INTERTWINED

HOW TO INDUCE NEUROPLASTICITY

A new approach to rehabilitating dystonias
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Joaquín Farias, Ph.D.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted,
in any form or by any means, without permission of the publisher

The opinions expresed in this book belong to the author and do not necesarily represent those of the author’s
collaborators.
Disclaimer: This book is not intended to diagnose or treat any condition. If you are affected by focal dystonia
please consult your physician prior trying any exercise contained in this book.

First Edition: February 2012

© Joaquín Farias Martínez

Cover image: Neurons: Patrick Hoesly. Digital Illustrator. www.ZooBoing.com

I.S.B.N.: 978-84-615-5124-8

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 To Pedro, the Rosetta Stone of dystonia
to Dominique, Tora, Leticia, David, Joe, Eeva and Maria
for sharing with me their way back home

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 Table of Contents

Prologue
Chapter I A new approach to rehabilitating dystonias

Adaptation
Under Construction
The ‘S’ addiction. A case of a six-year-old calligrapher.
The case of the cellist who pet his violoncello like a cat
The hypnotizing ball
Learning to be submissive
Paradox
Tremor
The number reader
The case of the archer who looked the other way
The case of the ankle resurrection
Over the moon
The case of the cursed bow
The shrinking piano
Lost
Orientation
The deformed hand
The case of the woman who was in denial
No limits
48 hours
Observing
Silent stroke
Accident
The case of the running hand
Reversal
The case of the Singer who couldn’t read sheet music
Genius
The erased lip
The hand that dropped the pick. Creating internal pressure scales.
Giant
Without symptoms
Change
Spain
Imagining
Phantom tension
The case of the two-fingered hand
The case of the giant thumb
A foreign body

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Recognizing
War
Unity
Grief at the bow
In utero
Regression
Withdrawal syndrome
Associations
Difficult words
Walking with giants
Dreams
Happiness
Dissociation
Mimesis
The hole
Marriage
Reacting
Abandonment

Chapter II How to induce a plastic change

Plasticity
Training
Resistance
Compensation
Classification
Learning movements
Rehabilitation
Phase I: analysis
Phase II: restitution
Variation
Rehabilitation techniques
Reconstruction
Synergy
EPILOGUE
APPENDIX I
Brodmann Areas
APPENDIX II
Treatment efficacy in an ecologically valid neuropsychological treatment program of
120 professional musicians with focal dystonia

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“Perhaps it is the very simplicity of the thing which puts you at fault”
Edgar Allan Poe

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 What do these have in common? A soprano who can’t sing from a printed score, a
violoncellist who can’t keep from crying while playing, a woman who can walk
backwards but not forwards, a man who can’t move his hands unless he’s playing the
violin, a priest who can’t say the words “you” or “we”, eyes that close, a dancer’s legs
that refuse to dance, and a magician’s hands that move on their own.

6
 PROLOGUE
“I learned very early the difference between knowing
the name of something and knowing something”.
Richard Feynman, What is Science?

Dystonia is defined as a movement disorder which causes involuntary muscle

contractions and spasms. The term originates from the Greek “dys-δυσ”, with the prefix
meaning difficulty or abnormality, and ton(o)- τόνος, meaning “tone” or “tension”. It
was recorded for the first time in 1911 as dystonia musculorum deformans, which is the
complete name of the inherited neurologic disorder that causes this disorder1 2.

When facing these types of concise and ambiguous definitions, a patient may
have many unanswerable questions.
Why does dystonia manifest itself in such a variety of ways? What do cervical
dystonia, writer’s cramp, and musical dystonia have in common? Is there only one kind
of dystonia or is each type of dystonia clinically different? Why are some people
affected but not others with the same genetic background? Which is a greater
determiner: individual predisposition or environment? Is focal dystonia an
occupational disease?
Is the patient in some way responsible for developing this disorder?
What happened in the lives of the patients during the weeks before the onset of
dystonia? Do patients show symptoms of the disorder years before it is diagnosed?
What is the first symptom? Does focal dystonia get worse?
Are emotions responsible for the disorder or is it only one factor in a complex
system of causes? Can certain movements alone produce dystonia?
Why does dystonia affect golfers, archers, and runners, but not soccer or
basketball players? Why do we find that musicians are affected to a greater degree?
During treatment, the most common questions are: Why are the majority of
treatments ineffective? Is it possible to develop more effective treatments in the future?
Is it possible that the answers to these questions lie in the collective experience
of the hundreds of thousands of patients in the world affected by dystonia and who live
with the disorder on a daily basis? The experiences of each individual are a piece of the
puzzle that only has meaning when it has been joined with all the others.

1
OPPENHEIM, H. “Über eine eigenartige Krampfkrankheit des kindlichen und jugendlichen Alters (Dysbasia lordotica
progressiva, Dystonia musculorum deformans)”. Neurologisches Zentralblatt, Leipzig, 1911, 30: 1090-1107.
2
Dystonia can also be produced by accidents, medication, exercise or stress.

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 This idea inspired me to initiate the Dystonia Project. This took place by making a
series of trips throughout the world looking for anonymous patients affected by dystonia
for whom the answer to these questions could be found in their daily lives. This is how I
met these extraordinary people whose clinical histories I examine in this book.
The Dystonia Project up to now has included 400 patients on five continents. Of
those, 120 have taken part in an experimental therapy program. The results of that
program are shown in Appendix II.

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 Adaptation

In a 1964 experiment by Wolfgang Kohler, the capacity for subjects to adapt to a

modified reality was evaluated using prismatic glasses that produced an inversion of
visual images. 3
A series of volunteers participated in the study. A projected image is turned
upside down on the retina, and the brain rights it, but the prismatic glasses inverted the
path of the rays. The subjects looking through the prismatic glasses saw an upside
down world. What was up, was down.
The subjects were asked to use the glasses throughout the day. On the first day,
they were unable to walk or orient themselves. After a few weeks of daily use, they
could drive, walk, and orient themselves without difficulty. An adaptation had taken
place. Some subjects were even able to ski or ride a bicycle. Then the glasses were
taken away, and the subjects were again unable to orient themselves or walk without
them.
After less than a week, their worlds returned to right again.

3 Kohler W. 1964. The information and transformation of the perceptual world. Psychological issues 3: 1-173.

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 Under Construction
Everything we are, our memories, fears, beliefs and dreams, are intertwined
within a network of 100 billion neurons which receive information, process it, and
generate reactions and memories through their connections. These connections are
constantly changing to produce pathways that compete with each other for dominance.
Each pathway is a possible route, a solution to a concrete problem. The most used
pathway will become the default, and the least used will be cast aside.
Everything we live and do changes us. There is no going backwards. In the
present, our brains create doors we can open in the future.

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“To state a theorem and then to show examples of it is literally to teach backwards”
E. Kim Nebeuts

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 I never wanted to practice the theory, but to theorize the practice. For this
reason, real examples are revealed first to be analyzed later.

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PART I: A new approach to rehabilitating dystonias

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 The ‘S’ addiction. A case of a six-year-old
calligrapher.
“Where you see the effect, I see the cause”

Ana was six years old when she learned to write with the help of her mother.
Her intellect, above average for her age, and her maturity enabled her to read and write
like a seven year old when she was five.
At six years old, she found that her classmates didn’t know how to write the way
she did, since in class they were beginning from zero by identifying letters and copying
them one by one in series of fifty. The teacher thought that even though she already
knew how to write, it wouldn’t do her harm to reinforce her writing by beginning from
zero. Ana wrote the series of numbers and letters. She wrote an ‘a’ and copied it fifty
times on a piece of graph paper, then moved on to the ‘b’ and so forth. After a certain
amount of time, she arrived at the ‘s’. She wrote pages and pages of this beautiful,
winding letter at home and at school.
Toward the end of the year, writing became a problem for her. Her writing
gradually became more imprecise and deformed. It was very difficult for her to
improve it. At the beginning of adolescence, she was diagnosed with writer’s cramp,
and for years she was treated with Trihexyphenidyl hydrochloride. She began by
receiving a low dose, but since it did not prove effective, it was increased to the
maximum allowed.
Ana entered the Dystonia Project when she was 17. At that time, she was not able to
write with her right hand without supporting it with the left. In this way she avoided
extending her wrist which would have completely prevented her from continuing to
write.

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 Our attention is drawn to the very large size and multiple disfigured strokes in Ana’s
writing

The first step, before beginning rehabilitation, was to analyze her writing; the
rhythms, posture, hand positions, angles, etc. The next step was to look at which
motions produced a dystonic response, caused spasms, tremors or dysfunctional
movements.
Upon finishing the assessment, it was found that the movements she could not make,
were those movements that included a straight downward stroke, because they produced
tremors and spasms. The pattern was very interesting: when beginning a downward
vertical stroke, her brain interpreted it as trying to make an ‘S’ and began a clockwise
semi-circular stroke. Ana, without knowing it, mechanically continued to draw ‘S’s’,
including when she didn’t want to, in a repeat of her past practice. This type of dystonia
could be called movement-related dystonia3.

3
Author-coined term.

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 A pattern can be seen from this exercise. The task required drawing a straight
upward line followed by a straight downward line. As can be seen, the mistakes were
made, in the majority of cases, in the downward strokes, changing the straight line into
a ‘j’. When these mistakes occur in upward strokes, they follow the same pattern, the
motion begins like that of a “j”.

This exercise shows how making the shapes of other letters that included vertical
strokes proved difficult as they were changed into ‘S’s’.

In these exercises, the same pattern can be seen while making circles and spirals,
where the descending stroke produces an involuntary movement as described above.

In this exercise, which evaluated the ability to connect upward strokes to downward
ones, we can see that when a dystonic reaction was produced, in this case spasms, the
length of the stroke increases due to the involuntary movement of the wrist.

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After one year of rehabilitation, the ‘sjf’ series became normal.

The series of spirals and circles improved considerably.

Finally, her writing became normal in size and became more precise.

Ana was able, therefore, to resume her studies.

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 It is usually thought that patients affected by writer’s cramp experience tremors or
spasms, taking for granted that they occur randomly, without a pattern, and that it is not
possible to control them nor purposely adjust them. They are usually treated with
medications.
The therapeutic approach taken in this case was extremely innovative given that, in
the rehabilitation, it is supposed that the spasms have a meaning, being logical but
untimely movements having to do with the patient’s past experiences. This logic could
be defined as previously programmed “stimulus response” associations, which would
correspond to the downward stroke in the first example and to the semi-circular
movements in the second. The precept that should guide the design of rehabilitation
protocols for patients affected by focal dystonia is: the movement is the aim and the
language.
In this case, the interaction between of automatic movement memories
performed to an extreme in the past produced a rigid response in the individual. This
rigidity is what characterizes a patient affected by focal dystonia. No other response to
this stimulus exists. This causes the patient to experience the spasm as an inevitable
response.

The rehabilitation, based on the response flexibility to the same stimulus, breaks
the rigidity of this response, making it possible to reprogram the kinetic sequences. In
this case, the descending stroke movement is associated with maintaining the direction
while training the inhibition of the dysfunctional association and retraining the proper
associations.
The learning procedure involves learning that the motor response takes place in
reaction to a sensory stimulation. This leads us to assess the association as being the
regulatory element that allows the learning to be committed to memory.
The neurologic mechanism that allows this type of learning was described by
Freud in his “Law of Association by Simultaneity” which states:
“when two neurons fire simultaneously, this firing facilitates their ongoing association”4

The association between “dysfunctional stimulus-response” is quite fixed within

the system in the case of patients affected by focal dystonia.

4
Amacher P. Freud’s neurological education and its influence on psychoanalytic theory. International Universities
Press. 57-59. Nueva York. 1965.

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 When a patient is able to react in another manner in response to the stimulation
which causes the spasm or tremor, the associative dysfunction gradually weakens,
following these general principles:
When two neurons fire separately, they disconnect.
Unused connections weaken and are finally lost.

Therefore, the rehabilitation process is based on creating and repeating functional

associations until they acquire dominance over the possible responses to stimulus. For
that reason, we try to achieve a default automatic response.

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 The case of the cellist who pet his violoncello
like a cat

Lydia was a mathematician. As a single 40 year old, she lived life to the fullest.
Since she had a lot of free time, she felt the need to “live” beyond the confinements of
her work. Therefore, she decided to return to the violoncello classes she had left in her
adolescence. From the beginning, she wanted to make up for the time she had lost and
practiced a great deal more than her classmates who were only ten years old. The
demands she placed on herself were so great that she finished with all the academic
requirements for students at her level, including public performances. The difference
was that the public performances didn’t mean as much to the children as they did to her.
She was aware that, on occasions, before a concert at an elementary school, she suffered
from insomnia for days.
One week, after a demanding week and an upcoming performance, she woke up
frightened in the middle of the night. Her arm was moving out of control. She
described it as a fish out of water. It twisted in all directions. After a few minutes of
pain and tension, her forearm turned excessively and painfully, and stayed that way for
hours. This painful turning of the left forearm continued throughout the next day,
letting up only on occasion. She was diagnosed with segmental dystonia, which was
treated with muscle relaxers.
Not being able to supinate her forearm prevented her from driving, and she even
had to learn to hold a cigarette differently in order to smoke. She was granted partial
disability a year later due to her impairment and the limitations it produced.

If we analyze this case from a different point of view, her dystonia was not a
random event, and the muscles it affected were not arbitrary. The maintained pronated
position her left arm took was due to the disconnect among the supinator muscles. This
is not strange, given that her violoncello practice required her to maintain a supinated
position of her left forearm.

20
 The overstimulation of the supinator muscles due to the practice of the violoncello
could have brought about the hypoactivity that leads to hyperactivity of antagonist
muscles.
The interesting thing about this pattern is that it only occurred when the forearm
took the position needed to play the violoncello, that is, with a maximum bending of the
elbow and turning of the forearm or identical positions such as driving or smoking.
Turning could be achieved when the elbow was bent or extended to a greater or lesser
degree.
In her case, simply by visualizing contact with the cello strings caused a
response of intense pronation, which appeared to be a movement to avoid the action.

Her therapy was based on gradually becoming used to the strings as a stimulus.
Lydia spent months caressing the cello inside its case in her lap, while watching
television or having a conversation. During the following months, she caressed the
strings without playing. The mere contact with the strings caused a reaction that, in
time, subsided. In the end she was able to come in contact with the strings to play in a
supinated position.
Lydia demonstrated a “tactile-stimulation movement” and “position-movement”
association. Within movement sequences, tactile is the first link. Before striking or
holding down a string, a tactile stimulation was made by touching it first.
In this case, as in the majority of dystonic piano players, an association exists
between touch and spasticity. This type of dystonic could be called touch-related
dystonia. Tactile stimulation generates a response or association characterized by
tensing and tremor that is fed by positive feedback or by compensating.
In the first place, it was necessary to disassociate contact with the string from
muscular tension in order to later eliminate the spastic response when the blocked
position occurred.

In the majority of patients affected by writer’s cramp or musician’s dystonia, touch-

related dystonias5 are present, sometimes in isolation, but in the majority of cases
coinciding with a position-related dystonia or a movement-related dystonia.

5
Author-coined term.

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 The hypnotizing ball

Daniel is a ping pong player, a member of his country’s national team. To the
surprise of his friends, he left his profession just when it was predicted that he would be
at the top of his career.
Daniel suffered from focal dystonia which affected the extensor muscles in his
forearm. Physical therapy treatments had provided no results. His case included one
peculiarity: he was able to perform all the movements without holding the paddle.
Even more peculiar was that he was able to perfectly perform the movements using the
paddle in the air.
As soon as a ball was bounced on the table, triggering the learned serve
response, his wrist extended uncontrollably. On occasions this happed so intensely that
he lost control and threw the paddle.
This case can again be explained by association and highlights the importance of
context. A predetermined context existed where his reaction was learned and inevitably
produced a dysfunctional connection. These contexts could become so specific that,
varying only in small details, the system did not recognize the context, leaving it to its
own associations. All of the elements present at the time the dysfunctional sequence
was programmed should appear in a concrete order in order to create the spasticity.
In this case, the dystonia was not in his hand, but in the ball.
This clue can be used when designing rehabilitation exercises, always seeking to
establish control within contexts not associated with spasticity in order to later confront
the conflictive contexts, modifying details so as to produce less extreme responses.

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 Learning to be submissive
Keiko started learning piano when she was four years old. Because of her talent,
her parents decided to look for a demanding teacher that would bring the most out of
her abilities.
Keiko admired and feared her teacher. He treated her like an adult from four
years old. When she made a mistake, she begged his pardon and bowed to him.
When Keiko entered the program, she was 27 and demonstrated a very
uncommon abdominal dystonia. The spasms only occurred when she was seated on a
piano bench, when a strong abdominal contraction made her body constrict. She
lowered her eyes, her shoulders folded, and her spine curved shortening her body to
protect her abdomen. This did not occur if she sat in any other type of seat. The
stimulus that triggered the dysfunctional response was extremely specific and singular.
After twenty years of daily submission, her body begged forgiveness, even in the
absence of the teacher.

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 Paradox

“How wonderful that we have met with a paradox.

Now we have some hope of making progress”
Niels Bohr

One puzzling aspect of dystonic behavior is that motor control changes

drastically, depending on the situation, in different contexts. The same patient can be
unable to make a specific movement while playing the guitar, but, on the other hand,
can be able to make the movement correctly while simulating it as if he were playing an
imaginary guitar. This phenomenon, known as “automatic-voluntary dissociation”
suggests that certain contexts and not others can trigger a dysfunctional response in
those patients.

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 Tremor

Lynda, a 45-year-old violinist, showed a task-specific dystonic tremor. This

condition prevented her from carrying out her work in a well-known orchestra in her
country. Her contract required her to play solos, on occasions, during symphonic
performances.
When she tried to play, her left hand began to tremble. The tremor was very
fast, which when in contact with the strings produced an exaggerated vibrato. Lynda
tried to stop the tremor, producing tension in the muscles of her left hand, until this
tension completely prevented her from playing the violin.
A tremor is an involuntary muscular movement, somewhat rhythmic, that
involves swinging or swaying movements in one or more parts of the body. It is the
most common involuntary movement and can affect the hands, the arms, the head, the
face, the vocal cords, the trunk, and the legs. The majority of tremors occur in the
hands. In some people, the tremor is a symptom of some other neurologic disorder.
The most common form of tremor, however, occurs in otherwise healthy people. A
tremor can result in embarrassment for some people and in difficulty performing daily
tasks.
The dystonic tremor can affect any muscle in the body and is most commonly
seen when the patient is in a certain position or moves in a certain way. The pattern of
the dystonic tremor can be differentiated from the pattern of the essential tremor.
Dystonias occur irregularly and sometimes can be relieved by complete rest. A tremor
can be an initial sign of localized dystonia in one particular area of the body.

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 Lynda’s case is a clear example of how symptoms appear, what could be called
the timeline of a patient affected by focal dystonia. The process begins with a
predystonic state, in which no physical demonstration of tremors or spasms yet exist,
but the patient perceives her hand or objects in contact with her hand as different. At
this time, the maladaptive plastic change or the degradation of the cortical
somatosensory representation has taken place. In the subsequent phase the patient tries
to align her distorted perception with outside demands. In this second phase, fast, mild
tremors primarily appear, which the patient tries to control, producing tension and
precipitating the third phase which is characterized by the presence of spasms that
completely hinder movement. So the first phase is basically perception; the second
shows a loss of control; and the third, immobility due to tension. Generally, the patient
seeks medical care when she is in the third phase.

In Lynda’s case, her treatment involved allowing the tremor to occur. During
the first days, when her hand began to tremble, she could not contain her tears and after
a few minutes of the tremor, she felt depressed. After a few days, her emotional
reaction changed, and she no longer felt anything when the tremor began. Finally the
tremor began to decrease until, after six months of daily practice, it disappeared. Lynda
was able to return to the orchestra. During the second year, she suffered a relapse of
one week during which the tremor returned just as it had begun. After that, normality
was the rule.

In this case, the association was produced upon contact with the strings, and the
tremor was the response, which produced a touch-related dystonia6. The hand position
needed to play the violin was not associated with the response, since Lynda, while
simulating the playing of an invisible violin, could perform the movements perfectly.
The response disappeared in this case by way of overstimulation, inducing an adaptation
to the system through habit. This plastic change involves an alternative proprioceptive
integration and the creation of new memories in which the contact is not associated with
the tremor.

6
Author-coined term.

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 In order to understand how the plastic change which occurred in this case works, we
need to be aware of the fundamental principles that govern the creation and
maintenance of connections.
This phenomenon, known as activity-dependent synaptic plasticity, is essentially
based on the reinforcement or weakening of the synapses between two neurons
depending on their activation time overlap.
In generic terms, a Hebbian principle has been formulated that reflects this
mechanism: “cells that fire together, connect.” Going even further, cells in contact that
don’t fire together because they don’t receive a synchronous signal very probably end
up having a restrictive relationship.
Therefore, even though these activity-dependent changes can be tremendously
temporary and fleeting, today we recognize that they are also the basis of long-term
learning, generating patterns of genetic cellular expression of great impact for neuronal
functionality. This type of functional plasticity could be responsible for many of the
changes in cortical reorganization and representation in somatosensory and motor
regions.

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 The number reader
Maria was pregnant. Her husband worked in an office, and she, in order to earn
extra money, accepted a job in a Bingo parlor. Her work consisted of taking out balls
and reading the numbers out loud. Again and again. After eight hours reading
numbers, she returned home hearing numbers and numbers in her head until she could
relax and sleep. 35, 43, 24, 70, 15, 9, 54…
One day she took out a 70, as she had many other times. She read it and
experienced intense pain. She had bitten her tongue and was bleeding. Her jaw
behaved like an out-of-control animal and bit it every time she tried to pronounce the
letter ‘t’. After various painful attempts, she decided to avoid the letter ‘t’. Her
attempts at moving her tongue so consciously caused her to lose the ability to articulate
in a few hours. One number had become the barrier between normality and incapability
to communicate.
Dystonic patterns are quite varied, which could mean that each pattern has been
produced by a specific activity. Dystonias exist for readers, archers, violinists, painters,
dancers, and at the same time the dystonias of each one are different from other people
in the same category. Dystonia always affects the movement that is most used, the
movement that is needed to carry out each activity.

