The neuroscience
Despite being widely recognized in the music community, the neuroscience of musicians' dystonia remains only partially understood. However, recent advancements in neuroscience have begun to shed light on the underlying mechanisms of this condition.
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Current research suggests that musicians' dystonia is a result of abnormal neural plasticity, which occurs when the brain reorganizes itself in response to repeated movements and motor activities. The basal ganglia, a group of nuclei in the brain that are involved in motor control, are thought to play a critical role in the development of musicians' dystonia. Abnormalities in the connections between the basal ganglia and other brain regions including the cerebellum and stratum have been identified as other potential root causes of the motor symptoms associated with this condition.
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Many highly trained activities including playing a musical instrument are performed semi-automatically, requiring little intentional effort. This implies a subconscious mechanism of activating a set of muscles specific to a particular automatic task (a motor subroutine)(Kaji et al., 2018). The motor subroutine in musicians’ focal dystonia is corrupted or disorganized at some level, with sensory inputs received from the muscles being processed and “mismatched” with the subsequent motor output. This in turn produces the tell-tale symptoms experienced by dystonic musicians.
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The primary somatosensory cortex of the brain is an area of interest for those suffering from the condition. Figure.1 shows the location of the somatosensory cortex together with three colored representations of the five fingers of the hand. The first representation (normal) shows a non-dystonic image of the fingers, each with a clear color boundary between them, where movements for each of the fingers remain distinctive. In the second representation (dystonic) there is a blurring or overlapping of the boundaries between fingers D2,3 and 4 where neuronal signaling between fingers has become mixed up or confused.
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A “disorganization” of sensory input and motor output occurs when the somatosensory cortex is in this state. Representations of individual finger movements overlap or encroach on one another and maladaptive plasticity results. Essentially, the brain accepts the blurred, dystonic state as being the norm. As the sufferer subconsciously executes the subroutine of movements for a particular sequence, the faulty, blurred circuitry is activated, and dystonic movements emerge.
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Figure.1
(Nudo, 2003)
(Figure. 1 shows finger representations D1-D5 on the surface of the somatosensory cortex showing D4 enlarged and overlapping into D3 and D5 in the dystonic state (center). (Click on the image to view the relevant .pdf)).
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As mentioned at the start of this section, focal dystonia is a “network disorder” involving several areas of the brain. The somatosensory cortex plays a significant part in the manifestation of focal dystonia, but it is not the full story. Discovering the complete etiology of focal dystonia essentially involves understanding what comes first, the chicken or the egg. Research suggests that the blurring of the sensorimotor cortex may occur in response to abnormalities at the sub-cortical level of the basal ganglia and cerebellum, re-enforcing the “network” theory. It has been surmised that the cortical events described above, occur “downstream” from the sub-cortical processes and are compensatory in nature (Kaji et al., 2018).
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The Role of the Cerebellum
A cerebellar origin of dystonia appears to be the most likely at the present time. Aberrant inputs conflict with output neuroplasticity causing the sensorimotor symptoms of focal dystonia. Provoking a tonic vibration response (TVR) in dystonic muscles through stimulation produces dystonic contractions. Blocking muscle spindle afferents by using botulinum toxin injections, temporarily stop these inputs. As these muscle spindle afferents are only perceived at the sub-conscious level and can remain present even in people with cortical lesions (including stroke patients), it can be surmised that the mechanism and pathway for this phenomenon are sub-cortical, pointing toward a cerebellar origin.
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The sub-cortical cascade process involves the interaction between the basal ganglia and cerebellum. The dentate nucleus within the cerebellum, and the striatum within the basal ganglia, are connected by intralaminar thalamic nuclei. A recent study by Chung (2019) has shown that "an aberrant cerebellar output from the lesion of the dentate nucleus may modulate the activity of the basal ganglia to cause dystonia".
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A further consideration for the cerebellar origin of dystonia may be in the processing of emotions and emotional experiences. Although more clearly thought of as being responsible for movement control, the functional role of the cerebellum in movement regulation is also of interest. Research has shown that a single exposure to acute stress may affect information processing.
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The Role of the Striatum
​The striatum, which is divided into two main sub-regions called the caudate nucleus and the putamen receives inputs from the cortex and thalamus and sends outputs to other regions of the basal ganglia and the thalamus.
The striatum acts as a relay station, processing incoming information and transmitting signals to other parts of the basal ganglia, such as the internal segment of the globus pallidus and the substantia nigra. These signals help to regulate the activity of the output nuclei of the basal ganglia, which in turn modulate the activity of the thalamus and the cortex, leading to the initiation and execution of movement.
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In this way, the striatum plays a crucial role in the regulation of the basal ganglia and helps to coordinate the complex processes involved in the control of voluntary movement and other functions. Any disruptions in the activity or structure of the striatum, such as those seen in focal dystonia in musicians, can have significant impacts on the function of the basal ganglia and the control of movement.
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Conclusion
In conclusion, the neurological underpinnings of musicians' dystonia are multifaceted and intricate. Our current understanding points toward aberrant neural plasticity and abnormalities in the neural networks within the basal ganglia and cerebellum as key contributing factors. The role of the primary somatosensory cortex and its interactions with other brain regions further complicate the manifestations of this disorder. The concepts of blurred representations in the somatosensory cortex, disorganization of sensory inputs, and the frustrated execution of motor subroutines suggest a complex interplay between cognition, sensory perception, and motor control. The evidence pointing towards a cerebellar origin of dystonia offers a potential clue concerning the inception of this condition - shedding light on the enigma that is neuron processing of emotions and stress to motor outputs. Despite these advancements, the neuroscience of musicians' dystonia is still a developing field. Further research is needed to fully understand the complex cascading sub-cortical processes, and how they contribute to the development and propagation of dystonic symptoms. Continued exploration of the relationships between different brain regions, the sub-conscious processing of sensory inputs, and the potential influence of emotional experiences warrant rigorous investigation. Ultimately, a more thorough understanding of these processes could pave the way for more effective treatments, offering hope to those suffering from this debilitating condition.
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