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PubMed1985

The degradation of phospholipids, formation of metabolites of arachidonic acid, and demyelination following experimental spinal cord injury.

Spinal cord injury has been studied using a cat compression model. Very early changes in lipid metabolism were found that compromise the integrity of the plasma membrane and decrease the activities of ATPases. Up to 18% of the ethanolamine plasmalogens are lost, with very marked elevations of the free fatty acids, arachidonic acid, diacylglycerols, prostaglandins, thromboxanes, and leukotrienes. These changes result in edema, inflammation, necrosis of oligodendroglia, demyelination, and paralysis.

Animals↗
PubMed2006

Therapeutic interventions after spinal cord injury.

Spinal cord injury (SCI) can lead to paraplegia or quadriplegia. Although there are no fully restorative treatments for SCI, various rehabilitative, cellular and molecular therapies have been tested in animal models. Many of these have reached, or are approaching, clinical trials. Here, we review these potential therapies, with an emphasis on the need for reproducible evidence of safety and efficacy. Individual therapies are unlikely to provide a panacea. Rather, we predict that combinations of strategies will lead to improvements in outcome after SCI. Basic scientific research should provide a rational basis for tailoring specific combinations of clinical therapies to different types of SCI.

Animals↗
PubMed2000

Olfactory ensheathing cells: bridging the gap in spinal cord injury.

Spinal cord injury (SCI) continues to be an insidious and challenging problem for scientists and clinicians. Recent neuroscientific advances have changed the pessimistic notion that axons are not capable of significant extension after transection. The challenges of recovering from SCI have been broadly divided into four areas: 1) cell survival; 2) axon regeneration (growth); 3) correct targeting by growing axons; and 4) establishment of correct and functional synaptic appositions. After acute SCI, there seems to be a therapeutic window of opportunity within which the devastating consequences of the secondary injury can be ameliorated. This is supported by several observations in which apoptotic glial cells have been identified up to 1 week after acute SCI. Moreover, autopsy studies have identified anatomically preserved but unmyelinated axons that could potentially subserve normal physiological properties. These observations suggest that therapeutic strategies after SCI can be directed into two broad modalities: 1) prevention or amelioration of the secondary injury, and 2) restorative or regenerative interventions. Intraspinal transplants have been used after SCI as a means for restoring the severed neuraxis. Fetal cell transplants and, more recently, progenitor cells have been used to restore intraspinal circuitry or to serve as relay for damaged axons. In an attempt to remyelinate anatomically preserved but physiologically disrupted axons, newer therapeutic interventions have incorporated the transplantation of myelinating cells, such as Schwann cells, oligodendrocytes, and olfactory ensheathing cells. Of these cells, the olfactory ensheathing cells have become a more favorable candidate for extensive remyelination and axonal regeneration. Olfactory ensheathing cells are found along the full length of the olfactory nerve, from the basal lamina of the epithelium to the olfactory bulb, crossing the peripheral nervous system-central nervous system junction. In vitro, these cells promote robust axonal growth, in part through cell adhesion molecules and possibly by secretion of neurotrophic growth factors that support axonal elongation and extension. In animal models of SCI, transplantation of ensheathing cells supports axonal remyelination and extensive migration throughout the length of the spinal cord. Although the specific properties of these cells that govern enhanced axon regeneration remain to be elucidated, it seems certain that they will contribute to the establishment of new horizons in SCI research.

Acute Disease↗
PubMed1993

Role of rehabilitation after spinal cord injury.

Spinal cord injury rehabilitation strives to provide the opportunity for persons with an acquired disability to lead a fruitful and satisfying personal and vocational life. The delivery of proper rehabilitation care to these patients involves the establishment of a continuum of services that includes the emergency medical system, the acute and rehabilitation hospital stay, and a program for lifetime health maintenance. As the patient regains health and confidence in his abilities, successful adjustment is promoted by separating the disabled person from a dependence on medical systems, redirecting the life focus back to family, and addressing vocational and social issues.

Counseling↗
PubMed1999

Induction of Eph B3 after spinal cord injury.

