Focal dystonia in the hands: a symptom and solution guide

[toggle title=”What’s all the fuss?”]

Focal dystonia is a neurological movement disorder, characterized by involuntary, uncontrollable, unwanted contracture of muscles which surround and usually accompany voluntary, intended contractions. These involuntary contractions characterize the debilitating effects of focal dystonia and act as the prime obstacle faced by those carrying out specific tasks that require a normal, efficient muscular function. The dystonic contractions can occur in any part of the body, but musicians, especially string players and keyboardists, are susceptible to developing dystonia of the hands, in which case the dystonic loss of extremely precise and fine motor control required for playing an instrument makes functional technique, and therefore proper performance on that instrument impossible (Altenmüller, Finger, & Boller, 2015, p. 94-95; Watson, 2009, p.260). Focal dystonia is not a disease that typically affects musicians who are beginners. It takes years to develop, and many of those who suffer from its ill-effects are often experienced musicians who have been practicing and performing at a high level for many decades, most of the time in mid-career (Watson, 2009, p. 262). Unfortunately, because of the slow developing nature of this disease, many musicians who have become affected by it never realized what was happening until the techniques used to make music were either too adversely affected, or actually worsened through further practice in desperate attempt to overcome the symptoms ( Altenmüller, Finger, & Boller, 2015, p. 94).

Focal dystonia concerns the neurophysiological connections between the brain and the contraction of muscles, and the affected areas are concentrated around muscles which have been trained over extended periods to the finest levels of motor control. Thus, the site and particular nature of dystonia for different musicians seems to be contextually correlated with the specific requirements imposed by the technique of each respective instrument. This is especially true when fine motor activities, when repeatedly and intensively practiced, are limited or deprived of flexibility- that is, to be aided by larger muscular movements. Examples of this include the left hand of the violinist, and the right hand of the classical guitarist, as represented in the section below. Focal dystonia is also highly task-specific, and the symptoms involving involuntary contraction, loss of control, and fatigue may not even appear during activities other than the one which the dystonia adversely affects. For instance, a person who experiences dystonic contractions in a certain area of the body while playing an instrument, may not have the same problem while using the same muscle groups to use a tool. Sometimes, this task specificity can also mean that dystonic symptoms don’t appear when playing another instrument, or when doing near entirely similar activities. For example, a brass player with embouchure dystonia may not have problems playing with another instrument or mouthpiece, an affected string player may show no sign of dystonia while playing a different instrument requiring slightly different motions, and keyboardist may not experience any problems while typing (Watson, 2009, p. 261-263).

In summary, focal dystonia develops over long periods of time through the intense practice of very specific, precise motions which engage very specific sets of muscle groups. The onset of symptoms is often gradual, with the notable characteristic of usually being painless. This painlessness, coupled with involuntary contracture is a generalized dystonic symptom. Likewise, the gradual deterioration of a precise, task-specific fine motor skill which was feasible in the past, the sense of fatigue only when applying that same skill, and the lack of improvement or even worsening of the condition with additional practice are all indicators that should hopefully serve as benchmarks to what focal dystonia feels like and how it develops. Writer’s cramp, tremors, embouchure dystonia, and musician’s hand dystonia are all essentially the same condition and operate on the same neurophysiological mechanism which we shall explore further. Controversially, traditional medicine has suggested that there is no known permanent “cure,” though in many cases, musicians have been able to recover by means of retraining the brain-muscle connections related to the dystonia (Solomon, 2007, p. 5). The dichotomy that exists between the conventional medical view of a proper cure for the disease (usually involving drug treatment), and long-term methods which involve retraining of the motor control in question will also be explored and examined.

 

The case in point

Here are two examples of professional musicians who have suffered from focal dystonia:

Dominic Frasca is a guitarist who specializes in contemporary music, using a ten string guitar and, in addition to a classically trained right hand finger picking technique, a vast array of extended techniques in order to perform nearly impossible technical feats. He developed severe dystonia of the right and left hands through the over-practice of these extended techniques, which has been reported as being sometimes up to fourteen hours per day. He was able to recover by taking a complete break from guitar playing, taking up Olympic weight training, and after a two-year period, subsequently retraining his technique (Griesgraber, 2005).

