scholarly journals Extensors respond faster than flexors for the MCP joints even under the loss of the corticospinal system

2021 ◽  
Author(s):  
Dongwon Kim ◽  
Raziyeh Baghi ◽  
Kyung Koh ◽  
Li-Qun Zhang ◽  
Jong-Moon Hwang
Keyword(s):  
Corticospinal Tract ◽  
Force Generation ◽  
Finger Movement ◽  
Neural Pathways ◽  
Neural Pathway ◽  
Paretic Side ◽  
Corticospinal System ◽  
Movement Smoothness ◽  
Measured Activation ◽  
Flexion And Extension

Damage in the corticospinal system following stroke produces imbalance between flexors and extensors in the upper extremity including the fingers, eventually leading to flexion-favored postures. The substitution of the reticospinal tract for the damaged corticospinal tract is known to excessively activate flexors of the fingers while the fingers are voluntarily being extended. Here, we questioned whether the cortical source or/and neural pathways of the flexors and extensors of the fingers are coupled and what factor of impairment influences finger movement. In this study, a total of 7 male participants with hemiplegic stroke conducted isometric flexion and extension at the MCP joints in response to auditory tones. We measured activation and de-activation delays of the flexor and extensor of the MCP joints on the paretic side, as well as, force generation and co-contraction between the flexor and extensor. All participants generated greater torque in the direction of flexion (p=0.017). Regarding co-contraction, coupled activation of the extensor is also made during flexion in the similar way to coupled activation of the flexor made during extension. As opposite to our expectation, we observed that during extension, the extensor showed marginally significantly faster activation (p=0.66) while it showed faster de-activation (p=0.038), in comparison to activation and de-activation of the flexor during flexion. But movement smoothness was not affected by those factors. Our results imply that the cortical source and neural pathway for the extensors of the MCP joints are not coupled with those for the flexors of the MCP joints and extensor weakness mainly contributes to the asymmetry between flexors and extensors.

Extensors respond faster than flexors for the MCP joints even under the loss of the corticospinal system

2021 ◽  
Author(s):  
Dongwon Kim ◽  
Raziyeh Baghi ◽  
Kyung Koh ◽  
Li-Qun Zhang ◽  
Jong-Moon Hwang
Keyword(s):  
Corticospinal Tract ◽  
Force Generation ◽  
Finger Movement ◽  
Neural Pathways ◽  
Neural Pathway ◽  
Paretic Side ◽  
Corticospinal System ◽  
Movement Smoothness ◽  
Measured Activation ◽  
Flexion And Extension

Damage in the corticospinal system following stroke produces imbalance between flexors and extensors in the upper extremity including the fingers, eventually leading to flexion-favored postures. The substitution of the reticospinal tract for the damaged corticospinal tract is known to excessively activate flexors of the fingers while the fingers are voluntarily being extended. Here, we questioned whether the cortical source or/and neural pathways of the flexors and extensors of the fingers are coupled and what factor of impairment influences finger movement. In this study, a total of 7 male participants with hemiplegic stroke conducted isometric flexion and extension at the MCP joints in response to auditory tones. We measured activation and de-activation delays of the flexor and extensor of the MCP joints on the paretic side, as well as, force generation and co-contraction between the flexor and extensor. All participants generated greater torque in the direction of flexion (p=0.017). Regarding co-contraction, coupled activation of the extensor is also made during flexion in the similar way to coupled activation of the flexor made during extension. As opposite to our expectation, we observed that during extension, the extensor showed marginally significantly faster activation (p=0.66) while it showed faster de-activation (p=0.038), in comparison to activation and de-activation of the flexor during flexion. But movement smoothness was not affected by those factors. Our results imply that the cortical source and neural pathway for the extensors of the MCP joints are not coupled with those for the flexors of the MCP joints and extensor weakness mainly contributes to the asymmetry between flexors and extensors.

