Neural Plasticity最新文献

Predicting upcoming sensorimotor events means creating forward estimates of the body and the surrounding world. This ability is a fundamental aspect of skilled motor behavior and requires an accurate and constantly updated representation of the body and the environment. To test whether these prediction mechanisms could be affected by a peripheral injury, we employed an action observation and electroencephalogram (EEG) paradigm to assess the occurrence of prediction markers in anticipation of observed sensorimotor events in healthy and brachial plexus injury (BPI) participants. Nine healthy subjects and six BPI patients watched a series of video clips showing an actor's hand and a colored ball in an egocentric perspective. The color of the ball indicated whether the hand would grasp it (hand movement), or the ball would roll toward the hand and touch it (ball movement), or no event would occur (no movement). In healthy participants, we expected to find distinct electroencephalographic activation patterns (EEG signatures) specific to the prediction of the occurrence of each of these situations. Cluster analysis from EEG signals recorded from electrodes placed over the sensorimotor cortex of control participants showed that predicting either an upcoming hand movement or the occurrence of a tactile event yielded specific neural signatures. In BPI participants, the EEG signals from the sensorimotor cortex contralateral to the dominant hand in the hand movement condition were different compared to the other conditions. Furthermore, there were no differences between ball movement and no movement conditions in the sensorimotor cortex contralateral to the dominant hand, suggesting that BPI blurred specifically the ability to predict upcoming tactile events for the dominant hand. These results highlight the role of the sensorimotor cortex in creating estimates of both actions and tactile interactions in the space around the body and suggest plastic effects on prediction coding following peripheral sensorimotor loss.

Background: The prevalence of comorbid pain after spinal cord injury (SCI) is relatively high in clinical observations and has continued to increase over time. Neuropathic pain (70.14%) is the most popular subject in academic journals after SCI. However, studies that used the bibliometric method to analyze comorbid pain after SCI are still lacking. This study is aimed at combining and integrating acquired information to analyze the global trends of research on the comorbidity of pain after SCI in the last three decades (1990-2019).

Methods: Systematic works of literature published from 1990 to 2019 were obtained from the Web of Science Core Collection. CiteSpace software was used to analyze the relationship of publication year with the country, institution, journals, authors, references, and keywords. The regression analysis is used to evaluate the percentage of the category increase or decrease over time significantly. IBM SPSS Statistics was used in the statistical analysis.

Results: A total of 730 publications were included in the analysis. A remarkable increase in the number of publications was observed in the study period (P < 0.05). A total of 202 academic journals focused on the categories of clinical neurology, neurosciences, and rehabilitation, and the annual growth rate of articles in these three categories was statistically significant (P < 0.05). The USA (356, 48.77%) and the University of Miami (64, 8.77%) were the country and institution with the highest number of publications, respectively. Spinal Cord, which was the main journal for research on pain after SCI, had the most publications (88, 12.05%). Burst keywords showed that the individual, inflammation, and central sensitization with pain after SCI are the research development trends and focus in this research field.

Conclusions: Overall, this study provides the latest research direction for pain after SCI. This historical overview of research into pain after SCI will be a useful basis for further research into development trends, focus issues, cooperators, and cooperative institutions.

Introduction: The transversus abdominis (TVA) and multifidus (MF) muscles are the main segmental spinal stabilizers that are controlled by the primary motor cortex of the brain. However, relocations of the muscle representation in the motor cortex may occur after chronic lower back pain (cLBP); it still needs more evidence to be proven. The current study was aimed at applying transcranial magnetic stimulation (TMS) to investigate the changes of representation of TVA and MF muscles at the cortical network in individuals with cLBP.

Methods: Twenty-four patients with cLBP and 12 age-matched healthy individuals were recruited. Responses of TVA and MF to TMS during muscle contraction were monitored and mapped over the contralateral cortex using a standardized grid cap. Maps of the center of gravity (CoG), area, volume, and latency were analyzed, and the asymmetry index was also computed and compared.

Results: The locations of MF CoG in cLBP individuals were posterior and lateral to the CoG locations in healthy individuals. In the healthy group, the locations of TVA and MF CoG were closed to each other in both the left and right hemispheres. In the cLBP group, these two locations were next to each other in the right hemisphere but discrete in the left hemisphere. In the cLBP group, the cortical motor map of TVA and MF were mutually symmetric in five out of eleven (45.5%) subjects and leftward asymmetric in four out of ten (40.0%) subjects.

