush' applies (groups 4 and 5), one may only need to
treat one of the two lesions to relieve all the symptoms,
regardless of which is the primary lesion of the two.

Can double crush mimic the symptoms of CTS?

23

Underlying this question is the unspoken idea that these

are two different diseases which can be mistaken for each
other (see above). If we ignore this misconception for the
moment the answers are: Symptoms - YES; Nerve conduction
studies - only if there really is a CTS. To amplify, root/plexus
disorders may produce symptoms which are very difficult to
distinguish from those of CTS, though I should emphasize that I
do not believe this to be common. Furthermore, it should be
remembered that the symptoms of CTS may be highly atypical
in a few cases. Root/plexus lesions do NOT produce the typical
nerve conduction findings of CTS at the wrist though they can
produce individual measurements which could be
misinterpreted as CTS if seen in isolation. Similar difficulties can
arise with generalized nerve disorders which makes it essential
to perform multiple nerve conductions when looking for CTS.
Anyone who relies on a single measurement (some people do
only the motor latency from wrist to Abductor Pollicis Brevis,
for example) will make mistakes.

How do RSI cases fit into all this?

24

The bottom line here obviously relates to the frequency

of occurrence of the various pathological groups outlined
above in the population of patients presenting with upper limb
symptoms which appear to be related to work. Some of the
published evidence has suggested that high proportions lie in
groups 1, 4 and 5 [1], other papers suggest that, out of all
patients with RSI the proportion of patients in groups 1, 2, 4, 5
and 6, i.e. those in whom CTS treatment may be justified, is
very low and are used as evidence against surgical treatment of
RSI. This same group of authors are fond of quoting the 'low
success rate' of carpal tunnel surgery.
There are no absolute answers to this, even combining
the wealth of published data already available but the views
expressed in the previous paragraph undoubtedly represent
one extreme and are, on that basis, fairly unlikely to be
completely correct. A few more observations may be relevant
however.
Many people presenting with work related upper limb
symptoms are under the age of 40, especially those who
identify themselves as RSI. In patients referred to Canterbury as
?CTS ie excluding those who had any other obvious
explanation for their symptoms, there was NCS evidence of CTS
in 355 out of 562 patients whose symptoms sounded plausibly
like CTS (63% compared to 72% in the over 40s). These younger
patients are thus less likely to have CTS and the real proportion
of work related symptoms in the under 40s due to CTS will be
considerably lower once we include all the other readily
recognisable pathologies. I therefore suspect that at least 60%
of all upper limb symptoms in this group are not due to CTS but
either arise in the roots/plexus, are due to other peripheral
25

nerve lesions, or are not nerve problems at all. Any surgical

series of patients drawn from this population and treated
indiscriminately for CTS will produce the 'poor success rate'
which is sometimes quoted unless great care is taken to filter
out only those patients with really convincing CTS for surgery.
The subjective success rate for surgical decompression of CTS
reported in the literature varies from 30% to 100% with an
overall average of 86%.
If 86% of patients gain good relief from treatment for CTS
then it is unlikely that Upton and McComas's figure of 75%
having significant double crush syndromes, such that diagnosis
and treatment of the proximal lesion too is needed, is correct.
My personal estimate would be that perhaps 30% of all
patients with NCS confirmed CTS have double crush in the
sense of there being some abnormality on cervical X-rays,
proximal EMG studies or stretch tests but that only about 10%
of these (i.e. 3% overall, roughly in line with some of the larger
studies quoted above) actually have proximal disease which
requires treatment in addition to treatment for the CTS in order
to relieve their symptoms. Readers of this paragraph who
immediately disagree should read it again and note that I am
talking about percentages of patients with PROVEN CTS, not
percentages of patients with RSI as a presentation - for that,
refer to the previous paragraph.

26

27

What is Carpal Tunnel Syndrome?

