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Results for “SPINAL CORD INJURIES”

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At least 19 recordsLinked to original sources
PubMed2002

Neurogenic bladder model for spinal cord injury: spinal cord microdialysis and chronic urodynamics.

We describe an animal model to study neurotransmitter changes in parallel with urodynamic testing following Spinal Cord Injury (SCI). Urodynamic access was achieved using a subcutaneously placed 7 French dual lumen portacatheter. Spinal cord injury was induced by weight drop technique onto exposed dura at T8. The L6-S1 detrusor nuclei were localized stereotactically and microdialysis probe placement was confirmed through histologic methods. Chronic urodynamics revealed detrusor hyperreflexia (DH) 14 days following SCI. In vivo microdialysis of spinal cord amino acids was performed using CMA 11 (240 uM) probes in halothane-anesthetized rats at baseline and intervals of 20-30 min following spinal cord injury. Significant increases in the excitatory amino acid glutamate, and the inhibitory amino acids, glycine and taurine, were seen following spinal cord injury. Amino acid levels peaked at approximately 40 min following contusion injury with glycine demonstrating the highest levels of all amino acids measured. This neurogenic rat model provides a useful means of examining the effects of spinal cord injury on bladder function. By utilizing spinal cord microdialysis, one could intervene at the level of the detrusor nuclei to modulate bladder function.

Animals↗
PubMed2000

Opioid peptide messenger RNA expression is increased at spinal and supraspinal levels following excitotoxic spinal cord injury.

Spinal cord injury in rats is known to cause anatomical, physiological and molecular changes within the spinal cord. These changes may account for behavioral syndromes that appear following spinal cord injury, syndromes believed to be related to the clinical condition of chronic pain. Intraspinal injection of quisqualic acid produces an excitotoxic injury with pathological characteristics similar to those associated with ischemic and traumatic spinal cord injury. In addition, recent studies have demonstrated changes in blood flow, neuronal excitability and gene expression in the brain following excitotoxic injury, indicating that behavioral changes may result from modification of neuronal substrates at supraspinal levels of the neuraxis. Because changes in spinal opioid peptide expression have been demonstrated in models of traumatic spinal cord injury and chronic pain, the present study investigated messenger RNA expression of the opioid peptides, preproenkephalin and preprodynorphin, at spinal and supraspinal levels following excitotoxic spinal cord injury. Male, Long-Evans rats were given three intraspinal injections of quisqualic acid (total 1.2 microl, 125mM). After one, three, five, seven or 10days, animals were killed and quantitative in situ hybridization performed on regions of the spinal cord surrounding the lesion site, as well as whole-brain sections through various levels of the thalamus. Preproenkephalin and preprodynorphin expression was increased in spinal cord areas adjacent to the site of quisqualic injection and in cortical regions associated with nociceptive function, preproenkephalin in the cingulate cortex and preprodynorphin in the parietal cortex, both ipsilaterally and contralaterally at various time-points following injury. These results further our knowledge of the secondary events that occur following spinal cord injury, specifically implicating supraspinal opioid systems in the CNS response to spinal cord injury.

Animals↗
PubMed2006

[Pathophysiology of acute spinal cord injury].

Spinal cord injury is one of the most devastating of all traumatic conditions that can be encountered by patients. Over the past years much research has been performed on elucidating the mechanisms of spinal cord injury. Experimental and clinical studies have suggested that acute spinal cord injury is a two-step process involving primary and secondary mechanisms. Primary injury of the spinal cord refers to the initial mechanical damage due to local deformation of the spine. Direct compression and damage of neural elements and blood vessels by fractured and displaced bone fragments or disc material occur after mechanical trauma. The secondary mechanism is initiated by the primary injury. The secondary mechanism includes a cascade of biochemical and cellular processes, such as electrolyte abnormalities, formation free radicals, vascular ischemia, edema, posttraumatic inflammatory reaction, apoptosis or genetically programmed cell death and another processes. This review describes the pathophysiology of acute spinal cord injury. Knowledge of the pathophysiology of the acute spinal cord injury is crucial for successful management of the patients with these injuries.

Adult↗
PubMed1994

Chronic spinal cord injury.

Spinal cord injuries predispose patients to numerous complications. The care of such patients requires attention to multiple bodily systems, sensitivity to the effects of interventions on function and lifestyle, and a special vigilance because of the tendency of spinal cord injuries to mask problems. Improved clinical care, however, has increased the life expectancy of people with spinal cord injuries and therefore the prevalence of such injuries. The Americans with Disabilities Act should make people with spinal injuries more visible, as they participate in and contribute to society in greater numbers. Maintenance of health brings greater opportunities for self-care and mobility through rehabilitation and may allow people with spinal cord injuries to take advantage of future opportunities for neurologic improvement or cure.

Chronic Disease↗
PubMed1984

A review of treatment of spinal cord injury.