Conclusions: Neural representations of TVA and MF muscles were closely organized in both the right and left motor cortices in the healthy group but were discretely organized in the left motor cortex in the cLBP group. This provides strong support for the neural basis of pathokinesiology and clinical treatment of cLBP.

Feature extraction is essential for classifying different motor imagery (MI) tasks in a brain-computer interface. To improve classification accuracy, we propose a novel feature extraction method in which the connectivity increment rate (CIR) of the brain function network (BFN) is extracted. First, the BFN is constructed on the basis of the threshold matrix of the Pearson correlation coefficient of the mu rhythm among the channels. In addition, a weighted BFN is constructed and expressed by the sum of the existing edge weights to characterize the cerebral cortex activation degree in different movement patterns. Then, on the basis of the topological structures of seven mental tasks, three regional networks centered on the C3, C4, and Cz channels are constructed, which are consistent with correspondence between limb movement patterns and cerebral cortex in neurophysiology. Furthermore, the CIR of each regional functional network is calculated to form three-dimensional vectors. Finally, we use the support vector machine to learn a classifier for multiclass MI tasks. Experimental results show a significant improvement and demonstrate the success of the extracted feature CIR in dealing with MI classification. Specifically, the average classification performance reaches 88.67% which is higher than other competing methods, indicating that the extracted CIR is effective for MI classification.

Nucleosomes composed of histone octamer and DNA are the basic structural unit in the eukaryote chromosome. Under the stimulation of various factors, histones will undergo posttranslational modifications such as methylation, phosphorylation, acetylation, and ubiquitination, which change the three-dimensional structure of chromosomes and affect gene expression. Therefore, the combination of different states of histone modifications modulates gene expression is called histone code. The formation of learning and memory is one of the most important mechanisms for animals to adapt to environmental changes. A large number of studies have shown that histone codes are involved in the formation and consolidation of learning and memory. Here, we review the most recent literature of histone modification in regulating neurogenesis, dendritic spine dynamic, synapse formation, and synaptic plasticity.

Skilled sensorimotor deficit is an unsolved problem of peripheral nerve injury (PNI) led by limb trauma or malignancies, despite the improvements in surgical techniques of peripheral nerve anastomosis. It is now accepted that successful functional recovery of PNI relies tremendously on the multilevel neural plasticity from the muscle to the brain. However, animal models that recapitulate these processes are still lacking. In this report, we developed a rat model of PNI to longitudinally assess peripheral muscle reinnervation and brain functional reorganization using noninvasive imaging technology. Based on such model, we compared the longitudinal changes of the rat forepaw intrinsic muscle volume and the seed-based functional connectivity of the sensorimotor cortex after nerve repair. We found that the improvement of skilled limb function and the recovery of paw intrinsic muscle following nerve regeneration are incomplete, which correlated with the functional connectivity between the primary motor cortex and dorsal striatum. Our results were highly relevant to the clinical observations and provided a framework for future investigations that aim to study the peripheral central sensorimotor circuitry underlying skilled limb function recovery after PNI.

Compared to relapsing-remitting multiple sclerosis (MS), progressive MS is characterized by a lack of spontaneous recovery and a poor response to pharmaceutical immunomodulatory treatment. These patients may, therefore, particularly benefit from interventions that augment training-induced plasticity of the central nervous system. In this cross-sectional double-blind cross-over pilot study, effects of transcranial direct current stimulation (tDCS) on motor sequence learning were examined across four sessions on days 1, 3, 5, and 8 in 16 patients with progressive MS. Active or sham anodal tDCS of the primary motor cortex was applied immediately after each training session. Participants took part in two experiments separated by at least four weeks, which differed with respect to the type of posttraining tDCS (active or sham). While task performance across blocks of training and across sessions improved significantly in both the active and sham tDCS experiment, neither online nor offline motor learning was modulated by the type of tDCS. Accordingly, the primary endpoint (task performance on day 8) did not differ between stimulation conditions. In sum, patients with progressive MS are able to improve performance in an ecologically valid motor sequence learning task through training. However, even multisession posttraining tDCS fails to promote motor learning in progressive MS.

