Neuronal activity and microglial activation support corticospinal tract and proprioceptive afferent sprouting in spinal circuits after a corticospinal system lesion

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.

Download Full-text

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

10.36227/techrxiv.17133251.v1 ◽

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.

Download Full-text

Development of the corticospinal system and hand motor function: central conduction times and motor performance tests

Developmental Medicine & Child Neurology ◽

10.1017/s0012162200000384 ◽

2000 ◽

Vol 42 (4) ◽

pp. 220-227 ◽

Cited By ~ 58

Author(s):

U M Fietzek ◽

F Heinen ◽

S Berweck ◽

S Maute ◽

A Hufschmidt ◽

...

Keyword(s):

Motor Function ◽

Motor Performance ◽

Performance Tests ◽

Corticospinal System

Download Full-text

Inflammational Animal Models for Schizophrenia

Zeitschrift für Psychologie ◽

10.1027/2151-2604/a000216 ◽

2015 ◽

Vol 223 (3) ◽

pp. 157-164 ◽

Cited By ~ 1

Author(s):

Georg Juckel

Keyword(s):

Animal Model ◽

Animal Models ◽

Immune Activation ◽

Microglial Activation ◽

Treatment Options ◽

Early Adulthood ◽

Brain Regions ◽

Synaptic Connections ◽

Preventive Interventions ◽

Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

Download Full-text