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 The case of the archer who looked the other way
“Inequality is the root of all local movements”
Leonardo Da vinci

Pablo was a professional archer. He dedicated more than five hours a day to
practice. It could be said that no one spends as much time looking to the left as an
archer. Pablo consulted a neurologist because when it came time to fire, he had begun
to experience something unusual. With the bow in his left hand and the arrow in his
right hand, he was unable to look to the left to aim. His head involuntarily turned until
he was looking in the opposite direction.
All movement is made up of synchronized operations, both the agonist muscles,
those that cause actions, and the antagonist muscles, those that oppose the action of the
agonist muscles.
The antagonist muscles control and brake the movement produced by the agonist
muscles so that they do not overcome the physical limits of the joints and, thereby cause
injuries to the musculoskeletal system. They should brake movement at their greatest
point, intervening only at the appropriate time. If they intervene too late, injury will be
caused, and if they intervene too early, they will oppose movement.
In the effects of focal dystonia, a co-contraction is observed. This consists of a
simultaneous contraction of the agonist muscles and the antagonist muscles while a
movement is being performed.
This case can be explained using the model of overstimulation: a deficit or hypo
activity is produced that accompanies an “agonist-antagonist” loss of balance, turning
into hyperactivity of the antagonist muscle. Not being able to turn to the left causes
turning to the right.

29
 The case of the ankle resurrection
“Walking is a controlled fall”

Claire was 56 years old. Her dystonia presented itself when she was 31, two
months before the birth of her first child. It worsened after her next two children were
born, and further worsened after menopause. Her dystonia was considered to be a result
of taking a prescription antihistamine.
Her ankle supinated involuntarily when she walked. This made it impossible for
her to place the sole of her foot on the floor, and she needed to use a cane to support
herself when she moved her right leg. She was not able to move forward but she could
walk backwards. She was able to walk up and down stairs. She always walked better if
she walked barefoot. Contact between her foot and the floor made her feel like she was
losing her balance and was about to fall.
Claire began a program of instruction based on not using her cane and the
multiple compensations she had developed during years of living with dystonia. The
first step was to rid her of her compensatory movements in order to clearly see what
percent of her movement was affected and work on her rehabilitation.
The restructuring of free movement is a chain reaction. Having the foot produce
correct support creates immediate changes in how the knees and hips function. After
the first element has been performed, the body remembers a sequence of movements.
Physical exercise allowed and induced a plastic change which enabled a full recovery of
functional movement. The memory that belongs to a movement, before the disorder
appeared, is a key piece in the construction of a reference upon which to model future
movement and make it functional again.
Clair went down stairs being conscious of each of her steps and paid great
attention to how she supported her right foot. To go down three steps, it previously
took her ten minutes to figure out what would be the sequence of movements and
translate them into a series of commands.

Another important aspect in her rehabilitation involved finding the tremors that
occurred prior to each of movement involved in taking a step. When the tremor was
found, the movement that caused it was prompted. In the majority of cases, initial
progress is rapid. The tremor pointed out the area that should be reorganized.

30
 The way to achieve the reorganization is stimulating, through movement, the
area in control of this specific movement. After a year of stimulation, waking slowly
but cleanly, without any compensation or abnormal movement, she was able to
normalize her step at a slow speed. Her walking is best when her mind is quiet, she is
focused, and she is not rushed or stressed.
Using slow motion is crucial in order to set motor schemas and make a diagnosis
regarding which points along the line of movement should be worked.
If we consider a movement as a line, we could say that the dystonic response is
not found all along it, but at certain points. Determining where these points are, make
rehabilitation more accurate, efficient, and faster.
Living with dystonia produces feelings of disconnection for the patient.
Bringing about the restructuring of movement after the restructuring of perception
caused the patient to describe the latter as “waking up her body”, a feeling of regaining
the whole.
Claire was surprised at how her childhood memories, such as walking with her
father, came back on their own during rehabilitation. Having to pay attention in order to
control each step was associated to early childhood memories of walking.

31
 Over the moon
Following the first manned space missions, it was noticed that the astronauts
who returned after experiencing long periods of weightlessness on a mission, needed to
go through a period of adaptation. During this time, they needed to consciously walk,
since the automatics of walking had not been used daily and had, therefore, become
diffused.

32
 The case of the cursed bow

Rainer was one of the most respected German violinists of the 1970s. When the
symptoms of his dystonia clearly presented themselves, it became impossible for him to
continue playing and opted to direct, thereby making over his career. Given that he no
longer played, he decided, as a symbolic act, to sell his bow.
This bow was bought and sold between European luthieres until it ended up in
Norway. Erika was looking for a bow and found this beautiful one two years later at a
luthieres in Oslo. Within a few weeks, Erika acquired the same dystonia that Rainer
had. The bow was slightly out of alignment.
String musicians often refer to bows as “balanced” or “unbalanced”. A bow can
be unbalanced when the center of balance becomes displaced in respect to the balance
point. Slight differences in weight between the head and the frog can allow the bow to
facilitate movements or hinder them.
The greater the virtuosity of the performer, the greater the demands will be that
the tools used must satisfy.
In this case, the subtly unbalanced work tool caused the feeling that the bow
might fall out of the user’s hand, which caused the players to modify their technique
and produced unnecessary tension in order to avoid it. These inconsistent technical
changes, while practicing, modify the automatized motor programs formed earlier in
childhood, causing dysfunctional associations between execution and excessive
muscular tension.

33
 The shrinking piano

“The ‘paradox’ is only a conflict between reality

and your feeling of what reality ‘ought to be’”
Richard Feynman. Lectures of Physics

Marc was a 38-year-old professional pianist affected by dystonia. For months

he had not been able to play the piano because he could not find the keys. He was
always coming up short when calculating finger placement and therefore hit two keys at
the same time.
Movement control happens through a process known as “feedback”. When we
carry out an action, we expect information about the result that it had, in this case the
feedback, and as a function of the results we receive, we perform the next movement.
This is only possible with simple movements carried out at slow speed. In the case of
complex movements, carried out at high speed by pianists, the process changes. The
movements that have become automatized work in parallel. They can be produced by
one system of movement, and the movements that require attention, proficiency and
continuous adaptations, by another. Regarding complex movements carried out at high
speed that do not allow patterning of the next through feedback, movements should be
carried out as a combination of motor sequences, preparing one combination while
performing another7.

All pianists can spread their fingers with precision with their eyes closed, placing
them in the positions that will result in their playing sixths, sevenths, octaves, etc. This
basic skill is based on using an internal tridimensional representation, created and
perfected during the first years of practice, that enable the player to calculate and adjust
distances, make vertical and horizontal readjustments, and visualize keyboard positions
when there is not time enough to see and feel the keyboard.

When Marc positioned his hands, using his internal representation as a reference, he
always came up short. His internal piano had shrunk and did not correspond to the
actual dimensions of the keyboard.
In analyzing this case, we find ourselves facing an unknown: When we move,
do we use the real object or our visualization of it as a reference? The answer is clear:
we first use our internal virtual model.

7
Lashley, K.S., “The problem of serial order in behaviour” en L.A Jeffress (Ed.), Cerebral Mechanisms and Behaviour.
New York: Wiley, 1951, pp.112-136.

34
 Marc knew that the keyboard had not shrunk, but he couldn’t help making an
error in his movements because he was basing them on erroneous references.
Four general regions of the neocortex are thought to produce the majority of our
voluntary movements. These regions are the prefrontal cortex, the premotor cortex
(Brodmann Area 68), the supplementary motor cortex (Brodmann Area 6), the primary
motor cortex (Brodmann Area 4), and the posterior sensory cortex.
The primary motor cortex and the premotor cortex contain a dictionary of
movements from which it chooses the most appropriate. The dictionary of movements
that the primary motor cortex has includes the more basic movements than those stored
in the dictionary in the premotor cortex. The premotor cortex and the primary motor
cortex receive instructions from the prefrontal cortex, which elaborates plans for
movements, and sends instructions from the prefrontal cortex to the premotor cortex and
to the primary motor cortex. The posterior sensory regions send information to the
primary motor cortex in order to perform relatively automatic movements, sending
information to the prefrontal cortex for the development of more complex movements.

In this manner, the selection of movement takes place in the prefrontal cortex.
The sequencing of this is organized by the premotor cortex. The individual elements of
the movement are produced by the primary motor cortex, and the posterior neocortex
functions to provide the sensory information needed to produce the movements.
For Marc, the process of movement development was faulty, since his internal
references had changed. In this case it was necessary to reconstruct his internal
representation of the keyboard by consciously scanning its distributions and heights, as
a blind pianist would do in his first piano classes. The training consisted of paying
attention to the feel of the finger placement on the keys and the feel of the keyboard, the
real one, and avoiding playing based on how the keyboard might have been, his internal,
virtual representation. This way, once a virtual representation of reality was
reconstructed, he was able to return to playing normally, basing his movements on an
appropriate virtual model.

8
Within the cytoarchitecture of the cerebral cortex, 52 regions have been defined, known as the Brodmann Areas, which are
differentiated from each other by the type of cells present. Thereby, Areas 1, 2, and 3 are somoesthetic areas, perceiving and
recognizing bodily sensations; Area 4 is the voluntary motor area; Area 6 is the premotor area, etc. More information about the
Brodmann Areas can be found in Appendix I at the end of this book.

35
 Lost

These newspaper articles illustrate problems caused by receiving improper feedback:

A guide dog leads his blind owner to the Friskies headquarters

“Police found M.B., a blind man in Castellbisbal (Barcelona) suffering
from symptoms of exhaustion and dehydration. It seems that this morning,
guided by his dog, instead of following his normal route, he had travelled
more than 30 kilometers on foot, crossing shrubs, wheat fields, and
dangerously traveling along the highway shoulder, ending up at the
headquarters of Nestle Purina, where a well-known brand of dog food is
produced.”

El Mundo Today 2011

A man dies after driving his car into a reservoir because his GPS showed the
wrong route
“A 37-year-old man died after driving his car into La Serena Reservoir, in Capilla
(Badajoz), while he was traveling on a short road. Apparently his car’s GPS
showed an old road that ended in the reservoir, but in the darkness of the night,
the driver was unable to stop his vehicle in time and was submerged in the water
within a few minutes.”

Europapress 2010

36
 Orientation
This article from a local paper, shows how internal representation can substitute
perception:

A blind man drives to work for a year without being discovered

“A.G., a 40-year-old resident of Madrid, was arrested last Friday for
reckless driving. A.G. had worked for 17 years in office near his home. He
had driven to his work every day. Two years ago, he lost his vision due to
an illness. When he was released from the hospital, he did not want to give
up driving his usual route to work. Since he had traveled the same route
thousands of times, he could mentally recreate every distance, remember
points of difficulty, and the hours of the greatest traffic.
He therefore decided to drive from memory and using his ability to
imagine what could be happening, based on his past experience. For one
year, he drove his route back and forth from his home to work without
anyone noticing and without any problem, until last week when the local
police stopped him for driving the wrong way on a one-way street which
had changed to the other direction the prior day.”

37
 The deformed hand

Kim was a stage magician who had stood out for her precise and elegant card
performance. During the last several months, her performance had become clumsy, and
she could no longer even shuffle the cards. She felt as if the fingers on her right hand
was opening involuntarily, and in order to avoid this, she squeezed it shut hard. In that
position, it was impossible for her to use her hand. The strange thing about this case
was that Kim was absolutely unconscious of what was happening. She saw that her
hand was not opened, but she felt that it was, and she couldn’t avoid fighting the
feeling.
In order to break this illusion, we used a confrontation technique. Kim opened
her hand voluntarily and felt the natural muscular tensions that were produced when she
made this movement. Then she relaxed her hand and compared the feelings.
Two very different perceptions were present. When she voluntarily opened her
hand, she felt the position and at the same time felt the muscular tension that was
necessary to produce the movement. The phantom tension was very different. She felt
as if her hand were opened, but didn’t feel that her extensor muscles were active.
In this way, Kim was able to differentiate when she produced the movement and
when it was an error in perception. Somehow Kim found a “marker” that allowed her to
differentiate between what was happening and what was only “noise”.

38
 The case of the woman who was in denial
Laura lives with her head tilted and turned to one side. She endures intense pain
caused by the contraction of her cervical muscles. Her head is in a position of negation
even during sleep. She was diagnosed with cervical dystonia eight years ago.
She remembers that her head suddenly began to shake one day after several
months of intense stress due to her divorce. During this period, she couldn’t sleep and
had to resort to antidepressants and sleeping pills in order to continue on with her life.
The initial shaking changed into a more intense spasm until looking straight ahead was
no longer an alternative. Her head was constantly in a position of negation. This
became a complex for her because she was unable to maintain eye contact when she
was speaking with someone. Her friends simply sat to her right, and she relaxed.
Although the spasm seemed to go on all day, many days she got up without it and could
move around the house for five or ten minutes as if she were recovered. After a few
short minutes, her head returned to its position of negation.

The dysfunctional response, in this case, was characterized by lateralization and a

rotation of the head. The muscles that produced the lateralization of the head to the left
lost activity, which caused a rebalancing of the antagonist muscles which drew the head
to the right. In her attempt to adjust the head position, and upon finding that the
muscles that carried out the action did not respond as they had before, she tried to make
the muscles that produced the rotation balance the situation, which caused an
interchange of functions. Far from solving the problem, these caused her to move from
the shaking phase to the more painful spasm phase, in which the tension and the co-
contraction was much greater.

This type of dystonia could be called dystonia associated with a mismatch of

internal axis,9 since the stimulus that triggers the response is distorted internal
references that cause the system to carryout positional adjustments by looking for a non-
functional balance.

9
Author-coined term.

39
 Laura demonstrated an inability to recognize the actual position of her head in
respect to her body. Occasionally we used a mirror for her to see the position of her
head, since it was difficult for her to determine where it was guided only by feel. Her
internal world had changed for Laura, and within this altered perception, what she did
was logical.
When the corporal topographic maps change, the system readjusts movements
using as a base is own distorted maps. Motor maps and location and position references
are subjective and individual. All individuals construct their own. Every movement
that we make must be imagined first, taking into account these internal virtual models
which are our references. It could be said that the internal virtual representation of the
body in space gets priority over the actual body position.

The problem is that I don’t know where my head is.

P: —“When your head is in the center and you are looking forward, what do you
feel?” —
R: —“I feel like my head is tilted to the left.”—.
P: —“When your head is tilted to the right, what do you feel?”—.
R: —“I feel uncomfortable, but at the same time I feel like I have to be that way.
This is my posture now, the one my body wants to be in. The problem is the pain”—.

40
 No limits

James was a professional athlete specializing in the triathlon who held the title
of Ironman. The Ironman competition is the most demanding of the triathlons. It
consists of 3,800 meters of swimming, 180 kilometers of cycling, and 42.2 kilometers
of running. The race has a time limit of 17 hours, average completion time is 12 hours,
and the present record is 8:04:08. In order to compete in these trials, an enormously
difficult training period that takes years is required.
This triathlon contest began in 1978 when Marine Corps Commander John
Collins proposed combining three existing competitions in order to determine the best
athletes in swimming, running, or cycling. The competitions were the Waikiki
Roughwater Swim which consisted of swimming 4 kilometers in open sea, the Around-
Oahu Bike Race which consisted of 80 kilometers on bicycle and the 42 kilometer, 195
meter Marathon of Honolulu. Collins proposed performing the three in a row. The
winner would be considered the “Ironman”. The Ironman Triathlon is a very
demanding race that takes its participants to their physical and mental resistance limits.
Nevertheless, some athletes find these distances small, and therefore do not participate
in them. Even so, events of greater physical challenge have been created, such as the
Double Ironman. Other more extreme formats have been developed for these, such as
the triple, quadruple, quintuple, deca, and the 15X events, which are multiple the
distance of the original Ironman.
James demonstrated a focal dystonia in his ankle. This condition prevented him
from even walking. We can just imagine how many flexo-extensions this ankle carried
out during the 17 hours that his last competition lasted. You might expect that given
this effort, an injury in the tendons would be suffered because of overuse, but that didn’t
happen. It would be expected that given this strain, an overload injury to the tendons
would happen. James’ physical strength allowed him to continue running, swimming,
and pedaling beyond what a normal athlete could have physically endured. This is why
he could surpass the neurological limits of movement.

41
 According to the research done until now, it appears that focal dystonia affects
athletes in certain disciplines and not others. Cases of developing focal dystonia are
known in sports that require ultra-repetitive practice, such as ping pong, resistance
races, golf, and target shooting10. It is possible that the monotony of the practice, one in
which a movement is repeated thousands of time without a break, puts the functional
stability of the system to the test, producing a maladaptive plasticity en certain cases.

10
Valerie L. Soland, Kailash P. Bhatia, Maria A. Volonte, and C. David Marsden. (1996). “Focal Task-Specific Tremors”.
Movement Disorders Vol. 1 1, N°. 6. 1996, pp. 665-670.

42
 48 hours
“No one can swim twice in the same river”.
Heracles

Anton holds the record for being the musician who developed dystonia in the
least amount of time. He remembers that he was then experiencing his best technical
and interpretive period. He had just won a place as clarinet soloist in a prestigious
orchestra, and instead of taking a break, he decided to shut himself in to master a
difficult trill. His plan involved playing the same trill eight hours a day. The trill
alternated between the pinky and ring fingers of his right hand.
In less than 48 hours, he had put in 16 hours of continuous practice of the same
trill, surpassing the barrier of 100,000 consecutive repetitions of the same movement
each day. At the end of the second day he was not able to control the movement of his
pinky finger as it caused involuntary movements of his ring finger.

In this case, the fast movement of repeatedly alternating between fingers, as

required in a trill, fused his two fingers.

Among patients who participated in the focal dystonia project and were affected
by musical focal dystonia, different fusions were observed which made the independent
movement of fingers impossible. In some cases, the index finger fused to the ring
finger and in others the ring finger fused to the middle finger or in less common cases
the thumb fused to the middle finger.

After an exhaustive study of patterns that each patient had used in the weeks
previous to their first symptoms, logic can be found. If they practiced ultra-repetitive
alternating fingerings, such as trills or scales on the guitar, those two fingers fused. If
they practiced chords that included pressing the index, middle and ring fingers
simultaneously, those three fingers fused. Descending tremolos and arpeggios on the
guitar caused fusions of the ring and middle finger. Ascending violin scales caused the
fusion of the middle, ring, and pinky fingers on the left hand. Right-handed ascending
scales on the piano produced fusions between the thumb and the index and middle
fingers. Depending on which instrument and on the sequence of movements needed to
play them, specific dystonic patterns were produced.

43
 The restructuring of perception and of movement was focused on the correct
performance of concrete patterns. Brain architecture is different among individuals.
Adult cortical maps are different and individual from each other and depend on stimuli
that have been received during life. Learning is individual. Stimulation generates a
determined brain architecture. Within just a few hours, the brain changes and adapts to
the subject’s needs. After a day of practice, our brain is not the same as it was
yesterday. The brain structure forms from the stimulus it perceives. Perception stimuli
develop the branching and interconnection of neurons. 11

11
J.L.Conel, The postnatal development of the human brain cortex. Harvard University Press, Cambridge, Mass, 1959.

44
 Observing
Danielle was a violinist and was affected by focal dystonia in the flexor muscles
of her fingers. After 40 years of playing the violin professionally, she had completely
forgotten how to play. Living with dystonia for 10 years had made it so that she could
not remember even the simplest of movements which she taught to her 4-year-old
students. She suffered a kind of confusion when she tried to play. Everything was
blurred. Her hand didn’t feel like it did before; the strings and the distances either.
Because of this, her movements were disordered and imprecise.
It was necessary to include in the rehabilitation program required daily video
viewing of great master violinists. Every day she viewed 30 minutes of visual
recordings of Menuhin, Perlmann, and Szigety. Little by little, her watching
transformed her movements, improved them, and helped her to remember her internal
dictionary of movements, her “lexicon”.

Presently, it is considered that this type of learning by imitation is based in the

activity of the mirror neurons. A mirror neuron is a neuron that fires when a person
performs the same act that person is observing being performed by another. They fire
when they see the action and also when they reproduce it, imitating what is perceived.
These are located in the inferior frontal gyrus and in the parietal lobe of human beings.
The mirror system allows the imitation of movements, feelings, and emotions of
others.
They capture things through senses, and what they capture is transformed into
movement. Mukamel and his colleagues measured the activity of 1177 neurons located
in the temporal and frontal cerebral cortex of 21 volunteers12. The subjects observed
actors on a computer screen smiling, frowning, grabbing an object with their fingers or
with their entire hand. They also saw words that described the actions. Four types of
mirror neurons that responded to different stimulus were found.

12
Mukamel, R., A.D. Ekstrom, J. Kaplan, M. Iacoboni & I. Fried. 2010. “Single-neuron responses in humans during
execution and observation of actions”. Current Biology 20: 750-756.

45
 The first type of neuron fires when an action is seen, but not when the action is
copied. Another type of neuron exists that fires only when the action is repeated and
not when it is seen. The third type of neuron fires when an action is seen and also when
another is repeated, but never the same that was seen. Finally, the fourth group of
neurons fire with the observation and execution of the same action.
Christian Keysers and Valeria Gazzola discovered the existence of “anti-mirror”
neurons. These are the ones that avoid there being a response after the activation of the
neurons that detect the action. According to Keysers and Gazzola, these “anti-mirror”
neurons allow us to mentally repeat an action without having the body move13.
It seems that strategies that activate the “action-observation” system of the
mirror neurons can be effective in the rehabilitation of focal dystonias.

13
Keysers, C. & V. Gazzola. 2010. Social neuroscience: Mirror neurons recorded in humans. Current Biology 20: R353-
R354.

