Obstacle avoidance movement-related motor cortical activity with cognitive task

Author(s):  
Akihiro Matsuura ◽  
Natsumi Sai ◽  
Ayaka Yamaoka ◽  
Tetsuya Karita ◽  
Futoshi Mori
2013 ◽  
Vol 33 (36) ◽  
pp. 14342-14353 ◽  
Author(s):  
A. Nelson ◽  
D. M. Schneider ◽  
J. Takatoh ◽  
K. Sakurai ◽  
F. Wang ◽  
...  

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Sergey D. Stavisky ◽  
Jonathan C. Kao ◽  
Paul Nuyujukian ◽  
Chethan Pandarinath ◽  
Christine Blabe ◽  
...  

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
John E. Downey ◽  
Lucas Brane ◽  
Robert A. Gaunt ◽  
Elizabeth C. Tyler-Kabara ◽  
Michael L. Boninger ◽  
...  

Author(s):  
Diego Orcioli-Silva ◽  
Rodrigo Vitório ◽  
Victor Spiandor Beretta ◽  
Núbia Ribeiro da Conceição ◽  
Priscila Nóbrega-Sousa ◽  
...  

Abstract Parkinson’s disease (PD) is often classified into tremor dominant (TD) and postural instability gait disorder (PIGD) subtypes. Degeneration of subcortical/cortical pathways is different between PD subtypes, which leads to differences in motor behavior. However, the influence of PD subtype on cortical activity during walking remains poorly understood. Therefore, we aimed to investigate the influence of PD motor subtypes on cortical activity during unobstructed walking and obstacle avoidance. Seventeen PIGD and 19 TD patients performed unobstructed walking and obstacle avoidance conditions. Brain activity was measured using a mobile functional near-infrared spectroscopy–electroencephalography (EEG) systems, and gait parameters were analyzed using an electronic carpet. Concentrations of oxygenated hemoglobin (HbO2) of the prefrontal cortex (PFC) and EEG absolute power from alpha, beta, and gamma bands in FCz, Cz, CPz, and Oz channels were calculated. These EEG channels correspond to supplementary motor area, primary motor cortex, posterior parietal cortex, and visual cortex, respectively. Postural instability gait disorder patients presented higher PFC activity than TD patients, regardless of the walking condition. Tremor dominant patients presented reduced beta power in the Cz channel during obstacle avoidance compared to unobstructed walking. Both TD and PIGD patients decreased alpha and beta power in the FCz and CPz channels. In conclusion, PIGD patients need to recruit additional cognitive resources from the PFC for walking. Both TD and PIGD patients presented changes in the activation of brain areas related to motor/sensorimotor areas in order to maintain balance control during obstacle avoidance, being that TD patients presented further changes in the motor area (Cz channel) to avoid obstacles.


NeuroImage ◽  
2011 ◽  
Vol 54 (4) ◽  
pp. 2915-2921 ◽  
Author(s):  
Leonardo Fazio ◽  
Giuseppe Blasi ◽  
Paolo Taurisano ◽  
Apostolos Papazacharias ◽  
Raffaella Romano ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Marsel Fazlyyyakhmatov ◽  
Nataly Zwezdochkina ◽  
Vladimir Antipov

The central brain functions underlying a stereoscopic vision were a subject of numerous studies investigating the cortical activity during binocular perception of depth. However, the stereo vision is less explored as a function promoting the cognitive processes of the brain. In this work, we investigated a cortical activity during the cognitive task consisting of binocular viewing of a false image which is observed when the eyes are refocused out of the random-dot stereogram plane (3D phenomenon). The power of cortical activity before and after the onset of the false image perception was assessed using the scull EEG recording. We found that during stereo perception of the false image the power of alpha-band activity decreased in the left parietal area and bilaterally in frontal areas of the cortex, while activity in beta-1, beta-2, and delta frequency bands remained to be unchanged. We assume that this suppression of alpha rhythm is presumably associated with increased attention necessary for refocusing the eyes at the plane of the false image.


Neuroscience ◽  
2017 ◽  
Vol 348 ◽  
pp. 143-152 ◽  
Author(s):  
George Mochizuki ◽  
Shaun G. Boe ◽  
Amanda Marlin ◽  
William E. McIlroy

2018 ◽  
Author(s):  
Ke Chen ◽  
Roberto Vincis ◽  
Alfredo Fontanini

ABSTRACTDysfunction of motor cortices is thought to contribute to motor disorders such as Parkinson’s disease (PD). However, little is known on the link between cortical dopaminergic loss, abnormalities in motor cortex neural activity and motor deficits. We address the role of dopamine in modulating motor cortical activity by focusing on the anterior lateral motor cortex (ALM) of mice performing a cued-licking task. We first demonstrate licking deficits and concurrent alterations of spiking activity in ALM of mice with unilateral depletion of dopaminergic neurons (i.e., mice injected with 6-OHDA into the medial forebrain bundle). Hemi-lesioned mice displayed delayed licking initiation, shorter duration of licking bouts, and lateral deviation of tongue protrusions. In parallel with these motor deficits, we observed a reduction in the prevalence of cue responsive neurons and altered preparatory activity. Acute and local blockade of D1 receptors in ALM recapitulated some of the key behavioral and neural deficits observed in hemi-lesioned mice. Altogether, our data show a direct relationship between cortical D1 receptor modulation, cue-evoked and preparatory activity in ALM, and licking initiation.SIGNIFICANCE STATEMENTThe link between dopaminergic signaling, motor cortical activity and motor deficits is not fully understood. This manuscript describes alterations in neural activity of the anterior lateral motor cortex (ALM) that correlate with licking deficits in mice with unilateral dopamine depletion or with intra-ALM infusion of dopamine antagonist. The findings emphasize the importance of cortical dopaminergic modulation in motor initiation. These results will appeal not only to researchers interested in cortical control of licking, but also to a broader audience interested in motor control and dopaminergic modulation in physiological and pathological conditions. Specifically, our data suggest that dopamine deficiency in motor cortex could play a role in the pathogenesis of the motor symptoms of Parkinson’s disease.


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