scholarly journals Neuromuscular Stimulation as an Intervention Tool for Recovery from Upper Limb Paresis after Stroke and the Neural Basis

2022 ◽  
Vol 12 (2) ◽  
pp. 810
Author(s):  
Shigeru Obayashi ◽  
Hirotaka Saito
Keyword(s):  
Neuromuscular Electrical Stimulation ◽  
Neural Mechanism ◽  
Neural Mechanisms ◽  
Stroke Severity ◽  
Neural Basis ◽  
Stimulation Parameters ◽  
Time Period ◽  
Function Recovery ◽  
Progress Rate ◽  
Upper Limb Paresis

Neuromodulators at the periphery, such as neuromuscular electrical stimulation (NMES), have been developed as add-on tools to regain upper extremity (UE) paresis after stroke, but this recovery has often been limited. To overcome these limits, novel strategies to enhance neural reorganization and functional recovery are needed. This review aims to discuss possible strategies for enhancing the benefits of NMES. To date, NMES studies have involved some therapeutic concerns that have been addressed under various conditions, such as the time of post-stroke and stroke severity and/or with heterogeneous stimulation parameters, such as target muscles, doses or durations of treatment and outcome measures. We began by identifying factors sensitive to NMES benefits among heterogeneous conditions and parameters, based on the “progress rate (PR)”, defined as the gains in UE function scores per intervention duration. Our analysis disclosed that the benefits might be affected by the target muscles, stroke severity and time period after stroke. Likewise, repetitive peripheral neuromuscular magnetic stimulation (rPMS) is expected to facilitate motor recovery, as already demonstrated by a successful study. In parallel, our efforts should be devoted to further understanding the precise neural mechanism of how neuromodulators make UE function recovery occur, thereby leading to overcoming the limits. In this study, we discuss the possible neural mechanisms.

Neural Mechanisms of Negative Symptoms

1989 ◽  
Vol 155 (S7) ◽  
pp. 93-98 ◽  
Author(s):  
Nancy C. Andreasen
Keyword(s):  
Frontal Cortex ◽  
Negative Symptoms ◽  
Neural Mechanism ◽  
Brain Regions ◽  
Brain Dysfunction ◽  
Neural Mechanisms ◽  
Dementia Praecox ◽  
Intellectual Abilities ◽  
The Brain ◽  
Psychic Mechanisms

When Kraepelin originally defined and described dementia praecox, he assumed that it was due to some type of neural mechanism. He hypothesised that abnormalities could occur in a variety of brain regions, including the prefrontal, auditory, and language regions of the cortex. Many members of his department, including Alzheimer and Nissl, were actively involved in the search for the neuropathological lesions that would characterise schizophrenia. Although Kraepelin did not use the term ‘negative symptoms', he describes them comprehensively and states explicitly that he believes the symptoms of schizophrenia can be explained in terms of brain dysfunction:“If it should be confirmed that the disease attacks by preference the frontal areas of the brain, the central convolutions and central lobes, this distribution would in a certain measure agree with our present views about the site of the psychic mechanisms which are principally injured by the disease. On various grounds, it is easy to believe that the frontal cortex, which is specially well developed in man, stands in closer relation to his higher intellectual abilities, and these are the faculties which in our patients invariably suffer profound loss in contrast to memory and acquired ability.” Kraepelin (1919, p. 219)

Neural Control of Swimming in Nudipleura Molluscs

2017 ◽  
pp. 438-450
Author(s):  
Paul S. Katz ◽  
Akira Sakurai
Keyword(s):  
Neural Control ◽  
Central Pattern Generators ◽  
Swimming Behavior ◽  
Neural Mechanisms ◽  
The Other ◽  
Neural Basis ◽  
Tritonia Diomedea ◽  
Pleurobranchaea Californica ◽  
Sea Slugs ◽  
Pattern Generators