Reinhard Goebel was a baroque violinist who gradually developed dystonia in his left hand after years of practicing for at least eight hours a day, forcing him to completely relearn the violin, playing left-handed (backwards). He was able to play in this backwards configuration for nearly a decade, but switched back despite the dystonia because he felt he couldn’t achieve his former musicality while bowing left-handed. Eventually, he quit playing violin completely and became a conductor. Interestingly, Goebel speaks about being able to relax the muscles in his hand, and thus reducing dystonic symptoms by taking Alzheimer’s medication, but claims that the medicine was negatively affecting his mental health and personality, as well as other aspects of his life (Todes, 2009).

The symptoms observed in these two cases are representative of a majority of dystonic patterns typically characteristic of guitarists and violinists who experience focal dystonia:

The technical approach to the classical guitar, which including the rapid, sequential rippling motion of the right hand fingers and thumb, is most commonly affected by focal dystonia, with the tendency over time for these contractions to become less independent, and therefore less properly coordinated. The individual finger contractions which make up the fluid plucking action of the right hand become smeared together, in addition to involuntary contractions of the thumb. Put simply, more fingers than what is intended “want” to pluck the strings of the guitar at the same time, and the sensibility of space, or timing between subsequent strokes of the fingers becomes uncontrollable, less deliberate, and less coordinated. Severe instances of such a dystonia would pose huge technical problems to the player in regard to what the music calls for, because every individual pluck, be it by the thumb or one of the fingers, should ideally have its own preparation stage, impulse (which coincides with contact with the string), and resolution towards the preparation of the next stroke. A good video example highlighting the recovery process of a patient of musician’s dystonia specialist Dr. Joaquin Fabra is shown below. Additionally, a simplification of a single dystonic contraction can be observed in the images in Figure 1.

 

[Video highlighting the improvements in a guitarist recoving from focal dystonia in the right hand. Pay close attention to the contrast between the before and after footage showing this musician’s progress, especially in regard to the ill effects the disease has on actual musical fluidity and expression in this particular case.]

 

Fig. 1

In classical guitarists with dystonia, the contraction of the right hand fingers and thumb is often affected.

 

 

 

 

 

 

 

 

 

 

 

 

In violin playing, there is a tendency for the fingers of the left hand to remain contracted, due to the position of hand and the way the instrument is held. After repetitive practice and the development of severe dystonia, the tendency is for the fingers to feel sluggish and heavy to lift off the fingerboard, which musically translates to a slowing and unraveling of the preparation stage of the individual muscles, which is necessary to play the next note or figure within a musical passage. Goebel, for example, said in the article linked above that he could not play trills with his dystonia: “I couldn’t play because my fingers were frozen on the fingerboard.” (Todes, 2009).

One might be filled with worry and concern after reading such stories about famous, accomplished musicians who seem to have inexplicably acquired such severe musical difficulties due to focal dystonia. With education, however, one might begin to realize that the most driven and hard-working practitioners of musical instruments are the most prone to dystonia. My own interest in focal dystonia was sparked back in 2012, when I noticed that the fingers of my left hand would become more sluggish, uncoordinated, and more difficult to lift off the fingerboard after repeating the same passage over and over throughout a half-hour practice session, even though I felt my hand wasn’t fatigued physically. It was around this time that Dr. Joaquin Farias (not to be confused with the aforementioned Joaquin Fabra), a world dystonia authority, came to Fredonia State University to do a lecture in which he elaborated upon the dangers of practicing in such a way. The key here is that I realized I was practicing complex passages with a very high number of repetitions and at tempos that were probably too fast to be considered healthy and efficient practice, for many hours a day, every day. It is uncertain and irrelevant whether or not I would have developed long-term focal dystonia if I had continued practicing as I did, but being educated about how dystonia develops has helped me to recognize yet another reason for musicians to constantly evaluate one’s own practice habits and patterns of learning, both mentally and physically. Within the context of focal dystonia, this reasoning boils down to a desire and curiosity- that is, to understand why and how many good musicians can potentially lose the ability to deliberately control the motions required to play their instruments as a result of a disease unrelated to concrete, physical trauma to the affected muscles, and to understand the means of preventing and recovering from such misfortune.[/toggle]