Carpal tunnel syndrome is a condition in which the
median nerve is compressed in the carpal tunnel that it runs
through in the front of the wrist. The median nerve transmits
sensations from the hand to the brain. It also controls muscle
activity on the thumb side of the hand. When the median nerve
is compressed, there may be tingling or numbness in the thumb
side of the hand. There may also be weakness and/or lack of
coordination in the actions of the thumb and adjacent fingers.

What Causes Carpal Tunnel Syndrome?

The median nerve can become compressed in the carpal
tunnel by thickening of the tendons of the muscles that share
the tunnel space with the nerve. This thickening can be caused
by tendonitis and/or by overuse of the muscles (often by
excessive keyboarding or use of industrial equipment)
combined with lack of stretching. Carpal tunnel syndrome can
also be caused by an increase in the fluid content of the body in
pregnancy as well as in some medical conditions.

Symptom Patterns in Carpal Tunnel Syndrome

Carpal tunnel syndrome can give a person weakness in
their grip (especially affecting the thumb), numbness and
tingling as well as pain. Each person may experience carpal
tunnel syndrome a little differently. The chart at the side shows
28

the idea that symptoms can be a pure experience of numbness,

pain or weakness. Alternatively, there may be a mixture of
symptoms.
It is important to have a good sense of what the
symptoms are, so that you can evaluate whether you are
getting better, staying the same, or getting worse.

Testing in Carpal Tunnel Syndrome

There are common physical tests for carpal tunnel
syndrome. In Phalens test the person pushes their two hands
together with their palms facing downward. If this creates the
uncomfortable sensation (or worsens the discomfort already
there) then you may have CTS. Some people have to hold the
position for a second or two only, while others need to hold the
position for 30 seconds to create discomfort. The more easily
this test creates symptoms, then the more irritable the
condition.
There are other physical tests that can be used to
measure the sensitivity of the median nerve in the carpal
tunnel as well as all along its course from the neck to the hand.
These tests can be used to guide hands-on treatment as well as
measure treatment success.
Medical evaluation for carpal tunnel syndrome may
involve Nerve Conduction testing and/or Ultrasound
evaluation. In Nerve Conduction testing an instrument is used
to evaluate whether the nerve is still conducting electricity
properly. In ultrasound assessment the size of the median
nerve, tendons inside the carpal tunnel, the roof of the tunnel
and the tunnel itself can be measured. Sometimes an x-ray will
29

reveal bony abnormalities in the tunnel such as an abnormal

bone and/or arthritis.
Some people opt for surgery immediately, but many
people (including many surgeons) attempt to deal with the
problem non-surgically and only proceed with surgery if the
symptoms are becoming progressively worse with conservative
care. The information on this page is to help people with
conservative care.
Many different hands on practitioners may be helpful
ranging from physiotherapists, chiropractors, osteopaths and
massage therapists. Since I am a massage therapist, my selfcare suggestions are shaped by my training and my experiences
with clients.

Hands on Treatment for Carpal Tunnel Syndrome

Hands therapy for carpal tunnel syndrome depends on
locating the most significant locations that the median nerve is
compromised. The following is a list of common locations that
the median nerve can be compressed:
1. In the neck, the roots of the median nerve can be
compressed by the spine.
2. Under the clavicle: It is common for upper extremity
nerves to be compressed between the clavicle and the
underlying first rib.
3. Under the pectoralis minor muscle. This muscle is
often short in people with forward-rounded shoulders.
30

4. Under the prontator teres muscle in the forearm. The

pronator teres muscle is responsible for twisting type
motions of the forearm and wrist. It is often tight in
people who use their hands for manual labor.
5. Under the flexor retinaculum. Finally, the median
nerve can be compressed in the palm side of the wrist.
Compression in any one location makes the nerve more
vulnerable to compression everywhere else along its course.
This has been termed the double crush phenomenon.
Effective therapy usually includes decompressing the nerve at
multiple sites along its course!

The image below shows hands on techniques to

release the flexor retinaculum

31

Self-Care for Carpal Tunnel Syndrome

There are often many factors that all add up to creating
symptoms in the median nerve in the hand. The chart below
outlines some of the common factors that contribute to carpal
tunnel symptoms.

