@article {3382, title = {Electrocorticographic activity over sensorimotor cortex and motor function in awake behaving rats.}, journal = {J Neurophysiol}, volume = {113}, year = {2015}, month = {04/2015}, pages = {2232-41}, abstract = {

Sensorimotor cortex exerts both short-term and long-term control over the spinal reflex pathways that serve motor behaviors. Better understanding of this control could offer new possibilities for restoring function after central nervous system trauma or disease. We examined the impact of ongoing sensorimotor cortex (SMC) activity on the largely monosynaptic pathway of the H-reflex, the electrical analog of the spinal stretch reflex. In 41 awake adult rats, we measured soleus electromyographic (EMG) activity, the soleus H-reflex, and electrocorticographic activity over the contralateral SMC while rats were producing steady-state soleus EMG activity. Principal component analysis of electrocorticographic frequency spectra before H-reflex elicitation consistently revealed three frequency bands: μβ (5-30 Hz), low γ (γ1; 40-85 Hz), and high γ (γ2; 100-200 Hz). Ongoing (i.e., background) soleus EMG amplitude correlated negatively with μβ power and positively with γ1 power. In contrast, H-reflex size correlated positively with μβ power and negatively with γ1 power, but only when background soleus EMG amplitude was included in the linear model. These results support the hypothesis that increased SMC activation (indicated by decrease in μβ power and/or increase in γ1 power) simultaneously potentiates the H-reflex by exciting spinal motoneurons and suppresses it by decreasing the efficacy of the afferent input. They may help guide the development of new rehabilitation methods and of brain-computer interfaces that use SMC activity as a substitute for lost or impaired motor outputs.

}, keywords = {brain-computer interface, cortex, H-Reflex, Motor control, Spinal Cord}, issn = {1522-1598}, doi = {10.1152/jn.00677.2014}, url = {http://www.ncbi.nlm.nih.gov/pubmed/25632076}, author = {Chadwick B. Boulay and Xiang Yang Chen and Jonathan Wolpaw} } @article {3377, title = {Novel inter-hemispheric white matter connectivity in the BTBR mouse model of autism.}, journal = {Brain Res}, volume = {1513}, year = {2013}, month = {06/2013}, pages = {26-33}, abstract = {Alterations in the volume, density, connectivity and functional activation of white matter tracts are reported in some individuals with autism and may contribute to their abnormal behaviors. The BTBR (BTBR T+tf/J) inbred strain of mouse, is used to model facets of autism because they develop low social behaviors, stereotypical and immune changes similar to those found in people with autism. Previously, it was thought a total absence of corpus callosal interhemispheric connective tissues in the BTBR mice may underlie their abnormal behaviors. However, postnatal lesions of the corpus callosum do not precipitate social behavioral problems in other strains of mice suggesting a flaw in this theory. In this study we used digital pathological methods to compare subcortical white matter connective tracts in the BTBR strain of mice with those found in the C57Bl/6 mouse and those reported in a standardized mouse brain atlas. We report, for the first time, a novel connective subcortical interhemispheric bridge of tissue in the posterior, but not anterior, cerebrum of the BTBR mouse. These novel connective tissues are comprised of myelinated fibers, with reduced myelin basic protein levels (MBP) compared to levels in the C57Bl/6 mouse. We used electrophysiological analysis and found increased inter-hemispheric connectivity in the posterior hemispheres of the BTBR strain compared with the anterior hemispheres. The conduction velocity was slower than that reported in normal mice. This study shows there is novel abnormal interhemispheric connectivity in the BTBR strain of mice, which may contribute to their behavioral abnormalities.