[toggle title=”How does this happen?”]

Neuroplasticity

Neuro – neuron, the nerve cells in our brains and nervous systems / Plastic – changeable, malleable, modifiable (Doidge, 2007, p. xv)

If focal dystonia develops so gradually, yet has such profoundly debilitating effects on musicians, then how does it happen and how is it allowed to happen by those affected by it? Solomon (2007), in his excellent guide geared towards guitarists recovering from focal dystonia, best personalizes the question over why some musicians get focal dystonia (and implicitly why others do not) as a simple begging for the answer to, “why me?” (p. 3). It has also been suggested, however with the notion that further research is needed in this regard, that some people are predisposed to the onset of focal dystonia (Watson, 2009, p. 264-266) with natural, personal inclinations towards perfectionism and anxiety and primarily contributing factors.

Studies in magnetic resonance imaging, such as the one conducted by Mohammadi et al. (2012) have revealed differences between healthy and dystonic subjects (writer’s cramp patients), in regard to the neural activation paths that stabilize the inhibitory response of neurons controlling muscle fibers which surround the muscles normally stimulated (contracted) directly by a voluntary nerve impulse. In the dystonic subjects, the inhibition of surrounding muscle contractions was found to be markedly reduced. This observation helps to partially explain why involuntary contractions usually occur in accompaniment to voluntary contractions in many types of dystonia, as well as the reasons behind why they only manifest within the contexts of extremely specific tasks. The study collected brain imaging from a resting-state in order to ensure that measured data would not be the ones associated to the activation of the brain adaptive mechanisms that would overcome dystonic patterns during movement. The fact that differences were still consistently visible between dystonic and healthy subjects may suggest that either many people who have dystonia are predisposed to it, or that these brain changes are simply positively reinforced by the dystonia, even though they may lie at the origin of the dystonia that develops in any particular person.

The question over whether certain people are naturally more predisposed than others in developing focal dystonia is a controversial one, and in need of further research to answer, but it is ultimately not so important when considering that there exists ever-increasing acceptance of scientific knowledge suggesting that focal dystonia “is primarily related to changes in parts of the brain that control and coordinate movement.” (Watson, 2009, p. 264). In short, musicians need to be aware that the problems they could be experiencing due to focal dystonia originates in the brain, and are not fundamentally related to muscle conditioning, overuse injury, trauma, or general weakness .

The key to understanding how dystonia originates in the brain is, of course, to understand the concept of neuroplasticity, the idea that the brain is highly dynamic and capable of changing on its own throughout a person’s entire life, whether these changes take place throughout a matter of minutes, days, weeks, months, or years. Doidge (2007) refers to neuroplasticity in contrast to the old doctrine of an unchangeable brain as one of the most remarkable discoveries of the twentieth century (p. xv) and takes pride in supporting its role in the many facets of physical, mental, and emotional function in human life:

“The idea that the brain can change its own structure and function through thought and activity is, I believe, the most important alteration in our view of the brain since we first sketched out its basic anatomy and the workings of its basic component, the neuron. … The neuroplastic revolution has implications for, among other things, our understanding of how love, sex, grief, relationships, learning, addictions, culture, technology, and psychotherapies change our brains.” (p. xvi)

