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The sequelae of Parkinson's disease (PD) includes both motor- and cognitive-related symptoms. Although traditionally considered a subcortical disease, there is increasing evidence that PD has a major impact on cortical function as well. Prior studies have reported alterations in cortical neural function in patients with PD during movement, but to date such studies have not examined whether the complexity of multicomponent movements modulate these alterations. In this study, 23 patients with PD (medication "off" state) and 27 matched healthy controls performed simple and complex finger tapping sequences during magnetoencephalography (MEG), and the resulting MEG data were imaged to identify the cortical oscillatory dynamics serving motor performance. The patients with PD were significantly slower than controls at executing the sequences overall, and both groups took longer to complete the complex sequences than the simple. In terms of neural differences, patients also exhibited weaker beta complexity-related effects in the right medial frontal gyrus and weaker complexity-related alpha activity in the right posterior and inferior parietal lobules, suggesting impaired motor sequence execution. Characterizing the cortical pathophysiology of PD could inform current and future therapeutic interventions that address both motor and cognitive symptoms., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Children with hearing loss (CHL) exhibit delays in language function relative to children with normal hearing (CNH). However, evidence on whether these delays extend into other cognitive domains such as working memory is mixed, with some studies showing decrements in CHL and others showing CHL performing at the level of CNH. Despite the growing literature investigating the impact of hearing loss on cognitive and language development, studies of the neural dynamics that underlie these cognitive processes are notably absent. This study sought to identify the oscillatory neural responses serving verbal working memory processing in CHL compared to CNH. To this end, participants with and without hearing loss performed a verbal working memory task during magnetoencephalography. Neural oscillatory responses associated with working memory encoding and maintenance were imaged separately, and these responses were statistically evaluated between CHL and CNH. While CHL performed as well on the task as CNH, CHL exhibited significantly elevated alpha-beta activity in the right frontal and precentral cortices during encoding relative to CNH. In contrast, CHL showed elevated alpha maintenance-related activity in the right precentral and parieto-occipital cortices. Crucially, right superior frontal encoding activity and right parieto-occipital maintenance activity correlated with language ability across groups. These data suggest that CHL may utilize compensatory right-hemispheric activity to achieve verbal working memory function at the level of CNH. Neural behavior in these regions may impact language function during crucial developmental ages., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Type 1 diabetes (T1D) has been linked to alterations in both brain structure and function. However, the neural basis of the most commonly reported neuropsychological deficit in T1D, psychomotor speed, remains severely understudied. To begin to address this, the current study focuses on the neural dynamics underlying motor control using magnetoencephalographic (MEG) imaging. Briefly, 40 young adults with T1D who were clear of common comorbidities (e.g., vascular disease, retinopathy, etc.) and a demographically-matched group of 40 controls without T1D completed an arrow-based flanker movement task during MEG. The resulting signals were examined in the time-frequency domain and imaged using a beamforming approach, and then voxel time series were extracted from peak responses to evaluate the dynamics. The resulting time series were statistically examined for group and conditional effects using a rigorous permutation testing approach. Our primary hypothesis was that participants with T1D would have altered beta and gamma oscillatory dynamics within the primary motor cortex during movement, and that these alterations would reflect compensatory processing to maintain adequate performance. Our results indicated that the group with T1D had a significantly stronger post-movement beta rebound (PMBR) contralateral to movement compared to controls, and a smaller neural flanker effect (i.e., difference in neural activity between conditions). In addition, a significant group-by-condition interaction was observed in the ipsilateral beta event-related desynchronization (bERD) and the ipsilateral PMBR. We also examined the relationship between oscillatory motor response amplitude and reaction time, finding a differential effect of the driving oscillatory responses on behavioral performance by group. Overall, our findings suggest compensatory activity in the motor cortices is detectable early in the disease in a relatively healthy sample of adults with T1D. Future studies are needed to examine how these subtle effects on neural activity in young, otherwise healthy patients affect outcomes in aging., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

The neuroimaging literature on cerebral palsy (CP) has predominantly focused on identifying structural aberrations within the white matter (e.g., fiber track integrity), with very few studies examining neural activity within the key networks that serve the production of motor actions. The current investigation used high-density magnetoencephalography to begin to fill this knowledge gap by quantifying the temporal dynamics of the alpha and beta cortical oscillations in children with CP (age = 15.5 ± 3 years; GMFCS levels II-III) and typically developing (TD) children (age = 14.1 ± 3 years) during a goal-directed isometric target-matching task using the knee joint. Advanced beamforming methods were used to image the cortical oscillations during the movement planning and execution stages. Compared with the TD children, our results showed that the children with CP had stronger alpha and beta event-related desynchronization (ERD) within the primary motor cortices, premotor area, inferior parietal lobule, and inferior frontal gyrus during the motor planning stage. Differences in beta ERD amplitude extended through the motor execution stage within the supplementary motor area and premotor cortices, and a stronger alpha ERD was detected in the anterior cingulate. Interestingly, our results also indicated that alpha and beta oscillations were weaker in the children with CP within the occipital cortices and visual MT area during movement execution. These altered alpha and beta oscillations were accompanied by slower reaction times and substantial target matching errors in the children with CP. We also identified that the strength of the alpha and beta ERDs during the motor planning and execution stages were correlated with the motor performance. Lastly, our regression analyses suggested that the beta ERD within visual areas during motor execution primarily predicted the amount of motor errors. Overall, these data suggest that uncharacteristic alpha and beta oscillations within visuomotor cortical networks play a prominent role in the atypical motor actions exhibited by children with CP.

Patients with Parkinson's disease (PD) often present with unilateral motor symptoms that eventually spread to the other side. This symptom lateralization is diagnostically important, as it serves to distinguish PD from other motor disorders with overlapping symptom profiles. Further, recent studies have shown that the side of symptom onset is important for prognosis, as there are differences in the rate of disease progression and the incidence of secondary symptoms between right- and left-dominant (RD, LD) patients. Physiologically, previous studies have shown asymmetrical decline in structure and metabolism throughout the basal ganglia, although connecting this directly to motor function has been difficult. To identify the neurophysiological basis of symptom laterality in PD, we recorded magnetoencephalography (MEG) during left- and right-hand movement paradigms in patients with PD who exhibited either RD or LD symptomatology. The beta oscillations serving these movements were then imaged using beamforming methods, and we extracted the time series of the peak voxel in the left and right primary motor cortices for each movement. In addition, each patient's symptom asymmetry was quantitated using the Unified Parkinson's Disease Rating Scale (UPDRS), which allowed the relationship between symptom asymmetry and neural asymmetry to be assessed. We found that LD patients had stronger beta suppression during movement, as well as greater post-movement beta rebound compared to patients with RD symptoms, independent of the hand that was moved. Interestingly, the asymmetry of beta activity during right-hand movement uniquely correlated with symptom asymmetry, such that the more LD the symptom profile, the more left-lateralized (i.e., contralateral to movement) the beta response; conversely, the more RD the symptom profile, the more right-lateralized (i.e., ipsilateral to movement) the beta response. This study is the first to directly probe the relationship between symptom asymmetry and the laterality of neural activity during movement in patients with PD, and suggests that LD patients have a fundamentally different and more "healthy" oscillatory pattern relative to RD patients.