What is Tarsal Tunnel Syndrome?

Tarsal tunnel syndrome is a condition in which the tibial
nerve is compressed in the bony/ligamentous tunnel that it
runs through on the inside of the ankle. The tibial nerve sends
sensory information from the heel and sole of the foot to up to
the spinal cord and brain. When the tibial nerve is compressed
and/or inflamed in the tarsal tunnel then the person may feel
aching, pressure, tingling and/or numbness in the heel and/or
sole of the foot.

32

What Causes Tarsal Tunnel Syndrome?

The tibial nerve can become compressed in the tarsal
tunnel by thickening of the tendons of the muscles that share
the tunnel space with the nerve. This thickening can be caused
by tendonitis and/or by overuse of the muscles (often by
excessive pronation of the foot during running.
The tarsal tunnel can become a tight corridor due to
excess fluid in the persons body generally, or a local injury,
ganglion, arthritis or many other factors. Some people develop
it due to poor footwear!
You should see your doctor if you think you have tarsal
tunnel syndrome for a medical diagnosis and possible
treatment.

Testing in Tarsal Tunnel Syndrome

There are common physical tests for carpal tunnel
syndrome. In the Dorsiflexion Eversion Test the examiner flexes
the ankle backward (dorsiflexion) and everts the ankle (turns
the ankle outward). When the ankle is dorsiflexed the tibial
nerve is placed on stretch in the area of the tarsal tunnel. At
the same time the eversion movement tenses the flexor
retinaculum. These two physical challenges stretching the

33

nerve and compressing it often create or worsen the pain of

tarsal tunnel syndrome.

Other physical tests include tapping or strumming the

nerve to determine if it is irritated. Medical evaluation may
include ultrasound or nerve conduction testing. If the nerve is
severely damaged and/or getting worse then surgery may be
the best option.
However, many people attempt to deal with the problem
non-surgically and only proceed with surgery if the symptoms
are becoming progressively worse with conservative care. The
information on this page is to help people with conservative
care.
Many different hands on practitioners may be helpful
ranging from physiotherapists, chiropractors, osteopaths and
34

massage therapists. Since I am a massage therapist, my selfcare suggestions are shaped by my training and my experiences
with clients.

Hands on
Syndrome

Treatment

for

Tarsal

Tunnel

The following techniques may be helpful in reducing

symptoms of tarsal tunnel syndrome. They may be in the order
below, or in a different order with different emphasis
depending on the clinical situation.
1.
2.
3.
4.
5.
6.

Milking fluid from the tarsal tunnel.

Releasing the flexor retinaculum.
Milking fluid from the ankle joint.
Milking fluid from within the tibial nerve.
Releasing the abductor hallucis muscle.
Neural sliding and gliding of the tibial nerve relative to
the flexor retinaculum.
7. Stretching the tibial nerve at the tarsal tunnel to
release adhesions within the nerve.
The You Tube video below demonstrates some of the key
interventions in lessening tarsal tunnel syndrome.

35

In this picture the Abductor Hallucis muscle, which

overlies the tibial nerve, is released and lengthened to
decompress the tibial nerve.

Tarsal Tunnel Home Care

Clients with tarsal tunnel syndrome may need to address
the following issues.
1. Chronic inflammation/swelling in the feet with better
supporting footwear and cool or cold foot baths.
2. Chronic foot pronation with orthotics.
3. Weak arches with the short foot exercise.
Sometimes tarsal tunnel syndromes come from nerve
compression or irritation further up the leg, as far as the hip or
low back. Your health care professional can help determine if
this is the case.
36

Symptom Profile
Although a patient may use many adjectives to describe
neural pain, it is often described as a deep burning, aching, or
heavy sensation. It can occur along the nerves pathway, jump
from one area to another, and clump around joint or tension
areas. It can be constant or intermittent, although a constant
pain is more indicative of inflammation and compressive
pathology. Sometimes the pain is worse at night, and
sometimes it is worse at the end of the day.
Pain that occurs because of local neural ischemia is
described as sharp or knifelike. Ischemia-related pain lessens
with easy motion and worsen with overuse. Sometimes an
inflammation can cause a sharp pain, but it is generally an ache
at the end of the day with stiffness in the morning or after
prolonged inactivity. An inflammation-based pain feels better
with gentle activity and worse with rest.
A good history of injuries and evaluation of the location
and patterns of pain can help detect the source of the patients
pain. The following types of pain should be evaluated for neural
origins: pain that occurs in susceptible neural tissue areas, such
as the carpal tunnel and fibular head; symptoms that do not
match the common pain patterns; and pain that follows a
dermatome, or sensory-nerve distribution.