46
 Silent stroke
In 2008, Das and his colleagues studied 2040 perfectly healthy middle-aged
adults. Surprisingly, they found micro-lesions in ten percent of the persons studied14.
Many strokes, ischemia as well as small hemorrhages, are asymptomatic and are
discovered in neuroimaging tests. The sum of these small silent strokes in the basal
ganglia and in the subcortical white matter produce a progressive motor deterioration,
without the patient ever showing any clinically relevant symptoms of acute stroke.

14
Das RR, Seshadri S, Beiser AS, Kelly-Hayes M, Au R, Himali JJ, Kase CS, Benjamin EJ, Polak JF, O’Donnell CJ,
Yoshita M, D Agostino RB, De Carli C, Wolf PA. Prevalence and correlates of silent cerebral infarcts in the Framingham
offspring study. Stroke. 2008 Nov; 39 (11): 2929-35.

47
 Accident

Carlo was a violinist. At 13 years old he was already considered a superb

violinist. He began a brilliant career as a concert performer, being recognized by critics
for his amazing technical ability and his profound musicality. Carlos didn’t remember
how he learned to play the violin. He knew that as a young boy he was already playing
and that he never had to work to learn any passage. The music flowed naturally from
his imagination and emotion and was unconsciously transformed into precise hand
movements.
When he was 40 years old, he had and accident on the way to the airport. The
crash was severe and the car badly damaged, but he was uninjured. He was surprised to
see that his violin appeared absolutely unaffected. He took it out of its case and found
that it had even stayed in tune. Since it seemed all right, he continued his trip, caught
his scheduled flight, and played that evening in a concert 8,000 kilometers away from
where the accident had occurred. During the concert, he noticed one passage seemed
uncomfortable to play, one that he must have played more than 500 times in concert
before. He didn’t understand why it seemed so suddenly difficult when it came to
controlling fast, refined movements such as vibrato or trills.
On occasions, the first signs of focal dystonia appear immediately following a
traffic accident. One of the explanations for this can be found in the latest studies on a
phenomenon known as postconcussion syndrome.
The existence of this syndrome has been recognized for several centuries, although
one of the first works that made specific reference to this problem was published in
1886 by Erichsen, On concussion of the spine, nervous shock, and other obscure
injuries to the nervous system15. Nonetheless, it was Straus and Savitsku, in 1934, who
were the first to name this combination of symptons as postconcussion syndrome or
disorder16.
Postconcussion syndrome is not only considered to strictly reflect brain damage,
but also the perceived stress and the abilities to cope with it, which compels us to take
into account the interaction between organic, psychological, and social factors of the
affected individuals, including those before and after the trauma.

15
Erichsen JD. On concussion of the spine, nervous shock and other obscure injuries to the
nervous system. Baltimore: William Wood & Co; 1886.
16
Watson MR, Fenton GM, McClelland RJ, et al. “The postconcussional state: neurophysiological
aspects”. Br J Psychiatry 1995; 167: 514-21.

48
 The present tendency is to consider that these organic factors play an essential role
in the appearance of the symptoms during the first few months, while psychological
factors have a fundamental role in explaining the continuation of, and even the increase
in, symptoms over time17.
Brain damage after a head trauma is the result of initial structural injuries and their
secondary complications. Because of the mechanisms of acceleration and deceleration
during the impact, contusions, lacerations, and intracranial hemorrhages are produced,
as well as a diffuse axonal injury. It not necessary that a direct blow to the head be
sustained; just the movements of acceleration, deceleration and rotation offset by other
reactive forces inside the brain can produce damage. Tissue damage resulting from
gradients of pressure created and the “traction-torsion” forces are produced on three
different levels: the surface of the brain develops cortical contusions; diffuse axonal
injury occurs in the white matter; and, even deeper, injury occurs in the basal ganglia
and in the axons of the brain stem. Blood vessels are also susceptible to initial
structural damage, producing micro and macro hemorrhages.
These injuries are known as primary injuries, since they occur at the time of
impact. Secondary injuries occur due to complications in the processes that were
initiated at the time of the first injury, but are not directly attributable to the impact.
Standing out among these are vascular diseases such as ischemia, the formation of
hematomas, and cerebral edema.
If macroscopic focal brain injuries, which are produced by contusions and lacerations or
by rupture or ischemia of large blood vessels, they are easily identified using
computerized tomographic techniques or magnetic resonance imaging. Diffuse injuries
involving white matter, the hippocampus, and the basal ganglia are more difficult to
identify.

We must remember that Carlo was diagnosed with dystonia because he was unable
to modulate his finger pressure with precision on the mast of the violin, which could
indicate a malfunction in the basal ganglia possibly being related to the traffic accident
he sustained.

17
King N. “Mild head injury: neuropathology, sequelae, measurement and recovery”. Br J Clin
Psychol 1997; 36: 161-84; Lishman WA. “Physiogenesis and psychogenesis in the
‘postconcussional syndrome’”. Br J Psychiatry 1988; 153: 460-9.

49
 The case of the running hand
“My hands want to run. I’m in a big hurry.”

Yumiko began to feel as if her right hand moved more slowly when she was
playing the piano. After a few weeks, her right hand was moving at a faster rate than
the left and was always rushing ahead of time.
In order to understand what was going on, we need to bring our attention to a
structure that has not usually been taken into account by studies about focal dystonia
until now: the cerebellum. The cerebellum is located at the bottom of the brain, with
the large mass of the cerebral cortex above it and the portion of the brainstem called the
pons in front of it. It is divided into two hemispheres and has approximately 50 percent
of all the neurons in the nervous system.
Keele and Ivry studied the function of movement control that the cerebellum carries
out, in particular its role as movement timekeeper18. The cerebellum functions as an
internal metronome controlling perceptions and movements so that they follow a time
graph (timing). This time graph shows step by step the time each movement takes and
the perception to carry out the task. The underlying deterioration in brain disorders is a
loss of timing, as much in movement as in perception. This faulty timing is very
common among those affected by focal dystonia and is very obvious in musicians.
Regarding Yumiko’s case, the timing breakdown affected only her right hand. Her
left hand carried out rhythmic and timing movement.
Rehabilitation in each of the cases should include exercises carried out following
strict rhythmic guidelines. This is the only way to restore internal timing.

18
Keele, S. Ivry R. “Does the cerebellum provide a common computation for diverse tasks? A
timing hipótesis”. In A.Diamond, Ed., The development and neural bases of higher cognitive
functions. Annals of the New York Academy of Sciences 608:197-211, 1991.

50
 Reversal
In his time, Mislav was a promising young violinist. When he was 25, he began
to experience the first symptoms of generalized dystonia in his arm. Within a short
time, his legs began to move involuntarily, and his arms crossed and knotted over each
other. He could not look forward because his head turned to the left and tilted
backwards. When his first symptoms appeared, he completely stopped playing the
violin. He couldn’t go to work because he couldn’t go down the stairs of his house.
Little by little, he isolated himself more and more until he fell into a deep depression.
He searched for the best neurologist in the Ukrane, and Mislav asked him if it
would be possible to play the violin. The neurologist told him to forget it; that he
should close that door in his past. He never again even tried it.
Mislav entered in the program three years later. In spite of his reluctance, after
many attempts, I was able to encourage him to try to play the violin for me.
To everyone’s surprise, Mislav stood up and played a Vivaldi piece for 15
minutes, performing scales and arpeggios scales and arpeggios in a coordinated, musical
fashion. While he played, his body straightened and most of his tension disappeared.
He was not there yet; the music took him to another place.
When he finished playing the Vivaldi piece, he put his violin in its case and returned
to sit in his wheelchair. His head returned to its turned position; his arms again lost
their coordination and ability to perform simple movements.
Mislav demonstrated a reversal of usual symptomatology. Contrary to the rest of the
cases related in this book, all the movements of his hands were difficult and spastic
except when he played the violin. Everything had been distorted by the dystonia except
the memories created when he was a child playing the violin, remaining intact in a sea
of dysfunctional connections.

51
 The case of the singer who couldn’t read music

Michiko was a baroque singer. Dysphonia overcame her during a very difficult
moment in her life in which personal problems and intense work kept her from sleeping.

What was very interesting about her case was that her inability to sing only
manifested itself when she was reading printed sheet music. When she improvised
without reading the music, or even when she was reading handwritten music, she could
regain control of her voice.

Michiko’s case shouldn’t be confused with agnosic alexia. In a pure alexia or alexia
without agraphia, the problem rests in the visual recognition of the letters, syllables, or
words. Nevertheless, patients can recognize these through other non-visual modalities
such as through touch or vision in motion (high road19). In these cases, the injury
occurs on a unilateral level in the left occipital and temporal lobes due to a infarct in the
posterior cerebral artery. It can be seen that when an injury occurs, not only are these
areas of the lobes affected, but the back of the corpus callosum (splenium) is also
altered. Therefore, the print (visual input) isn’t able to be moved from the injured areas
of the occipital lobe to Bordmann’s Area 39, and hence, the person cannot recognize
letters, producing agnosic alexia. If the person recognized words through tactile
pathways, there is no problem since the information from the somatosensory area passes
through the uninjured middle of the corpus callosum by way of Area 39. The person can
also recognize words in motion, because the uninjured high road is used, which arrives
to the Area 39 by passing through the anterior area of the corpus callosum.

19
At the level of cortical processing, there are two pathways that are responsible for processing visual
information. Both originate in the occipital striate cortex. The first is the high road or via the Where. The
high road, part of the occipital lobe, goes through the parietal lobe and ends in the frontal lobe. It
processes the information that determines the position of objects in space and if they are in motion or not.
The second is the low road or via the What, which starts in the occipital lobe and goes to the temporal
lobe. It is responsible for processing information about shapes, faces, and colors. It reports what people
are watching.

52
 Michiko could recognize the characters, but suffered a spastic dysphonia that kept
her from singing. Spastic dysphonia is a disorder of the voice caused by an interruption
of laryngeal control, in which the involuntary movements of the laryngeal musculature
originates during phonation. These involuntary movements can be of two types:
excessive closure or incomplete closure. Excessive glottal closure occurs more
frequently and is characterized by excessive tension of the thyroarytenoid laryngeal
muscle20 which gives the voice an abnormally deep tone and a strangled quality.

In Michiko’s case, an incomplete closure and irregular approximation of the vocal

cords was produced, which caused a reduction in voice quality and uncontrollable
increases in fundamental frequency and “airy” voice.

Michiko’s dysphonia was characterized by being attached to an association within a

very precise context. The process of the underlying association made Michiko react
differently to handwritten music than she did to a printed piece of music. Each dystonia
is different and personal. Associations follow a pattern. This pattern is made up of
dysfunctional associations that repeat in a predetermined sequence. Therefore, the time
of programming this response probably coincided in Michiko’s life with singing,
reading, and a series of factors such as emotional distress, all of which was conditioned
by sleep deprivation.

20
The thyroarytenoid muscle originates from the inner side of the sheet of thyroid cartilage and the
outer surface of the cricovocal membrane and is inserted into the anterolateral surface of the arytenoid
cartilage. It has two parts: half (test vowel) and lateral (muscle pull). It forms the body of the vocal cord.
It relaxes and shortens the vocal cords.

53
 Genius
Glenn Gould, a mythical Canadian pianist, followed a ritual when recording. He put
his hands in very hot water for five minutes. He played for twenty minutes, and put his
hands in the water for another five. All his recording sessions were like this. Glenn
Gould felt it necessary to have his hands extremely relaxed in order to assure himself of
absolute control and precision.
Gould’s international career did not last very long and was marked by a variety of
injuries which caused him insecurity and stress.
The first problem to appear was an intense pain in his shoulder, possibly a result of
his unusual posture while playing. Following this was a right ulnar nerve entrapment.
This caused pain and a loss of sensitivity in his right ring and pinky fingers21. The
nerve entrapment was not the last problem that he would suffer, and with time, he began
to suffer symptoms of dystonia, such as a loss of trill control, inability to regulate sound
volume and involuntary movements. Facing these symptoms, Dr. Stein, a neurologist in
Philadelphia who was unaware of what focal dystonia was, diagnosed Gould with
conversion hysteria.
On April 10, 1964, Gould played in public for the last time.
In his diary begun in 1977, we can read a chronicle of his fight to regain control,
reestablish uniformity in his attacks, independent control of his fingers, and steadying
his wrist22

We can also find there his complaints about the apparent uselessness of his efforts,
his desperation and his frustration. His writings show that from that time until his
death, he was fighting for recovery, trying to reeducate himself. These long hours of
rehabilitation, by himself, searching in silence, allowed him to regain enough control to
record for the second time Goldberg Variations in April and May of 1981, which is
considered by many to be his masterpiece. On October 4, 1982, one of the great
musicians of history left us, just a few days after having recorded Piano Sonata in B
Minor Op. 5 by Richard Strauss in New York.
Glenn Gould was able to overcome a difficult dystonia and maintained intact his
love of music, which allowed him to developed a despair proof resiliency until the end
of his life.
21
Ostwald P (1997) Glenn Gould: The ectasy and tragedy of genius. New York: W.W. Norton
&Company.
22
National Library of Canada. Glenn Gould: Descriptive Catalogue of the Glenn Gould
Papers/Catalogue raisonné du Fonds Glenn Gould, ed. Ruth Pincoe and Stephen C. Willis, 2 vols.
(1992) [incl. chronology, bibliography, discography, and lists of writings, compositions, concerts,
radio and TV broadcasts, and films].

54
 The erased lip

Arturo was a trombonist. Since childhood, he showed great facility while

playing. It could be said that he could do whatever he wanted. He passed all his
auditions and was chosen to play in the very prestigious Youth Orchestra in Europe. At
the height of his career, dystonia overcame him and he completely lost control of his
embouchure. He could no longer control his lips, which distorted his sound. He had
completely lost the sensitivity in the central part of his upper lip. He felt as if a part of
his body has been erased.

The only way he was able to play was by crossing the street and going to a
construction site where they were breaking the asphalt using a jackhammer. With so
much noise, he could not hear his own sound, and that instantly returned control over
his muscles to him.

Just as with patients who stutter, many dystonic musicians improve or normalize
their performance when they cannot hear the sound they produce. This could occur
because by blocking the action, positive feedback is produced. Positive feedback is
defined as a mechanism though which the effects or output from a system cause
accumulated effects on the input. A system which presents an unstable balance point
has positive feedback, since any minute variation makes the system move away from
this state of balance. In this case, positive feedback is produced in the following way:
the brain orders the motor muscles of the lip and tongue to produce the position and
movements wanted. The basal ganglia are in charge of regulating the force exerted in
each movement, estimating the force required to carry out each action. The cerebellum
is in charge of giving precision to the movements, correcting any errors in measurement
produced by the other parts.

Haslinger and collaborators studied the brain activity of metal wind instrument
players who were affected by embouchure dystonia coming to the conclusion that the
sensorimotor hyperactivity that characterized these patients could reflect insufficient
subcortical and intracortical inhibition as well as abnormal sensorimotor integration23.

23
Haslinger B, Altenmüller E, Castrop F, Zimmer C, Dresel C., “Sensorimotor overactivity as a
pathophysiologic trait of embouchure dystonia”. Neurology. 2010 Jun 1; 74(22):1790-7.

55
 In this case, the first sound that is produced is identified as incorrect and is
dysfunctionally modified producing another sound even further from the one sought.
This process is repeated as a dysfunctional loop many times per second until a distortion
of the lip position is reached so that sound is not possible. Arturo’s lip position being
correct when he couldn’t hear himself play could reflect that the first sound and the first
position were correct. Could Arturo be adjusting a position that was correct?
Whenever a correct action or position is corrected, an incorrect result is obtained.

56
 The hand that dropped the pick.
Creating internal pressure scales.
The nervous system learns by comparing. In essence, we perceive tension as an
entity which opposes relaxation. We could not perceive one without the other. When
Hideaki played the guitar before the onset of focal dystonia, he was not only able to
produce a movement, but he could also modulate it.
If we analyze the ability to produce different sounds with the guitar, this
depends largely on the pressure that is exerted on the strings. We produce diverse
pressures and therefore we attain diverse colors and refinements.
Hideaki was a Japanese heavy metal guitarist. He had never received any formal
musical education, but thanks to his natural gifts, he had reached great virtuosity and
therefore collaborated with some of the best bands in his country. Hideaki had to stop
playing one day because the pick fell from his hand while he was playing at practice.
From that moment on, he was not able to play without making great effort not to let the
pick fall, which completely blocked his playing. Within weeks, he was not able to play
even the simplest passages.
He thought he had gone crazy, squeezing the pick so hard as he held it that it
seemed that it would break. After a number of years without knowing what was going
on, he was diagnosed with dystonia of his right thumb and index finger.
In order to analyze this case, we are going to analyze how the central nervous
system carries out pressure control:
Muscles are composed of muscular fibers. These can’t be activated individually
but can be activated in groups. Depending on the number of groups that are activated,
we put the muscle into action at 50 percent, 60 percent, etc., of its contraction potential.

This is possible thanks to internal pressure scales. These internal scales are internal
virtual models that have been acquired during years of movement during which they
have compared tension and relaxation. These scales are our internal reference, making
necessary adjustments possible which allow us to calculate the amount of force required
for an action and the amount of force we produce.

57
 The first internal scale is perfected by us as children when we learn to adjust the
pressure in relation to the objects we manipulate, cuddle, or squeeze.
With practice, this internal scale expands until it enables more than 50 different
pressures, as is the case of finger movement. The larger the range of tensions that we
can consciously control, the greater the precision of our movements will be.
The structures in charge of modulating movement, generating the force
necessary for each correct motion, are called the basal ganglia. The basal ganglia are a
group of nuclei in the forebrain that connect the motor cortex with the mid-brain. When
these structures are not working properly, they give two types of errors in movement:
the erroneous movements that use excessive force, and the erroneous movements that
use insufficient force. The movements produced in the cortex are modulated by two
pathways in the basal ganglia. According to Alexander and Crutcher, the indirect
pathway has a stimulating effect, while the direct pathway has an inhibiting effect on
the inner part of the globus pallidus. If inhibition overrules, the thalamus is shut down
and the cortex is incapable of producing movement. If stimulation overrules, the
thalamus can become hyperactive, increasing movement beyond what is necessary24.
Hideaki showed a distorted internal pressure scale which was restricted to action
of holding the pick while he played (thumb-index finger grip). Hideaki could control the
pressure exerted using another type of grip such as, for example, thumb-middle finger.
He was even able to control the same grip (thumb-index finger) perfectly well in other
contexts, grasping other objects. If the object grasped had the shape of a pick, its
weight and feel, his control faded. It was as if his internal pressure scale had been
erased only and precisely for this action.

In Hideaki’s case, the reconstruction of his internal scale produced during conscious
exercises that exerted gradual and selective pressure following a progression from the
most simple to the most complex with an end of acquiring the dexterity that would
allow him to use the tension necessary for each movement. Hideaki applied different
degrees of pressure using his internal subjective scale. This scale needs to include at
least ten pressures classified from least to most, with his proprioception the only guide
in completing the exercise. As the exercise progressed the aim became sensing and
making a larger number of different pressures until reaching the number 30.
This type of exercise allowed the basal ganglia activity to become regulated making
it possible for Hideaki to play the electric guitar applying the necessary pressure each
time using the thumb-index finger grip to hold the pick in his right hand.

24
Alexander, R.E. and Crutcher M. “Functional architecture of basal ganglia circuits: Neural
substrates of parallel processing”. Trends in Neuroscience 13:266-271, 1990.

58
 Giant

Andre was 1.95 meters tall and weighed 120 kilos. He was a musician and a
weightlifter. Included among his daily exercises were squats with 200 kilos and bench
presses with 180 kilos.
It’s not known whether dystonia was caused by his efforts during practices or by
his divorce.
While he was seated in front of me, he said, “I can’t play the oboe because I
have no strength.”

59
 Without symptoms
Manuel was the first patient affected by dystonia who visited me without
symptoms. His hand moved normally, and he was able to play the guitar, but he felt as
if the strings had changed in thickness and tension within the past few days. He knew
this was impossible because he was aware that it hadn’t happened.
In this case, the mechanism that allows us to be aware of pressure
(proprioception) and the volume of objects (exteroception) was failing. Proprioception
is defined as the perception of our body and our actions. Exteroception is the
perception of the environment in which we interact. Proprioception and exteroception
are related but independent processes. This relationship can be summarized like this:
the motor areas of the frontal lobe organize movement. The spinal cord transmits the
information to the hand. The motor neurons transmit the message to the muscles of the
hand and the forearm. The sensory receptors in the fingers send the message to the
sensory cortex which confirms that the movement has been completed. The medulla
transmits the sensory information to the brain. The basal ganglia judge the force of
pressure, and the cerebellum corrects errors of movement. The sensory cortex receives
the message that the movement has been carried out.
Tinazzi and his collaborators studied and tested the proprioception of patients
affected by focal dystonia of the hands, concluding that a change was present in the
timing process for muscular activity, as well as for spatial discrimination for cutaneous
stimuli25.
In Manuel’s case, his internal world changes when he makes contact with the
guitar string. His internal pressure scales blurred only in this specific context. His
ability to judge the qualities of other objects, such as weight or shape and volume were
intact. He was even able to perfectly judge the resistance of a piano key or the keys of a
clarinet.

25
Tinazzi, M., Fiorio, M., Stanzani, C. Moretto, G., Smania, N., Fiaschi, A., Bhatia, K.P. and
Rothwell, J.C. (2006), “Temporal discrimination of two passive movements in writer’s cramp”.
Movement Disorders, 21:1131-1135.