It would seem as though the brain’s plastic (flexible, malleable, modifiable) capabilities are intrinsically linked and necessarily involved with learning, and as we are concerned with focal dystonia, the learning and retention of fine-motor tasks. The mechanism of motor learning is responsible for why a non-musician would feel physically awkward and enfeebled when trying to hold and play a musical instrument, whereas for an experienced player of that instrument, the feeling is natural and facile. Ironically, the same neuroplastic processes that contribute to the learning of motor skills, including those used to play an instrument, are also responsible for the development of (or in effect, the learning of) dystonia. In severe cases, the effect is such that because of its ingrainability and plastic nature, the dystonia appears to reduce the abilities of a skilled musician to that of a beginner. Joaquin Farias, in the lecture I attended at SUNY Fredonia, poetically likened the learning process of dystonia to building a house of cards, in which adding to many cards cause the entire thing to topple over, contrary to the view that learning a skill is a merely additive process, like building a stone wall. He also emphasizes the role of memory in the processes of learning and unlearning, the processes which constitute the definition of the brain’s plasticity:

“Every act carried out produces a memory; it is not possible to repeat an act without remembering it. The action generates memories and the memory enables the acts. Focal dystonia resides in the memory pattern prior to the action. Learning and forgetting are two related processes; one is not possible without the other. Learning is necessary in order to forget and, on many occasions, forgetting in order to learn. ” (Farias, 2006, p. 56)

Realistically, an understanding of dystonia is reached by studying series of brain changes that can occur as motor skill is acquired, from the beginning stages when the motion is very deliberate and cognitively involved, to the mature stages of near automatic facility.

 

The properties of long-term potentiation

One important neuroplastic element of motor learning to understand is long-term potentiation (LTP). We know that the contraction of muscles is controlled by electro-chemical impulses and signals sent by the brain down the spinal cord. According to Leonard (1998), long-term potentiation is a physiological mechanism through which the neural pathways in the brain (specifically, the motor cortex, the main center for the conscious control of motion) become more excitable with repeated stimulation (p. 210). Long-term potentiation has two properties that are important to understanding the development of focal dystonia: the consolidation of procedural memory, and synaptic associativity.

It is through procedural memory that we are able to learn new motor skills and form habits (Leonard, 1998, p. 207). A synapse, or connection between nerve cells, that is very active will become more excitable over time, and thus contribute to the enhancement and muscular memory of the task by which it is activated. This would explain why the fine motions of playing a musical instrument, when repeated in sequence over a long period of time (habit), are strengthened and become integrated into that sequence of motion (Leonard, 1998, p. 216). In other words, the exacting manner or gesture of a specific motion becomes embedded into the memory of enacting that procedure or task. This is also likely the reason why the involuntary contractions and loss of control in focal dystonia usually only appear within the very specific contexts of certain activities. A diagram illustrates this process in Figure 2.

 

Fig. 2

 

Fig. 3

 

Associativity, on the other hand, “is a selective LTP property by which a weak stimulus, if it is consistently paired with a strong stimulus, becomes potentiated and thus strengthens its synapse over time.” (Leonard, 1998, p. 216). A diagram illustrates this process in Figure 3. Because the practice of musical instruments requires that extremely fine motions be performed in such rapid sequence, it is very well possible that surrounding contractions become associated with each other which otherwise wouldn’t normally be, accounting for the reduced inhibition of surround muscle contraction observed in the aforementioned writer’s cramp study by Mohammadi et al. This would also account for how surrounding muscle contraction begins to become involuntary, accompanying the voluntary contractions in cases of focal dystonia. According to Farias (2006), the relationship between opposing muscles is also affected:

“In the case of musicians suffering from focal dystonia, a change in the principle of reciprocal innervation (when a muscle contracts, its opposing muscle relaxes), known a co-contraction, is observed. The phenomenon of co-contraction consists in that during the execution of a movement, both the agonist and antagonist muscles contract simultaneously.” (p. 68).