Contralateral Movement and Extensor Force Generation Alter Flexion Phase Muscle Coordination in Pedaling

2000 ◽  
Vol 83 (6) ◽  
pp. 3351-3365 ◽  
Author(s):  
Lena H. Ting ◽  
Steven A. Kautz ◽  
David A. Brown ◽  
Felix E. Zajac
Keyword(s):  
Muscle Activity ◽  
Tibialis Anterior ◽  
Rectus Femoris ◽  
The Body ◽  
Force Generation ◽  
Mechanical Transmission ◽  
Electromyographic Activity ◽  
Neural Pathways ◽  
Control Mechanisms ◽  
Muscle Coordination

The importance of bilateral sensorimotor signals in coordination of locomotion has been demonstrated in animals but is difficult to ascertain in humans due to confounding effects of mechanical transmission of forces between the legs (i.e., mechanical interleg coupling). In a previous pedaling study, by eliminating mechanical interleg coupling, we showed that muscle coordination of a unipedal task can be shaped by interlimb sensorimotor pathways. Interlimb neural pathways were shown to alter pedaling coordination as subjects pedaling unilaterally exhibited increased flexion-phase muscle activity compared with bilateral pedaling even though the task mechanics performed by the pedaling leg(s) in the unilateral and bilateral pedaling tasks were identical. To further examine the relationship between contralateral sensorimotor state and ipsilateral flexion-phase muscle coordination during pedaling, subjects in this study pedaled with one leg while the contralateral leg either generated an extensor force or relaxed as a servomotor either held that leg stationary or moved it in antiphase with the pedaling leg. In the presence of contralateral extensor force generation, muscle activity in the pedaling leg during limb flexion was reduced. Integrated electromyographic activity of the pedaling-leg hamstring muscles (biceps femoris and semimembranosus) during flexion decreased by 25–30%, regardless of either the amplitude of force generated by the nonpedaling leg or whether the leg was stationary or moving. In contrast, rectus femoris and tibialis anterior activity during flexion decreased only when the contralateral leg generated high rhythmic force concomitant with leg movement. The results are consistent with a contralateral feedforward mechanism triggering flexion-phase hamstrings activity and a contralateral feedback mechanism modulating rectus femoris and tibialis anterior activity during flexion. Because only muscles that contribute to flexion as a secondary function were observed, it is impossible to know whether the modulatory effect also acts on primary, unifunctional, limb flexors or is specific to multifunctional muscles contributing to flexion. The influence of contralateral extensor-phase sensorimotor signals on ipsilateral flexion may reflect bilateral coupling of gain control mechanisms. More generally, these interlimb neural mechanisms may coordinate activity between muscles that perform antagonistic functions on opposite sides of the body. Because pedaling and walking share biomechanical and neuronal control features, these mechanisms may be operational in walking as well as pedaling.

scholarly journals The neural pathway midline crossing theory: a historical analysis of Santiago Rámon y Cajal’s contribution on cerebral localization and on contralateral forebrain organization

2019 ◽  
Vol 47 (3) ◽  
pp. E10
Author(s):  
Carla Mora ◽  
Carlos Velásquez ◽  
Juan Martino
Keyword(s):  
Brain Plasticity ◽  
Great Influence ◽  
Optic Chiasm ◽  
Compensatory Mechanism ◽  
Neural Pathways ◽  
Neural Pathway ◽  
Cortical Function ◽  
Cerebral Lateralization ◽  
Midline Crossing ◽  
Crossing Theory

Throughout history, many scientists have wondered about the reason for neural pathway decussation in the CNS resulting in contralateral forebrain organization. Hitherto, one of the most accepted theories is the one described by the renowned Spanish physician, Santiago Rámon y Cajal at the end of the 19th century. This Nobel Prize winner, among his many contributions to science, gave us the answer to this question: the key lies in the optic chiasm. Based on the fact that the ocular lenses invert the image formed in the retina, Cajal explained how the decussation of the fibers in the optic chiasm is necessary to obtain a continuous image of the outside in the brain. The crossing of the tactile and motor pathways occurred posteriorly as a compensatory mechanism to allow the cortical integration of the sensory, motor, and visual functions. This theory had a great influence on the scientific community of his time, and maintains its importance today, in which none of the theories formulated to date has managed to entirely refute Cajal’s. In addition, the decussation of neural pathways plays a significant role in different diseases, especially in the recovery process after a hemispheric lesion and in several congenital pathologies. The advantages of cerebral lateralization have also recently been published, although the evolutionary connection between fiber decussation and cortical function lateralization remains a mystery to be solved. A better understanding of the molecular and genetic substrates of the midline crossing processes might result in significant clinical advances in brain plasticity and repair.

