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 …