This article compares the neural basis for swimming in sea slugs belonging to the Nudipleura clade of molluscs. There are two primary forms of swimming. One, dorsal/ventral (DV) body flexions, is typified by Tritonia diomedea and Pleurobranchaea californica. Although Tritonia and Pleurobranchaea evolved DV swimming independently, there are at least two homologous neurons in the central pattern generators (CPGs) underlying DV swimming in these species. Furthermore, both species have serotonergic neuromodulation of synaptic strength intrinsic to their CPGs. The other form of swimming is with alternating left/right (LR) body flexions. Melibe and Dendronotus belong to a clade of species that all swim with LR body flexions. Although the swimming behavior is homologous, their swim CPGs differ in both cellular composition and in the details of the neural mechanisms. Thus, similar behaviors have independently evolved through parallel use of homologous neurons, and homologous behaviors can be produced by different neural mechanisms.

scholarly journals The neural mechanism of aesthetic judgments of dynamic landscapes: an fMRI study

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xueru Zhao ◽  
Junjing Wang ◽  
Jinhui Li ◽  
Guang Luo ◽  
Ting Li ◽  
...  
Keyword(s):  
Visual Processing ◽  
Occipital Lobe ◽  
Neural Mechanism ◽  
Aesthetic Judgment ◽  
Neural Mechanisms ◽  
Middle Temporal Gyrus ◽  
Dynamic Stimuli ◽  
Dynamic Landscapes ◽  
The Aesthetic ◽  
Aesthetic Judgments

AbstractMost previous neuroaesthetics research has been limited to considering the aesthetic judgment of static stimuli, with few studies examining the aesthetic judgment of dynamic stimuli. The present study explored the neural mechanisms underlying aesthetic judgment of dynamic landscapes, and compared the neural mechanisms between the aesthetic judgments of dynamic landscapes and static ones. Participants were scanned while they performed aesthetic judgments on dynamic landscapes and matched static ones. The results revealed regions of occipital lobe, frontal lobe, supplementary motor area, cingulate cortex and insula were commonly activated both in the aesthetic judgments of dynamic and static landscapes. Furthermore, compared to static landscapes, stronger activations of middle temporal gyrus (MT/V5), and hippocampus were found in the aesthetic judgments of dynamic landscapes. This study provided neural evidence that visual processing related regions, emotion-related regions were more active when viewing dynamic landscapes than static ones, which also indicated that dynamic stimuli were more beautiful than static ones.

scholarly journals Cooperative defence operates by social modulation of biogenic amine levels in the honey bee brain

2018 ◽  
Vol 285 (1871) ◽  
pp. 20172653 ◽  
Author(s):  
Morgane Nouvian ◽  
Souvik Mandal ◽  
Charlène Jamme ◽  
Charles Claudianos ◽  
Patrizia d'Ettorre ◽  
...  
Keyword(s):  
Honey Bee ◽  
Honey Bees ◽  
Alarm Pheromone ◽  
Neural Mechanism ◽  
Isoamyl Acetate ◽  
Neural Mechanisms ◽  
Response Threshold ◽  
Defensive Behaviour ◽  
Personal Risk ◽  
Main Component

The defence of a society often requires that some specialized members coordinate to repel a threat at personal risk. This is especially true for honey bee guards, which defend the hive and may sacrifice their lives upon stinging. Central to this cooperative defensive response is the sting alarm pheromone, which has isoamyl acetate (IAA) as its main component. Although this defensive behaviour has been well described, the neural mechanisms triggered by IAA to coordinate stinging have long remained unknown. Here we show that IAA upregulates brain levels of serotonin and dopamine, thereby increasing the likelihood of an individual bee to attack and sting. Pharmacological enhancement of the levels of both amines induces higher defensive responsiveness, while decreasing them via antagonists decreases stinging. Our results thus uncover the neural mechanism by which an alarm pheromone recruits individuals to attack and repel a threat, and suggest that the alarm pheromone of honey bees acts on their response threshold rather than as a direct trigger.

