Special Issue "Pathophysiology of Spinal Cord Injury (SCI)"
Deadline for manuscript submissions: 31 January 2022.
Interests: spinal cord injury; axon regeneration; aging; gene therapy; drug discovery; cardiometabolic disease; bowel dysfunction
Interests: spinal cord injury; neural control of breathing; plasticity; axonal regeneration and sprouting; personalized medicine
Spinal cord injury (SCI) leads to paralysis, sensory, and autonomic nervous system dysfunctions. However, the pathophysiology of SCI is complex, not limited to the nervous system. Indeed, several other organs and tissue are also affected by the injury, directly or not, acutely or chronically, which induces numerous health complications. While a lot of research has been performed to repair motor and sensory functions, SCI-induced health issues are less studied, although they represent a major concern among patients. There is a gap of knowledge in pre-clinical models studying these SCI-induced health complications that limits translational applications in humans.
In this Special Issue of Biology, we encourage the submission of manuscripts on any aspects of the pathophysiology of spinal cord injuries. This includes, but is not limited to, the impact of SCI on cardiovascular function, bladder and bowel function, risk of infections associated with SCI, liver pathology, metabolic syndrome, bones and muscles loss, and cognitive functions. We welcome original research articles, review articles, and short communications. This Special Issue will provide an overview of the pre-clinical models available to study the pathophysiology of SCI, and bring experts in the field to discuss what is needed to increase the research and translational potential of SCI-induced health complications.
Dr. Cédric G. Geoffroy
Dr. Warren Alilain
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- spinal cord injury
- cardiovascular function
- bladder function
- bowel function
- liver pathology
- metabolic syndrome
- bone loss
- muscle loss
- cognitive functions
- sexual functions
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Monoaminergic Influence on Spinal Cord Injury: The Upside of Descending Spared Fibers
Authors: Gizelle N. K. Fauss and James W. Grau
Affiliation: Department of Psychological and Brain Sciences, Texas A&M University, College Station, TX, USA
Abstract: Spinal cord injury (SCI) often leads to the disruption of descending modulatory fibers. Indeed, secondary complications following the initial trauma such as inflammation, neuropathy and axotomy can lead to an exaggerated loss of descending regulation. Serotonin, dopamine and noradrenaline are common modulatory neurotransmitters that regulate various spinal functions through supraspinal systems. The loss of descending control over these processes after SCI can lead to hyperexcitability and central sensitization, the reduction of inhibitory regulation, and maladaptive plasticity. In fact, monoaminergic neuromodulators have been implicated in the propagation of neural damage, the development of allodynia and hyperalgesia, and the dysregulation of autonomic output. While extensive work has been conducted to determine the cellular mechanisms that underlie these modulators on neuropathic pain, locomotion, and autonomic function, little attention has been given to the body of literature that explore the impact of disrupted descending pathways on the maintenance of homeostatic processes such as neuroplasticity and cell survival in the context of SCI. This overview will focus on the consequences of monoaminergic dysregulation after SCI and how this influences cell loss, plasticity, and peripheral processes. We will consider the neuromodulatory fiber pathways that mediate these maladaptive effects and provide a discussion of potential therapeutic interventions that improve functional recovery.
Title: Osteopenia in a Mouse Model of Spinal Cord Injury: Effects of Age, Sex and Motor Function
Authors: Michelle Hook 1,*, Alyssa Falck 2, Ravali Dundumulla 1, Mabel Terminel 1, Cédric G. Geoffroy 1 and Dana Gaddy 2
Affiliation: 1 Neuroscience & Experimental Therapeutics, 8447 Riverside Pkwy, Bryan, TX 77807, USA
2 Department of Veterinary Integrative Biosciences, College of Veterinary Medicine, Texas A&M University, 4458 TAMU, College Station, TX 77845, USA
Abstract: After spinal cord injury (SCI), 80% of individuals are diagnosed with osteopenia or osteoporosis. The dramatic loss of bone after SCI increases the potential for fractures 100-fold, with post-fracture complications occurring in 54% of cases. With the age of new SCI injuries increasing, we hypothesized that a SCI-induced reduction in weight bearing could further exacerbate age-induced bone loss. To test this, young (2-3 months) and old (20-30 months) male and female mice were given a moderate spinal contusion injury (T9-T10), and recovery was assessed for 28 days (BMS, rearing counts, distance traveled). Tibial trabecular bone volume was measured after 28 days with ex vivo microCT. While BMS scores did not differ across groups, older subjects travelled less in the open field and there was a decrease in rearing with age and SCI. Older subjects also had decreased bone volume, and SCI further reduced bone volume in females, with a trend in males. Interestingly, both rearing and total activity correlated with decreased bone volume. These data underscore the importance of load and use on bone mass. While partial weight-bearing does not stabilize/reverse bone loss in humans, our data suggest that therapies that simulate complete loading may be effective after SCI.
Keywords: spinal cord injury; osteopenia; bone loss; recovery of function
Title: The Effect of Chronic Spinal Cord Injury Severity on Cardiometabolic Function
Authors: Adel. B. Ghnenis 1, Calvin. L. Jones 1, Arthur Sefiani 1, and Cédric. G. Geoffroy *
Affiliation: Department of Neuroscience & Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, Bryan, TX 77807, USA
Abstract: Changes in cardiometabolic function contribute to morbidity and mortality after chronic spinal cord injury (SCI). We examined the effects of SCI severity overtime on cardiac and liver function, body composition, glucose metabolism, and functional recovery following moderate and severe thoracic SCI in mice. We observed significant structural and functional cardiac changes with increased prevalence of liver echogenicity and fibrosis in mice with severe SCI. Moreover, there were significant changes in body composition (fat and lean %) and functional recovery in response to SCI severity. We demonstrated that disturbances in cardiometabolic function following thoracic SCI vary significantly depending upon the severity of the injury.