Treatment
Treatment can be either direct or indirect. Direct
treatment techniques are the same as those used in evaluation
or neural tissue. Indirect treatment techniques can be as simple
as changing posture and often involve altering a soft-tissue
37

structure, which affects the nerve. A hamstring stretch can

affect the sciatic nerve, and cervical stretch can affect the
brachial plexus.
There are several different direct neural mobilization
techniques. Only a few of the more common ones are
discussed here. Before these techniques are discussed,
however, you should understand that neural mobilization in sot
a common treatment and should be used only as a last resort.
Any of the neural techniques can easily injure the patient, so
extreme caution must always be used in deciding whether and
when to apply the technique and in applying the treatment
have failed and only when benefit to the patient from its
application is strongly indicated. It is used always with extreme
caution, because it can further injure the patient. Precautions
and contraindications are discussed later in this chapter. Neural
mobilization techniques should be used only when the sport
rehabilitation specialist knows the pattern of application and
the expected outcome of the treatment.

Neural Tension Test

Introduction
The Upper Limb Tension Tests (ULTTs) are also known as
Brachial Plexus Tension or Elvey Test. These tests are designed
to put stress on neurological structures of upper limb. These
tests were first described by Elvey and hence also known as
Elvey test but most commonly called ULTT. The shoulder,elbow,
forearm,wrist and fingers are kept in specific position to put
stress on particular nerve (nerve bias) and further modification
38

in position of each joint is done as "sensitizer". The ULTT's are

equivalent to the straight leg raise designed for the lumbar
spine.

Purpose
These tension tests are performed to check the peripheral
nerve compression or as a part of neurodynamic assesment.
The main reason for using a ULTT is to check cervical
radiculopathy. These tests are both diagnostic and therapeutic.
Once the diagnosis of cervical radiculopathy is made the tests
are done to mobilise the entrapped nerve.

Types
The test is divided into 4 types and examine the different
nerve.
ULTT 1 for Median nerve, anterior interosseous nerve
(C5,C6,C7).
ULTT 2 for Median nerve, musculocutaneous nerve,
axillary nerve.
ULTT 3 for Radial nerve.
ULTT 4 for Ulnar nerve, C8, T1 nerve root.

Method to Perform
Each test is done on normal side first. The order for
positioning the joint first is shoulder followed by forearm, wrist,
fingers, and last by elbow. Each sensitizer is added until the
pain is provoked or produced. To further sensitize the test side
flexion of cervical spine can be added. If the pain comes in the
39

very initial position then there is no need to add further

sensitizers.
If pain or sensations of tingling or numbness are
experienced at any stage during the positioning into the test
position or during addition of sensitization manoeuvres,
particularly reproduction of neck, shoulder or arm symptoms,
the test is positive; this confirms a degree of mechanical
interference affecting neural structures.
All test are done in supine lying and while applying the
shoulder depression it should be maintained even while
applying shoulder abduction.

ULTT 1: for Median nerve, anterior interosseous nerve

Shoulder

Depression and abduction (110 degree).

Elbow

Extension.

Forearm

Supination.

Wrist

Extension.

Fingers and thumb Extension.

Cervical spine

Contralateral side flexion.

