scholarly journals Spinal Cord Injury and Bladder Dysfunction: New Ideas about an Old Problem

2011 ◽  
Vol 11 ◽  
pp. 214-234 ◽  
Author(s):  
Célia Duarte Cruz ◽  
Francisco Cruz
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Bladder Function ◽  
Neuronal Circuits ◽  
Therapeutic Approaches ◽  
Cord Injury ◽  
New Ideas ◽  
The Central Nervous System ◽  
Induced Changes

Control of the lower urinary tract (LUT) requires complex neuronal circuits that involve elements located at the peripheral nervous system and at different levels of the central nervous system. Spinal cord injury (SCI) interrupts these neuronal circuits and jeopardizes the voluntary control of bladder function. In most cases, SCI results in a period of bladder areflexia, followed by the emergence of neurogenic detrusor overactivity (NDO). Only recently, researchers have started to have a clearer vision ofthe mechanisms of SCI-induced changes affecting LUT control. For example, changes in the urothelium have recently been described and proposed to play a role in NDO. As such, a better understanding of NDO has generated new opportunities to investigate novel therapeutic approaches for NDO.In the present paper, we aim to update recent data concerning SCI-induced LUT dysfunction and therapeutic approaches commonly used to deal with NDO. We make a brief description of LUT control and changes occurring after SCI, and refer to new therapeutic options, including vanniloids and botulinum toxin. Finally, we discuss mechanisms of spinal cord repair, an interesting and very active area of investigation that has obtained some promising results in the recovery of LUT control.

scholarly journals Acellularized spinal cord scaffolds incorporating bpV(pic)/PLGA microspheres promote axonal regeneration and functional recovery after spinal cord injury

RSC Advances ◽  
2020 ◽  
Vol 10 (32) ◽  
pp. 18677-18686
Author(s):  
Jia Liu ◽  
Kai Li ◽  
Ke Huang ◽  
Chengliang Yang ◽  
Zhipeng Huang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Axonal Regeneration ◽  
Traumatic Injury ◽  
High Rate ◽  
Plga Microspheres ◽  
Cord Injury ◽  
The Central Nervous System

Spinal cord injury (SCI) is a traumatic injury to the central nervous system (CNS) with a high rate of disability and a low capability of self-recovery.

scholarly journals Neuroplasticity After Spinal Cord Injury and Training: An Emerging Paradigm Shift in Rehabilitation and Walking Recovery

2006 ◽  
Vol 86 (10) ◽  
pp. 1406-1425 ◽  
Author(s):  
Andrea L Behrman ◽  
Mark G Bowden ◽  
Preeti M Nair
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Paradigm Shift ◽  
Clinical Findings ◽  
Cord Injury ◽  
Rehabilitation Concepts ◽  
The Central Nervous System ◽  
Walking Recovery ◽  
Physiologically Based Approach

AbstractPhysical rehabilitation after spinal cord injury has been based on the premise that the nervous system is hard-wired and irreparable. Upon this assumption, clinicians have compensated for irremediable sensorimotor deficits using braces, assistive devices, and wheelchairs to achieve upright and seated mobility. Evidence from basic science, however, demonstrates that the central nervous system after injury is malleable and can learn, and this evidence has challenged our current assumptions. The evidence is especially compelling concerning locomotion. The purpose of this perspective article is to summarize the evidence supporting an impending paradigm shift from compensation for deficits to rehabilitation as an agent for walking recovery. A physiologically based approach for the rehabilitation of walking has developed, translating evidence for activity-dependent neuroplasticity after spinal cord injury and the neurobiological control of walking. Advanced by partnerships among neuroscientists, clinicians, and researchers, critical rehabilitation concepts are emerging for activity-based therapy to improve walking recovery, with promising clinical findings.

Adaptive trial designs for spinal cord injury clinical trials directed to the central nervous system

Spinal Cord ◽  
2020 ◽  
Vol 58 (12) ◽  
pp. 1235-1248
Author(s):  
M. J. Mulcahey ◽  
Linda A. T. Jones ◽  
Frank Rockhold ◽  
Rϋediger Rupp ◽  
John L. K. Kramer ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Clinical Trials ◽  
Nervous System ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Adaptive Trial

scholarly journals The role of connexin43 in neuropathic pain induced by spinal cord injury

2019 ◽  
Vol 51 (6) ◽  
pp. 555-561 ◽  
Author(s):  
Anhui Wang ◽  
Changshui Xu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Cell Metabolism ◽  
Pain Models ◽  
Cord Injury ◽  
The Central Nervous System ◽  
And Function

Abstract Neuropathic pain is caused by the damage or dysfunction of the nervous system. In many neuropathic pain models, there is an increase in the number of gap junction (GJ) channels, especially the upregulation of the expression of connexin43 (Cx43), leading to the secretion of various types of cytokines and involvement in the formation of neuropathic pain. GJs are widely distributed in mammalian organs and tissues, and Cx43 is the most abundant connexin (Cx) in mammals. Astrocytes are the most abundant glial cell type in the central nervous system (CNS), which mainly express Cx43. More importantly, GJs play an important role in regulating cell metabolism, signaling, and function. Many existing literatures showed that Cx43 plays an important role in the nervous system, especially in the CNS under normal and pathological conditions. However, many internal mechanisms have not yet been thoroughly explored. In this review, we summarized the current understanding of the role and association of Cx and pannexin channels in neuropathic pain, especially after spinal cord injury, as well as some of our own insights and thoughts which suggest that Cx43 may become an emerging therapeutic target for future neuropathic pain, bringing new hope to patients.