}, keywords = {Analysis of Variance, Animals, Autistic Disorder, Brain, Corpus Callosum, Disease Models, Animal, Electroencephalography, Enzyme-Linked Immunosorbent Assay, Female, Functional Laterality, Image Processing, Computer-Assisted, Male, Mice, Mice, Inbred C57BL, Mice, Neurologic Mutants, Microtubule-Associated Proteins, Myelin Basic Protein, Nerve Fibers, Myelinated, Neuroimaging, Spectrum Analysis}, issn = {1872-6240}, doi = {10.1016/j.brainres.2013.04.001}, url = {http://www.ncbi.nlm.nih.gov/pubmed/23570707}, author = {Miller, V M and Disha Gupta and Neu, N and Cotroneo, A and Chadwick B. Boulay and Seegal, R F} } @article {3093, title = {Trained modulation of sensorimotor rhythms can affect reaction time.}, journal = {Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology}, volume = {122}, year = {2011}, month = {09/2011}, pages = {1820{\textendash}1826}, abstract = {OBJECTIVE: Brain-computer interface (BCI) technology might be useful for rehabilitation of motor function. This speculation is based on the premise that modifying the EEG will modify behavior, a proposition for which there is limited empirical data. The present study examined the possibility that voluntary modulation of sensorimotor rhythm (SMR) can affect motor behavior in normal human subjects. METHODS: Six individuals performed a cued-reaction task with variable warning periods. A typical variable foreperiod effect was associated with SMR desynchronization. SMR features that correlated with reaction times were then used to control a two-target cursor movement BCI task. Following successful BCI training, an uncued reaction time task was embedded within the cursor movement task. RESULTS: Voluntarily increasing SMR beta rhythms was associated with longer reaction times than decreasing SMR beta rhythms. CONCLUSIONS: Voluntary modulation of EEG SMR can affect motor behavior. SIGNIFICANCE: These results encourage studies that integrate BCI training into rehabilitation protocols and examine its capacity to augment restoration of useful motor function.}, keywords = {brain-computer interface, EEG, Reaction Time}, issn = {1872-8952}, doi = {10.1016/j.clinph.2011.02.016}, url = {http://www.ncbi.nlm.nih.gov/pubmed/21411366}, author = {Chadwick B. Boulay and Sarnacki, W. A. and Jonathan Wolpaw and Dennis J. McFarland} } @article {3104, title = {A novel P300-based brain-computer interface stimulus presentation paradigm: moving beyond rows and columns.}, journal = {Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology}, volume = {121}, year = {2010}, month = {07/2010}, pages = {1109{\textendash}1120}, abstract = {OBJECTIVE: An electroencephalographic brain-computer interface (BCI) can provide a non-muscular means of communication for people with amyotrophic lateral sclerosis (ALS) or other neuromuscular disorders. We present a novel P300-based BCI stimulus presentation - the checkerboard paradigm (CBP). CBP performance is compared to that of the standard row/column paradigm (RCP) introduced by Farwell and Donchin (1988). METHODS: Using an 8x9 matrix of alphanumeric characters and keyboard commands, 18 participants used the CBP and RCP in counter-balanced fashion. With approximately 9-12 min of calibration data, we used a stepwise linear discriminant analysis for online classification of subsequent data. RESULTS: Mean online accuracy was significantly higher for the CBP, 92\%, than for the RCP, 77\%. Correcting for extra selections due to errors, mean bit rate was also significantly higher for the CBP, 23 bits/min, than for the RCP, 17 bits/min. Moreover, the two paradigms produced significantly different waveforms. Initial tests with three advanced ALS participants produced similar results. Furthermore, these individuals preferred the CBP to the RCP. CONCLUSIONS: These results suggest that the CBP is markedly superior to the RCP in performance and user acceptability. SIGNIFICANCE: The CBP has the potential to provide a substantially more effective BCI than the RCP. This is especially important for people with severe neuromuscular disabilities.}, keywords = {brain-computer interface, brain-machine interface, EEG, event-related potential, P300, Rehabilitation}, issn = {1872-8952}, doi = {10.1016/j.clinph.2010.01.030}, url = {http://www.ncbi.nlm.nih.gov/pubmed/20347387}, author = {Townsend, G. and LaPallo, B. K. and Chadwick B. Boulay and Krusienski, D. J. and Frye, G. E. and Hauser, C. K. and Schwartz, N. E. and Theresa M Vaughan and Jonathan Wolpaw and Sellers, E. W.} }