Spinal cord injury remains a devastating event to the person sustaining the injury. Not only the cost of acute and rehabilitation care, but also the loss of productivity of the victims who are often young men injured at a highly productive period of their lives are a costly illness for society as a whole. In the past 20-30 years, there has been continual improvement in the morbidity and mortality from spinal cord injury with the improvement in prevention of a second injury, prevention of secondary renal, pulmonary and cutaneous complications, better techniques for stabilization of the spinal column, and more effective utilization of remaining neurological function with improved rehabilitation therapy. It remains, however, difficult to demonstrate an effect from a wide range of 'acceptable' medical or surgical care on the resultant loss of spinal cord function. The lack of improvement in preventing or reversing the loss of spinal cord function in spite of marked variations in acute spinal cord injury care indicate that acceptable data are still lacking to determine the role of aggressive and conservative management. The need for a more organized approach to the problem is obvious.

Animals↗
PubMedDate not supplied

Unique issues in pediatric spinal cord injury.

Spinal cord injuries are devastating events, and they are particularly tragic when they affect children or adolescents who have barely had an opportunity to experience life. Of the approximately 10,000 individuals who sustain spinal cord injury each year in the United States, 3% to 5% occur in individuals younger than 15 years of age and approximately 20% occur in those younger than 20 years of age (Nobunaga, Go, & Karunas, 1999). Because of the growth and development inherent in children and adolescents and the unique manifestations and complications associated with spinal cord injuries, management must be developmentally based and directed to the individual's special needs (Vogel, 1997). The many unique facets of pediatric spinal cord injuries are addressed in this article. They clearly delineate the need for care that is responsive to the dynamic changes that occur with growth and development. The multidisciplinary team, combined with a focus on family-centered care, is essential in pediatric spinal cord injuries.

Adolescent↗
PubMed2006

Male fertility and sexual function after spinal cord injury.

Spinal cord injury has an enormous impact upon the sexual relationship of a man and his partner. Erection may be partial or absent, orgasm altered or impossible, and fertility severely impaired. New understanding of the physiology of sexual function and improved treatment can enable most cord-injured men to achieve erections suitable for sexual satisfaction. Modern methods of sperm collection and fertility treatment mean that many can also be fathers. The best results are obtained by a team approach involving rehabilitation and reproductive medicine clinicians, nurses, spinal cord injury specialists and counselors with the cord-injured man and his partner. Erections can be achieved by drugs, such as sildenafil, that block phosphodiesterase 5, prolonging the action of nitric oxide with resultant smooth muscle relaxation. Intracavernosal prostaglandin E1 and mechanical systems, such as vacuum pumps and constriction rings, are also effective. Sexual gratification can be promoted in the context of an understanding relationship in which the cord-injured person can gain pleasure from pleasing his partner and also from his partner's exploration of erotogenic areas not affected by the spinal cord injury. An emphasis on the broader view of sexuality in relationships allows for a continuance and strengthening of bonds between the couple. Vibration ejaculation or electroejaculation can be used to collect semen. For a limited period in the acute phase, usually for about 6-12 days after injury, normal semen can be obtained by electroejaculation from some cord-injured men. With chronic spinal cord injury the semen is of variable quality. Some patients have necrospermia, which may be improved by regular ejaculation. Others have poor quality semen or spermatogenic disorders and, in this situation, in vitro fertilization techniques must be used to achieve parenthood. Trials of assisted ejaculation help individualize cost-effective management of the infertility.

Autonomic Nervous System↗
PubMed2002

Non-surgical management of spinal cord injury.

Spinal cord injury remains a devastating neurological condition with limited therapeutic opportunities. Since decompressive surgery and high-dose methylprednisolone have limited utility for most patients, spinal cord injury clearly represents a major medical challenge. Experimental evidence has suggested that secondary cellular injury processes may be a realistic target for therapeutic intervention with the goal of inhibiting the progression of detrimental changes that normally follows traumatic injury to the cord. Preventing or reducing this delayed cellular injury may alone improve neurological recovery or facilitate future regenerative approaches to the injured cord. This review summarises recent advances in the development of pharmacological agents targeting the acute phase of spinal cord injury as well as potential strategies to facilitate regeneration of the spinal cord.

Clinical Trials as Topic↗
PubMed1980

Effects of hypertension and hypercarbia on spinal cord tissue oxygen in acute experimental spinal cord injury.

Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.

Animals↗
PubMedDate not supplied

Degenerative and spontaneous regenerative processes after spinal cord injury.

Spinal cord injury results in acute as well as progressive secondary destruction of local and distant nervous tissue through a number of degenerative mechanisms. Spinal cord injury also initiates a number of endogenous neuroprotective and regenerative responses. Understanding of these mechanisms might identify potential targets for treatments after spinal cord injury in humans. Here, we first discuss recent developments in our understanding of the immediate traumatic and subsequent secondary degeneration of local tissue and long projecting pathways in animal models. These include the inflammatory and vascular responses during the acute phase, as well as cell death, demyelination and scar formation in the subacute and chronic phases. Secondly, we discuss the spontaneous axonal regeneration of injured and plasticity of uninjured systems, and other repair-related responses in animals, including the upregulation of regeneration-associated genes in some neurons, increases in neurotrophic factors in the spinal cord and remyelination by oligodendrocyte precursors and invading Schwann cells. Lastly, we comment on the still limited understanding of the neuropathology in humans, which is largely similar to that in rodents. However, there also are potentially important differences, including the reduced glial scarring, inflammation and demyelination, the increased Schwannosis and the protracted Wallerian degeneration in humans. The validity of current rodent models for human spinal cord injury is also discussed. The emphasis of this review is on the literature from 2002 to early 2005.