Wrist Posture Does Not Influence Finger Interdependence

2019 ◽  
Vol 35 (6) ◽  
pp. 410-417
Author(s):  
Niranjan Chakrabhavi ◽  
Varadhan SKM
Keyword(s):  
Metacarpophalangeal Joint ◽  
Neural Mechanisms ◽  
Finger Movement ◽  
Current Experiment ◽  
Healthy Human ◽  
Involuntary Movements ◽  
Human Participants ◽  
Middle Ring ◽  
Flexion And Extension

A task involving an instructed finger movement causes involuntary movements in the noninstructed fingers of the hand, also known as finger interdependence. It is associated with both mechanical and neural mechanisms. The current experiment investigated the effect of finger interdependence due to systematic changes of the wrist posture, close to neutral. Eight right-handed healthy human participants performed submaximal cyclic flexion and extension at the metacarpophalangeal joint at 0° neutral, 30° extension, and 30° flexion wrist postures, respectively. The experiment comprised of an instruction to move one of the 4 fingers—index, middle, ring, and little. Movements of the instructed and noninstructed fingers were recorded. Finger interdependence was quantified using enslavement matrix, individuation index, and stationarity index, and it was compared across wrist postures. The authors found that the finger interdependence does not change with changes in wrist posture. Further analysis showed that individuation and stationarity indices were mostly equivalent across wrist postures, and their effects were much smaller than the average differences present among the fingers. The authors conclude that at wrist postures close to neutral, the finger interdependence is not affected by wrist posture.

Neurologic Findings of Craniovertebral Junction Disease

Neurosurgery ◽  
2010 ◽  
Vol 66 (suppl_3) ◽  
pp. A13-A21 ◽  
Author(s):  
David Benglis ◽  
Allan D. Levi
Keyword(s):  
Corticospinal Tract ◽  
Craniovertebral Junction ◽  
Sensory Function ◽  
Neural Pathways ◽  
Tract Tracing ◽  
New Developments ◽  
The Past ◽  
Central Cord Syndrome ◽  
Lesion Studies ◽  
Neurologic Findings

Abstract IN THIS REVIEW, we explain the origins of central cord syndrome and Bell's cruciate paralysis and the intricate detail of neural pathways located in this region and their influence on motor and sensory function. Although lesion studies and tract tracing studies on primates over the past 50 years refute the theory of a somatotopically organized corticospinal tract, this concept continues to pervade many neuroanatomic texts. We categorized the various pathologies of the craniovertebral junction and their unique neurologic presentations. New developments in the fields of neuroscience of spinal tract lesioning are also discussed.

scholarly journals Lesion Area in the Cerebral Cortex Determines the Patterns of Axon Rewiring of Motor and Sensory Corticospinal Tracts After Stroke

2021 ◽  
Vol 15 ◽  
Author(s):  
Tokiharu Sato ◽  
Yuka Nakamura ◽  
Akinori Takeda ◽  
Masaki Ueno
Keyword(s):  
Cerebral Cortex ◽  
Brain Injuries ◽  
Corticospinal Tract ◽  
Cervical Spinal Cord ◽  
Neural Substrates ◽  
Neural Pathway ◽  
Lesion Area ◽  
Basic Principles ◽  
Corticospinal Tracts ◽  
Small Stroke

