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Title: Mismatch negativity in health and dystonia and its modulation by non-invasive brain stimulation
Author: Chen, J.
Awarding Body: University College London (University of London)
Current Institution: University College London (University of London)
Date of Award: 2014
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MMN has been characterized as an automatic, pre-attentive, error detection mechanism that may aid switch in attention towards a salient stimulus as well as assisting with contrast enhancement of sensory data. There is interest clinically in the MMN given its abnormality in a number of neurological/neuropsychiatric disorders. This thesis explores tDCS as a practical tool to modulate MMN in health, to assess impaired somatosensory error detection as an explanation of the underlying mechanism of dystonia by utilising somatosensory mismatch negativity (MMN) and to explore the role of the cerebellum in both error detection and dystonia using tDCS. We found that tDCS is a reliable way to alter the generation of MMN perhaps through homeostatic interaction in frontal auditory MMN generator. Subsequently, we found a reliable way to generate somatosensory MMN and then by using tDCS stimulation were able to give more evidence of the relationship between the cerebellum and somatosensory MMN. Finally, we have demonstrated an abnormality in somatosensory MMN in patients with dystonia which is strongly correlated with somatosensory temporal discrimination threshold. Additionally, we showed that there was no modulation of sMMN after cerebellar tDCS in patients with dystonia. This thesis suggests that, in health, tDCS is able to modulate both auditory and somatosensory MMN. These experiments provide evidence for a new way in which MMN might be modulated for experimental purposes and potentially for clinical/therapeutic purposes. The finding of reduced somatosensory MMN (but not auditory MMN) in dystonia suggests a specific deficit in error detection in the somatosensory domain in dystonia. The correlation of somatosensory MMN with somatosensory temporal discrimination threshold, which is robustly abnormal in dystonia, implies a shared mechanism between the two phenomena. We suggest that somatosensory temporal discrimination could be subsumed within somatosensory MMN as an error detection task. The dependence we have demonstrated for somatosensory MMN on the cerebellum in healthy people fits with a role for the cerebellum in the pathophysiology of dystonia. We could not modulate somatosensory MMN in patients with dystonia with tDCS as we could in healthy people, and this provides some additional evidence that cerebellar dysfunction might be relevant both for the abnormal somatosensory MMN in dystonia but also for the clinical manifestation of dystonia itself.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available