Considering the plastic mechanism of synaptic associativity, it is easy to imaging how the involuntarily co-contraction of opposing muscles becomes ingrained by activities such as the rapid-fire execution of left hand fingering patterns (basically, the sequentially dense retraction and extension of the fingers on and off the strings), resulting in cases similar to Reinhard Goebel’s in which he felt his fingers were frozen to the fingerboard. The same can be said about the involuntary loss of control over retraction and extension in a guitarist’s plucking hand, observable in the video example provided above.

 

The brain areas in question

Another singularly important aspect of the brain to discuss is the plastic deformation of the sensory and motor homunculi (singular: homunculus). The homunculus is basically a representation, or map of the entire human body that exists in the sensory and motor cortices. Specific parts of the body correspond directly to points on this map in these cortices. Nicholls et al. (2001) say “Cells from which the pathway originates are arranged in an orderly matter to form a somatotopic pattern in the primary motor cortex. This can be demonstrated by electrical stimulation of small regions of cortex to activate muscle.” (p. 464). Additionally:

“Functional MRI and trans-cranial magnetic electrical stimulation, as well as other techniques, have been used to show that the map of motor cortex is plastic and can be altered following peripheral lesions. Indeed, alterations of the cortical map can even be demonstrated as a consequence of practice to acquire a novel skill. It has been suggested that synaptic rearrangements within the primary motor cortex constitute one substrate of motor learning.” (p. 465).

Solomon (2007) says that in cases of focal dystonia, the neural representation of the fingers in this map can become “blurred or smeared” (p. 3), such that the brain cannot distinguish individual motions between separate fingers. This statement is supported echoed by Watson (2009), suggesting there is also some sensory component that indicates changes in the sensory and motor cortices:

“We have already seen that the wiring of the brain is not fixed, but can be shaped by experience and that this plasticity can alter the sensory and motor maps within the cortex. Studies of the brain of monkeys and humans with focal dystonia reveal changes in the organization of the area of the primary sensory cortex receiving information from the affected region. In monkeys that develop dystonia after being trained to carry out repetitive hand, there is a degradation in the sensory map of the hand. The near-simultaneous stimulation of adjacent fingers during tasks that require close attention to maintain accuracy appears to be the most significant factor underlying these changes. The receptive fields of the nerve cells that map the fingers onto the cortex can be enlarged by a factor of ten to twenty, resulting in considerable overlap between the representation of adjacent fingers and even between the front and back of the hand. Receptive fields may also grow to cover several finger joints. The end resent is that the brain can no longer tell what part of the finger,or even which finger, is being touched. Investigations of musicians and nonmusicians with focal dystonia of the hand reveal similar maladaptive changes in the cortical mapping. The finger representations of the dystonic hand are much closer together and either overlap or appear in random order.” (p. 264).

Watson (2009) has also recognized research which provides evidence that similar body maps exist in certain brain areas outside of the cortex, such as the basal ganglia system, a mysterious section of the brain which is thought to be involved with maintaining the activity within the cortex and the collective fluidity of individual motions within sequences and gestures. In dystonic situations, this system has been shown to exhibit a disorganized map on the side of the brain controlling the dystonic limb, but not on the other side (p. 265). A study examining similar extracortical changes in writer’s cramp patients suggested that this may have to do with the maladaptation of striatal pathways in order to reach equiperformance in affected tasks (Gallea et al., 2015, p. 180, 189-190). Another study, employing a technique known as voxel-based morphometry to examine the volume of the gray matter around the basal ganglia system, also found that changes in the level of activity in this area could indicate a compensatory phenomenon, in addition to a predisposing factor in the development of focal dystonia (Zeuner et al., 2015).

Here is a short summary of the possible neuroplastic changes and concepts covered so far which could account for the onset and development of dystonic symptoms:

– Changes to the neural inhibition of surrounding muscles in both resting-state (Mohammadi et al., 2012) and while applying dystonically affected motions to a specific task. Watson (2009) suggests that the intense training that musicians undergo effectively forces muscles that aren’t normally active together to be active at the same time, causing the inhibitory processes between surrounding, as well as agonist and antagonist muscles to degenerate into a hyper-sensitive, maladaptive state (p. 265-266).

