Chapters authored
Pharmacological and Nonpharmacological Therapeutic Strategies Based on the Pathophysiology of Acute and Chronic Spinal Cord Injury By Elisa Garcia, Roxana Rodríguez-Barrera, Jose Mondragón-Caso,
Horacio Carvajal and Antonio Ibarra
Spinal cord injury (SCI) induces a series of anatomic and physiological disorders which have severe repercussions on neural function. SCI is classified chronologically into an acute (primary and secondary phase) and a chronic phase. The primary phase results directly from the initial trauma and is comprised of disturbances in neural tissue (mainly axons), blood vessels, and spinal shock. Secondary injury results from a series of time-dependent pathophysiological changes, beginning in the first minutes after SCI and lasting days and weeks. This phase is characterized by biochemical and immunological alterations in the injury site and periphery, leading to neuronal over-excitation, apoptosis, and axonal demyelination. In chronic stages, the pathophysiology consists of disturbances in fiber organization, oligodendrocyte apoptosis, fibroglial scar formation, and cyst formation, leading to parenchymal alterations such as syringomyelia and hydromyelia hindering the possibility for functional basal axonal regeneration. This chapter will review a wide range of pharmacological and nonpharmacological therapeutic strategies in preclinical and clinical phases, each targeting different pathological mechanisms of SCI in acute and chronic stages of SCI; taking into account limitations, advances, scope, and new trends. The chapter focuses on the general aspects of SCI pathophysiology, pharmacological and nonpharmacological treatments acute and chronic stages of SCI.
Part of the book: Essentials of Spinal Cord Injury Medicine
Transplantation or Transference of Cultured Cells as a Treatment for Spinal Cord Injury By Roxana Rodríguez-Barrera, Karla Soria-Zavala, Julián García-Sánchez, Lisset Karina Navarro-Torres, Estefanía de la Cruz Castillo and Elisa García-Vences
Spinal cord injury (SCI) involves damage to the spinal cord causing both structural and functional changes, which can lead to temporary or permanent alterations. Even though there have been many advances in its treatment, the results of clinical trials suggest that the current therapies are not sufficiently effective. Recently, there has been a lot of interest in regulating this harmful environment by transplanting cultured cells and boosting their antiinflammatory cytokines and growth factors production. Several types of cells have been studied for SCI therapy including, Schwann cells (SC’s), olfactory ensheathing cells (OECs), choroid plexus epithelial cells (CPECs), and immune cells (ICs) (lymphocytes, dendritic cells and alternative macrophage and microglia phenotypes). These treatments have shown to be promising and in this chapter, we will review the general aspects of transplanting these cells for SCI therapy as well as the neuroprotective and regenerative responses that different types of cells have reached in different SCI models. The mesenchymal stem cells (MSC) are one of the most well studied cell types; however, they were not included in this section because they will be reviewed in another chapter of this book.
Part of the book: Spinal Cord Injury Therapy
Beyond the Quality of Life in Bowel Dysfunction after Spinal Cord Injury: Approaches to the Consequences in Motility, Immune System, and Microbiome By Estefanía de la Cruz-Castillo and Elisa García-Vences
Spinal cord injury (SCI) is a harmful event that involves several repercussions on sensory and motor function that affects the quality of life (QoL) of patients. After SCI, many damage mechanisms are activated that impact on both autonomous extrinsic and intrinsic innervation toward the gut, and these changes modify the gut motility causing bowel dysfunction (BD), an entity that affects 40% of patients with SCI, being the second comorbidity after loss of mobility with no recognized cure. The severity of complications is ruled by the level and severity of injury, having a worse prognosis with an injury that is the most proximal to the brain. In the last 5 years, some experiments have tried to elucidate the consequences of dysbiosis in the gut and aggregated proinflammatory processes. The goal of this chapter is to establish the importance of bacterial composition and immune system repercussions in bowel dysfunction after SCI and how could it give rise to new therapies.
Part of the book: Paraplegia
Rehabilitation Therapies in Spinal Cord Injury Patients By Brenda Rodríguez-Mendoza, Paola A. Santiago-Tovar, Marco A. Guerrero-Godinez and Elisa García-Vences
Spinal cord injury (SCI) represents a neurological life-changing condition that causes devastating physical, social, psychological, and economic consequences in the injured patient. It is due to traumatic causes that affect the motor and sensory functions, limiting daily life activities. Since rehabilitation is a fundamental process of recovery, this chapter will review diverse approaches in rehabilitation to restore or improve patients’ capability. In the first section, functionality and quality of life tools will be discussed. Subsequently, rehabilitation strategies and their adoption will be explained. Ultimately, rehabilitation goals, according to the level of injury, will be reviewed.
Part of the book: Paraplegia
Cytokines in Scar Glial Formation after an Acute and Chronic Spinal Cord Injury By Roxana Rodrígez-Barrera, Adrián Flores-Romero, Julián García-Sánchez, Lisset Karina Navarro-Torres, Marcela Garibay-López and Elisa García-Vences
The inflammatory response after a spinal cord injury (SCI) is a secondary mechanism of damage, this involves alterations at the local and systemic level, and it is mediated by cytokine participation that takes part actively. The excessive inflammatory response causes an autoreactive response that targets against components of the nervous tissue; this response lengthens the inflammatory process initiated during the acute phase. The participation of immune cells in acute phases is characterized by the arrival of neutrophils, macrophages, and microglia, as well as T lymphocytes, which express their peaks on different days post-injury (1st, 3rd, and 11th respectively). The chronic phase of the injury begins 14 days after it occurred, reaching its highest point at 60 days, and can still be detected the following 180 days. One of the outcomes of the inflammatory process and cytokine synthesis is the generation of glial scar. In this chapter, we will review the different cytokine mechanisms involved in the formation of glial scar in acute and chronic phases, as well as the modulating treatments of glial scar.
Part of the book: Cytokines
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