40

'ULTT 2': 'Median nerve, musculocutaneous nerve,

axillary nerve
Shoulder

Depression and abduction (10 degree)

Elbow

Extension

Forearm

Supination

Wrist

Extension

Fingers and thumb Extension

Shoulder

Lateral rotation

Cervical spine

Contralateral side flexion

ULTT 3: Radial nerve

Shoulder

Depression and abduction (10 degree)

Elbow

Extension

Forearm

Pronation

Wrist

Flexion and ulnar deviation

Fingers and thumb Flexion

Shoulder

Medial rotation

Cervical spine

Contralateral side flexion

41

ULTT 4: Ulnar nerve

Shoulder

Depression and abduction (10-90 degree)

hand to ear

Elbow

Flexion

Forearm

Supination

Wrist

Extension and radial deviation

Fingers and thumb Extension

Shoulder

Lateral rotation

Cervical spine

Contralateral side flexion

42

Neural Tension Tests

{1} Passive Neck Flexion
PNF can be used by itself to assess spine disorders or
along with the lower limb or upper-limb tests. PNF can be
performed with the patient sitting or lying supine. In the supine
position, the patient lies supine without a pillow. The patient
initiates the motion by lifting his or her head off the table. The
sport rehabilitation specialist places his or her hands under the
head to support it and moves the neck into flexion while the
patient remains relaxed.

43

{2} Straight-Leg Raise

Straght-let raise (SLR) is sometimes referred to as
Leseagues test or Lazarevics test. The patient lies supine
without a pillow, and the sport rehabilitation specialist places
one hand on the foot and the other on the quadriceps just
proximal to the patella. The leg is lifted by the hand on the
Achilles, while the hand on the quadriceps keeps the knee from
bending. If enough flexibility is present, the heel may be placed
on the sport rehabilitation specialists shoulder. Neural tension
may be increased in the SLR with the addition of ankle
dorsiflexion, ankle plantar flexion with inversion, hip adduction,
hip internal rotation, or passive neck flexion, individually
combination.

44

{3} Prone Knee Bend

Prone knee bend (PKB) is similar to a quadriceps stretch.
With the patient prone and his or her head turned to the side
being treated, the sport rehabilitation specialist grasps the
lower leg above the ankle and flexes the knee to move the heel
toward the buttock while maintaining slight hip extension. PKB
is used to treat anterior thigh and groin pain.

45

{4} Slump Test

The slump test should not be used on patient who have
an irritable disorder. With the patient sitting on a table in a
slumped or sagging position and his or her hands behind the
low back, the sport rehabilitation specialist applies pressure to
the shoulders to bow the spine without changing the hip
position. The patient then brings the chin down to the chest,
and the sport rehabilitation specialist applies slight
overpressure to the head. The patient then extends on knee
and follows this motion with ankle dorsiflexion while keeping
the knee extended (Fig. 6-4b). Neck flexion pressure is released
slowly. This technique must be applied with extreme caution; it
is used as a test, not a treatment, because of its forceful
application. It is used to assess the response of the nervous
system to treatment. If the patient reports results before the
entire technique is applied, it is not necessary to go through the
full procedure. This procedure is not recommended for patients
with a suspected disk injury.

46

Application
Tension tests should be performed before all neural
mobilization treatments to determine the appropriate force to
apply during treatment. Pretreatment and post-treatment
tension test should be used to assess the patients symptom
response and the resistance of the tissue. Symptom responses
include pain, numbness, and tingling; the sport rehabilitation
specialist must know when and where in the motion these
symptoms may occur to avoid them during the treatment.
Identifying where tissue resistance occurs determines the
extent of application for the mobilization technique and helps
the specialist evaluate the results of treatment.
Extreme caution must be employed when using neural
mobilization to treat irritable conditions that affect
neurophysiology unless the sport rehabilitation specialist has
taken postgraduate courses on this topic, he or she should
refrain from using neural mobilization on irritable conditions.
Caution also should be taken when using neural
mobilization techniques to treat nonirritable conditions. These
conditions are likely to have pathomechanical causes and
secondary fibrosis, connective-tissue adhesions, and restriction
of normal tissue adhesions, and restriction of normal tissue
mobility Neural Mobilization HI and IV motions, but pain should
still be avoided. As a rule, grade in motions produce less pain
than grade IV.
Throughout the treatment the patients symptoms must
be monitored Initial treatment should not cause or increase
symptoms. A constant dull ache and sensation of pins and

