Brain Sciences

Background/Objectives: This study examined whether swimming experience is associated with better sensorimotor control in water by comparing joint position sense, cortical activity, and subjective workload across training backgrounds and environments. Methods: Thirty-six participants (12 swimmers, 12 Chinese Wushu (Wushu) athletes, and 12 untrained individuals) performed continuous shoulder and elbow joint-position-reproduction tasks on land and in water. Joint-angle errors, resting-state and task-related α- and β-band EEG power, and NASA Task Load Index scores were assessed using cluster-based permutation tests and mixed analyses of variance with multiple-comparison correction. Results: Environment affected left-elbow absolute error (p = 0.0015) and constant error at all four joints (all corrected p ≤ 0.0028), without a swimming-specific accuracy advantage. Wushu athletes had lower signed left-shoulder and left-elbow constant errors than swimmers. Swimmers showed a greater water–land increase in resting-state α power than untrained participants before right-side tasks (Holm-adjusted p = 0.0048). Task-related α desynchronization was weaker in water during left-shoulder and left-elbow tasks; no corrected training-related effects emerged for task-related α or β power. Physical demand and perceived performance showed group × environment interactions (both corrected p = 0.0458); swimmers reported lower physical demand than untrained participants in water. Conclusions: Swimming experience was associated with distinct pre-task resting-state α responses, but not better joint-position accuracy or distinct task-related cortical activity modulation. Long-term training in different environments appeared to reduce the physical demand of sensorimotor tasks performed in the familiar environment. These findings provide limited support for swimming-specific sensorimotor advantages in water.

Background: Mirror therapy is widely used in stroke rehabilitation, yet its immediate task-related cortical responses remain incompletely characterized. We used functional near-infrared spectroscopy (fNIRS) to characterize cortical hemodynamic responses during a mirror task in patients with stroke. Methods: Fifty-one stroke patients with upper limb dysfunction were recruited. Participants performed both a mirror task and a control task, while hemodynamic changes in regions of interest were simultaneously recorded using a 43-channel fNIRS device. General linear model (GLM) analysis was used to compare differences in activation intensity between the mirror task and control task in the cortical regions of interest. Results: Compared with the control task, the mirror task significantly activated 10 channels: CH2, CH3, CH5, CH9, CH11, CH19, CH24, CH25, CH32, and CH33. The activated brain regions were concentrated in the bilateral premotor cortex/supplementary motor area (PMC/SMA), ipsilesional supramarginal gyrus (SMG), ipsilesional primary somatosensory cortex (S1), and contralesional primary motor cortex (M1). Conclusions: The mirror task elicited greater activation than the control task across a distributed cortical network involving bilateral PMC/SMA, ipsilesional SMG/S1, and contralesional M1 in patients with stroke. These findings demonstrate that fNIRS can objectively characterize task-related cortical hemodynamic responses during mirror tasks and provide a basis for future studies linking these cortical response patterns to rehabilitation outcomes.

Background/Objectives: Sleep–wake states strongly influence seizure susceptibility, but the circuit mechanisms linking arousal regulation to seizure burden in chronic temporal lobe epilepsy (TLE) remain unclear. This study investigated whether hypothalamic orexin neurons regulate sleep architecture, spontaneous seizures, and epileptic network activity in a kainic acid (KA)-induced chronic TLE model in male mice. Methods: Continuous video-EEG/EMG recordings were used to quantify sleep–wake states, circadian seizure distribution, and seizure burden. Orexin neurons were bidirectionally manipulated in KA-treated Hcrt-Cre mice using Cre-dependent hM3Dq or hM4Di chemogenetic tools. Orexin receptor 1 signaling was pharmacologically blocked with SB334867. Power spectral density and phase–amplitude coupling analyses were performed across wakefulness, non-rapid eye movement sleep, and rapid eye movement sleep. Results: Spontaneous seizures occurred predominantly during wakefulness and non-rapid eye movement sleep, with no seizures observed during rapid eye movement sleep. Seizure occurrence was greater during the dark phase and remained higher during wakefulness after correction for state occupancy. Chemogenetic activation of orexin neurons increased wakefulness, reduced sleep, and increased seizure count and total seizure duration, whereas chemogenetic inhibition produced opposite effects. SB334867 promoted sleep and reduced seizure count and total seizure duration. Chronic KA mice showed state-dependent spectral remodeling and enhanced delta–high-gamma coupling, which was partially attenuated by SB334867 during non-rapid eye movement and rapid eye movement sleep. Conclusions: These findings suggest that orexin signaling is associated with sleep–wake regulation, abnormal network coupling, and seizure burden in chronic TLE. Modulating orexin signaling may represent a potential direction for future therapeutic investigation aimed at improving sleep disruption and reducing seizure burden.