– Long-term potentiation, or increased excitability of neural pathways by means of repetitive external stimulation, subsequently strengthening the procedural memory of specific tasks, as well as the association, or pairing between different neural connections. (Leonard, 1998, p. 210-217)

– Changes of the sensory-motor maps within the primary motor cortex (Solomon, 2007, p. 3) and putamen/basal ganglia system (Watson, 2009, p. 265)

– Abnormal overactivity of the basal ganglia system (Gallea et al., 2015) suggesting a perpetuation of dystonic contractions through the process of motor-learning.

It is difficult to tell for certain in which of these components dystonia originates, or if it is even important to try to isolate the origins of dystonia as a specific order or long-term chronology of neurophysiological events. The most useful observation stemming from the study of these changes is that the vast majority of dystonic cases (those which don’t involve someone born with a dystonic disease, or those involving a known source of brain trauma) arise through repetitive, over-intense practice of extremely fine motor skills over a course of many years. I am also inclined to emphasize that while these brain changes may appear as separate components, they are interrelated in the sense that many areas of the brain exhibit an adaptive response to different environments, different requirements for successfully executing different motor tasks, and compensatory activity due to changes in corresponding brain areas (Doidge, 2007, p. xv). [/toggle]

[toggle title=”What to do”]

For a musician who has identified his/her problems as dystonic, and trying to recover, a neurologist coming from a conventional medical point of view would most likely recommend treatments which would best serve the interests of the medical establishment. In contrast, treatments which are underpinned by the research principles of neurorehabilitation (Altenmüller, Finger, & Boller 2015, p. 237-248) and sensorimotor retraining represent the cutting edge towards a cure for dystonia are still relatively recent, relative to traditional views that existed before what Doidge (2007) describes as the “neuroplastic revolution.” (p. xiiv-xvi). It would appear that in numerous cases, doctors unfamiliar with treating a disorder which is essentially rooted in a nueroplastic problem, would typically recommend either drug treatments or surgery (Farias, 2006, p. 26; Solomon, 2007, p. 2-4; Todes, 2009).

Under the premise of research which shows that dystonia originates from the plasticity of the brain, considering these options as a true “cure” for the disease is logically incorrect because they would, at best, alleviate some of the symptoms, but not fix the source of the problem. Surgery on a dystonically functioning hand or limb is probably a waste as well as a huge risk, because any physical alteration or manipulation implies diagnosis of a muscular or nerve problem at that particular site, and not the brain. Besides the qualitative differences between a brain problem and a local problem at the site of the symptoms, such a diagnosis also ignores the discrepancy between the age difference that exists between the onset of typical overuse injuries (younger and more active) and the onset of dystonia (older and more experienced) (Watson, 2009, p. 264).

In addition to Reinhard Goebel’s remarks about trying and discontinuing the use of Alzheimer’s medication to relax his muscles, Jason Solomon has commented on the common treatment of injecting diluted botulinum toxin (commercially branded as Botox) into the dystonic muscles. This treatment essentially blocks the signal sent by the brain at the sight of the injected muscle, which stops it from contracting involuntarily. Solomon remarks that Botox injections helped his dystonia while playing guitar, but the injections were painful and expensive, in addition to not addressing the root of the problem. He explains that in actuality, his brain was probably still sending all the neural signals responsible for the dystonic contractions, though their effect on the muscles was weakened and alleviated by the drug (Solomon, 2007, p. 4-5). The study by Mohammadi et al. (2012) has also observed that injections of the botulinum toxin produces no changes in brain networks during a resting state, implying that the drug has no effect on underlying dysfunction of the motor cortex (p. 845).