The corticospinal tract (CST) is an essential neural pathway for reorganization that recovers motor functions after brain injuries such as stroke. CST comprises multiple pathways derived from different sensorimotor areas of the cerebral cortex; however, the patterns of reorganization in such complex pathways postinjury are largely unknown. Here we comprehensively examined the rewiring patterns of the CST pathways of multiple cerebral origins in a mouse stroke model that varied in size and location in the sensorimotor cortex. We found that spared contralesional motor and sensory CST axons crossed the midline and sprouted into the denervated side of the cervical spinal cord after stroke in a large cortical area. In contrast, the contralesional CST fibers did not sprout in a small stroke, whereas the ipsilesional axons from the spared motor area grew on the denervated side. We further showed that motor and sensory CST axons did not innervate the projecting areas mutually when either one was injured. The present results reveal the basic principles that generate the patterns of CST rewiring, which depend on stroke location and CST subtype. Our data indicate the importance of targeting different neural substrates to restore function among the types of injury.

scholarly journals Brain micro-inflammation at specific vessels dysregulates organ-homeostasis via the activation of a new neural circuit

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Yasunobu Arima ◽  
Takuto Ohki ◽  
Naoki Nishikawa ◽  
Kotaro Higuchi ◽  
Mitsutoshi Ota ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Neural Circuit ◽  
Gastrointestinal Disease ◽  
Third Ventricle ◽  
Neural Pathways ◽  
Neural Pathway ◽  
Dorsomedial Nucleus ◽  
Boundary Area ◽  
Gastrointestinal Failure ◽  
The Brain

Impact of stress on diseases including gastrointestinal failure is well-known, but molecular mechanism is not understood. Here we show underlying molecular mechanism using EAE mice. Under stress conditions, EAE caused severe gastrointestinal failure with high-mortality. Mechanistically, autoreactive-pathogenic CD4+ T cells accumulated at specific vessels of boundary area of third-ventricle, thalamus, and dentate-gyrus to establish brain micro-inflammation via stress-gateway reflex. Importantly, induction of brain micro-inflammation at specific vessels by cytokine injection was sufficient to establish fatal gastrointestinal failure. Resulting micro-inflammation activated new neural pathway including neurons in paraventricular-nucleus, dorsomedial-nucleus-of-hypothalamus, and also vagal neurons to cause fatal gastrointestinal failure. Suppression of the brain micro-inflammation or blockage of these neural pathways inhibited the gastrointestinal failure. These results demonstrate direct link between brain micro-inflammation and fatal gastrointestinal disease via establishment of a new neural pathway under stress. They further suggest that brain micro-inflammation around specific vessels could be switch to activate new neural pathway(s) to regulate organ homeostasis.

scholarly journals A neural pathway superposition model and the explanation of depression and human behaviour

2019 ◽  
Author(s):  
Alex Lee
Keyword(s):  
Neural Circuit ◽  
Neural System ◽  
Death Sentence ◽  
Neural Pathways ◽  
Superposition Model ◽  
Neural Pathway ◽  
Huge Amount ◽  
The Future ◽  
Future Child ◽  
Commit Suicide

Some depressed people committed suicide, why their consciousness can not defeat the suicide? The author gives a neural pathway superposition model to explain it. If one thing happens in front of a child and an adult, the adult’s neural pathway about this thing is actived , the child copies the same neural pathway as this adult, this copy includes copy the predictions of the future, child can copy different people’s neural pathways. So the number of one neural pathway can be superposed from one to several even more. The superposition of one neural pathway causes the superposition of the chemistry emission of the neural pathway in brain. After many generations, if there are huge numbers of the superposition of the neural pathway in one person’s brain, there are huge amount of chemistry emission in brain. If this neural pathway emits poison or negative chemistry, the superposition of the poison or the negative chemistry to a large quantity makes this person can not bear, the suicide is the end of the emission of so much poison in neural system. For an individual, when the same neural circuit is superimposed to tens of thousands, he will feel that tens of thousands of people think that something should be guilty or should commit suicide or in the future he will be die, It is difficult for individuals to fight against the death sentence or prediction of 10,000 individual. The neural editing can cure depression. Another method is not to edit the end connection of the neural circuit, but to remove the neural circuit that secretes negative chemicals, which can completely treat depression.

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