scholarly journals Neural Mechanisms of Reward Prediction Error in Autism Spectrum Disorder

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Maya G. Mosner ◽  
R. Edward McLaurin ◽  
Jessica L. Kinard ◽  
Shabnam Hakimi ◽  
Jacob Parelman ◽  
...  
Keyword(s):  
Prediction Error ◽  
Autism Spectrum ◽  
Neural Mechanisms ◽  
Reward Learning ◽  
Prediction Errors ◽  
Frontal Pole ◽  
Neural Basis ◽  
Reward Prediction ◽  
Behavioral Impairments ◽  
Adults With Asd

Few studies have explored neural mechanisms of reward learning in ASD despite evidence of behavioral impairments of predictive abilities in ASD. To investigate the neural correlates of reward prediction errors in ASD, 16 adults with ASD and 14 typically developing controls performed a prediction error task during fMRI scanning. Results revealed greater activation in the ASD group in the left paracingulate gyrus during signed prediction errors and the left insula and right frontal pole during thresholded unsigned prediction errors. Findings support atypical neural processing of reward prediction errors in ASD in frontostriatal regions critical for prediction coding and reward learning. Results provide a neural basis for impairments in reward learning that may contribute to traits common in ASD (e.g., intolerance of unpredictability).

Congenital Mirror Movements: Behavioral, Neural, Genetic, and Clinical Issues

2018 ◽  
Vol 2 (Fall 2018) ◽  
pp. 23-33
Author(s):  
Jordan R. Gardner ◽  
Elizabeth A. Franz
Keyword(s):  
Somatosensory System ◽  
Clinical Importance ◽  
Neural Mechanism ◽  
Neural Mechanisms ◽  
Future Research ◽  
Life Outcomes ◽  
Mirror Movements ◽  
Corticospinal Tracts ◽  
Heterogeneous Nature ◽  
Causal Genes

Non-syndromic congenital mirror movements (CMM) is a rare neurological condition, either inherited or sporadic, in which affected individuals lack independent dexterity of hand and finger movements. With all volitional movements of the hands and fingers, unintentional mirroring occurs in the opposite-side homologous effectors. A hallmark neural mechanism of CMM is abnormal, active, extra ipsilateral corticospinal tracts. Mutations in four different causal genes have been identified so far. The present review considers the physiology underlying CMM, including its implicated neural mechanisms and clinical relevance. The heterogeneous nature of the condition is highlighted, particularly in terms of the clinical importance of factors associated with the mirroring phenotype or phenotypes. Speculation about the possible effects of CMM on the somatosensory system is also included as a prospective direction for further study. Despite some inconvenience and occasional discomfort associated with CMM, the potential for highly positive life outcomes is illuminated. Lastly, CMM management is discussed as a key goal toward which future research should stride.

Social cognition, brain networks and schizophrenia

2004 ◽  
Vol 34 (3) ◽  
pp. 391-400 ◽  
Author(s):  
K.-H. LEE ◽  
T. F. D. FARROW ◽  
S. A. SPENCE ◽  
P. W. R. WOODRUFF
Keyword(s):  
Prefrontal Cortex ◽  
Social Cognition ◽  
Literature Review ◽  
Social Functioning ◽  
Frontal Lobe ◽  
Temporal Cortex ◽  
Neural Mechanisms ◽  
Neural Basis ◽  
Future Studies ◽  
Shed Light

Background. A better understanding of the neural basis of social cognition including mindreading (or theory of mind) and empathy might help to explain some deficits in social functioning in people with schizophrenia. Our aim was to review neuroimaging and neuropsychological studies on social cognition, as they may shed light on the neural mechanisms of social cognition and its dysfunction in patients with schizophrenia.Method. A selective literature review was undertaken.Results. Neuroimaging and neuropsychological studies suggest convergence upon specific networks for mindreading and empathy (the temporal cortex, amygdala and the prefrontal cortex). The frontal lobe is likely to play a central role in enabling social cognition, but mindreading and empathic abilities may require relatively different weighting of subcomponents within the same frontal-temporal social cognition network.Conclusions. Disturbances in social cognition may represent an abnormal interaction between frontal lobe and its functionally connected cortical and subcortical areas. Future studies should seek to explore the heterogeneity of social dysfunction within schizophrenia.

