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Hyperkinetic disorders such as chorea, ballism and dystonia can be observed after lesions (usually small strokes) affecting the thalamus, basal ganglia and related circuits.1 Neural circuit models of basal ganglia circuitry suggest that these result from disinhibition of thalamo-cortical projections because of a reduction in inhibitory output from the internal pallidal segment. Increased thalamo-cortical drive may lead to an increase in the excitability of excitatory and inhibitory circuits of the frontal areas of the cortex,2,3 including M1, that may contribute to hyperkinesia.
Circuits of the human motor cortex can be activated non-invasively with transcranial magnetic stimulation (TMS) of the brain,4 and because the excitability of neural circuits in the cerebral cortex is not static, repetitive TMS (rTMS) can produce changes in neurotransmission that outlast the period of stimulation.5–7
rTMS has been proposed as a therapeutic tool in several psychiatric and neurological disorders, and a recent review suggested that the best effects of therapeutic rTMS are seen when protocols that depress network excitability are used to treat disorders characterised by cortical hyperexcitability.8
A recent study showed that excitability of the motor cortex can be reduced for 30–60 min after application of a novel paradigm of rTMS termed continuous θ burst stimulation (cTBS).9,10 This protocol leads to a decrease in the excitability of excitatory and inhibitory cortical circuits that is long lasting. Thus, after TBS, there is a decrease in the amplitude of the corticospinal volleys evoked by transcranial stimulation,10 and the size of the resulting motor-evoked potentials.9 In addition, a reduction in excitability of intracortical inhibitory circuits was shown by a decrease in short latency intracortical inhibition, a putative marker of γ aminobutyric acid transaminase-A activity.9
The aim of this preliminary study was to investigate whether …