47

needles should be avoided. The patient should be relaxed

throughout the treatment.
The duration, amplitude, and number of repetitions can
be changed as treatment progresses and the patient responds
positively to treatment. A sequence of slow oscillations can last
20 to 30 s, followed by a reassessment of the patients
condition. A sustained movement should be released if
symptoms occur and should last no longer than 10 s even
without symptoms. Sustained movement and oscillations can
be repeated a number of times as the treatment progresses so
that the treatment lasts for several minutes. The amplitude can
be increased until some symptoms are produced, although the
minimal force needed to achieve a positive muscle energy,
myofascial mobilization, cross-friction massage, and neural selfmobilization, can also be added.

Self-Mobilization
If neural mobilization techniques provide positive results,
it may be beneficial for the patient to perform self-treatment
techniques. Along with these techniques, the patients program
should include therapeutic exercises and corrective techniques
that can resolve the problems precipitating factors.
Self-mobilization techniques for the lower limbs are easier
to apply than those for the upper limbs. One of the more
difficult tasks in self-mobilization of the upper limb is
maintaining scapular depression during the activity. Specific
instructions on correct application and proper sequencing must
be given to the patient to ensure the best results. It is
important that the patient demonstrate proper execution of
48

the technique to the sport rehabilitation specialist before he or

she attempts the technique without supervision. Demonstrates
lower- and upper-limb tension techniques.

49

Precautions
Again, neural mobilization techniques should be applied
only as a last resort after other treatment techniques have
been unsuccessful. These techniques should be used only with
extreme caution and continual feedback from the patient about
the areas response to the treatment. Reproduction of painful
symptoms should be avoided, especially numbness and tingling
sensation. The slump test and the upper-limb tension tests are
complex maneuvers that can involve many structures and
therefore require consistent care and discretion. It is much
easier to irritate upper-limb nerves than lower-limb nerves,
because the upper-limb nerves are smaller and traverse more
complicated paths around bones and through muscles than
those of the lower limbs.
A worsening disorder, indicated by increased symptoms,
is an indication to stop the technique. The sport rehabilitation
specialist should always apply treatment carefully are err on
the side of caution if he or she has any doubts about the
treatment.
Diabetes, AIDS, and other systemic diseases can weaken
the nervous system. Extra care should be taken when applying
neural mobilization techniques to patients with these
conditions.
Whereas the circulatory system closely follows the
nervous system throughout the body, care should be taken
with individuals who have circulatory system disturbances. If a
nerve is mobilized, the circulatory structure next to it is also
mobilized.
50

Contraindication
Contraindications to neural mobilization include
malignancies of the nervous system or vertebral column, acute
inflammatory-

-infections, areas of instability, and spinal cord injuries.

Suspected disk lesions, cauda equine lesions (suggested by
changes in bowel or bladder function or changes in perineal
sensations),

-dizziness related to vertebral artery insufficiencies, and any

central nervous system disorder, such as spina bifida or
51

multiple sclerosis are also contraindications. Worsening

neurological signs are another important contraindication.

52

Reference
1.
2.
3.
4.
5.
6.
7.
8.

9.

Mobilization of the nervous system by David Butler.

www.nervemobilization.com
Wizebedia\neuralmobilization.
Youtube\neuralmobilization.
Basmajian J, Nyberg R. Rational manual therapies
Baltimore, Williams & Wilkins 1993.
Handbook of Physical Therapy and Rehabilitation
Krusen, Knottke, ELL wood M.D. PH.D., 1978.
Jehnv. Basmajian, Rich Nyberg Rational Manual
Therapy.
Kisner Carolyn and Colby Lynn Allen Therapeutic
exercise foundations and techniques 6th edition,
David company, Philadelphia, 2012.
Powers S, Howley E. Exercise physiology, Theory and
application to fitness and performance. United State,
Brown & Benchmark 1997.

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