The real cure to focal dystonia seems to be retraining the sensorimotor portions of the brain, principally utilizing, to one’s own advantage, the neuroplastic processes which gave rise to the dystonia in the first place. It is important to understand, however, that recovering from dystonia is a very daunting and seemingly insurmountable challenge for many musicians, and because the disease takes so many years to mature, it may also take years to recover from it through a wisely guided rewiring of the brain. It should also be noted that this retraining or rewiring may be a multi-stage process which requires an initial period of rest, or in other words, a complete break from the task that is affected by dystonia. The reason behind this is so that the neural pathways and associations that cause task-specific dystonia will have time to whither away and weaken in the absence of that task. If you are a musician severely affected by dystonia, this could mean taking a break from playing your instrument for a length of time spanning anywhere from a few months to a few years, and then slowly reintroducing regular practice, but perhaps with less frequency, less intensity, and more mindfulness and awareness than before. The worst case is when a musician, unaware of the nature of his/her dystonia, becomes alarmed at the problem, and increases the intensity of practice with the blind hope that this will make the problem go away.

I would encourage everyone to read Jason Solomon’s excellent guide, as he has produced some very useful advice for any musician looking to understand the nature of dystonic disorders and recover. He also includes applied technique-specific advice for guitarists, based on what worked for him throughout the course of his own recovery, which in itself was guided by the research of Dr. Nancy Byl. Although Solmon’s advice, which is condensed into thirteen points, is geared towards guitarists, the material is useful in promoting an understanding and awareness of how changing one’s habits of practice can have a profoundly positive effect on the recovery process.

One of Solomon’s most prominent recovery methods involves scratching and stimulating the individual fingertips of the dystonic hand with a toothpick at regular intervals throughout the day (Solomon, 2007, p. 5-6). This stimulation, called “passive touch,” is combined with “active touch,” in which the fingers of the dystonic hand are used to reach out and individually stroke and touch everyday objects or textured surfaces. Special importance is placed on very careful concentration and attention to the sensations felt by each individual finger, in effort to remind the brain that they are separate. Solomon (2007) also makes a wonderful remark about changing one’s thoughts towards instrumental playing itself:

“Many of these suggestions require you to reconceptualize how you approach producing sound on the instrument. For example, I no longer think to myself: “I will now practice the guitar.” Instead, I think: “I will now touch my guitar.” I consider practicing to be a form of sensorimotor training. I firmly believe that success in playing any instrument begins with a proper physiological understanding of exactly how it is that you draw sound from the instrument.” (p. 7).

I would like to draw a parallel to the success Mr. Solomon has found in the sensory aspect of his retraining method, with a series of finger motion and isometric exercises advocated by renowned the viola da gamba player, Prof. Catharina Meints. Meints, who has practiced these exercises for years, gives credit to these exercises for increasing instrumental facility while away from the instrument, developing and maintaining finger independency, and contributing to the general longevity of technique over the course of many years of dedicated practice. Prof. Meints demonstrates and explains the use of these exercises in an instructional video titled “Finger Exercises Away from Your Instrument” which can be found on the Viola da Gamba Society of America’s online teaching videos page.

Another practical tip offered by Solomon is to use larger muscles to aid and increase the efficiency of the extreme fine-motor flexion of the finger muscles of both hands (Solomon, 2007, p. 12-13). He summarizes his advice nicely in stating that one should feel all motions originating in the palms and forearms. David Leisner explains this concept further in the video below:

In terms of my own recent experience in trying to increase the integration of my left arm to assist the fingers, I can attest to the helpfulness of the larger muscle groups extending sequentially from my forearm, upper arm, and back. When employed with the appropriate motion, the larger areas of the body serve to relax and reduce unnecessary tension, as well as the manic focus that consumes the activity of the fingers during passages that require repetitive or complex musical acrobatics. In a lesson I took with renowned viola da gamba player Vittorio Ghielmi, he described the basic carriage of the left hand fingers as a “comb” that rocks back and forth as a fluid extension of the arm. In the animations in Figure 4, I’ve tried to demonstrate an example of a slight modification in left hand technique which engages larger motions and muscles in the arm and back, assisting the technical requirements of the fingers themselves. It should be noted that in addition to alleviating some of the stresses imposed upon the small tendons and muscles in the fingers and wrist (thus avoiding overuse injury), one also alleviates intense stress on the nervous system and suppresses the development of focal dystonia by modifying a technical habit in this way.