60
 Considering that musician’s focal dystonias always start out this way, it can be said
that the patient goes through and invisible phase of the disorder when the deficit is
simply perceptive. In general, this phase doesn’t last more than a few days. Due to the
compensation process of the nervous system which tries to carry out the movements
basing them on erroneous perceptions, the dysfunctional movements don’t take long to
appear. It is only at this time that the patient tends to be conscious that something is
going on.
Another similar case was that of Michael. Michael’s feelings changed like clouds in
the sky while he was playing. These feelings changed every three minutes; they went
from feeling heaviness to clumsiness, from clumsiness to weakness, from weakness to
tension, from tension to instability, and from instability to heaviness again.
The interesting thing about these cases is that the process halted in the beginning,
which is why the patients remained stuck in the initial perception-only phase (invisible)
and didn’t show any tremors or spasms associated with the normal development of the
disorder (visible phase that affects motor control).
In these cases, rehabilitation focuses on the restructuring of perception, producing a
plastic change in the somatosensory areas only.
Both Manuel and Michael had to re-learn to feel and familiarize themselves with the
new feelings they were experiencing when they used their hand. It could be said that
the success of the rehabilitation was based in the adaptation of a new reality.

61
 Change
“The more I wanted to look, the less I found.
When I least wanted it, I had it all without trying.”
San Juan de la cruz

Francisco was 34 years old. Until recently, he had enjoyed a promising career
as a percussionist. He contracted focal dystonia in the months following the death of
his father.
When he tried to play, his right hand seemed to take on a life of its own and took
positions that did not adapt themselves to his performance. His fingers extended as if
taken by some unknown logic.
He completely left playing in concerts, and we devoted ourselves to searching
for a procedure that would return control to his own hands. After years of searching, we
discovered a clue: Francisco admitted to his duality.
The procedure was baffling but effective. When he sat before his instrument, he
said to himself: “Let my body move any which way. I won’t do anything.”
Before our amazed eyes, his movements recovered fluidity.
When he said to himself, “I’m going to play myself…”
He instantly lost his ability to perform in a coordinated manner…

In order to evaluate how Francisco was able to willingly and alternatively

produce dystonic and functional movements, a study was performed using functional
magnetic resonance imaging.

Functional magnetic resonance imaging (FMRI) is a clinical study procedure

that allows images to be displayed of the regions of the brain that carry out a determined
task. The objective was to be able to determine which areas of the brain were involved
when Francisco produced a dystonic movement and which areas take part at the same
time when a rehabilitated movement was performed.

62
 Functional magnetic resonance cannot detect the activity of different brain regions in
absolute terms. It can only detect differences in activity under different given
conditions. While the FMRI images were being taken, Francisco was asked to perform
movements necessary to play percussion instruments. This task is called the
experimental condition. The experimental condition was alternated with the control
condition, where Francisco remained relaxed and resting with the drumstick in his hand,
looking at a fixed static point.
Both the task and the control were repeated various times separated by breaks.
The combination of all these conditions studied are known as an FMR paradigm.
The final image is obtained through a statistical process of subtraction. The image
obtained in the control condition is taken away from the image obtained in the
experimental condition. The subtraction produces an image somewhat different each
time that the subject performs an action. The final image is the statistical average of all
the recorded images.
This process does not provide a specific list of areas that take part in a particular
activity, but an indication of the areas that become more or less active when a task is
performed.
The region of the brain that controls hand movement will suffer vasodilation, and
brings about a change in the concentration of local deoxyhemoglobin. This will cause a
change in local magnetism that in turn is detected by the resonator. In this way, the area
can be shown in color over the gray background of the conventional resonance.

63
The image obtained when Francisco performed dystonic movements with his right hand
shows intense activity in the motor and sensory cortex of both hemispheres.

The image obtained when free normal movement (rehabilitated) was performed
showed less cortical area activity and did not show bilateral (both hemispheres)
activation. This image corresponds to the expected image for this movement in a
healthy subject.

64
The following images can be compared with the previous ones; they were obtained by
performing the same movement with the unaffected left hand.

The success in rehabilitation is linked to some type of change in the cells of the
nervous system. These changes are thought to make up a neurologic record of learned
information. The human brain contains billions of neurons connected by multiple
synapses (installed capacity), much of these being multiplied or repeated (redundancy).
Neuronal connections exist which increment their activity level when the group of
neurons that were originally in charge of a certain function become inactive
(compensatory unmasking).
The plastic changes induced in the motor and sensory cortex through rehabilitation,
which are observed in the case of Francisco can be due to a process of unmasking silent
synapses26.

26
Silent synapses are defined as specialized structures for the neurotransmission that do not produce a
physiological response in the receiving nerve cell. The silent synapse does not function because it has not
been activated. Stimulation through rehabilitation can, in some cases, activate the silent synapse. This
process is called unmasking silent synapses.

65
 Spain
In order for us to perform the gestures necessary to write with precision, a
process of feedback and error correction needs to be given. The cerebellum is the
structure charged with carrying out this process.
When we write, two versions of each movement are generated. One is the
movement that we intended to make, and the other is the movement that we really
made, received by the sensory receptors in the hand, forearm, etc. The cortex sends
instructions to the spinal cord to carry out the movement. At the same time, it sends a
copy of this information to the cerebellum, which receives information about the
instructions sent to the motor neurons through the inferior olivary nucleus. When the
movement is produced, the sensory receptors in the hand and fingers send a message
that refines the movement made.

The cerebellum processes these versions of the same movement, comparing the
information about the intended movement and the one actually carried out. Through the
comparison, it calculates the error and proposes a correction that is sent to the cortex to
improve the precision of the next movement. If the movement was correctly made, no
correction or adjustment is necessary.

In the case of patients affected by writer’s cramp, although movement is correctly

begun, a distorted process in the cerebellum could perceive the movement as incorrect,
calling for an adjustment to be made.

The unneeded adjustment would cause muscles that shouldn’t take part in the
movement to become active. This adjusted movement is not part of those necessary to
write, and the print becomes distorted.

66
 When Victoria began her rehabilitation, the first word she wrote was “Spain”. The
distortion in this case is very clear through the displacement of the line of text, which
descends do to the unnecessary involvement of other muscles.

Victoria related that when she tried to write correctly, her hand felt “unstable” and
this was why she changed her writing posture and made multiple compensatory
movements. This completely distorted her writing. Functional magnetic resonance
images obtained when she was carrying out the dysfunctional response in writing with
her right hand show activity in the motor and sensory cortex in both hemispheres as
well as a great deal of activity in the right side of the cerebellum.

67
 Her rehabilitation centered around having Victoria be conscious that the process of
movement control was malfunctioning, and that it gave an error signal when in reality
the movement was correct. Victoria learned to write ignoring the feeling of instability
and curbing any adjustment in her beginning direction. In a way, it was like driving
blind, giving preference to the information intended and ignoring the information from
the sensory receptors. Through practice, her writing improved considerably.

In the magnetic resonance produced after her training, we can see that her movement
regularized, since it no longer generated activity in the cerebellum, possibly due to this
way of writing “in radar silence”.

68
 Imagining
“Slow movement is superior to rapid movement.
Inmobility is superior to slow motion.
Look for movement in inmobility.”
Wang Xiangzhai

Nyberg and his collaborators made a comparison between evoked brain activity
produced while carrying out a movement and brain activity produced while imagining
it. Images were obtained through positron emission tomography in subjects while they
were rolling a ball with their right hand.

These images were later compared to those obtained while the subjects were
mentally rehearsing this motion (covert movement).
The most active areas of the brain while the task was being carried out were the
sensory and motor cortex, the premotor cortex in the left hemisphere, and the
cerebellum in the right hemisphere.

The most active areas of the brain during the mental task also included the
somatosensory and motor cortex, although to a lesser extent, but the cerebellum was not
included. This shows that similarities exist in the neocortical activation produced by
real and imagined movements.

As we recall, in the case of Francisco, his dystonia occurred as a strong contraction

of the extensor muscles of the forearm during any attempt to make a percussive motion
using a flexion movement. Francisco volunteered for an experiment that observed the
way in which focal dystonia patients imagined their movements.

Before carrying out this study, two questions were posed:

Do patients imagine movements correctly, but they are not able to carry them out?
Or is it the opposite: they imagine the movements incorrectly, with this affecting their
later performance?

69
 When Francisco made a dystonic movement, these functional magnetic resonance
images were obtained that show activity in the right hemisphere as well as the left.

This pattern is characteristic of dystonic movement, which is distinguished from

what would be expected of healthy movement in that the movement of striking with the
drumstick using the right hand would only show activity in the left hemisphere and in
the right cerebellum.

When Francisco imagined the movement but didn’t carry it out, this image was
obtained in which the dysfunctional bilateral activity can be observed once again.

This shows that Francisco imagined his movements dystonically even when he
thought he was imagining them correctly.

70
 After rehabilitation, Francisco imagined his movements correctly. His imagination
became free of the dysfunctional movements.
In this last image, the absence of significant activity is noticeable, which in a healthy
subject would be unusual, since the covert movement (mental rehearsal) normally
shows activity in the sensory, motor, premotor, and frontal cortex.
During years of training to inhibit dysfunctional muscle activity, Francisco
discovered that if instead of imagining that he was making a movement, he imagined
that the movement was happening on its own, he was able to carry out the movement
correctly.
Surprisingly, imagining a movement happening on its own, a concept very close to
the practice of the zen tradition of martial arts, does not produce an activation which is
different from a resting position.

71
 Phantom tension
“Reality is merely an illusion, albeit a very persistent one.”
Albert Einstein
Patrick had been affected by drummer’s dystonia for 20 years.
He agreed to collaborate in a study about the perception of tension in patients
affected by dystonia. The protocol that we designed included various movements and
positions that Patrick needed to carry out, while at the same time needing to judge the
subjective force used in each position using a scale from zero to ten, with zero as no
tension at all and ten as maximum tension. His brain activity would be measured using
functional magnetic resonance images.

In the first position, he needed to remain completely relaxed. Patrick evaluated his
force at zero. The image of his brain activity and his perception corresponded, with no
activity registered.

72
 In the next experiment, he was asked to remain relaxed, but in this case he needed to
establish tactile contact with the drumstick. Patrick perceived tension in his forearm
and hand evaluating his force of tension as a 4 on a scale of 0 to 10.

The surprising thing in this case is that the image of his brain activity again showed
no significant activity.

In the last experiment, Patrick was asked to hold the drumstick with his fingers.
Patrick evaluated the tension in his arm and forearm at a level of 10. Again, the
image of his brain activity showed the same absence of significant activity.

73
 In order to understand what was going on, we need to remember that the final image
in each case is obtained by subtracting the activity of the control condition (in the
resting state) from the active condition (while carrying out the movement). That the
image does not register activity does not mean that no brain activity exists; it means that
it’s the same as the activity in the resting state or that it no significant differences exist.
It’s true that tension existed in his arm, but this tension was not as different as he
thought the tension was when his arm was at rest.
Possibly due to of a malfunction of his basal ganglia, Patrick was not able to
conclusively evaluate the force that the muscles of his hand and forearm were exerting.
His subjective internal references were maladjusted.

74
 The case of the two-fingered hand
Joao was a Bossa Nova guitarist. He didn’t know why one day while he was
playing the guitar he became unable to control his hand. The lack of control progressed
until he was unable to move his fingers independently.
Joao compared the dysfunctional movements of his hand to a lobster claw.
He was only able to feel two of his fingers: his thumb and “big finger”.
When he referred to “the other” or his “big finger”, he was referring to his index
fingers, middle, ring, and pinky, which he perceived as just one finger.
This particular fusion did not allow him to feel his fingers independently nor
move them independently. His hand felt like a lobster claw, and moved as such.

In the primary somatosensory cortex (Areas 1, 2, 3a, 3b) a somatotopically

organized representation of the human body exists. The different parts of the body are
represented in an ordered manner, but it is inverted in relation to their normal body
position. This representation is called the Sensory Homunculus. In this area, the
representation of the surface of the body is conditional upon the density of the
somatosensory receptors, varying greatly from place to place. The hand represents a
third of this area.

Each one of the areas shaping the primary somatosensory cortex is dominated by
responses to a type of body receptor. Area 3a represents muscular feeling (position and
movement of the muscles), Area 3b represents slow as well as fast adapting cutaneous
receptors and Area 2 represents the feeling of deep pressure and joint pressure. It is
presently thought that Areas 1, 2, 3a, and 3b contain a specific homunculus in each.

The sensory systems develop many maps that are the topographical representations
of the outside world. The body’s areas of representation can be modified through
sensory stimulation. Elbert and his collaborators examined the somatosensory maps of
musicians with hand focal dystonia and found that the distances between representations
of the fingers were less than normal27.

27
Elbert T, Heim S, Rockstroh B. 2001. Neural plasticity and devolpment. In Nelson and M Lucian, Eds Handbook of
Developemntal Cognitive Neuroscience . Cambridge: MIT Press, 2001. 191-204.

75
 The enlargement of the area of representation for one finger can cause this to overlap
with the adjoining area. The borders between areas of representation for each of the
fingers become blurred producing a fusion. Due to his long hours of practice repeating
Bossa Nova chords in which he used his index, middle, and ring fingers in percussive
functions, an enlargement of the cortical representation of these fingers was produced,
creating a joined representation.
In this case, the image of the hand used as an internal reference (cortical
representation) doesn’t match the real hand.

It is important to point out that this fusion only occurs when certain passages are
played on the guitar, and not others. Additionally, it does not occur when any other task
is carried out with the fingers, including playing the piano, which requires a great deal
of finger independence and dexterity.
How can this happen?
If the somatotopical maps of the fingers have degraded due to a maladaptive
neuroplastic change, such as Elbert and his collaborators suggest, how can Joao play the
piano with complete finger independence? One way to explain this paradox, which
often occurs in those affected by focal dystonia, would be to consider that the system
creates as many different maps as tasks we carry out. This way, we can have only two
fingers with which to play the guitar and five with which to play the piano. These maps
are modified with experience and store context associations with the task in which they
created. In this way, input, in this case a specific task, carries with it a load of files
which include not only the automatic associations, but also maps of the body itself as
well as the outside world. Other cases explained in this book could also support this
hypothesis.

In this case, the job of rehabilitation consisted of inducing a plastic change in the
distorted somatotopical map through passive movement and proprioceptive stimulation.
To accomplish this, it was necessary to feel the different joints and be able to move
the fingers independently holding back the movements of the other fingers playing the
guitar. In this way, the association was broken by making small fisions that weakened
the initial fusion, drawing the boarders of each of the fingers once more. The virtual
representation of the hand was gradually changing until one was achieved that matched
the real hand.

This stimulation should be very selective and precisely applied to the associated task.
This could be an explanation for why general mobility intervention programs have not
had success up to now.

76
 The case of the giant thumb
Sasha was a pianist, gave classes in an important Russian conservatory, and
combined his teaching with giving concerts. He specialized in Chopin, Rachmaninov
and Prokofiev. For a time, he played in pain due to median nerve entrapment (carpal
tunnel syndrome). He kept the pain in his forearm a secret, and didn’t cancel any of his
concerts. After a summer of rest, the pain subsided but was replaced with a strange
feeling. His thumb had grown. When he looked at it in the mirror, it seemed to be the
same as before, but it felt much larger than his left thumb, and much heavier. To move
this giant thumb took Herculean effort. After a few weeks of trying to play like this, the
tension in his forearm got to such a level that it turned into strong involuntary spasms.
At the end of the year he was diagnosed with focal dystonia of the forearm flexor
muscles.

Cases in which a traumatic arm injury precedes the onset of focal dystonia are
common. Other cases of musicians who took part in the program are:

Richard was a Jazz guitarist and ice hockey player. One day during a game, he
received a strong blow to the middle finger of his left hand. The finger swelled, and his
fingertip was so bruised it was almost black.
Richard couldn’t let himself touch anything, so for weeks he played the guitar
avoiding the use of this finger, although sometimes by mistake a string hit his finger and
caused intense pain. When his finger got better, he found that the ring and middle
fingers of his left hand bent toward his palm, keeping him from being able to play.
Months later he was diagnosed with focal dystonia.

In the case of Stuart, a bagpiper and boxer, dystonia appeared suddenly after
breaking a carpal bone while boxing.

A traumatic ulnar fracture during a fall preceded the dystonia that a traditional music
guitar player, Albert, suffered.

77
 The relationship between injuries and the onset of focal dystonia can be explained in
light of recent studies about neuroplasticity induced by injuries. When a peripheral
nerve is temporarily blocked by using a local anesthesia, important changes in the
receptive fields of somatosensory neurons can be noted.

The temporary loss of sensory afferents from a small area of skin induces a
reversible reorganization of the receptive fields of the cortical and subcortical neurons.
During this time, the neurons adopt new receptive fields that respond to the tactile
stimulation of the skin surrounding the anesthetized area. Once the effects of the
anesthetic subside, the receptive fields of the cortical and subcortical neurons return to
their normal sizes. This event makes an area of anesthetized skin seem to feel
disproportionately large.

Merzenich and his collaborators studied plasticity in somatosensory representations

and showed that the organization of the maps could become altered if the afferent
stimuli going to the cortex is manipulated28.

All the musicians affected by focal dystonia who participated in the study that gave
rise to this book showed proprioceptive disorders. These could make it difficult to
perceive the position of the fingers, the work of the flexor musculature, or the work of
the extensor musculature. None of these showed symptoms of peripheral nerve
entrapment at the time of rehabilitation, although in ten percent of cases, they had
suffered from carpal tunnel or cubital tunnel syndrome or in the weeks before the onset
of the first symptoms of dystonia. It is possible that the time they spent practicing their
instruments coincided with the recuperation period for a peripheral nerve entrapment,
which could have induced a learned paralysis29.

28
Merzenich, M.M, Jenkins M. 1993. Reorganization of cortical representations of the hand following alterations of skin
inputs induced by nerve injury, skin island transfers, and experience. Journal of hand therapy 6:89-104.
29
Ramachandran VS. Behavioral and magnetoencephalographic correlates of plasticity in the adult human brain. (review).
Proc Natl Acad Sci USA 1993b; 90: 10413-20.

78
 The concept of learned paralysis was defined for the first time by Dr. Vilayanur S.
Ramachandran and could be applied in these cases to explain what occurred. The
process might be produced in the following form:
During the period of recuperation from a nerve entrapment in which pain and the loss
of sensitivity in the affected area are present, each time the patient attempts to use the
groups of muscles innervated by the compressed nerve, he receives sensory information
telling him that the muscles are not responding. This information remains fixed in the
cerebral circuit through a process of associative learning. This learned paralysis leads to
the implementation and learning of a series of compensations which consist of using
some muscle groups to make up for the lack of function of others.
For example, if it is not possible to play the piano by flexing the fingers, the player
will try to play by flexing the wrist. When the injury has recuperated and the nerve
recovers its function, instead of returning to make the movement correctly, the subject
persists in using the compensations because he had learned that the recovered
musculature was not available.

Rehabilitation consisted of stimulating and using the musculature perceived as “not

available” with the intention of inducing a “relearning of availability”.

79
 A foreign body

Fernando has a prosperous downtown store. As a youth, he was very athletic.

His first symptom of dystonia occurred when he was completing his military
instruction. His hand trembled and moved involuntarily when he had to salute a
superior, which was considered to be a joke and resulted in his being detained.
When he got out of the military, he was diagnosed with hand dystonia.
Five years later, his dystonia progressed and affected his vocal cords.

The first symptom of dysphonia appeared suddenly while he was having a

conversation with a friend. He felt that he had a foreign body in his throat. He was able
to continue talking, but he had the feeling of having swallowed a piece of cotton that
had become stuck somewhere, which caused him to use more pressure to speak.
Continuing with the conversation became an exhausting effort for him. He hurried to
the bathroom to try to vomit in order to get it out. Days later the doctor confirmed that
there was nothing there, but he felt it in the same place. Fernando didn’t recognize his
own vocal cords, and he perceived them as a foreign body.

Commonly in patients affected by dystonia, they refer to different parts of their

bodies as foreign bodies. The tertiary sensitive area (Areas 39, angular gyrus; and 40,
supramarginal gyrus) presents a design of the body. Errors in processing in this area
could make the patient not recognize parts of his own body.

80
 Recognizing
On occasion, patients who have suffered the amputation of a limb continue to
feel as if the missing limb were still part of their body. It seems that if patients suffer
pain in an injured arm before its amputation, this pain can persist in the body part’s
absence because the brain retains the last sensory experience as a fossil record of
information (nociceptive memory).
This phenomenon, known as phantom limb, was described for the first time as
“ghost sense” by Ambroise Paré in 1551. But it was the North American neurologist,
Silas Weir Mitchell who conducted the in depth studies on the subject, helping soldiers
who suffered amputations during the United States Civil War. Mitchell, who worked in
Turner’s Lane Hospital in Philadelphia, observed that the great majority of soldiers had
developed ghost senses shortly after the loss of a limb.

Patients affected by dystonia are characterized by suffering from an illusion

which is inversed from the one experienced by Phantom Limb patients.
In Phantom Limb cases the limb can be felt, and in some cases patients can feel
the limb move, although it is no longer there. In dystonia cases, the arm is there,
perfectly healthy, but the brain doesn’t recognize it.

If we can’t perceive a part of our own bodies, in order to return it to form part of
us, we need to initiate a recognition process similar to the one carried out by computers
when new hardware is installed.

A similar process of recognition is produced in hand transplants. The transplant

of forearms and hands are quite recent, but the first hand transplant was performed in
Louisville, United States, in 1998. During this type of intervention, structures are
severed reciprocally so that the lengths are correct and then the bones are connected
with plates and screws, the veins, nerves and arteries are microscopically repaired, and
the skin is closed, and the patient is woken up. It has been observed that six months
after the operation patients normally finalize the recognition process and feel and move
the forearm, hand, and fingers with precision.

If it is possible to wake up and recognize an arm that was not ours in such a
short period of time, the possibility of returning feeling to our own hand becomes
something achievable.

81
 War
“The organs weep the tears that the eyes refuse to shed.”
Sir William Osler (1849-1919)

Rachel is a clarinet player. She lives in New York, in the southern part of
Manhattan, known as Lower Manhattan. On September 11, 2001, Rachel left her
children at a day care near the World Trade Center, when from her home she heard the
impact of the first airplane hit the North Tower. She can’t remember precisely what
happened that morning, only the anguish and uncertainty. Although no one in her
family was hurt, she, like the major part of the residents of Manhattan, could not sleep
for weeks, and the smallest sound woke her up in a state of alert. Following this long,
sustained period of anxiety, dystonia suddenly appeared in the fingers of her right hand,
making her have to give up the clarinet.