Depression is a common psychological and mental disorder, characterized by low mood, slow thinking and low will, and even suicidal tendencies in severe cases. It imposes a huge mental and economic burden on patients and their families, and its prevention and treatment have become an urgent public health problem. It is worth noting that there is a significant gender difference in the incidence of depression. Studies have shown that females are far more likely to suffer from depression than males, confirming a close relationship between estrogen and the onset of depression. Moreover, recent studies suggest that the brain-derived neurotrophic factor- (BDNF-) mammalian target of rapamycin complex-1 (mTORC1) signaling pathway is a crucial target pathway for improving depression and mediates the rapid antidepressant-like effects of various antidepressants. However, it is not clear whether the BDNF-mTORC1 signaling pathway mediates the regulation of female depression and how to regulate female depression. Hence, we focused on the modulation of estrogen-BDNF-mTORC1 signaling in depression and its possible mechanisms in recent years.

Background: Bodily self-perception is an important concept for several neurological disorders, including spinal cord injury (SCI). Changing one's bodily self-perception, e.g., via rubber hand illusion (RHI), induces alterations of bottom-up and top-down pathways and with this the connectivity between involved brain areas. We aim to examine whether (1) this process can be manipulated by changing cortical excitability, (2) connectivity between relevant brain areas differ when the RHI cannot be evoked, and (3) how this projection differs in a patient with SCI.

Method: We applied RHI and facilitatory theta burst stimulation (TBS) on the right primary somatosensory cortex (S1) of 18 healthy participants and one patient with incomplete, cervical SCI. During RHI, we recorded high-density electroencephalography (HD-EEG) and extracted directed and nondirected connectivity measures.

Results: There is no difference in connectivity between sham and real TBS or in the effectivity of RHI. We observed a higher laterality in the patient, i.e., higher connectivity of the right and lower of the left hemisphere. Besides this, connectivity patterns do not differ between healthy participants and the patient.

Conclusion: This connectivity pattern might represent a neuroplastic response in the attempt to overcome the functional impairment of the patient resulting in a similar overall connectivity pattern to the healthy participants, yet with a higher sensitivity towards RHI and a higher laterality. The cortico-cortical communication was not altered depending on whether the illusion was provoked or not; hence, the perceptory illusion could not be observed in the EEG analysis.

Electroacupuncture (EA) improves hypothalamic-pituitary-adrenal (HPA) axis disorder by reducing corticotropin-releasing hormone (CRH) synthesis and release in the paraventricular nucleus (PVN). However, the potential mechanism underlying CRH regulation remains unclear. Secretagogin (SCGN) is closely related to stress and is involved in regulating the release of CRH. We hypothesized that SCGN in the PVN might trigger the HPA system and be involved in EA-mediated modulation of HPA dysfunction caused by surgical trauma. Serum CRH and adrenocorticotropic hormone (ACTH) and plasma corticosterone (CORT) levels at 6 h and 24 h after hepatectomy were determined by radioimmunoassay. CRH and SCGN protein levels in the PVN were detected by western blot and immunofluorescence, and CRH and SCGN mRNA levels in the PVN were determined by means of real-time polymerase chain reaction (RT-PCR) and in situ hybridization (ISH). Our studies showed that serum CRH, ACTH, and CORT levels and PVN CRH expression were significantly increased at 6 h and 24 h after hepatectomy in the hepatectomy group compared with the control group, and those in the EA+hepatectomy group were decreased compared with those in the hepatectomy group. The protein and mRNA levels of SCGN in the PVN were also increased after hepatectomy, and their expression in the EA+hepatectomy group was decreased compared with that in the hepatectomy group. When SCGN expression in the PVN was functionally knocked down by a constructed CsCI virus, we found that SCGN knockdown decreased the serum CRH, ACTH, and CORT levels in the SCGN shRNA+hepatectomy group compared with the hepatectomy group, and it also attenuated CRH expression in the PVN. In summary, our findings illustrated that EA normalized HPA axis dysfunction after surgical trauma by decreasing the transcription and synthesis of SCGN.