Fig.4

 

 

 

 

 

 

 

The same principle is easily applied to the left or right arm of a plucked instrument, as well as many other examples. I would be interested, however, in hearing suggestions as to how a violinist could more easily employ a more integrated and fluid left arm in order to assist the fingers in such a fashion, since the violin is normally held in an ergonomically less-favorable way than most string instruments.

I would also highly recommend that anyone seeking further knowledge on the nature of dystonic disorders to read some of the references cited in this blog. The book written by Doidge (2007) is an excellent, inspiring introduction to neuroplasticity, that shows interested readers many ways in which the highly dynamic human brain can change, to either ill or healing effect. Prof. Isabelle Cossette, the teacher of the McGill University seminar MUGT613 – Understanding the Performing Body, and organizer of this blog, has also spoken highly of the writings and research of Dr. Eckart Altenmüller, one of the world’s foremost experts on music-related brain plasticity, including movement disorders affecting musicians. Upon Prof. Cossette’s recommendation, I would advise those looking for a comprehensive overview of musicians’ dystonia, as well as music-related neuroplastic therapy, to read chapters 5 and 12 from the reference listed below (Altenmüller, Finger, & Boller, 2015).[/toggle]

[toggle title=”Concluding remark”]

It is utterly disturbing to hear claims that focal dystonia is an incurable disease, especially when such claims come from the mouth of such an esteemed artist and figure as Reinhard Goebel: “Nobody I know has recovered from focal dystonia. It is the most dangerous thing you can have. Some say, ‘I’m fully recovered,’ but it stays, in my experience.” (Todes, 2009). Through association with him, as well as other teachers and role models in the field of early music, a young baroque violinist suffering from focal dystonia, might therefore be led to believe that his/her condition is devastating and incurable. The possibility of such a situation is merely hypothetical, but irrational in principle, as numerous musicians have have reported to have recovered through neurorehabilitative means (a demographic which seems to have been irrationally ignored by Goebel, and probably by his doctors too), whereas Goebel has not, to my knowledge, spoke of any further attempt to overcome his dystonia after realizing the shortcomings of his medical treatment.

Comprehensive education about the neurophysiological reasons behind focal dystonia can be a confusing and often discouraging prospect on the surface; there seems to be a limitless number of brain structures, pathways, and plastic changes to study in order to find the answers and keys to a solution. The clearest extraction, from varied study on musician’s dystonia as well as other dystonias, may very well be that there is no one magic bullet that provides an instant cure to the problems brought about by this mysterious disease. Just as learning to perform on a musical instrument at the highest level is, one must realize that the road to recovering from focal dystonia is long and arduous, with a willingness to accept the supposition that dystonia is actually in most cases a learned illness due to the brain’s incredible plasticity. One might wisely say that the root of dystonia is impatience, and if impatience is allowed to dominate behaviors and mindsets during any learning or recovery process, then the only result can be failure. Often, it isn’t the aptitude, but rather the attitude that can make the biggest difference in enhancing any activity or achieving any goal.

I hope I have provided a useful and thorough introduction to this fascinating subject. -Ryan Gallagher

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[toggle title=”References”]

 

Altenmüller, E., Finger, S., & Boller, F. (2015). Music, neurology, and neuroscience: Evolution, the musical brain,

medical conditions, and therapies. Amsterdam, Netherlands : Elsevier.

 

Doidge, N. (2007). The brain that changes itself. New York, NY: Viking.

 

Farias, J. (2006). Rebellion of the body: Understanding musician’s focal dystonia. Seville, Spain: Galene Editions.

 

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