Omar was a respected musician of traditional Middle Eastern music who lived in
Bagdad and lived with his family when the city was bombed during the Second Gulf
War. Following the anguish, anxiety, and fear, dystonia appeared in his hands making
it impossible within a few weeks to continue his profession as an instrumentalist.

In recent years, lines of research support that being exposed to intense stress can
be sufficient cause to trigger some forms of dystonia in those who are susceptible.
Dr. Khodakhah and his team studied RDP (rapid-onset dystonia-parkinsonism)
at the Albert Einstein College of Medicine in New York. RDP is a rare, inherited
illness that combines symptoms of dystonia and Parkinson’s, such as slow, rigid
movements. These symptoms initially appear in a subtle manner after exposure to
intense emotional or physical stress, fever, childbirth, or extreme strenuous exercise.
The symptomology can become more severe and permanent.
Dr. Khodakhah researched the implications of a hormone named ouabain in
30
RDP . Ouabain (g-strophanthin) is a substance that is found in the ripe seeds of
African plants Strophanthus gratus and the bark of Acokanthera ouabaio.
The name comes from the Somali waabaayo and means arrow poison. From
times before memory, Somali tribal hunters extracted ouabain to poison their arrows.
It’s thought that a dart with a concentrated dose of ouabain could kill a hippopotamus,
by causing cardiac arrest.

30
Calderon DP, Fremont R, Kraenzlin F and Khodakhah K. "The neural substrates of rapid-onset dystonia-parkinsonism."
Nature Neuroscience, March 2011, Vol. 14(3), pp. 357-65.

82
 Dr. Khodakha’s team discovered that by using a perfusion of low doses of
ouabain, dystonia could be induced in lab rats. Ouabain was injected directly into the
brain and the basal ganglia. With low doses, the rat did not develop dystonia unless it
was also exposed to a high degree of stress.
In 1991 Hamlyn and his collaborators identified endo-ouabin as an endogenous
hormone that our bodies synthesize in the adrenal gland31. This hormone, similar to
ouabain, is naturally produced by our bodies in high-stress situations. It’s starting to be
thought that it could play a role in the appearance of RDP in genetically susceptible
people.

Emotions could not only play a role in the onset of the illness, but they could
also be of maximum importance during the process of rehabilitation.
Let’s remember that the operation of the neuroendocrine system involves
diverse hormones to regulate key processes during the inducement of plastic changes in
rehabilitation. The afferent cholinergic, adrenergic, and serotonergic modulate the
reorganization of the cortical plasticity. Taking into account that the behavioral tone
regulates these substances, it can be understood how decisive the emotional state of the
patient during rehabilitation is, since depression inhibits many of the neuronal
recuperation mechanisms.

The two hormones that are thought to play a fundamental role in neuroplasticity
are serotonin and noradrenaline due to their double hormonal-neurotransmitter function.
Serotonin (5-hydroxytryptamine, or 5-HT) is a monoamine neurotransmitter
synthesized in serotonergic neurons in the central nervous system (CNS) and
enterochromaffin cells (Kulchitsky cells) in the gastrointestinal tract of humans. It
takes part in the inhibition of anger and aggression; humor; sleep; vomit; sexuality; and
appetite. It controls body temperature, motor activity, and cognitive and perceptive
functions.
Serotonin is necessary for both the elaboration of melatonin, a non-protein hormone
made in the pineal gland, and for regulating sleep. Serotonin amounts increase in the
evenings since melatonin is synthesized through it at night.
The amount of melatonin decreases at dawn when the synthesis of it is inhibited, in
this way increasing the amount of serotonin that is not turned into melatonin. Serotonin
as a neurotransmitter acts as an internal clock determining sleep and wake cycles.

31
Hamlyn JM et al.: Identification and characterization of an ouabain-like compound from human
plasma. Proceedings of the National Academy of Sciences of the United States of America 88
(14): 6259-63, 1991.

83
 The internal clock is in charge of coordinating various biological functions such as
body temperature; the stress hormone, cortisol; and sleep cycles. The proper
coordination of these four elements makes it possible for us to sleep profoundly and
wake rested. Men produce up to 50 percent more serotonin than women; therefore,
women are more sensitive to the changes in serotonin levels.

Noradrenalin (or norepinefrin) is an adrenergic hormone that is synthesized in the

adrenal medulla, having the double function of hormone and neurotransmitter.
Noradrenalin affects parts of the body where attention and response to actions are
controlled. Together with adrenalin, noradrenalin also intervenes in the “flight or fight”
response, directly increasing the cardio pulse rate, causing the release of glucose which
acts as energy reserves, and increasing blood flow to the skeletal muscle.
A high secretion level of noradrenalin increases wakefulness, which increases
the subject’s state of alertness, and also facilitates the ability to act on a stimulus. Low
levels of noradrenalin are associated with the onset of depression.

Recent studies concerning dystonia conducted by the National Institute of

Neurological Disorders and Stroke indicate that a defect in the body’s ability to process
certain neurotransmitters that assist brain cells to communicate with each other could be
one of the fundamental causal factors to dystonia. Specifically, the levels of
noradrenalin and serotonin that act as chemical inhibitors which assist the brain in
regulating acetylcholin, an excitatory chemical which upon release at the nerve endings,
is responsible for muscle contraction.

84
 Unity
Jorgos was affected by hand dystonia. Not only had he lost control of the
fingers of his right hand, but he also showed other symptoms. He had the same
repeated thoughts day and night. He was depressed and was not able to pull himself out
of it. During his professional life previous to the onset of dystonia, he had traveled a
great deal. He had lived in a variety of places and had learned English, German, and
Japanese. Now he could not make decisions. He stood still in the street because he was
not able to decide if he should go left or right.

Focal dystonia is thought to be due to a functional anomaly of the basal ganglia

in the brain. Presently, the role that the basal ganglia play in its connections to the
limbic system and prefrontal cortex is being studied in its relationship to
pathophysiologic processes involved in disorders such as anxiety, depression, and
obsessive compulsive disorder32. The basal ganglia are better known for their role in
the planning and execution of movements, but they are also related to other processes
such as emotional behavior and cognitive functions for instance, making decisions,
monitoring, and inhibitory control. Therefore, a functional anomaly of the basal ganglia
could affect the generation, maintenance, and change of emotions, thoughts, and
movements33.

In this way, the borders between that which is emotional, mental, and motion
blur, making it imperative to consider these three elements as one. In essence, the
experience of not being able to stop thinking, feeling, or moving is due to these same
processes. We need to explore the interrelationships among emotion, thought, and
movement during rehabilitation in order for it to be effective.

32
Stathis P, Panourias IG, Themistocleous MS, Sakas DE. Connections of the basal ganglia with the limbic system:
implications for neuromodulation therapies of anxiety and affective disorders. Acta Neurochir Suppl. 2007;97(Pt 2):575-
86.
33
Saint-Cyr JA, Taylor AE, Nicholson K. Behavior and the basal ganglia. Adv Neurol. 1995;65:1-28.

85
 Grief at the bow
On one of my trips to Japan, a music professor introduced me to one of his
students. It seemed that she could not play the violoncello because just placing the bow
to the string caused her to cry uncontrollably and feel such profound sadness that she
needed to abruptly stop playing.
According to what I was told, Fumiko had begun to study violoncello very
young.
When she was 12 years old, she showed such talent that her teachers and parents
decided to send her to the United States to study. It was decided that she would go
alone to live in Minnesota where a prestigious professor was living. No one asked her,
and before she knew what was going on, she found herself in a strange country, isolated
in a cold winter separated from her parents and friends in a rented room.
She spent her days and nights crying and playing her violoncello.
When she couldn’t stand it any longer, she had a nervous breakdown, and her
parents brought her back to Japan. She never played the violoncello again.
The day that I met her, she seemed to me to be a lively young girl, happy and
very well mannered. I asked Fumiko to play for me. Just as I had been told, when she
began to play, her face changed and the tears began to run down her cheeks. She
suddenly stopped playing and explained that she couldn’t continue. Tension had
paralyzed her.
I asked her to play and cry; to not try to contain it; to not interrupt the music; to
use the music to close the wound.
Fumiko played BWV 1008 Suite for solo cello no. 2 in D minor by J.S. Bach. I
still remember the knot in my throat that was caused by the serene and profoundly sad
music that Fumiko was able to coax from that cello. It was a sound that flowed from
deep inside her and created an image of a frozen, deserted field from those isolated
winters of her youth. I never again heard such a compelling rendition of that music.
A year later, she returned to the university to continue her violoncello studies.
It seemed that her wound had closed since she had cried enough.

86
 In utero

Louis is an apparently normal two year old. Louis is only dystonic while he
sleeps. When he sleeps, he displays symptoms of a generalized dystonia that disappears
when he wakes up.
How it is possible for him to move normally during the day and only suffer from
a generalized dystonia while he is sleeping is an enigma that specialists have not been
able to resolve.
Some recent studies defend a psychogenic hypothesis of dystonias34. The term
“psychogenic” is used as a general term to designate those pathological processes that
originate from a psychological cause. This is different from physiogenic or
somatogenic, which are terms referring to processes which have physical or somatic
causes. In light of the psychogenic hypothesis, being exposed to psychological traumas
could be connected as one of the trigger factors within the complex network of causes
leading to the onset of dystonia.
Could a child of this age have been exposed to such an extreme psychological
trauma? Or perhaps it wasn’t the child who was exposed to it.

Dr. Engel and his collaborators at Mount Sinai School of Medicine in New York
studied pregnant women who suffered psychological trauma during their pregnancy due
to the September 11, 2001, World Trade Center attacks in New York35. They studied
187 mothers who were living or working near the World Trade Center the day of the
attacks. These children who suffered a psychological trauma in utero were born with
smaller cranial circumferences than is usual at birth. This could influence subsequent
neurocognitive development.

Dr. Marcus of the University of Michigan carried out a study of mothers who
had suffered severe depression during pregnancy and evaluated the impact of this on
their children at the moment of birth. Compared with children born at the same time of
gestation, the children of these mothers were born with smaller cranial circumferences
and with lower birth weights36. Additionally, these children were born in less healthy
states as evaluated by their Apgar scores, a scale which evaluates five physioanatomical
parameters: skin color, heart rate, reflexes, muscle tone, and respiration.

Could it be possible that Louis was reliving an in utero trauma while he sleeps?

34
Hawley J, Weiner WJ. Psychogenic dystonia and peripheral trauma Neurology August 2, 2011 vol. 77 no. 5 496-502
35
Engel SM, Berkowitz GS, Wolff MS, Yehuda R. Psychological trauma associated with the World Trade Center attacks
and its effect on pregnancy outcome. Paediatr Perinat Epidemiol. 2005 Sep;19(5):334-41.
36
Marcus SM. Depression during pregnancy: rates, risks and consequences--Motherisk Update 2008.Can J Clin
Pharmacol. 2009 Winter;16(1):e15-22. Epub 2009 Jan 22. Review.

87
 Regression
Daniel is a dancer specializing in contemporary dance. A year ago, he was
victim of a mugging. He received multiple kicks to his head and abdomen, was taken to
the emergency room, and was hospitalized.
He didn’t seem to have any after effects except for being afraid to walk alone in
the city at night. Something had changed in his life, however. Now when he dances, he
produces strange involuntary movements which he describes as a regression to an
animal state. His dystonia includes a strong contraction of the dorsal interossei and
extensor muscles of his fingers which causes his hand to make a clawing position. He
also suffers from abdominal contractions which causes him to leave an upright position,
and take on a four-footed one. Daniel notices what is happening to him when he
dances, and tries to integrate these strong contractions into his dance.
During aggression, two drives coexist yet oppose each other. One is the
possibility to defend oneself against the attack, and the other is to flee. A person’s
reaction will depend on the intensity each of these takes.
The defensive response is produced when the circumstances reach the point of
no return and the victim, conscious of not being able to flee, decides that there is no
other way out but to fight.
There are people who have a greater predisposition to fight and others with a
greater predisposition to flee. In cases like Daniel’s, not have the possibility to escape
relentlessly produces the fight response.
Conflictive situations, marked by high levels of stress, pain, and fear, cause a
lowering of the “response threshold”37 making it easier for defensive responses to come
forth.

It seems that the aggression he suffered caused a lowering of his response

threshold, and he now reacts in an extreme way to low levels of stress in his daily life.
Daniel redirects his emotional state through his dance, although this activity is not a
generating stimulus for his behavior.
The greater the excitement, the greater the probability to redirect the aggression will
be.

37
The term “response threshold” refers to the speed and intensity with which on responds to a determined stimulus.

88
 Withdrawal syndrome
William is a surgeon who has had dystonic symptoms since he was very young.
They started to show themselves when he was an adolescent and would return from
time to time, especially when he was tired, anxious, or sleep deprived. During his
adolescence, he had difficulties doing sports and in motor activities such as dance. His
main problem is right hand dystonia, which is directly related to writing and also affects
his ability to manipulate certain surgical instruments such as forceps or scissors. In the
last seven years, there has not been one single day when he has been symptom-free.

As has already been mentioned in this book, anomalies in basal ganglia function
are very closely related to the existence of disorders such as focal dystonia or task-
specific tremor. The basal ganglia are involved in both habit formation and in
addictions38. The process of focal dystonia rehabilitation has various points in common
with the treatment of addictions.
It could be said that patients affected by focal dystonia are muscle tension
addicts.
Dysfunctional muscle tension is produced because of a feeling of need to
generate it. This need is so strong that it makes the patient, once able to inhibit the
dysfunctional tension, experience something similar to withdrawal syndrome. The
fundamental objective during rehabilitation is the inhibition of the dysfunctional
response, characterized by the production of spasms. Three phases can be identified in
the rehabilitation process. In the first phase, the patient feels the need to produce
tension, and it is produced automatically without the possibility of stopping it. In the
second phase the patient feels the need to produce the tension, but is now able to stop it.
In this stage, it is very common that the tension becomes “displaced”. For example, if a
spasm is stopped in the wrist muscles, the tension moves to another area.
Displaced tension can appear in the shoulders, toes, or abdomen. This new
tension is usually easily inhibited since it is not yet set into the system. We need to be
very meticulous and pay attention to each new tension and relax them sequentially as
soon as they show. The third and final phase in the rehabilitation process is
characterized by the absence of the need to produce dysfunctional tensions.

38
Belin D. Jonkman S. Dickinson A. Robbins T. Everitt B. Parallel and interactive learning processes within the basal
ganglia: Relevance for the understanding of addiction. Behavioural Brain Research.Volume 199, Issue 1, 12 April 2009.
89–102.

89
 Associations
Lucia developed a tremor in her arm after having been raped. Tremors
commonly appear in patients affected by post-traumatic stress and are considered to be
characteristic diagnostic signs39.
Dr. Peter Levine, a specialist in the rehabilitation of patients affected by post-
traumatic stress, proposes that the key to overcoming traumatic events is the capacity to
break the paralysis induced by the trauma and to recover mobility and functionality40.
The tremor could be a natural mechanism to resolve the somatic manifestation of
trauma (paralysis) and, in this way, reestablish balance.
In Lucia’s case, the association between the trauma and the tremor is not as
obvious, since it only occurs when she tries to play the violin.
Although it might appear that these two contexts, the trauma and playing the
violin, are not related, they could be. Lucia’s tremor appeared suddenly weeks after her
traumatic experience. In point of fact, during her period of shock, she played the violin
as a way to think about something else. Could Lucia have created a connection between
the violin and the rape?

We must recall that the limbic system manages the physiologic responses to
emotional stimuli. The limbic system includes various interrelated structures called the
hippocampus, the cingulate gyrus, and the amygdala. The amygdala intervenes in the
somatic expression of emotion, and is made up of different nuclei with fibers that
connect to the hippocampus, basal ganglia, hypothalamus, thalamus, and brainstem
nuclei. It plays a fundamental role in emotional processing, learning, and modulation of
attention. The amygdala associates emotions with memories.

In this case, her memories are also movements, and the basal ganglia have a
large role in their creation. The basal ganglia take part in initiating movements, muscle
tone control, posture, and the creation of motor sequences. The basal ganglia are
involved in the formation of habits and behaviors that are a consequence of stimulus
and response associations, in emotional behavior, and in addictive behaviors. Tremors,
spasms, and involuntary movements are a consequence of the errors in function of the
basal ganglia.

39
The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR, 2000).
40
Levine, P. (2002). Waking the tiger: Healing trauma: The innate capacity to transform overwhelming experiences.
Berkeley, CA: North Atlantic Books.

90
 Therefore, we find ourselves facing a traumatic experience that produces an
emotional and somatic response, which is associated by simultaneity with motor
memories.
A dysfunctional association endures in the memory making her avoid a neutral
activity because it is linked to emotions in her memory.
In Latin the word “remember” comes from “recordare” which means “pass through
the heart once again”.

In order to recover, Lucia needs her prefrontal cortex to intervene making it

possible for her to inhibit the automatic response and monitor her behavior as a function
of perception. The prefrontal cortex is responsible for joining cognitive abilities that
allow foresight and goals setting, designing plans and programs, self-regulating and
monitoring of tasks, precisely selecting behaviors and conduct, and the flexibility of
cognitive work, in order to obtain efficient results to solve problems.

91
 Difficult words

Mathew’s case was very uncommon. He had left his work due to a focal
dystonia of the lips. He remembered that his symptoms had appeared after a time of
spiritual retreat in which he had prayed intensely. His symptoms appeared selectively
in certain lip positions, which were needed to produce certain sounds, phonemes, and
words. Mathew made me a list of the difficult words he could not pronounce because
they produced great tension in his face, tongue and lips.

In principle, he could have avoided these blocked words and replace them with
synonyms made up of other phonemes.

I discovered that this was not possible because Matthew was a priest, and
because the first two words on his list were “you” and “we”.

92
 Walking with giants

Dolores told me that one day she woke up and her body seemed to be smaller.

When she walked down the street, the sidewalks seemed higher than yesterday,
the streets wider, and the people she met were enormous.

This feeling created panic for her and she didn’t want to leave her house.

93
 Dreams

Dominique dreamed that she was playing the violin with a cucumber.

Claudio dreamed that his bow had shrunk.

Laura dreamed that her fingers were carrots.

Each of these happened before the first symptom of their disorder appeared.

94
 Happiness
Not all dystonia patients have been through traumatic experiences. In some
cases the months prior to the onset of dystonia were some of the happiest of their lives.
Maria was in love. Monique gave birth to her first child. Tom got the job he
had fought so hard for. All of these people developed a dystonia which came about at
the same time as these events.
What do these have in common: a mother that just gave birth to her first child, a
man in love, a woman who was attacked, and a student finishing her doctoral thesis?
There is an enormous span of emotions that these patients might be going through, but
what they all have in common is sleep deprivation.
Sleep deprivation is a repeated element in almost all the cases I have studied and
should be taken into consideration as a causal factor.

95
 Dissociation

Sofia told me a Native American story:

In this story, a wise man dreamed that he was split into two dogs.
One dog was violent and dark.
The other was calm and was self-controlled.
There came a time when the two dogs began to fight. The battle lasted days.

“And who won?”

“The one who was fed the most…”

We have the opportunity to choose how to act.

Only in the present can we change the past and create the future.

96
 Mimesis

Maria uses a cane. She doesn’t really need it. She can walk without it. The
dystonia that affects her ankle doesn’t make her loose her balance, but it requires her to
walk very slowly so she can appropriately support her foot at each step. She discovered
that when she used her cane, drivers didn’t blow their horns when she slowly crossed a
crosswalk.
Many dystonia patients suffer because their disorder is not visible to others and
they feel misunderstood because, as they seem to be completely sane, they don’t receive
adequate social support, being pressured on many occasions to behave normally, when
this is not possible for them.

97
 The hole

Sarah felt unsupported and frustrated when she tried to encourage and explain to
others how she had recovered from a focal dystonia in her hand.

One day she told me a history that explains how she felt:
“Imagine there was a neurological disorder which meant that you were constantly
seeing a hole in the sidewalk and falling as you approached it, though there was no hole.
And imagine someone trained you to walk as if there was no hole, until eventually you
didn't see it anymore. And then imagine, after this wonderful deliverance, that people
came to you and said 'prove it! Show me that you don't see a hole! I want to see you
walk and not see a hole and not fall! If you don't do this I will call you a liar!'

That's kind of what it feels like.

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 Marriage
Erika and Marco are married. Both of them have focal dystonia of the third
finger of the left hand. When they met, neither was affected. Dystonia appeared in both
cases with little difference at the same time as the birth of their last child.
Erika and Marco do not share genetics, since they are from two different
countries and are two different ethnicities. They share one marriage and one life.

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 Reacting
Pedro could be considered the Rosetta Stone of focal dystonia. Throughout his
life, he has been affected by embouchure dystonia in his lips, a segmental forearm
dystonia, writer’s cramp, and a computer keyboard dystonia.
To understand his case is to understand the connection between the different
types of focal dystonia.
Pedro showed the first symptoms of dystonia more than twenty years ago. He
remembers that his lip movements became uncontrollable when he decided to advance
from playing his trombone just for fun –to playing without errors. Playing the trombone
with involuntary movements caused him anxiety, so he decided to change specialties
and begin a career as percussionist, where the facial muscles were not necessary. He
began to play percussion intensely, advancing very quickly. When it became necessary
for him to play serious orchestra solos, the symptoms of a strong segmental right
forearm dystonia began.
Since he could no longer play percussion, he took a management position in an
education center. He didn’t need to play, so for some time, he was able to work without
problems. When he had to sign important documents, the symptoms of writer’s cramp
appeared. He stopped writing by hand and began to use a computer. At first he was
able to use the keyboard without problems. Once again, spasms appeared in this
context after a few months of having to input data while dealing with parents and
teachers.
In Pedro’s case, it is possible that a highly reactive personality can be generating
multiple maladaptive responses when faced with situations that can produce a high
level of psychological tension for him. This reactivity evolves to increase or decrease
depending on his daily life. Each time a dysfunctional response to a stimulus is
produced, a reactive person becomes more vulnerable and demonstrates a greater
tendency to react this way in the future in similar situations. It’s like a snowball that
rolls down a hill, growing and moving faster and faster. We must remember that when
we react one way to one situation, it is a decision. If we react the same way three times,
it is a tendency. If our reaction remains the same over time, our response will become
predetermined.
Therefore, it is of great importance to rehabilitate all the affected contexts in a
pressure-free environment. In fact, during therapy, the less you expect, the more you
achieve.

