Re-emergent Tremor in Parkinson's Disease: The Role of the Motor Cortex.

BACKGROUND: Parkinson's disease patients may show a tremor that appears after a variable delay while the arms are kept outstretched (re-emergent tremor). The objectives of this study were to investigate re-emergent tremor pathophysiology by studying the role of the primary motor cortex in this tremor and making a comparison with rest tremor. METHODS: We enrolled 10 Parkinson's disease patients with both re-emergent and rest tremor. Tremor was assessed by spectral analysis, corticomuscular coherence and tremor-resetting produced by transcranial magnetic stimulation over the primary motor cortex. We also recorded transcranial magnetic stimulation-evoked potentials generated by motor cortex stimulation during rest tremor, tremor suppression during wrist extension, and re-emergent tremor. Spectral analysis, corticomuscular coherence, and tremor resetting were compared between re-emergent tremor and rest tremor. RESULTS: Re-emergent tremor showed significant corticomuscular coherence, causal relation between motor cortex activity and tremor muscle and tremor resetting. The P60 component of transcranial magnetic stimulation-evoked potentials reduced in amplitude during tremor suppression, recovered before re-emergent tremor, was facilitated at re-emergent tremor onset, and returned to values similar to those of rest tremor during re-emergent tremor. Compared with rest tremor, re-emergent tremor showed similar corticomuscular coherence and tremor resetting, but slightly higher frequency. CONCLUSIONS: Re-emergent tremor is causally related with the activity of the primary motor cortex, which is likely a convergence node in the network that generates re-emergent tremor. Re-emergent tremor and rest tremor share common pathophysiological mechanisms in which the motor cortex plays a crucial role. © 2020 International Parkinson and Movement Disorder Society.

Somatosensory temporal discrimination threshold in Parkinson's disease parallels disease severity and duration.

OBJECTIVE: To investigate whether the somatosensory temporal discrimination threshold (STDT) is already altered at the clinical onset of Parkinson's disease (PD) and whether STDT abnormalities correlate with disease progression we tested STDT values in patients with different severity of disease. METHODS: We prospectively and consecutively enrolled 63 PD patients: 26 drug-naive PD patients with symptom onset no longer than two years prior to inclusion in the study (early-phase), 37 PD patients with varying degrees of disease severity and 51 age-matched healthy subjects. The STDT was tested on the index finger of both hands, and on both sides of the face. Twelve out of 26 early phase PD patients were re-tested two years after the initial diagnosis. RESULTS: PD patients as a whole displayed higher STDT values than healthy subjects. STDT values did not significantly differ between early-phase PD patients and healthy subjects, whereas they were significantly higher in patients with mild/moderate and advanced PD. In early-phase PD patients STDT values at the two years-follow up assessment did not statistically differ from those obtained at baseline. Considering the whole group of PD patients STDT abnormalities significantly correlated with duration and severity of the disease. CONCLUSIONS: STDT increases as disease progresses. In early-phase PD patients STDT values are still statistically similar to those of healthy subjects, thus implying that dopaminergic depletion alone may not be sufficient to cause STDT abnormalities. SIGNIFICANCE: Our study gives new insight into the sensory abnormalities in PD.