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Anxiety in Parkinson disease (PD) negatively impacts quality of life. While research predominantly focuses on central nervous system changes, some evidence suggests a connection between peripheral autonomic dysfunctions and PD-related anxiety. The role of the peripheral autonomic nervous system in this context may be overlooked. This study explores the link between anxiety symptoms and cardiac sympathetic denervation in PD using 11C-meta-hydroxyephedrine ([11C]HED) PET cardiac imaging. We studied 34 non-demented PD subjects, assessing anxiety levels through the Spielberg Anxiety State-Trait test trait section (STAI-T). Patients underwent comprehensive assessments along with [11C]HED cardiac and [11C]DTBZ brain PET. To identify subdimensions of STAI-T, we employed principal components analysis (PCA). We examined associations between the anxiety subdimensions and two measures of cardiac sympathetic denervation from [11C]HED PET. We utilized correlation and linear regression models for these analyses. PCA revealed two STAI-T results components: anxiety-depressive and pure anxiety subcomponents. Only pure anxiety significantly correlated with measures of cardiac sympathetic denervation (rhos −0.40, p = 0.018; 0.35, p = 0.043). Regression models confirmed a significant association, with cardiac sympathetic denervation explaining ∼20 % of pure anxiety variance, independent of sex, dopaminergic impairment, and anxiolytic treatments. This study provides preliminary evidence of peripheral autonomic nervous system abnormalities contributing to PD-related anxiety, suggesting dysregulation in peripheral autonomic functions influencing anxiety perception. • STAI-T total scores represent a combination of depression and pure anxiety. • Depression subdimension was not associated with cardiac sympathetic denervation. • Pure anxiety scores were associated with cardiac sympathetic denervation. • Cardiac sympathetic denervation-anxiety association is dopamine deficit-independent. [ABSTRACT FROM AUTHOR]

We evaluated the role of cerebellum in defensive responses, by recording the Hand Blink Reflex (HBR) and modulating cerebellar activity with transcranial Direct Current Stimulation (tDCS). The active electrode was centered on the median line 2 cm below the inion and the return one over the right shoulder. Direct current was applied for 20 min with an intensity of 1.5 mA, both for cathodal and anodal stimulation. For the recording of HBR, we stimulated electrically the median nerve at the wrist and recorded EMG activity from the orbicularis oculi muscle bilaterally. Depending on the hand position respective to the face, we assessed four different conditions: “hand-far”, “hand-near” (eyes-open), “hand-side”, “hand-near” (eyes-closed). EMG signals were high-pass filtered (55 Hz), full-wave rectified, and averaged separately for the four conditions at the ipsilateral and contralateral recording sides. The anodal stimulation reduces the magnitude of the HBR, as measured by the Area Under the Curve (AUC), and increased the HBR latency in the “hand-side” and “hand-near” (eyes-closed) conditions (HBR magnitude: p = 0.004 and p < 0.0001; HBR latency: p = 0.023 and 0.002, respectively). These results support a critical role of the cerebellum in the defensive responses within the peripersonal space, thus selectively modulating defensive behavior when the visual feedback is missing. [ABSTRACT FROM AUTHOR]

The cerebellum is involved in a number of integrative functions, but its role in pain perception and nociceptive processing is poorly understood. We evaluated the effects of transcranial cerebellar direct current stimulation (tcDCS) by studying changes in perceptive threshold (PT), pain intensity (VAS) and laser evoked potentials (LEPs). Twenty-five subjects were studied before and after anodal, cathodal and sham tcDCS. LEPs were obtained using a Nd:YAP laser. VAS was evaluated by delivering laser pulses at two different intensities, respectively two and three times the PT. Cathodal polarization dampened the perceptive threshold and increased the VAS score, while anodal one had opposite effects (p < 0.001, two-way repeated measures ANOVA, “time” × “stimulation”). Cathodal tcDCS increased LEPs amplitudes and decreased their latencies, whereas anodal polarization elicited opposite effects (p < 0.0001). Motor thresholds assessed through transcranial magnetic stimulation were not affected by tcDCS. tcDCS modulates pain perception and its cortical correlates. As it is effective on N1 and N2/P2 components, we speculate that the cerebellum modulates the activity of both somatosensory and cingulate cortices, thus interfering with the sensory-discriminative and affective-emotional dimensions of pain. Our findings prompt investigation of the tsDCS as a novel and safe therapeutic tool in pain syndromes. [ABSTRACT FROM AUTHOR]

Cerebellum is involved in a wide number of integrative functions, most of them unknown. Particularly, its role in pain processing has only poorly understood. We evaluated the effects of cerebellar transcranial direct current stimulation (c-tDCS) on pain perception by assessing changes in laser evoked potentials (LEPs) parameters (perceptive threshold, N1–N2/P2 amplitudes and latencies) by stimulating the left hand. Materials and Methods: Twelve healthy subjects were enrolled and studied before and after anodal, cathodal and sham tDCS (20’, 2.0 mA). LEPs were obtained using a neodymium:yttrium–aluminium–perovskite (Nd:YAP) laser. While cathodal c-tDCS improves amplitudes (N1: F (2,66) = 23.3, p < 0.0001; N2/P2: F (2,66) = 19.1, p < 0.0001) and decreases LEPs latencies (N1: F(2,66) = 7.7, p = 0.001; N2/P2: F (2,66) = 5.4, p = 0.007) compared with sham condition, anodal c-tDCS elicits opposite effects ( p < 0.001 for all the comparisons). Anodal polarization dampens perceptive threshold, while the cathodal stimulation increases it ( p < 0.001). The main finding of our study is that cerebellar direct current polarization is able to modulate pain perception in humans. As c-tDCS was effective on N1 and N2/P2 components, we speculate that cerebellum is engaged in pain processing dynamically modulating the activity of both secondary somatosensory and cingulate cortices. [ABSTRACT FROM AUTHOR]