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 Abandonment
Naoko was affected by a flutist focal dystonia. Her first symptoms appeared
suddenly after a traffic accident in which she was uninjured. For two years, she tried
multiple therapies with no results. When she began her rehabilitation program, she
started to make progress, but very slowly. It seemed it was not time to try it. After a
year of rigorously attempting, she left it. She took a year off for herself, in which she
was going to try it without hurry and without pressure. She returned home to her family
and trained to be a master mechanic for musical instruments. During her year of
training, she hardly touched her flute nor practiced exercises. When she finished her
training, her life had changed. She was no longer an aspiring orchestral flautist. Now
she was a sought-after instrument mechanic. The pressure to achieve at a high level
when she played the flute disappeared, and with it, the dystonic symptoms. Now she
was able to play the flute normally. Naoko is one of the people who can say that she is
completely recuperated after having suffered from focal dystonia. She is happy and
tries to avoid stress and anxiety in her life.

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Part II: How to induce a plastic change

102
 Plasticity

The inherent capacity of brain cells to modify themselves and their functions
allowing us to learn, change, and adapt is known as brain neuroplasticity. The
modification of neuronal connections makes the repair of cortical and subcortical
circuits, the integration of alternative cortical areas in order to carry out modified
functions, and recovery from brain injuries possible.
In spite of the fact that the brain is typically thought of as static and unalterable,
today we know this is not true. Brain plasticity is possible in adults, although it is more
limited than in children.
The different areas of the brain are genetically determined to take part in specific
functions; however, in the cerebral cortex in particular, modulation and modification
through experience and learning are possible.
Neuroanatomical, neurochemical, and functional changes that occur during
plastic reorganization allow for the recovery of affected functions. In this case, it is
known as physiological or adaptive plasticity. In cases where as a consequence of this
reorganization certain functions become more difficult and others are favored, a
maladaptive plasticity is produced.
The brain adapts and reorganizes itself to allow functionality though different
neuronal mechanisms. The first mechanism is the creation of new synapses through the
sprouting of dendrites, aimed at helping to recover function. A second option includes
the functional reorganization between different neuronal areas or groups within the
preexisting neural network. Redundant circuits exist in the brain which perform similar
functions in parallel form. An injury to one of these pathways makes the other
completely take over the transmission of the information and develops pathways that
previously existed but were underused or had become inactive.

It is also possible to incorporate new areas to form part of the previously

established network, or to use a network that was not usually used for this function and
was in charge of completely different functions. This might imply the learning and use
of new strategies.
In other cases, different regions of the brain, which were in charge of carrying
out completely different functions, are “recruited” to compensate for losses due to an
injury.

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 Finally, occasionally neighboring or contralateral (another hemisphere) areas
provide the function because of a functional reorganization of the cortex, perhaps
through the activation of redundant pathways and circuits.

Neurotransmission systems play a very important role as mediators in these

processes, since they are involved in the maintenance and cessation of neuronal
plasticity, setting the limits for the critical period.

The neurotransmission systems involved in plasticity are:

• N-Methyl-D-Aspartate System (NMDA), a glutamate receptor that is involved in
intracortical facilitation and inhibition mechanisms; It is able to block the
capacity for plasticity in the cortex.
• Cholinergic System (ACh), along with the glutaminergic system, this plays a role
in cortical morphogenesis
• Serotonin System, is involved in the formation and maintenance of new synapses
• GABAergic System (GABA), the inhibition exerted by the GABA system is
overcome by neurochemical changes following an injury in which glutamate is a
part, to allow necessary plastic changes required for rapid plasticity recovery. In
the long run, the decrease of GABA-mediated inhibitory tone precedes the
unmasking of silent synapses and the consolidation of alternative neighboring or
contralateral pathways to preserve or replace the damaged function. There is
evidence that both sensory deprivation and stimulation cause changes in different
directions on GABAergic activity.

We could say that the N-Methyl-D-Aspartate System, the Cholinergic System,

and the Serotonin System are like fertilizer in a garden, which allows the creation of
new connections. On the other hand, the GABAergic System would be like an anti-
fertilizer that preserves what is already acquired. In this way, balance between creation
and preservation in the central nervous system reigns. In the case of rehabilitation, it is
necessary to start the mechanisms of change and establish and stabilize balance.

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 Training
“It’s not easy. It’s not simple. But it’s not impossible.”
Mario Pergolini

As opposed to physical training, brain training is discontinuous and

unpredictable. If we analyze the progress made during the first six months of
reeducation, we can see that in the great majority of patients the progress is made in an
unexpected way after weeks of apparently ineffective training. This progress is
preceded by incubation periods during which connections are made and silent pathways
are unmasked so necessary advancements can be made.

It is important to point out that these types of interventions cause exhaustion in

patients after weeks of intense physical and intellectual work. When patients are
exhausted after weeks of progress, they experience a decrease in performance, which
tends to be interpreted as a step backwards or regression in their progress. We need to
be aware of the fact that this decrease in performance is due fundamentally to
exhaustion. In general, after a week or two of appropriate rest, patients recuperate to the
level they had prior to their exhaustion.

Many patients, when trying to rehabilitate themselves alone without a coach,

confront this phenomenon and interpret it as the system they are following being
inadequate. They therefore become discouraged and abandon or modify their practice
exercises.

The exercises should be maintained during enough time to accomplish results. If we

modify exercises every day, we do not give enough time for the system to establish the
progress for one process that is needed to move on to the next.

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 It is very important to establish realistic goals to guide your progress.
Obviously, the ultimate goal is normalized movement and the absence of tremor and
dysfunctional movements. Although this is our ultimate goal, in daily work we focus
on partial goals, with our objective being to achieve the greatest degree of fluidity and
relaxation possible today.

We must concentrate on the present and try to do each of the daily exercises
without putting too much pressure on the process. At first, it is not important if the
exercises are not done perfectly. The important thing is to try it, because after weeks or
months of trying, these movements can be recovered.

Some patients have unrealistic ideas about what the rehabilitation process
consists of. They think that the movements are either poorly performed or well
performed. This simplification doesn’t match actual experience because in order to
reach 100 percent recovery, you previously need to make movements at 50 percent, at
60 percent, at 75 percent, at 90 percent, etc. Each one of the phases should be
consecutively achieved, and moving on to the next one should be considered as an
achievement that improves the quality of life.

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 Resistance
“To arrive at what you do not know,
you have to go where you do not know.”
San Juan de la Cruz

Occasionally, patients are resistant to the process of rehabilitation. The most

common are characterized by their opposition to progress and could be described by the
following list:
I can’t do it
In the majority of cases this affirmation is based more on fear of failure and
uncertainty than it is on a real impossibility. If the patient can pass this first stumbling
block, decide to make a first step, and complete the task that seemed impossible, other
resistances appear that need to be conquered sequentially. For example, when a patient
with ankle dystonia says that he can’t correctly take a step and you convince him to do
it, if the result is positive, he will say that one step is possible, but two are not. Two
steps should be attempted, and when two are made, he will say that two are possible but
not three. This way tasks are tailored to the size of the resistance in a zone of proximal
development, and the patient gradually regains his lost self-esteem.

I prefer to go on as I am
This is not an option. As small as the improvements achieved are, they are
worth it because they determine our daily life.

I tried this before and it didn’t work

Just because you tried it before without results doesn’t mean that it won’t work
now since you and the circumstances have changed.

Rehabilitation makes me nervous. I don’t like to relax. I feel odd.

This feeling is perfectly natural and you don’t have to fight it. The loss of
control of your own movements generates great anxiety.
If we live in a state of constant anxiety, it is difficult to be conscious of it. On
the other hand, when we are able to relax, even a little bit, we suddenly get a new
perspective and recognize our own anxiety because now we are in another state that we
can compare to our usual one. Rehabilitation that allows improvement in control is the
best way to alleviate this anxiety produced by its loss.

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 If I can’t do it perfectly right now, I prefer not to try
The rehabilitation process is begun in order to improve our quality of life. If
there is something we are unable to do or if we have lost control of some part of our
body, it’s worth the effort to try. Rehabilitation allows us to work on the past in the
present in order to make a better future.

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 Compensation
If the patient is crying, would you treat his eyes?

To help understand how the first phase of the disorder works, we can use the
following metaphor:

Imagine that Patient X suddenly loses 60 percent of her hearing while she’s sleeping.

The first words she speaks when she gets up will sound to her strangely like a
whisper. Unconsciously she will adjust her sound (she will shout) to hear her speech
the same way she did the previous day. (Adjustment: normalizing perception by
modifying later movements.) From her point of view, it will have normalized.

An external observer only knows that Patient X has begun to shout, but he
doesn’t know why.

If we ask Patient X, she will say that she is not shouting, that she is speaking in
the same way as yesterday.
Surprisingly, Patient X won’t consult a doctor looking for help for her hearing
problems except for seeking to find out why she goes to bed hoarse each night.

This example helps us to understand the essence of the compensation process.

To begin with, it is not a conscious process.

It’s logical, from a certain point of view, but it can be highly unproductive and
dysfunctional, as in the case of Patient X, who instead of seeking assistance aggravates
the problem.

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 What has been Patient X’s error? Due to her lack of awareness about her deficit,
Patient X has taken it for granted that she is healthy and that nothing has changed.
Based on this erroneous appraisal that makes her think her hearing is the same as
yesterday, she evaluates what is happening and comes to the conclusion that if her
perception is adequate, what must be wrong is the action (motor pathway). This leads
her to make an adjustment to the movement (increased work for her vocal chords),
which in turn generates more incapacity. Patient X has modified her movement to keep
her proprioception stable.

What should have been Patient X’s correct reaction in this case?

If Patient X gets assistance from a rehabilitator, that will help her become aware
of her deficit and to understand that although it seems to her to be insufficient, the
volume of her voice when she doesn’t shout is, in fact, more than sufficient for her to be
heard well.
To do this, she must go through training to hypersensitize herself. When she realizes
she is speaking and she can’t hear herself, it means that she is speaking at a low volume.
When she hears herself a little, it means that her volume is adequate. And when she
hears herself well, that means that she is shouting. In this case, the movement is not
modified, and the perception is worked on in order to produce an adaptation and plastic
change in the way in which she perceives. Movement is not modified in order to
modify proprioception.

Patients affected by dystonia are not conscious of the tension that they are
producing, where it is being produced, nor when. The process of restructuring
proprioception aims to recover awareness of the tension that is produced, in order to
adjust it or inhibit it.

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 Classification
As has been explained in the previous case analyses, the symptoms of dystonia
are caused by dysfunctional associations created by a maladaptive plasticity. These
dysfunctional associations can be of a variety of types. In my daily practice, I have
classified them as follows:

Position Reaction: In this case, a certain position produces dysfunctional

tension associated with a position. This is the case of some guitarists who only have to
hold the guitar to have spasms in the musculature of their fingers begin.

Contact Reaction: In this case, it is the contact with a specific object that
produces associative dysfunctional tension. This type of reaction can be seen in some
cases of writer’s cramp, when contact with the pen produces spasms in the musculature
of their fingers, or in the case of violinists where contact with the string produces
tremors.

Pressure Reaction: In these cases putting pressure on something with a specific

finger produces dysfunctional tension. It can be seen in writer’s cramp when the writer
uses a computer keyboard, where the hand can rest on the keyboard, but putting
pressure on it makes the patient lose movement control.

Movement Reaction: In these cases, making a certain movement produces the

dysfunctional tension. This can be observed in cases of writer’s cramp when a specific
stroke triggers spasms in the musculature of the fingers or forearm.

Goal-oriented reaction: In these cases it is the mental image of performing a

certain movement that produces an associative dysfunctional tension. This can be
observed in patients affected by writer’s cramp and very clearly in percussionists who
are able to grasp the drumstick in a playing position without symptoms if they think
they are not going to play. If they are told to play after counting to five, they
immediately lose control of their movements.

111
 The different types of reactions present in each case allow us to make a
classification within each type of dystonia. In this way, we can speak of a patient that
has writer’s cramp with position reaction or the case of a trombonist who only displays
a goal-oriented reaction. It is also possible that patients have a variety of reactions in a
single case.

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 Learning movements
Learning complex and refined movements, such as writing or playing a musical
instrument, consists of building systems of programs that become automatic so that later
they can be triggered in different ways.
Basic and complex programs exist with complex ones being created in a
combination of basic ones. In order to write, it is necessary to be able to make
horizontal and vertical strokes. It is also necessary to be able to change the position of
the forearm resting on the paper to move the tip of the pen from left to right on each
line.
These movements are based on basic programs which include the selective
activation of some musculatures and inhibition of others. These programs that allow
basic movement are called Level 1 Programs.
Once this skill is acquired and individual coordination of Level 1 Programs is
perfected, we move on to the combination of a variety of simple movements such as, for
example, when we make diagonal strokes combined with the movement of a vertical
stroke along with a horizontal stroke. These combinations create curves, waves, etc. If
we write a line of “a’s”, we will be combining vertical strokes and horizontal strokes
along with wrist and forearm movements.
These programs, composed of a variety of subprograms that are carried out
following a choreography, are called Level 2 Programs.

Automatization is achieved through the repetition of Level 2 Programs. This

includes creating a unit of information (a file) that, upon being selected, performs a
complete chain of information (combination of Level 2 movements). These chains of
movement are called Choreographed Sequences or Kinetic Melodies (Level 3). In the
case of focal dystonias, the loss of control is due to the distortion of basic movements
(Level 1) and not Choreographed Sequences (Level 3) as has been thought. In fact, the
term “writer’s cramp” implies that the writing is the problem, when actually it is not the
writing that is the problem. It happens when it comes time to make a basic movement
that is part of writing, which is also part of other complex Choreographed Sequences.
Therefore, rehabilitation should not be restricted to writing, but should develop
exercises to rehabilitate movement affected within a wider context, carrying out other
Choreographed Sequences that involve this basic movement, such as drawing, coloring,
shaping clay, etc.

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 Rehabilitation

“Don’t try to calm the ocean. Learn to swim between the waves.”
Japanese Proverb

Producing neuroplasticity is like sailing without knowing where we are going.

Dystonia rehabilitation is a long and difficult process. It requires from a patient a great
psychological resiliency to discouragement. The sooner the reeducation begins, the
more favorable the outcome will be. On the other hand, in many cases, after having
suffered from dystonia for more than ten years, it is possible to achieve a complete
recovery, but more effort is necessary along with an appropriate guide so that no errors
are committed which would impede progress.
The minimum amount of recovery time observed has been six months in young
women who started their rehabilitation a few months after the onset of the disorder. In
the rest of the cases, times vary between one and eight years.
Left-handed women have a greater possibility of achieving success, followed by
right-handed women, left-handed men, and right-hand men. The younger the patient is,
the easier it is to produce a plastic change. This phenomenon is known as the Kennard
Principle. The Kennard Principle is not met in all cases. Young patients are found who
are incapable of adapting or changing, and patients who are more than 50 years old who
are able to make great progress are also found.
Patients who spoke a variety of languages before the onset of the disorder, and
who have had a life characterized by adaptation, such as in the case of having lived in
different countries with different cultures, show a greater facility during training.
Depressed patients rarely finish the process and don’t tend to make rapid
progress. In these cases, it is better to treat the depression first and then start training
when the behavioral tone is appropriate.
Patients who are optimistic and fighters are the perfect candidates for this type
of reeducation.

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 Phase One: Analysis
“If it can be seen, it is not dystonia.”
The first step in rehabilitation is to distinguish between what is happening and
what the patient thinks is happening. In order to do this, an analysis is conducted to
determine which muscles are more active than they should be and which muscles are
less active than they should be.

Generally in focal dystonia, only one muscle is affected. The other muscles that
appear to be affected are making compensations looking for balance or adjusting the
movement. In most cases, the muscle responsible is always the least obvious one.

The musculoskeletal system is designed following the rule of specificity.

A certain movement (Movement A) is produced by a group of specific muscles
working together. If one of these muscles is not working, it is not possible to carry out
Movement A. We can carry out a similar movement, but not one that is the same (A’).
We can limp, but we can’t walk.
It could be said that exchanging is not allowed.
Through compensation, we try to break the rule of specificity.
Producing an exchange, fighting without success to make a movement carried
out before dystonia.

The process of reducing muscle tension which compensation carries out is

gradual and should be done in backward order, reversing the timeline of its creation.
For example, if in order to avoid a slight tremor we produce a dysfunctional tension in
Muscle A, this will produce an imbalance in movement in general. Trying to
reestablish this balance will produce tension in Muscle B, and follows successively in a
compensation sequence A-B-C-D-E. These dysfunctional tensions are not produced in
a random fashion but follow an invariable and predetermined sequence in a domino
effect.

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 Phase Two: Restitution
“Look for the tremor; it is reorganization”
Inhibition should be carried out in reverse order from that in which these
tensions were programmed. This means that tensions learned in A-B-C-D-E order
should be inhibited in E-D-C-B-A order.
If in the A-B-C-D sequence the C element is not produced, element D will not
be produced either. If sequence A is not produced, the sequence chain will not be
produced.

Once the compensation has been removed (going backwards on the timeline) we
find the primary dysfunctional movement or tension.
The process is illustrated by this metaphor:
Imagine a Russian doll: those wooden dolls that have other smaller ones stacked
inside. When you open the first one, you can take out the next identical but smaller one,
which also can be opened and has another identical but smaller one. If we continue
opening the dolls, we get to the last doll, which is very small. When we open that one,
we find only empty space.
In many focal dystonia cases, there is just a group of compensations, including
what seemed to be the initial dysfunctional tension (since this was the first one
clinically noted) that was at the same time a compensation for a movement that was not
carried out.

Once all the compensations have been inhibited, movement is freed.

Given this, the following questions come up: Why does the patient produce
compensations, if their presence makes the desired movement difficult or impedes it,
and its absence frees movement? The answer is that the patient produces a
compensation because he feels that he needs it, since when he doesn’t compensate, he
experiences unpleasant sensations. Because of this, in many cases compensations are
due to avoidance strategies of certain neural connections. When performing certain
movements, the unpleasant sensations that patients refer to tend to be described as
“instability”, “emotional distress” or “strangeness” and in some cases “a pain that’s not
anywhere”.

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 In the book The man with a shattered world, Alexander Luria describes the recovery
of his patient, Lyova Saletsky, a chemist who fought on the Western Front during
WWII and who sustained a gunshot wound. Saletsky slowly recovered his ability to
read and write. Luria described these compensatory strategies to recover function as a
way to “surround the acid zones”.

Patients affected by focal dystonia also notice these acid zones which they try to
avoid using compensations.

Is it possible to recover these unstable connections?

This process is called restitution and results from reconstructive neuroplasticity.
The process of restitution consists of inhibiting the attempts to “avoid compensating”
and confront the functional movement that is produced through these “noisy” or
unstable neural pathways in order to recover functionality and stability of these
connections through a process of rehabilitation. This technique involves the precise
activation of the malfunctioning brain areas in order to, in some cases, gain normal
function.

In order to achieve this activation with surgical precision, we must select

appropriate movements using appropriate speed intensities and rhythms. This is why
the quality of rehabilitation is primary, because the movements performed by the patient
are one way of stimulating and restoring precise neural connections. Simple finger
movements can reorganize complex networks of brain neural connections.

It is common after inhibiting compensations that muscles relax, and upon using
the unstable neural connections, tremors of varied intensity and speed are observed.
Superficial, fast tremors are a good sign since they appear in the last phases of
reorganization when it is then possible for the muscle to relax. Slower and heavier
tremors characterize the previous phases where a large dose of dysfunctional tension in
the musculature still exists. This is the why we should look for the movements that
produce tremors, because they are a positive sign of reorganization, and although it
appears that the movement is out of control, it is just adjusting itself.

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 This process should be guided by an experienced rehabilitator since the patient
is in an extremely fragile state and is unable to determine whether the unpleasant
sensations he’s feeling when he performs a movement mean that he should stop making
it or the opposite, that they are inherent to a process of cortical-subcortical
reorganization. It is imperative to dismiss peripheral nerve entrapment or other
pathologies that can produce paresthesias in order to clearly distinguish these from the
uncomfortable “phantom tension” and “siren’s songs” that disorient a patient affected
by dystonia in her search of normalizing perception.

At the beginning of rehabilitation, the patient feels the incorrect (dystonic)

movements as correct and familiar. On the other hand, the recovered (functional)
movements feel unfamiliar, strange, and uncomfortable at first, which is paradoxical
since the patient is able to feel and evaluate that these are more fluid movements and
that the muscles are more relaxed.

This rejection while producing an appropriate and functional movement is one

of the biggest impediments in rehabilitation of patients affected by focal dystonia.

In order to confront this rejection, it is very useful to employ a three-question

strategy. The three questions are:
How was the movement, taking into consideration the muscular sensation?
How did you see the movement: was it fluent or uncoordinated?
How did you feel?

A person without dystonia who responds to the first question by saying that the
movement was easy and relaxed and to the second by saying that the movement was
fluent will not add new information to the third answer since a relaxed, fluent
movement produces a familiar and normal sensation. A patient affected by focal
dystonia might answer that the movement was performed in an adequate manner, that it
was fluent and relaxed, and that she does not want to repeat it because she felt an
unpleasant sensation that is difficult for the patient to describe. The three questions
should be used to make the patient aware that she shouldn’t avoid performing those
movements because they produce uncomfortable “noisy” sensations and that this noise
will lessen with practice.

