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We have previously demonstrated that, in rested subjects, extensive practice in a motor learning task increased both electroencephalographic (EEG) theta power in the areas involved in learning and improved the error rate in a motor test that shared similarities with the task. A nap normalized both EEG and performance changes. We now ascertain whether extensive visual declarative learning produces results similar to motor learning. Thus, during the morning, we recorded high-density EEG in well rested young healthy subjects that learned the order of different visual sequence task (VSEQ) for three one-hour blocks. Afterward, a group of subjects took a nap and another rested quietly. Between each VSEQ block, we recorded spontaneous EEG (sEEG) at rest and assessed performance in a motor test and a visual working memory test that shares similarities with VSEQ. We found that after the third block, VSEQ induced local theta power increases in the sEEG over a right temporo-parietal area that was engaged during the task. This local theta increase was preceded by increases in alpha and beta power over the same area and was paralleled by performance decline in the visual working memory test. Only after the nap, VSEQ learning rate improved and performance in the visual working memory test was restored, together with partial normalization of the local sEEG changes. These results suggest that intensive learning, like motor learning, produces local theta power increases, possibly reflecting local neuronal fatigue. Sleep may be necessary to resolve neuronal fatigue and its effects on learning and performance., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Ricci, Tatti, Nelson, Panday, Chen, Tononi, Cirelli and Ghilardi.)

Beta oscillations (13.5-25 Hz) over the sensorimotor areas are characterized by a power decrease during movement execution (event-related desynchronization, ERD) and a sharp rebound after the movement end (event-related synchronization, ERS). In previous studies, we demonstrated that movement-related beta modulation depth (peak ERS-ERD) during reaching increases within 1-h practice. This increase may represent plasticity processes within the sensorimotor network. If so, beta modulation during a reaching test should be affected by previous learning activity that engages the sensorimotor system but not by learning involving other systems. We thus recorded high-density EEG activity in a group of healthy subjects performing three 45-min blocks of motor adaptation task to a visually rotated display (ROT) and in another performing three blocks of visual sequence-learning (VSEQ). Each block of either ROT or VSEQ was followed by a simple reaching test ( mov ) without rotation. We found that beta modulation depth increased with practice across mov tests. However, such an increase was greater in the group performing ROT over both the left and frontal areas previously involved in ROT. Importantly, beta modulation values returned to baseline values after a 90-min of either nap or quiet wake. These results show that previous practice leaves a trace in movement-related beta modulation and therefore such increases are cumulative. Furthermore, as sleep is not necessary to bring beta modulation values to baseline, they could reflect local increases of neuronal activity and decrease of energy and supplies., (Copyright © 2020 Tatti, Ricci, Nelson, Mathew, Chen, Quartarone, Cirelli, Tononi and Ghilardi.)

Stroke survivors show greater postural oscillations and altered muscular activation compared to healthy controls. This results in difficulties in walking and standing, and in an increased risk of falls. A proper control of the trunk is related to a stable walk and to a lower falling risk; to this extent, rehabilitative protocols are currently working on core stability. The main objective of this work was to evaluate the effectiveness of trunk and balance training performed with a new robotic device designed for evaluation and training of balance and core stability, in improving the recovery of chronic stroke patients compared with a traditional physical therapy program. Thirty chronic stroke patients, randomly divided in two groups, either underwent a traditional rehabilitative protocol, or a robot-based program. Each patient was assessed before and after the rehabilitation and at 3-months follow-up with clinical and robot-based evaluation exercises focused on static and dynamic balance and trunk control. Results from clinical scores showed an improvement in both groups in balance and trunk control. Robot-based indices analysis indicated that the experimental group showed greater improvements in proprioceptive control, reactive balance and postural control in unstable conditions, compared to the control group, showing an improved trunk control with reduced compensatory strategies at the end of the training. Moreover, the experimental group had an increased retention of the benefits obtained with training at 3 months follow up. These results support the idea that such robotic device is a promising tool for stroke rehabilitation., (Copyright © 2020 De Luca, Squeri, Barone, Vernetti Mansin, Ricci, Pisu, Cassiano, Capra, Lentino, De Michieli, Sanfilippo, Saglia and Checchia.)

Beta power over the sensorimotor areas starts decreasing just before movement execution (event-related desynchronization, ERD) and increases post-movement (event-related synchronization, ERS). In this study, we determined whether the magnitude of beta ERD, ERS and modulation depth are linked to movement characteristics, such as movement length and velocity. Brain activity was recorded with a 256-channels EEG system in 35 healthy subjects performing fast, uncorrected reaching movements to targets located at three distances. We found that the temporal profiles of velocity were bell-shaped and scaled to the appropriate target distance. However, the magnitude of beta ERD, ERS and modulation depth, as well as their timing, did not significantly change and were not related to movement features.

Recently we found that modulation depth of beta power during movement increases with practice over sensory-motor areas in normal subjects but not in patients with Parkinson's disease (PD). As such changes might reflect use-dependent modifications, we concluded that reduction of beta enhancement in PD represents saturation of cortical plasticity. A few questions remained open: What is the relation between these EEG changes and retention of motor skills? Would a second task exposure restore beta modulation enhancement in PD? Do practice-induced increases of beta modulation occur within each block? We thus recorded EEG in patients with PD and age-matched controls in two consecutive days during a 40-min reaching task divided in fifteen blocks of 56 movements each. The results confirmed that, with practice, beta modulation depth over the contralateral sensory-motor area significantly increased across blocks in controls but not in PD, while performance improved in both groups without significant correlations between behavioral and EEG data. The same changes were seen the following day in both groups. Also, beta modulation increased within each block with similar values in both groups and such increases were partially transferred to the successive block in controls, but not in PD. Retention of performance improvement was present in the controls but not in the patients and correlated with the increase in day 1 modulation depth. Therefore, the lack of practice-related increase beta modulation in PD is likely due to deficient potentiation mechanisms that permit between-block saving of beta power enhancement and trigger mechanisms of memory formation.

The present study was aimed to evaluate the malvidin's protective effects on damage induced by 30 min bilateral common carotid artery occlusion (BCCAO) and 60 min reperfusion (RE) in rat pial microcirculation. Rat pial microcirculation was observed using fluorescence microscopy through a closed cranial window. Western blotting analysis was performed to investigate the endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS) and matrix metalloproteinase 9 (MMP-9) expression. Moreover, MMP-9 activity was evaluated by zymography. Finally, neuronal damage and radical oxygen species (ROS) formation were assessed. In all animals, pial arterioles were classified in five orders of branching according to Strahler's method. In hypoperfused rats, 30 min BCCAO and 60 min RE caused a decrease in arteriolar diameter, an increase in microvascular leakage and leukocyte adhesion, accompanied by decreased capillary perfusion and red blood cell velocity (VRBC). Moreover, marked neuronal damage and evident ROS generation were detected. Conversely, malvidin administration induced arteriolar dilation in dose-related manner, reducing microvascular leakage as well as leukocyte adhesion. Capillary perfusion and VRBC were protected. Nitric oxide (NO) synthase inhibition significantly attenuated malvidin's effects on arteriolar diameter. Western blotting analysis revealed an increase in eNOS and p-eNOS expression, while zymography indicated a decrease in MMP-9 activity after malvidin's administration. Furthermore, malvidin was able to prevent neuronal damage and to decrease ROS generation. In conclusion, malvidin protects rat pial microcirculation against BCCAO/RE injury, preventing blood-brain impairment and neuronal loss. Malvidin's effects appear to be mediated by eNOS activation and scavenger activity.