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.
AimsTo quantify extra-valvular cardiac damage associated with severe aortic valve stenosis (AS), a novel staging model was proposed. This study aimed to validate this model in patients undergoing transcatheter aortic valve replacement (TAVR) as well as to assess its prognostic impact.Methods and resultsBased on echocardiographic findings, the following stages were applied: isolated AS (stage 0), left ventricular (LV) damage (stage 1), left atrial or mitral valve damage (stage 2), pulmonary hypertension or tricuspid regurgitation (stage 3), or right ventricular dysfunction (stage 4). The primary endpoint was 2-year all-cause mortality. The distribution across stages was 0.8% at stage 0, 7.5% at stage 1, 63.3% at stage 2, 18.3% at stage 3, and 10.1% at stage 4. All-cause mortality increased at all stages 1–4 (12.1%, 18.2%, 26.6%, and 28.2%; p = 0.023). In the multivariate model, the stage of cardiac damage, age, New York Heart Association (NYHA) class III/IV, peripheral artery disease, and previous pacemaker were independent predictors of the primary endpoint.ConclusionsPatients treated for severe AS show a high prevalence of extra-valvular cardiac damage. An increase in stage is associated with higher 2-year all-cause mortality. The application of this staging model may add value to current treatment algorithms.
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