scholarly journals Neural Basis for Regulation of Vasopressin Secretion by Anticipated Disturbances in Osmolality

2021 ◽  
Author(s):  
Angela Kim ◽  
Joseph C. Madara ◽  
Chen Wu ◽  
Mark L. Andermann ◽  
Bradford B. Lowell
Keyword(s):  
Water Balance ◽  
Arcuate Nucleus ◽  
Feedback Regulation ◽  
Neural Mechanisms ◽  
Neuron Activity ◽  
Neural Basis ◽  
Water Excretion ◽  
Hypothalamic Arcuate Nucleus ◽  
Vasopressin Secretion ◽  
Renal Water Excretion

AbstractWater balance, tracked by extracellular osmolality, is regulated by feedback and feedforward mechanisms. Feedback regulation is reactive, occurring as deviations in osmolality are detected. Feedforward or presystemic regulation is proactive, occurring when disturbances in osmolality are anticipated. Vasopressin (AVP) is a key hormone regulating water balance and is released during hyperosmolality to limit renal water excretion. AVP neurons are under feedback and feedforward regulation. Not only do they respond to disturbances in blood osmolality, but they are also rapidly suppressed and stimulated, respectively, by drinking and eating, which will ultimately decrease and increase osmolality. Here, we demonstrate that AVP neuron activity is regulated by multiple anatomically-and functionally-distinct neural circuits. Notably, presystemic regulation during drinking and eating are mediated by non-overlapping circuits that involve the lamina terminalis and hypothalamic arcuate nucleus, respectively. These findings reveal neural mechanisms that support differential regulation of AVP release by diverse behavioral and physiological stimuli.

scholarly journals Neural mechanisms of oculomotor abnormalities in the infantile strabismus syndrome

2017 ◽  
Vol 118 (1) ◽  
pp. 280-299 ◽  
Author(s):  
Mark M. G. Walton ◽  
Adam Pallus ◽  
Jérome Fleuriet ◽  
Michael J. Mustari ◽  
Kristina Tarczy-Hornoch
Keyword(s):  
Visual Cortex ◽  
Eye Movements ◽  
Nonhuman Primate ◽  
Neural Mechanisms ◽  
Sensitive Period ◽  
Compelling Evidence ◽  
Neural Basis ◽  
Brain Areas ◽  
Oculomotor Nuclei ◽  
Oculomotor Abnormalities

Infantile strabismus is characterized by numerous visual and oculomotor abnormalities. Recently nonhuman primate models of infantile strabismus have been established, with characteristics that closely match those observed in human patients. This has made it possible to study the neural basis for visual and oculomotor symptoms in infantile strabismus. In this review, we consider the available evidence for neural abnormalities in structures related to oculomotor pathways ranging from visual cortex to oculomotor nuclei. These studies provide compelling evidence that a disturbance of binocular vision during a sensitive period early in life, whatever the cause, results in a cascade of abnormalities through numerous brain areas involved in visual functions and eye movements.

How do we see what is not there?

1998 ◽  
Vol 21 (6) ◽  
pp. 773-774
Author(s):  
Lothar Spillmann ◽  
John S. Werner
Keyword(s):  
Long Range ◽  
Neural Mechanism ◽  
Neural Mechanisms ◽  
Range Interaction ◽  
Perceptual Completion ◽  
Long Range Interaction

Pessoa et al. provide a valuable taxonomy of perceptual completion phenomena, but it is not yet clear whether these phenomena are mediated by one kind of neural mechanism or more. We suggest three possible neural mechanisms of long-range interaction to stimulate further perceptual and neurophysiological investigation of perceptual completion and filling-in.

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