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 It is very important to understand that if the movement is appropriate and we are
more relaxed even though we feel strange, we should persist until normalization is
achieved. In this way, we move from performing bad movements that feel good to
performing good movements that feel bad to finally performing good movements that
feel good. This is a difficult journey without an appropriate guide and without
performing all the steps in the correct order at the necessary time. The reason why focal
dystonia rehabilitation systems have been ineffective until now might be due to not
taking into account the complexity of the process that affects multiple functions and
should be rehabilitated in an extremely precise and controlled fashion in order not to
create dysfunctional plasticity.

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 Variation
“The definition of insanity
is doing the same thing over and over again
and expecting different results.”
Albert Einstein

The activity of the nervous system is economic. The system is limited to

repeating what has been learned and structured (preservation mode), since that way it
uses less energy.
In this way the same neuronal connections are always used when no active
process of change has been initiated.
The learning mode (neuroplasticity) is characterized by using more energy
whereby our tendency is to be in repetition mode most of the time. Neuroplastic
processes that produce a deep restructuring of neuronal activity, such as is the case in
the rehabilitation of dystonia, have a huge impact on the nervous system.
The process of plastic change cannot be taken for granted, since it is not
spontaneously produced unless it is actively initiated through stimulation and enhanced
through daily practice.
In order to initiate a plastic change, it is necessary to induce a complex chain
reaction that optimizes neural connections. This adjustment and optimization reaction
to the connections is what makes rehabilitation of motor control possible.
The inducement of the process is begun when the system is forced to change
upon being faced with an adaptive challenge, which requires something different.
In this way, the art of plastic change inducement consists of choosing when and
how to take the system to the adaptive change situation, through small challenges,
which in this case are the exercises or the different ways of perceiving movement.
These challenges should be programmed cautiously, because if they are not reasonable
at any given time, they could cause maladjusted responses, and if they are too simple,
they won’t take advantage of the moment when conditions are right to produce a
change.

The challenge proposed by the exercise forces the system to consider other
possibilities and explore new solutions, unmasking silent synapses and allowing
sprouting of axons and dendrites. This phase of the plastic process is characterized by a
great deal of neural activity and could be called Search Phase and Options Trial.

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 When the intended organization is achieved, learning should be integrated and made
automatic (Stabilization Phase).
Fifteen minutes of stimulation is sufficient to produce great changes in neuronal
activity.
What counts is not the amount of stimulation time, but the variety, the selection
of exercises and that they are carried out at the appropriate time.

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 Rehabilitation Techniques

The dysfunctional associations between movements should be extinguished

though a process of counterconditioning. The object is not to repeat rigid, conditioned
responses already in place in the system, but to produce multiple responses to a
determined stimulus with the aim of making the response flexible as a phase prior to
ending it.
For example, if the patient produces a dysfunctional tension in his finger when
he flexes his elbow, he should perform exercises that require the flexion of the elbow
without allowing the tension in the fingers.
Through the years, I have developed different counterconditioning exercises that
allow dysfunctional associations to be broken, as is outlined below. If a patient presents
Position Reaction, Contact Reaction and Pressure Reaction, these associations should be
broken in this order.
As has been mentioned previously, flexibility of response exercises should be
completed first in order to move on to Extinguishing Exercises later.

Flexibility of Response Techniques:

Imitation: This technique consists of consciously creating the dysfunctional tension
without the presence of the stimulus that generates this response. The patient
consciously imitates herself producing the spasm. She can also consciously produce the
spasm in the unaffected hand and evaluate how it feels. This technique is not advisable
when the patient is working alone, but it is highly effective when performed in the
presence of an experienced therapist.

Retrogradation: The retrogradation technique consists of reversing the order in

which the tensions occur. If Movement A (elbow flexion) produces Movement B
(finger tension), we first produce the tension in the fingers and then the flexion of the
elbow. In this way, the input does not precede the output, but the other way around.

Mirror: This technique consists of performing the correct movements with the
unaffected hand and later attempt to perform them with the affected hand, evaluating the
differences. This technique provides accurate feedback in the first phases of
rehabilitation.

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 Variation: This technique consists of reacting in different ways to a conditioned
stimulus. For example, if the fingers contract when the elbow flexes, we flex the elbow
and extend the fingers. In the case, Movement A is not followed by B, but by X.

Flexibility of Response-Extinction Techniques

Once the variation exercise has been successfully performed, the patient can move on
to Switch-on and Switch-off exercises. These exercises consist of producing Movement
A followed by B, then A followed by X, A followed by B, A followed by X, and finally
A followed by no movement. In this way we achieve the first extinction through
inhibition after flexibility training. I have observed that this way of proceeding is the
shortest route to achieve inhibition of dysfunctional responses.

Sequenced response inhibition exercises: The inhibition of the dysfunctional

response becomes reality in the first rehabilitation sessions, but it should not be forced
and it’s best to gradually establish control. In this way, the capacity to inhibit the
response is not only strengthened, but it is weakened if not fully performed. Sequenced
response inhibition exercises consist of allowing the response only within certain
default temporal parameters. These exercises should be performed within very precise
rhythmic pauses in order to develop adequate “in time” movement control in the patient.
If after Movement A the patient produces Movement B, we will ask that he perform
Movement A, count “one and two” and then allow movement B. The wait time
between stimulus and response should be lengthened according to the rehabilitator’s
criteria, moving from a minimum of one second to ten seconds. When the patient has
passed the ten-second barrier, the response will have been weakened since the urgency
to react is one of the characteristics of being affected by focal dystonia. The ability to
postpone the response indicates that the recovery of control process is being established.

Exercises for stimulation and modification of internal scales:

Movement is learned through a process of trial and error. Something very similar to
playing “guess the number”. If you have to guess the number “15”, and you say, “20”,
and you didn’t go over, then you know you can throw out all the numbers over “20”. If
you say, “10” and the number is higher, the range will be reduced to just a few numbers.
In this process, the errors are more important than the correct guesses, since they allow
us to get closer to the desired result. This is the same process that the nervous system
uses to look for the most adequate tension for each movement. Through each attempt
the range of possibilities becomes less, and the movement becomes more refined and
controlled.

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 Reconstruction
I developed the clone file technique to assist in cases in which the patient
displayed a goal oriented dystonia or dystonia appears in conjunction with another
injury or the patient displayed a very aggressive response that could cause him to injury
himself.
In these cases a process of gradual reduction to the dysfunctional tension
response was not possible since the response was so intense that if it were produced, it
could cause injury or aggravate current joint, muscle or tendon pathologies.
If Stimulus A produces dysfunctional Reaction B which we don’t want to allow,
the way to proceed in this cases would be to avoid A.
Let’s analyze the process: If Stimulus A, which generates a dysfunctional
response, is the idea of starting, for example in the case of a walker affected by
dystonia, how can we avoid this stimulus?
Many people think that the only option would be not to walk.
In fact, another option exists that allows walking and avoiding Stimulus A at the
same time.
It consists of creating another starting stimulus in another location (with another
file name) which produces the movements of starting to walk. If facing the idea of
“start to walk” (generating stimulus) the system produces a dysfunctional reaction, we
can create a new access route to functional movement.

We program another generating stimulus that is not called “start to walk” but
“allow moving ahead”, for example. This new mental scheme, not associated with any
response, is associated with a chain of functional movements learned from zero as a
new sequence (even though it is a duplication of information present in the system--the
mechanism of walking). In this way an access route to the movement is produced that
surrounds and avoids dysfunctional associations. The neural route A-B is substituted by
A’-B’, with the patient able to perform a movement identical to the one performed pre-
dystonia. Although outside observers do not notice it, this movement uses new
pathways. Surprisingly, patients are able to perceive that they are using a new
alternative pathway to perform the same movement. When we speak of recovering the
ability to walk, in reality it is beginning from zero. This process used to produce the
plastic change is analyzed in the chapter called Change.

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 Synergy
It is possible to improve the effectiveness of each and every rehabilitation
technique through multimodal (visual, tactile, auditory, kinesthetic) integration
exercises.
For example, if we need to relax the musculature of the fingers, and we
concentrate on the sensations of musculature tension, we can achieve our objective. If
in addition, we imagine our fingers changed into over-cooked spaghetti, long and soft, it
might be easier to achieve optimal relaxation.
The brain has the capacity to link and integrate stimuli. Using this ability of
association, which is one of the pillars of our cognitive abilities, we can very effectively
surpass rehabilitation goals.
Patients who naturally use these procedures show a greater ability when it comes
to solving the diverse problems posed during rehabilitation.
Some patients solved problems playing the violin by using analogies to cooking
techniques; some solved problems walking using past experience riding horses. Colors
helped understand emotions; music helped understand movement and painting, feeling;
poetry helped understand abstract concepts about neurology.

Rehabilitation is not separated nor is it isolated from life. All past experiences
(visual, tactile, auditory, emotional, and kinesthetic) can and should be used to enhance
the integration of learning.

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 Epilogue
"Two roads diverged in a yellow wood, and I
I took the less traveled by,
And that has made all the difference.”
Robert Frost. The road not taken

To all those who have read this book looking for help for their own
rehabilitation, Have courage!
Much patience is required to reach the end of the road.
An appropriate guide is of vital importance to help us maintain a firm focus on
our final objective and to make progress when we are disoriented or have lost hope.
During this process it is fundamental to maintain good spirits and keep perspective.
One patient asked me once if dystonia was a spiritual disorder. I don’t know
how to answer this question, but what is certain is that in order to recover it is necessary
to cultivate virtues such as patience, self-understanding, self-control, hope, resiliency,
and happiness.
Make your recuperation process a route to personal transformation and an
opportunity to learn.

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 Aknowledgements

I would like to aknowledge the support and collaboration of NISA Hospital of

Seville in making it possible to take the fMRIs that appear in this book.
Thank you to Dr. Rodriguez Navarro and the neurophysiology and radiology
unit at NISA Hospital and especially to Dr. Giamelli, Dr. Viñuela and Dr. Jimenez.
Thank you to the memory clinic team at NISA Hospital.
Thank you to Dr.Yoshie at Tokyo and Osaka University for her advice and help.
Thank you to Lynda Franco and Estefanía Farias for their help in the translation and
editing of this book.
Thank you to all my patients and students who have been my true teachers all this
time.

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 About the author

Dr.Joaquín Farias is a leading specialist in neuropsychological rehabilitation in

focal dystonias, biomechanist, ergonomist, psychosociologist, musician, martial arts
instructor, shiatsu therapist, traveller, researcher and advocate for a patients’s right to
receive the least aggressive treatment available.
He believes that patients are not just subjects, but are people, and when a life is
reduced to a clinical history, many times the most important facets of the person are
overlooked.
He believes that rehabilitation experiences are not reproducible because each person
is unique and different and that life doesn’t repeat itself.
He believes in the humanization of science and in the integration of all disciplines
because the patient lives in a world that cannot be divided.
He believes that questions without answers could be resolved if we were not in such
a hurry and it wasn’t so important to be completely right all the time.

For further information, go to: http://www.focaldystonia.net

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APPENDIX I

129
Brodmann’s Areas

130
Lateral view

Medial view

131
1, 2, 3 Primary somatosensory cortex

4 Primary motor cortex

5y7 Somatosensory association cortex

6 Suplementary motor cortex

9 Dorsolateral prefrontal cortex

10 Anterior prefrontal cortex

11, 12 Orbitofrontal area

17 Primary visual cortex

18 Secondary visual cortex
19 Associative visual cortex

22 Superior temporal gyrus

39 Angular gyrus
40 Supramarginal gyrus
41, 42 Primary and Auditory Association Cortex
43 Primary gustatory cortex

44 Broca’s area
45 Pars triangularis Broca’s area

Image: Brodmann areas: Gray's Anatomy of the Human Body, 1918

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APPENDIX II

133
 Treatment efficacy in an ecologically valid neuropsycological
treatment program of 120 professional musicians with focal
dystonia

Farias J, Ph.D.* Yoshie M, Ph.D.**

* Dystonia Research Project. Seville. Spain

**Japan Society for the Promotion of Science. Japan
Department of Life Sciences. Graduate School of Arts and Sciences. The University of
Tokyo. Japan
Department of Psychiatry. Brighton and Sussex Medical School. United Kingdom.
Dynamic Brain Network Group. Graduate School of Frontier Biosciences. Osaka
University. Japan

Keywords: Anosognosia, Focal Dystonia, Sleep Hygiene, Neuronal Plasticity,

Proprioception, Neuropsychological Rehabilitation

ABSTRACT:

This study evaluates the efficiency of a new ecologically valid neurospycological

treatment for musicians with focal dystonia. Intervention is based on motor-
specific restructuring of proprioception and rehabilitation of awareness of
deficits.

The participants included 120 musicians affected by dystonia who represented

a wide range of styles and instruments, including string instruments, guitars,
piano, harpsichord, harp, woodwind, and bagpipes. All of them were selected
randomly from the population of dystonic musicians in Europe, Japan, U.S.A,
Canada and Australia.

The research was conducted from 2000 to 2011. A training protocol was
designed in order to restructure proprioception through exercises and context-
specific retraining. All subjects followed an individualized retraining protocol
that lasted one year, during which improvements in musical performance were
evaluated. Participants’ progress was assessed three times: once at the
beginning, once after six months, and once after one year of training.

It was observed that 100 percent of the subjects presented deficits in

proprioception in certain areas of the body at the beginning of the study. In all
cases patients also presented anosognosia and were unaware of their
neurologic functional deficits, which were proprioceptive.

After the completion of the one-year retraining protocol, a dramatic

improvement was observed in 90 percent of participants (108 subjects out of
120). In 27.5 percent of the cases, a complete recovery was observed.

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INTRODUCTION:

Focal Dystonia in musicians is a task-specific movement disorder which is

characterized by a loss of voluntary motor control in movements developed over
a long period of time.

Until now, it has caused many musicians to terminate their careers due to their
inability to maintain an appropriate technical level. It is under-diagnosed due in
large part to musicians not seeking medical attention because they attribute
symptoms to a lack of practice.

The musician’s focal dystonia pathophysiology has been defined as including

reduced inhibition in different levels of the central nervous system, maladaptive
plasticity, and alterations in sensorimotor processing; however, the root causes
are yet to be determined [1].

A direct comparison of fMRIs of healthy patients and musicians affected by

dystonia shows that dystonic musicians exhibited greater activity in the
premotor ipsilateral area while tapping the fingers of their left hand. When
these patients performed this movement with both hands, they exhibited less
activity in the left cerebellum. Additionally, dystonic musicians exhibited irregular
activation patterns in their associative-motor systems [2].

These findings suggest that the irregular neural activation patterns in dystonic
patients might reflect poor neural functioning due to their dystonia and the
resulting compensatory activity in order to maintain appropriate voluntary
movement.

In a study of note, focal dystonia was produced in the hand of a monkey by

inducing continual repetitive movements [3]. The movements that degraded the
cortical topography in this study were highly repetitive, monotonous and
synchronized in a way similar to those performed by musicians during their daily
practice.

Treatment options for musicians affected by focal dystonia include

pharmacological interventions such as the use of Trihexyphenidyl or Botulinum
Toxin-A as well as retraining programs and ergonomic changes in the
instrument. Other treatment attempts include surgical nerve decompression,
physical therapy, anticholinergic medication, and splint devices [4].

Regarding the different treatments based on reeducation through exercises, the

available systems are:

Rehabilitation through physiotherapy based on rectifying abnormal

postures and reeducation of the impaired motions using stretching,
removable ortheses, and specific exercises targeting the whole body and
not restricted to the affected areas.[5]

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 Other retraining systems propose immobilizing by splints one or more
digits other than the focal dystonic finger. This finger carried out repetitive
exercises in coordination with one or more of the other digits [6].

Other approaches used sensorimotor training based on the principles of

neuroplasticity carried out within the context of a wellness program
(aerobics, postural exercises, stress-free hand use), and supervised,
attended, individualized, repetitive sensorimotor training activities [7].

Applied pedagogical retraining and sensorimotor reorganization by

proprioceptive training using hand muscle vibration [8].

Rehabilitation programs based on the use of slow motion movements [9].

The current rehabilitation systems are not acceptable to professional musicians

due to the fact that they have little ecological validity, are not integrated into a
musical context, employ therapists without enough instrumental/musical training
to solve specific technical issues, use immobilization devices such as splints,
and, most importantly, require restrictive training protocols that preclude
practice during long periods of time, which is not compatible with professional
activity in the majority of cases.

The number of musicians who made complete recoveries or were able to return
to their professional activities employing these systems has been relatively low.

The objective of this study was to evaluate the effect of retraining methods
based on proprioception stimulation, the reduction of spasticity, and the
improvement of musical performance in musicians affected by dystonia. The
hypothesis proposed considered the proprioceptive deficit to be the primary
cause of involuntary movements with these becoming the
adaptation/compensation of the distorted proprioception.

PATIENTS AND METHODS

To complete this study, data from 120 professional musicians from Europe,
Japan, Australia, U.S.A and Canada diagnosed with focal dystonia by a
neurologist. Subjects gave informed consent to the study, which was approved
by the local ethics committee and conforms to the Declaration of Helsinki.
Patients included in this study were affected by focal dystonia during at least
one year prior to the initiation of the study.

The diagnostic procedure included a complete neurological examination

conducted by a neurologist and in 20% of cases, the diagnosis also included an
M.R.I. A movement analysis was also conducted by an expert in musical
ergonomics, during which subjects played their respective instruments. This
analysis included a clinical history which gathered personal and work
information on subjects. These interviews were taped and transcribed.

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Study subjects represented a wide range of styles and instruments, including
classical guitar, flamenco guitar, rock and jazz electrical guitar, electric bass,
piano, harpsichord, violin, viola, violoncello, clarinet, flute, bagpipes, and harp.
Clinical features of the 120 patients are summarized in Table I.

METHOD
Training with an instructor

Subjects underwent five two-hour sessions over the first six months of therapy,
during which they played their repertory for the instructor. The instructor guided
the retraining providing information about fluidity of movement and musical
results of performance. This information acted as a feedback. Afterwards, the
instructor asked the subject to play the musical passages making the necessary
adjustments.

The therapist/instructor required the subject to perform conscious movements

as well as automatic movements which produced fluid movements with
marginal use of will. This was achieved by passively guiding the subject’s
movements.

The subject was taught to perform a complete sequence of movements from

beginning to end. Initially, training was divided into different steps, which were
taught individually and then joined in correct order. Once the first passage was
performed correctly, the next passage was added. Each step was performed
without errors, since the passage was begun again from the beginning
whenever an error was made. The component passages comprising each
kinetic sequence were added progressively until the subject could repeat the
action without errors.

Sessions were recorded by video camera in order to evaluate the evolution in

their playing. Subjects watched these video recordings as a supplementary
feedback, which was a crucial component of the anosognosia rehabilitation.

After each session, subjects were asked to sleep 20 minutes. During the study,
subjects slept an average of at least 8 hours a night.

Training using exercises

Subjects followed the protocol described below 30 minutes each day during 12
months.
The training consisted of two series of exercises: slow-movement exercises and
pressure exercises.

Slow-movement exercises (20 minutes a day)

These movements were performed very slowly to enhance proprioception.

Subjects worked on both hands, the affected and unaffected hand. Movements
speed was approximately 0.5 cm per second.

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The following movements were worked on: flexions, extensions, and circular
movemens of the metacarpophalangeal and interphalengeal joints, wrist and
elbow; forearm subination; and abuctions and aductions of the shoulder.
Circular movements alternated between clockwise and counterclockwise.

Pressure exercises (10 minutes a day)

Subjects were asked to apply different amounts of pressure using a subjective

internal scale.
The scale required at least 10 presses, classified from least to most, with their
proprioception being the only guide to classification. The musicians practiced
this exercise until they were able to perceive 30 perceptive degrees in finger
pressure.

In order to assess the general progress of performance, subjects used the

Tubiana and Chamagne Scale (TCS) [10].

The TCS is based on a six-point scale:

0 Unable to play.
1 Play several notes but stops because of blockage or lack of facility.
2 Plays short sequences without rapidity and with unsteady fingering.
3 Plays easy pieces with restrictions. Rapid sequences stir up motor problems.
4 Nearly normal playing but avoids technically difficult passages for fear of
motor problems.
5 Normal playing. Returns to concert performances.

General progress was evaluated using the TCS three times: at the beginning,
after six months, and at the end of twelve months of training.

To complement the TCS, an assessment was designed to specifically evaluate

improvement in control during performance. This assessment specifically
evaluated two technical variables related to musical performance: the ability to
perform technical movements fluently during performance at different speeds
(peak number of notes per minute—speed) and the ability to maintain fluent
performance (endurance). This assessment was based on the observation of
musical performance and was carried out by an expert in musical movement.
The evaluation was completed directly during subjects’ performance and later
through observations of fast motion video recordings.

Through this analysis of movement and the later corresponding interview, these
could be determined:

1 Location and movement that produced co-contractions

2 Location of the areas of proprioceptive deficit.

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Statistical Analysis

The Friedman test was used followed by the Wilcoxon test after which the
Bonferroni correction was applied to calculate differences between variables
(Tubiana, endurance and speed, and the ratios of speed and endurance). The
Spearman correlative coefficient was calculated by evaluating the relationships
between the TCS and the technical musical variables. The Mann Whitney test
was used to assess gender differences. The α level was fixed at <0.05 in order
to rule out the null hypothesis.

RESULTS

The Mann Whitney test showed significant differences between gender, age,
and experience. Women subjects were significantly older and had greater work
experience than the men. On the other hand, no functional differences existed
between genders as a variable (Tubiana, endurance and speed). Regarding
the functional progress of musicians with dystonia, the distribution on the TCS
scale is shown on Table II, Figure 1.