scholarly journals Rho activation patterns after spinal cord injury and the role of activated Rho in apoptosis in the central nervous system

2003 ◽  
Vol 162 (2) ◽  
pp. 233-243 ◽  
Author(s):  
Catherine I. Dubreuil ◽  
Matthew J. Winton ◽  
Lisa McKerracher
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Axon Growth ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Cord Injury ◽  
The Central Nervous System

Growth inhibitory proteins in the central nervous system (CNS) block axon growth and regeneration by signaling to Rho, an intracellular GTPase. It is not known how CNS trauma affects the expression and activation of RhoA. Here we detect GTP-bound RhoA in spinal cord homogenates and report that spinal cord injury (SCI) in both rats and mice activates RhoA over 10-fold in the absence of changes in RhoA expression. In situ Rho-GTP detection revealed that both neurons and glial cells showed Rho activation at SCI lesion sites. Application of a Rho antagonist (C3–05) reversed Rho activation and reduced the number of TUNEL-labeled cells by ∼50% in both injured mouse and rat, showing a role for activated Rho in cell death after CNS injury. Next, we examined the role of the p75 neurotrophin receptor (p75NTR) in Rho signaling. After SCI, an up-regulation of p75NTR was detected by Western blot and observed in both neurons and glia. Treatment with C3–05 blocked the increase in p75NTR expression. Experiments with p75NTR-null mutant mice showed that immediate Rho activation after SCI is p75NTR dependent. Our results indicate that blocking overactivation of Rho after SCI protects cells from p75NTR-dependent apoptosis.

scholarly journals Investigating Mimetics of a Peptide Derived from the Effector Domain of MARCKS as Possible Therapeutics for Spinal Cord Injury

2021 ◽  
Vol 1 (3) ◽  
Author(s):  
Monica Tschang ◽  
Melitta Schachner
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Female Mice ◽  
Blood Brain ◽  
Cord Injury ◽  
The Central Nervous System

Like other conditions affecting the central nervous system, spinal cord injury (SCI) is difficult to treat with molecular therapies because the blood-brain barrier makes intravenous treatments largely ineffective. For example, a synthetic peptide chain derived from the effector domain (ED) of myristoylated alanine-rich C-kinase substrate (MARCKS) has been found to improve functional recovery after SCI in female mice; however, peptides do not always pass the blood-brain barrier and are easily degraded due to natural proteases and are excreted during kidney filtration. Therefore, the ED peptide cannot access the central nervous system to exhibit its effects if administered intravenously. Instead of injecting the ED peptide into the bloodstream, we propose to find compounds that can pass the blood-brain barrier in place of the ED peptide, improving treatment compatibility. To find such alternatives, we screened compound libraries via competitive enzyme-linked immunosorbent assay (ELISA) and identified five potential ED peptide mimetics—compounds that mimic the structure and function of the ED peptide. We then used another competitive ELISA to verify their structural similarity to the peptide. After performing toxicity tests to determine the appropriate concentrations of the mimetics to use in functional assays, we found that all five mimetics trigger a significant increase in neurite length in neurons from female mice, but not male mice, when compared to the vehicle control solution. Although more functional tests are necessary, these results suggest that these mimetics trigger ED peptide functions and may provide a more efficient treatment alternative for SCI.

scholarly journals Cosine tuning determines plantarflexors' activities during human upright standing and is affected by incomplete spinal cord injury

2020 ◽  
Author(s):  
Kai Lon Fok ◽  
Jae W Lee ◽  
Janelle Unger ◽  
Katherine Chan ◽  
Daichi Nozaki ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Knee Extension ◽  
Medial Gastrocnemius ◽  
Quiet Standing ◽  
Incomplete Spinal Cord Injury ◽  
Cord Injury ◽  
The Central Nervous System

Plantarflexors such as the soleus (SOL) and medial gastrocnemius (MG) play key roles in controlling bipedal stance; however, how the central nervous system controls the activation levels of these plantarflexors is not well understood. Here we investigated how the central nervous system controls the plantarflexors' activation level during quiet standing in a cosine tuning manner where the maximal activation is achieved in a preferred direction (PD). Further, we investigated how spinal cord injury affects these plantarflexors' activations. Thirteen healthy adults (AB) and thirteen individuals with chronic, incomplete spinal cord injury (iSCI) performed quiet standing trials. Their body kinematics, kinetics as well as electromyography signals from the MG and SOL were recorded. In the AB-group, we found that the plantarflexors followed the cosine tuning manner during quiet standing. That is, MG was most active when the ratio of plantarflexion torque to knee extension torque was approximately 2:-3, while SOL was most active when the ratio was approximately 2:1. This suggests that the SOL muscle despite being a monoarticular muscle is sensitive to both ankle plantarflexion and knee extension during quiet standing. The difference in the PDs accounts for the phasic activity of MG and for the tonic activity of SOL. Unlike the AB-group, the MG's activity was similar to the SOL's activity in the iSCI-group, and the SOL PDs were similar to the ones in the AB-group. This result suggests that chronic iSCI affects the control strategy, i.e., cosine tuning, for MG, which may affect standing balance in individuals with iSCI.

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