Date of Award

2006

Degree Type

Thesis

Degree Name

Bachelor of Science Honours

Faculty

Faculty of Computing, Health and Science

First Advisor

Dr Dylan Edwards

Abstract

AIMS: Transcranial Magnetic Stimulation (TMS) has been recently demonstrated to have potential therapeutic benefits by promoting cortical plasticity through modulation of corticospinal excitability. We have previously shown in healthy adult subjects that paired-pulse TMS (1.5ms ISI) applied over Ml at 0.2Hz for 15min (known as iTMS), can raise corticospinal excitability for a period (~10min) that outlasts the intervention. Since interhemispheric changes in corticomotor excitability are considered to have fundamental importance in the control of voluntary movement, and recovery of motor function following unilateral damage, importance is placed on understanding the mechanisms involved. The aims of the current study were therefore to investigate if the raised corticomotor excitability following iTMS intervention over Ml will be paralleled by an increase in contralateral M1, and whether this may be brought about by a reduced transcallosal inhibition. Method; STUDY ONE: In eleven healthy adult volunteers (7 Male, 18-45yrs), the mean amplitude of the MEP was recorded (single pulse, 110% resting motor threshold, optimal site for first dorsal interosseous muscle on each hemisphere) pre and post 15 min of iTMS (left hemisphere, 100% of resting motor threshold). STUDY TWO: In six healthy adult volunteers (2 Male, 19-36yrs), Transcallosal Inhibition was investigated pre and post 15 minute iTMS, by delivering a conditioning pulse over the comparable site on the contralateral cortex at 110% resting motor threshold (RMT) between 9-13ms lSI. The effect of the conditioning stimulus on the test stimulus MEP amplitude was compared pre and post iTMS and was expressed as an index of lnterhemispheric Inhibition. Results: iTMS applied over the left M1 (Primary motor cortex) during study one, produced a post intervention increase in MEP amplitude for RFDI in the first post collection of 227%±34% SEM (p<0.000) of baseline, with a corresponding increase of 123.8% ±12% (p<0.001) in the contralateral hemisphere. Similarly during study two, MEP amplitude for first collection following 15 minutes iTMS produced increases of 197%±26% (p<0.001) and 125%±14% SEM (p<0.05) for the intervened and non intervened hemispheres respectively. IHI following 15 minutes iTMS was significantly reduced by 20% (pre intervention: 57±12%, post intervention: 77±14%, p<0.05). Conclusion: These studies have reliably produced raised corticomotor excitability following iTMS, and have demonstrated that this effect is not confined to the stimulated area. The findings support that the effects of repetitive TMS can be distributed across motor networks, with raised excitability being partially transferred to the contralateral cortex. Whilst facilitatory interhemispheric pathways may be involved in this phenomenon, it can be confirmed that the observation of bilateral increase in corticomotor excitability ' does involve transcallosal inhibitory pathways, and that the contralateral cortex is disinhibited. Such findings may be of importance for therapeutic TMS application where the aim is to enhance corticospinal output, and due to the nature of lesion, stimulation over the lesioned cortex is not possible or contraindicated.

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