Animals↗
PubMed2001

Epidemiology, demographics, and pathophysiology of acute spinal cord injury.

Spinal cord injury occurs through various countries throughout the world with an annual incidence of 15 to 40 cases per million, with the causes of these injuries ranging from motor vehicle accidents and community violence to recreational activities and workplace-related injuries. Survival has improved along with a greater appreciation of patterns of presentation, survival, and complications. Despite much work having been done, the only treatment to date known to ameliorate neurologic dysfunction that occurs at or below the level of neurologic injury has been intravenous methylprednisolone therapy. Much research over the past 30 to 40 years has focused on elucidating the mechanisms of spinal cord injury, with the complex pathophysiologic processes slowly being unraveled. With a greater understanding of both primary and secondary mechanisms of injury, the roles of calcium, free radicals, sodium, excitatory amino acids, vascular mediators, and apoptosis have been elucidated. This review examines the epidemiology, demographics, and pathophysiology of acute spinal cord injury.

Age Factors↗
PubMed2003

Endometrial cancer of the uterus in a patient with spinal cord injury.

Spinal cord injury occurs predominantly in males, and endometrial cancer in a patient with spinal cord injury is very rare. A 71-year-old woman, gravida 7, para 4, who had incomplete quadriplegia due to a spinal cord injury, was admitted with a complaint of genital bleeding. Biopsies of the cervix and the endometrium revealed endometrioid adenocarcinoma. Total abdominal hysterectomy was performed under general anesthesia. Pathohistological analysis revealed endometrial adenocarcinoma (G1) with squamous metaplasia and International Federation of Gynecology and Obstetrics (FIGO) surgical stage 2b. Local recurrence was not obvious after the surgery. However, lung metastasis appeared on postoperative day 225, and she died from dyspnea on day 277. Uterine cancer screening is more necessary in long-term bedridden women.

Aged↗
PubMed2006

Mechanisms controlling normal defecation and the potential effects of spinal cord injury.

Spinal cord injury frequently leads to bowel dysfunction with the result that emptying the bowel can occupy a significant part of the day and reduce the quality of life. This chapter contains an overview of the function and morphology of the normal distal gut in the human, and of gut behaviour in normal defecation. In humans, this can be monitored and is described, but knowledge of the mechanisms controlling it is limited. Work on animals has shown that the intrinsic activity of the smooth muscles and their interactions with the enteric nervous system can program the activity that is necessary to expel waste material, but the external anal sphincter is controlled through somatic nerves. The gut however also receives input from the central nervous system through autonomic nerves, and a spinal reflex centre exists. Voluntary effort to induce defecation can influence all the control mechanisms, but the precise importance of each is not understood. The behaviour and properties of the individual muscles in the normal human rectum and anal canal are described, including their responses to intrinsic nerve stimulation and adrenergic and cholinergic agonists. The effects of established spinal cord injury are then considered. For convenience, supraconal and conal/cauda equina lesions are considered as two categories. Prolongation of transit times and disordered defecation are common problems. Supraconal lesions result in reduced resting anal pressures and increased risk of fecal incontinence. The acute effects of spinal cord injury are described, with injury causing ileus (prolonged total gastrointestinal transit times), constipation (prolonged colonic transit times) and fecal incontinence (passive leakage).

Cholinergic Agonists↗
PubMedDate not supplied

Clinical fundaments for rehabilitation treatment in spinal cord injury.

Spinal cord injury leads to a severe disabling syndrome, which most often affects the young. The major etiologic factor in spinal cord injuries is trauma. Patients' rehabilitation is started in the acute phase, soon after the trauma occurs, mainly through preventive care against the formation of pressure sores, deformities of the palsy segments, proper vesical and bowel emptying and care with vasomotor alterations. The rehabilitation process continues at a specialized rehabilitation center, searching the best functional performance of each patient, according to the type and level of the spinal cord injury. This work shows fundaments for the rehabilitation treatment.

Electric Stimulation Therapy↗
PubMed2000

Cellular transplantation and spinal cord injury.

Spinal cord injury is often characterized by immediate and irreversible loss of sensory and motor functions below the level of injury. Cellular transplantation in various experimental models of spinal cord injury has been used as a strategy for reducing deficits and improving functional recovery. The general strategy has been aimed at promoting regeneration of intrinsic injured axons with the development of alternative pathways that facilitate a partial functional connection. Other objectives of cellular transplantation studies have included replacement of lost cellular elements, alleviation of chronic pain, and modulation of the inflammatory response after injury. This review focuses on the cell types that have been used in spinal cord transplantation studies in the context of evolving biological perspectives, technological advances, and new therapeutic strategies and serves as a point of reference for future studies.

Animals↗