In accordance with the Friedman test followed by the Wilconxon test plus the
Bonferroni correction, significant differences were found (p<0.001) in endurance
(Table III) in addition to in endurance-ratio (Figure 2) between the pre-
intervention and the first, second, third, and fourth months of intervention as
well as in relation to the post-intervention. Significant differences (p<0.001)
were found in the speed (peak) (Table III) and in the speed (peak)-ratios (Figure
2) between the pre-intervention and the third, fourth, and sixth months as well
as in relation to the post-intervention. The mean and standard deviation of
absolute values for endurance and speed are shown in Table III. Significant
differences were found on the TCS (p<0.001). Significant differences were
found between the TCS values on the pre-intervention and the values at six
months and between these values and the post-intervention.

DISCUSSION

To carry out this study, a neuropsychologic training program was designed with
the intention of restructuring proprioception in order to reduce or inhibit dystonic
movements.

This program training program has ecologic validity, which allows improvements
from the first sessions and is integrated into the subject’s musical performance
routine. The training is applied indiscriminately to various types of dystonia that
affect musicians and is effective in treating players of guitar, piano, woodwinds,
strings, etc., as well as in cases of dystonia prolonged over many years.

This program of intervention allows musicians to return to their careers, as well

as possible (taking into account that it will be a gradual process). This
reincorporation takes place in steps during the first year, and in some cases
during the first six months in order to meet dates imposed by health insurers.

139
On the other hand, a model that would allow complete recoveries and not just
partial improvements in control and movement is being sought.

All study subjects were affected by deficits in proprioception and anosognosia.

The subjects were divided into groups who experienced difficulty in perceiving
finger position (n=5), difficulty in perceiving when flexor muscles are active
(n=3), difficulty in perceiving when extensor muscles are active (n=111).
Subjects perceived their hands as belonging to another person. At the end of
treatment, subjects reported that they had adjusted their perception to normal
levels, perceiving their hand as belonging to them.

The treatment program proposed consisted of stimulating and using the muscle
groups in which the proprioceptive deficit occurred as was referred to as
“unavailable” by patients. Through proprioceptive stimulation in these cases, a
“re-learning of availability” may have been induced. The assumption is that the
lack of coordination is due principally to the loss of the capacity to integrate the
sensorimotor inputs, rather than the capacity to modulate the sensorimotor
output. Therefore, our work is not based on rectifying conflicting positions as
asserted by other specialists [5], but on correcting the perceptual deficit that
produces them. Consequently, analysis of musical performance is necessary in
order to identify all the compensations that are masking the dysfunction.

The treatment program proposed includes adequate sleep hygiene.

A variety of studies describe sleep-dependent learning processes in the motor

system [11]. Two stages of motor-skill learning have been defined: the first
stage during training is characterized by rapid learning, and the second occurs
throughout a night of sleep [12]. We considered it fundamental to assure that
our subjects got adequate sleep to stabilize the improvement produced during
training.

Table II shows that all subjects demonstrated improvements during the first six
months of treatment. The majority (67.5%) improved from a level of 0-1-2-3 on
the TCS to level 4, and 20% improved from a level of 4 to 5 on the TCS. By
comparing these improvements with those achieved between the sixth month
and the end of treatment in the twelfth month, we see that 16 subjects (13.3%)
who were at TCS levels of 2, 3 or 4 improved to levels of 3, 4, or 5.

These results show that the first six months of treatment are critical and that for
the majority of subjects, the plasticity changes that allowed recovery occurred
during this timeframe. Studies related to recovery after brain damage show that
after brain damage occurs, spontaneous recovery of functioning occurs
between 6 months and one year following the injury. A variety of factors affect
recovery, including the type of injury, which areas are affected, the degree of
injury, etc., and the age, gender, and personality of the subject at the time of the
injury [13].

In the case of apraxia, there is agreement that spontaneous recovery tends to

occur during the first 6 months after the onset of apraxia [14,15]. In the case of
our study, spontaneous recovery could not have occurred because all of the

140
subjects had a history of being affected by focal dystonia during at least one
year before treatment was begun, which allows us to eliminate this type of
recovery as related to treatment, which might have affected the validity of study
results.

A striking aspect of our results is that 20% of study subjects were able to
achieve a level of 5 on the TCS after the first 6 months of treatment, taking into
account that previous studies indicated that a treatment period between 1 and 8
years was necessary [1,9,6].

When we look at the improvements of all subjects from the beginning of

treatment to the end, we find that improvement occurred in 100% of musicians
and that 29.9% achieved a TCS level of 5, which implies that they no longer
showed symptoms and returned to performing. For 60.8% of subjects, a TCS
level of 4 was reached, and 12% reached a TCS level of 4.

In order to evaluate the progress of study subjects and collect data, three
fundamental values were analyzed: playing time without involuntary
movements, peak speed (notes per minute), and values achieved on the TCS.
Table III shows that playing time without involuntary movements improved
sharply during the first four months of treatment and then leveled off after the
fifth month of treatment. Speed values achieved a huge increase during the
first month of treatment, leveled off, and again showed great improvement after
the fifth month of treatment. The first large jump in speed and fluidity between
pre-intervention and the first month of treatment is attributed to the reduction or
inhibition of compensatory movements. Between the first and third months of
treatment, fluidity and performance control increased when playing at a medium
speed when it is easier to inhibit dysfunctional movements. Between the third
month and the end of treatment, speed progressively increased because control
had been achieved.

Study subjects improved throughout the 12 months of this study, with the first
months showing the most marked improvements. Treating professional
musicians might have been one factor contributing to these results compared to
those of other studies, due to their cognitive reserve prior to the onset of
dystonia. One hopeful aspect of our results is that great improvements were
achieved in patients exhibiting focal dystonia for periods of 20 to 30 years and
whose dysfunctional movements where very solidified.

Some of the factors that trigger focal dystonia are trauma, nerve entrapment
and overuse injury [16]. In a previous study that evaluated treatment options for
violin and viola players affected by focal dystonia such as nerve
decompression, physical therapy, anticholinergic medication, and the use of
botulinum toxin injections, improvements were gained in 38% of patients
affected by dystonia in the left hand. Patients affected by bow arm dystonia
showed no benefit from the treatment [4]. In our study, we observed that 64.7%
of violin and viola players affected by left-hand dystonia showed great
improvement and were able to return to their professional careers (CTS=5);
50% of violin and viola players with right-hand bow arm dystonia showed great
improvement and were able to return to their professional activities (CTS=5).

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With respect to woodwinds, our treatment proved highly effective by achieving
one level of improvement in 42.8% of subjects (CTS=5) after six months of
treatment and in 50% by the end of one year of treatment. These outcomes are
very positive considering that treatments proposed previously had focused on
pianists and guitarists achieving little results for woodwinds [6, 9, 17].

The positive outcomes achieved in this study could be due in great measure to
including treatment of anosognosia for the first time and to giving restructuring
proprioception priority. Tinazzi, et. al. studied and assessed proprioception of
patients affected by focal dystonia of the hands, and concluded that a change
was present in time perception in muscular activity such as in temporal and
spatial discrimination from cutaneous stimulation [18]. Therefore, treatment with
an instructor is essential, as proposed in this study, since the subjects exhibited
difficulty in evaluating and identifying their own movements. It is usual that
subjects affected by musical focal dystonia rate adequate movements as
inadequate and reject feelings that could produce functional movements.
Patients’ rejections of correct movements have been observed in other studies
[9]. Therefore the feedback from a therapist allows for learning without the error
becoming an indispensable key element in determining the effectiveness of
treatment.

Taking into account previous behavioral approaches to the treatment of focal

dystonia [5,6,9], our treatment approach presents many benefits for musicians
with focal dystonia, requiring less time and effort by the patients. Musicians are
more receptive to our treatment since it is ecologically valid. They go through
the rehabilitation process in a musical context that they are familiar with,
minimizing anxiety.

One of the disadvantages of our treatment approach is that the person who
oversees the process needs to have expertise in musical performance and
processes involved. The trainer needs to be able to offer technically
appropriate solutions, which can be difficult when you are working with top-level
performers. A trust-based relationship must be established in order to assure
that the patient is going to follow the instructor’s guidance.

Psychological conditions such as performance anxiety and perfectionist

tendencies are related to focal dystonia. These conditions make the musician
vulnerable to the disorder, due to the creation of associations between emotions
and motor memories [19]. Perfectionist tendencies might drive musicians to
repetitively, continually and obsessively practice a musical phrase, which is a
possible cause of focal dystonia. On the other hand, compulsive practice is
linked to high levels of anxiety and increases the risk of suffering from this
movement disorder [20, 21, 22]. Additionally, heightened anxiety found in
musicians has been related to patterns of hyperactivity and muscle contraction
during musical performance [22].

A large survey involving 2,212 musicians from 47 orchestras showed that 17%
of the musicians suffered depression and 13% suffered acute anxiety [23]. In
the present study, on the other hand, 35.8% of the dystonic patients were
affected by depression and 29.2 % by anxiety. Both incidence rates were more

142
than twice as high as the rates reported in their study. Although it is impossible
to determine whether these psychological conditions are the cause or
consequence of focal dystonia, we obtained evidence of a significant link
between emotional disturbances and focal dystonia in musicians.

Professional musicians tend to demonstrate high levels of occupational stress,

with public performance being the primary stressor leading to anxiety [25-29].
Musicians frequently must deal with conflicting information provided by
supervisors, other players, and orchestra directors, which produces increased
psychosocial stress levels [22, 27-29]. The subjects of the present study
exhibited a high incidence of occupational stress (95%).

Changing work schedules were a source of occupational stress for musicians

[28, 29]. In the present study, 80.8% of subjects worked shifts (18.3% night
shifts) and 15.8% had only temporary work.

Frequent travel and tours are a source of anxiety and create difficulties in
organizing family life [28,29].

Besides occupational stress, economic challenges were another source of

stress. The coordination of work life and family life is difficult due to erratic work
schedules [28,29]. In the present study, 74.2% of subjects were fathers or
working mothers worried by financial or family problems. Interpersonal stress
affected 82.5% of subjects with 40.8% becoming separated or divorced in the
months preceding the onset of dystonia. Other significant conflictive situations
subjects reported as occurring in the months prior to the onset of dystonia
included death in the family (16.4%) and birth of a child (9.7%).

Like us, other researchers have concluded that it is possible to normalize the
topography of the sensory-motor representation of the fingers after a behavioral
therapy in musicians, substantiating the idea that cortical map alteration can be
induced by practice [6,8,30]. Focal dystonia in musicians seems to be a result
of intense, repetitive practice. Other factors such as ergonomic risks,
psychosocial factors, depression, and anxiety may form part of the causal
network that is the source of this disorder.

While further investigation is needed, the results obtained in this study suggest
that neuropsychological training protocols with ecological validity that include
specific motor retraining, proprioceptive restructuring, awareness training, and
appropriate sleep hygiene should be incorporated in the treatment of musicians
affected by focal dystonia.

143
 REFERENCES

1. Jabusch H.C, Altenmüller E. Focal dystonia in musicians: From

phenomenology to therapy. Advances in cognitive phsychology 2006
volume 2 ; 2-3: 207-220.
2. Kadota H, Nakajima Y, Miyazaki M, Sekiguchi H, Kohno Y, Amako
M, et al. An fMRI study of musicians with focal dystonia during tapping
tasks. J Neurol 2010; 257:1092–1098.
3. Byl N. N., Merzenich M. M., Jenkins W. M. A primate genesis
model of focal dystonia and repetitive strain injury: I. Learning-induced
dedifferentiation of the representation of the hand in the primary
somatosensory cortex in adult monkeys. Neurology 1996;47:508-520.
4. Schuele S, Lederman R. J. Long-term outcome of focal dystonia
in string instrumentalists. Mov. Disord 2004;19: 43-8.
5. Chamagne P. Functional dystonia in musicians: rehabilitation.
Hand Clin 2003; 19: 309-316.
6. Candia V, Elbert T, Altenmüller E, Rau H, Schäfer T, Taub E. A
constraint-induced movement therapy for focal hand dystonia in
musicians. Lancet 1999; 353: 42.
7. Byl NN, Nagarajan S, Mckenzie AL. Effect of sensory
discrimination training on structure and function in patients with focal
hand dystonia: a case series. Arch Phys Med Rehabil 2003.
Oct;84(10):1505-14.
8. Rosenkranz K, Butler K, Williamon A, Cordivari C, Lees AJ,
Rothwell JC. Sensorimotor reorganization by proprioceptive training in
musician's dystonia and writer's cramp. Neurology 2008 Jan
22;70(4):304-15.
9. Sakai N. Slow-down exercise for the treatment of focal hand
dystonia in pianists. Med. Probl. Perform. Art. 2006; 21: 25-28.
10. Tubiana R.Dystonia, Incidence: classification of severity and
results of therapy. In Winspur I, Wyn Parry C.B. The musician’s hand. A
clinical guide. London: Martin Dunitz td 1998:164-167.
11. Walker M.P, Brakefield T, Morgan A, Hobson J.A, and Stickgold
R. Practice with sleep makes perfect: Sleep dependent motor skill
learning. Neuron 2002; 35: 205–211.
12. Walker M.P, Brakefield T, Seidman J, Morgan A, Hobson J.A,
Stickgold R. Sleep and the Time Course of Motor Skill Learning. Learn.
Mem 2003;10:275-284.
13. Rains, G.D. Principios de neuropsicología humana. México:
McGraw_Hill; 2003.

14. Heilman, K.M., Valenstein, E. Clinical Neuropsychology. Nueva

York: Oxford University Press; 2003.
15. Van Heugten, CM. Rehabilitation and management of apraxia
after stroke. Reviews in Clinical Gerontology 2001; 11, 177-184.

144
16. Jabusch H. C., Altenmüller E. Anxiety as an aggravating factor
during onset of focal dystonia in musicians. Med. Probl. Perform. Art.
2004A; 19: 75-81.
17. Candia V, Schaefer T, Taub E, et al: Sensory motor retuning: a
behavioral treatment for focal hand dystonia of pianists and guitarists.
Arch Phys Med Rehabil 2002; 83:1342-1348.

18. Tinazzi, M., Fiorio, M., Stanzani, C. Moretto, G., Smania, N.,
Fiaschi, A., Bhatia, K.P. and Rothwell, J.C. (2006), Temporal
discrimination of two passive movements in writer’s cramp. Movement
Disorders, 21:1131-1135.

19. Mor S, Day H.I, Flett G.L, Hewitt P.L. Perfectionism, control, and
components of performance anxiety in professional artists. Cognitive
Ther. 1995; Res. 19: 207-225.
20. Kenny D. T, Davis P, Oates J. Music performance anxiety and
occupational stress amongst opera chorus artists and their relationship
with state and trait anxiety and perfectionism. J. Anxiety Disord 2004; 18:
757-777.
21. Stoeber J., Eismann. U. Perfectionism in young musicians:
Relations with motivation, effort, achievement, and distress. Pers. Indiv.
Differ 2007; 43: 2182-2192.
22. Yoshie M., Kudo K., Ohtsuki T. Effects of psychological stress on
state anxiety, electromyographic activity, and arpeggio performance in
pianists. Med. Probl. Perform. Art 2008a; 23: 120-132.
23. Fishbein M, Middlestadt S. E, Ottati V, Straus S, Ellis A. Medical
problems among ICSOM musicians: Overview of a national survey. Med.
Probl. Perform. Art.1988; 3: 1-8.
24. Dews C. L. B., Williams M. S. Student musicians' personality
styles, stresses, and coping patterns. Psychol. Music 1989;17: 37-47.
25. Steptoe A. Stress, coping and stage fright in professional
musicians. Psychol. Music 1989;17: 3-11.
26. Steptoe A. Negative emotions in music making: The problem of
performance anxiety. In: Juslin PN, Sloboda JA (eds.) Music and
emotion: Theory and research (Series in affective science). Oxford:
Oxford University Press; 2001: 291-307.
27. Yoshie M, Shigemasu K, Kudo K, Ohtsuki T. (2008b).
Multidimensional anxiety and music performance: An exploratory
application of the Zones of Optimal Functioning model. In: Buchwald P,
Ringeisen T, Eysenck M (eds) Stress and anxiety: Application to life span
development and health promotion. Berlin: Logos Verlag; 2008b: 163-
171.

145
28. Yoshie M, Shigemasu K, Kudo K, Ohtsuki T. Effects of state
anxiety on music performance: Relationship between the Revised
Competitive State Anxiety Inventory-2 subscales and piano performance.
Music. Sci. 2009;13: 55-84.
29. Parasuraman S, Purohit Y. S. Distress and boredom among
orchestra musicians: The two faces of stress. J. Occup. Health Psychol
2000;5: 74-83.
30. Candia V, Wienbruch C, Elbert T, Rockstroh B, Ray W. Effective
behavioral treatment of focal hand dystonia in musicians alters
somatosensory cortical organization. Proc. Natl. Acad. Sci. USA 2003;
100: 7942- 7946.

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 Table I
Years of
n(%) Age Range (ages) Practice

Mean sd Minimum Maximum Mean sd

Sample 120 (100) 36,5 7,9 24 62 26,1 8,4

Male 98 (81,66) 35,4 7,3 24 62 24,7 7,8

Female 22 (18,33) 41,3 8,6 28 62 32,7 8,3

Instrumentalists Guitar Keyboard Strings Woodwinds Harp Bagpipe

n 76 7 19 14 2 2

% 63,3 5,8 15,8 11,6 1,6 1,6

Dystonia
location Flexors Extensors

n 109 11

% 90,8 9,2
Dystonia r
location Der. R. 1 R.3 R. 4 R. 5 L.3 L. 4 L. 5

n 14 34 32 2 23 2 5

% 13 30 29 2 21 2 4
Proprioceptive Finger
deficit Flexors Extensors position

n 3 111 6

% 2 87 5

Clinical history Overuse Tendonitis UTS CTS Fractures Bursitis Tremor

n 24,0 38,0 1,0 8,0 3,0 2,0 8

% 31,6 50,0 0,69 10,5 3,9 3,0 6

Depression Anxiety

n 43,0 35,0

% 48,3 39,3

Technical
changes
Work history WRS Competition Shifts Dual roles Exams

n 114,0 6,0 97,0 88,0 14,0 53,0

% 25,0 1,3 21,3 19,3 3,1 11,6

Interpersonal Family Death in
Personal History stress illness Childbirth Divorce the family

n 99,0 5,0 20,0 49 34,0

% 47,8 2,4 9,7 24 16,4

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 Table II
Tubiana and Chamage Scale (TCS) Number of subjects (n)

TCS Preintervention (n) Month 6 (n) Post-intervention (n)

0 15

1 83

2 20 2

3 2 13 12

4 81 73

5 24 35

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 Table III

Performing Time Speed (peak)

Mean SD min max Mean SD min max

Pre-intervention 6,5*** 3,6 2,0 18,0 142,2 66,4 40,0 500,0

Month-1 21,3*** 12,3 10,0 60,0 462,6 167,8 100,0 800,0

Month-2 37,0*** 16,4 10,0 90,0 458,0 178,4 45,0 800,0

Month-3 45,4*** 17,7 10,0 90,0 451,3 207,1 100,0 800,0

Month-4 59,9*** 17,7 10,0 90,0 590,2*** 151,5 100,0 800,0

Month-5 59,7 18,2 10,0 90,0 684,3*** 103,6 180,0 880,0

Month-6 60,7 17,0 15,0 90,0 696,8*** 95,5 200,0 800,0

Post-intervention 71,4 18,3 30,0 90,0 716,4*** 96,6 200,0 800,0

Time values are expressed in minutes. Speed values are expressed in notes/minutes.
Standard deviation (SD). Minimum (min).Maximum (max)
Significant differences (***, p<0.001 **, p < 0,01 *, p < 0,05)

149
 Figure 1

Tubiana and Chamage Scale (TCS) Number of subjects (%)

Tubiana and Chamage Scale (TCS)

preintervention 6th month postintervention

Mean 21,50 *** 81,17*** 83,83***
sd 11,93 12,24 11,97
min 0 40 60
max 60 100 100

150
 Figure 2

Performing time Speed (Peak)

Mean SD min max Mean SD min max
Pre-intervention 6,5*** 3,6 2,0 18,0 142,2 66,4 40,0 500,0
Month-1 21,3*** 12,3 10,0 60,0 462,6 167,8 100,0 800,0
Month-2 37,0*** 16,4 10,0 90,0 458,0 178,4 45,0 800,0
Month-3 45,4*** 17,7 10,0 90,0 451,3 207,1 100,0 800,0
Month-4 59,9*** 17,7 10,0 90,0 590,2*** 151,5 100,0 800,0
Month-5 59,7 18,2 1,3 90,0 684,3*** 103,6 180,0 880,0
Month-6 60,7 17,0 15,0 90,0 696,8*** 95,5 200,0 800,0
Post-intervention 71,4 18,3 30,0 90,0 716,4*** 96,6 200,0 800,0

Pre-intervention (PREINT). Post-intervention (POSTINT).

Time values are expressed in minutes. Standard deviation (SD). Minimum (min).Maximum (max)
Significant differences (***, p<0.001).

151
 Spearman Correlation

time (minutes) Speed

pre-int 6th month post-int pre-int 6th month post-int
pre-intervention,
TCS -0,084 -0,158 -0,169 ,683** -0,221** -0,158**

6th month, TCS 0,029 0,369** 0,419** -0,225 0,699** 0,688**

post-intervention,
TCS 0,084 0,433** 0,483** -0,223 0,650** 0,804**

ratio-time
month-4 month-5 month-6 post- int
pre-intervention, TCS -0,066 -0,056 -0,045 -0,048

6th month, TCS 0,200* 0,240** 0,209* 0,183*

post-intervention, TCS 0,174 0,210* 0,173 0,148

Speed-time
month-4 month-5 month-6 post- int
pre-intervention, TCS -0,56** -0,63** -0,65** -0,65**

6th month, TCS ,357** ,427** 0,423** 0,438**

post-intervention, TCS ,327** 0,417** 0,404** 0,466**

(***, p<0.001 **, p < 0,01 *, p < 0,05)

152