6.1 Conclusions
As mentioned in the Introduction, the aims of the current thesis were to (1) show the effect of altered sensory feedbacks in MD in a more comprehensive way, and to (2) help to elucidate the differences in long-range neural orchestration between the healthy pianists and MD patients under different types of sensory feedback during piano playing.
The hypothesis for (1) was that altered auditory feedback and altered somatosensory feedback may act as successful sensory tricks in MD. But the results from the behavioural study in this thesis demonstrated that the altered sensory feedback did not bring any beneficial effect to the fine motor control of our patients on a group analysis level. Both groups of participants had deteriorated fine motor control under the delayed auditory feedback. Neither the AAF (either MUTE or DELAY) nor the altered tactile feedback (GLOVE) acted as a successful sensory trick and improved the fine motor control of pianists suffering from MD significantly.
Therefore the results were against our hypothesis. It should be mentioned, however, that one individual suffering from focal dystonia benefitted from the MUTE condition and 3 out of 12 patients had significantly improved motor control under GLOVE condition. This points toward the heterogeneity in neural and /or behavioural organisation of musician’s dystonia.
After concluding for the first aim, an EEG study was carried out for the second aim, with the hypotheses that the degree of inter-regional phase synchronisation between the cortical regions involved in the sensorimotor network is altered in MD patients, and the patterns of such alteration are dependent on the sensory feedback. As a result, the comparison of EEG
data revealed that in MD patients, there were higher degrees of inter-regional phase synchronisation between the frontal and parietal regions and between the temporal and central regions in conditions that are relevant to the long-trained auditory-motor coupling (normal auditory feedback and complete deprivation of auditory feedback). Importantly, such abnormalities are decreased in conditions with delayed auditory feedback and altered tactile feedback. These findings support the hypothesis that the impaired sensorimotor integration of MD patients is speci fic to the type of overtrained task that the patients were trained for and can be modi fied with altered sensory feedback.
The findings of these studies add to the previous research on the sensory deficits in MD, or in focal dystonia in general. In the research field of focal dystonia, there is currently a lack of neuroimaging studies related to the sensory deficits and task-specificity of the disorder.
Furthermore, the only neuroimaging study related to the sensor trick phenomenon was the PET study published by Naumann and his colleagues (2000). The EEG study in the present thesis enabled the precise monitor over the dynamics of neural network under various altered auditory feedback conditions without the noise in fMRI studies, offered novel evidences for the sensory feedback-dependent neural de-orchestration in MD.
To conclude, neither did the altered auditory feedback nor did the altered tactile feedback employed in the present thesis improve MD patients’ symptoms. This project did not find a successful sensory trick in MD. However, the evidence of feedback-depend long-range phase synchronisation contributes to the basic research in the pathophysiology of MD, and it leads to more studies in the sensorimotor integration and task-specificity of MD in near future.
6.2 Outlook
Behavioural Study. The findings imply that it might be necessary to employ more diverse motor tasks/motor patterns for experimental material and more forms of altered auditory feedback for the future behavioural studies. Although the Scale Analysis paradigm itself has been proved to be a robust and objective measurement for quantifying dystonic symptoms and it has been suggested that with MD the symptoms are more easily triggered by scale/scale-like playing (see Rosenkranzet al. 2009 for using C major scale-like sequence as their experimental material), the high heterogeneity and task-specificity of MD symptoms makes it difficult to conclude the effect of a single motor pattern has a similar effect on all the patients. It is similar in the case of the temporal asynchrony and types of delay for the altered auditory feedback. More lengths of duration and more types of delayed auditory feedback should be involved in future experiments (ex. random delay, adaptive delay), and even faster
tempi of playing would be preferred for MD symptoms are usually triggered by fast tempi.
Furthermore, more diverse paradigms than synchronisation or synchronisation-continuation paradigms may also be considered in future experiments.
EEG phase synchronisation Study.The analysis of the altered neural network in FHD is gaining its importance since the abnormal reorganisation of functional cortical networks in FHD has been shown (ex. Jinet al. 2011; Mooreet al. 2012). Studying how different parts of the neural system are abnormally orchestrated together in terms of their temporal co-ordination can help us better understand the rich phenomenology of dystonia, and probably a dynamic, systematic view of the disorder is more important than studying a single isolated deficit in the whole system in the case of dystonia. The next step of analyses should be focused solely on the patterns of local and long-range cortical dynamics of the healthy pianists performing under different sensory feedback, so the further comparison between the healthy controls and the patients can lead to more fruitful results.
Dystonia is a complex movement disorder and it can only be understood with a broader view of how different parts of the neural system work together. MD, as a form of dystonia, is one of the best examples of how complex the disorder is and it further provides us with invaluable insights into the neuroscience of musical excellence in healthy expert musicians. Although the mechanisms of sensory trick remain elusive, I hope the studies in this thesis can contribute a tiny piece to the puzzle of the pathophysiology of dystonia.
7
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