Abstract
Abnormal oscillatory activity in the subthalamic nucleus (STN) may be relevant for motor symptoms in Parkinson's disease (PD). Apart from deep brain stimulation, transcranial magnetic stimulation (TMS) may be suitable for altering these oscillations. We speculated that TMS to different cortical areas (primary motor cortex, M1, and dorsal premotor cortex, PMd) may activate neuronal subpopulations within the STN via corticofugal neurons projecting directly to the nucleus. We hypothesized that PD symptoms can be ameliorated by a lasting decoupling of STN neurons by associative dual-site repetitive TMS (rTMS). Associative dual-site rTMS (1 Hz) directed to PMd and M1 (“ADS-rTMS”) was employed in 20 PD patients treated in a blinded, placebo-controlled cross-over design. Results: No adverse events were noted. We found no significant improvement in clinical outcome parameters (videography of MDS-UPDRS-III, finger tapping, spectral tremor power). Variation of the premotor stimulation site did not induce beneficial effects either. A single session of ADS-rTMS was tolerated well, but did not produce a clinically meaningful benefit on Parkinsonian motor symptoms. Successful treatment using TMS targeting subcortical nuclei may require an intervention over several days or more detailed physiological information about the individual brain state and stimulation-induced subcortical effects.
Highlights
Bradykinesia and tremor impair quality of life in patients suffering from Parkinson’s disease (PD), [1]
The off-motor state has been linked to abnormal beta-oscillatory neuronal activity in a network comprising basal ganglia and motor cortical regions, with the strength of these oscillations being correlated to motor impairment [3,4,5,6,7] and dopamine replacement therapy [8,9,10,11,12]
At the start of the transcranial magnetic stimulation (TMS) intervention we identified the hot spot for stimulation of the abductor pollicis brevis muscle (APB) employing low frequency (
Summary
Bradykinesia and tremor impair quality of life in patients suffering from Parkinson’s disease (PD), [1]. Some motor symptoms can successfully be ameliorated by deep brain stimulation (DBS) of the subthalamic nucleus [2], many patients are reluctant to undergo invasive procedures or are not eligible. In those patients, add-on therapies based on noninvasive brain stimulation techniques may be a promising alternative. The off-motor state has been linked to abnormal beta-oscillatory neuronal activity in a network comprising basal ganglia and motor cortical regions, with the strength of these oscillations being correlated to motor impairment [3,4,5,6,7] and dopamine replacement therapy [8,9,10,11,12]. Tass [13] and Popovych and Tass [14] have hypothesized that
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