Spinal cord injury (SCI) in adult rats initiates a cascade of events producing a nonpermissive environment for axonal regeneration. This nonfavorable environment could be due to the expression of repulsive factors. The Eph receptor protein tyrosine kinases and their respective ligands (ephrins) are families of molecules that play a major role in axonal pathfinding and target recognition during central nervous system (CNS) development. Their mechanism of action is mediated by repellent forces between receptor and ligand. The possible role that these molecules play after CNS trauma is unknown. We hypothesized that an increase in the expression of Eph proteins and/or ephrins may be one of the molecular cues that restrict axonal regeneration after SCI. Rats received a contusive SCI at T10 and in situ hybridization studies 7 days posttrauma demonstrated: (i) a marked up-regulation of Eph B3 mRNA in cells located in the white matter at the lesion epicenter, but not rostral or caudal to the injury site, and (ii) an increase in Eph B3 mRNA in neurons in the ventral horn and intermediate zone of the gray matter, rostral and caudal to the lesion. Immunohistochemical analyses localizing Eph B3 protein were consistent with the mRNA results. Colocalization studies performed in injured animals demonstrated increased Eph B3 expression in white matter astrocytes and motor neurons of the gray matter. These results suggest that Eph B3 may contribute to the unfavorable environment for axonal regeneration after SCI.

Animals↗
PubMed2005

From discovery to clinical trials: treatment strategies for central neuropathic pain after spinal cord injury.

Spinal cord injuries (SCI) result in a devastating loss of function below the level of the lesion in which there are variable motor recoveries and, in the majority of cases, central neuropathic pain syndromes (CNP) develop several months to years following injury. Unfortunately, the study of chronic pain after SCI has been neglected in the past due in part to the lack of good animal models but largely due to the clinically held dogma that CNP is not a real phenomenon and is psychogenic in nature rather than based on described pathophysiological mechanisms. The purpose of this article is to offer standardized terminology of pain, insight into animal modeling issues of CNP, descriptions of current clinical therapies and to discuss the pathophysiological mechanisms that provide the substrate for CNP that will lead to innovative new therapies. It is hoped that this information will give insight for research strategies as well as better care not only of SCI individuals, but is generalizable to many other CNP syndromes.

Central Nervous System↗
PubMed2004

Effect of combined treatment with melatonin and methylprednisolone on neurological recovery after experimental spinal cord injury.

Spinal cord injury (SCI) results in the loss of function below the lesion. Secondary injury following the primary impact includes a number of biochemical and cellular alterations leading to tissue necrosis and cell death. Methylprednisolone (MP), by reducing edema and protecting the cell membrane against peroxidation, is the only pharmacological agent with a proven clinically beneficial effect on SCI. Melatonin, known as a free radical scavenger, has been shown to have an effect on lipid peroxidation following experimental SCI. The purpose of this study was to examine the effect of MP and melatonin on neurological, ultrastructural, and electrophysiological recovery. Female albino rats weighing 200-250 g were randomized into five groups of 18 rats each and six rats for the control group. Weight-drop trauma was performed for each group and a 30-mg/kg single dose of MP for rats in group 1, a 10-mg/kg single dose of melatonin for rats in group 2, and MP and melatonin in the same doses for rats in group 3 were administered immediately after trauma. The rats in group 4 were the vehicle group (treated with ethanol) and group 5 was the trauma group. The motor and somatosensory evoked potentials were recorded at the 4th hour, the 24th hour, and on the 10th day of the study for six rats in each group. Posttraumatic neurological recovery was recorded for 10 days using "motor function score" and inclined plane test. After electrophysiological study the rats were terminated for an analysis of lipid peroxidation level of the injured site of the spinal cord. Electron microscopic studies were performed to determine the effects of melatonin, MP, and the combined treatment with MP and melatonin on axons, neurons, myelin, nucleus, and intracytoplasmic edema. The groups treated with MP, melatonin, and a combination of both had significantly enhanced electrophysiological, biochemical, and neurological recovery and also showed better ultrastructural findings than the trauma and vehicle groups. Although combined treatment was significantly more effective on lipid peroxidation than melatonin or MP treatments alone, at the 10th day, neurobehavioral, electrophysiological, and ultrastructural recovery were at the same level. In conclusion, MP, melatonin, and MP and melatonin combined treatment modalities improved functional recovery at the same level. Future studies involving different doses of melatonin and different dose combinations with MP could promise better results since each drug has a different anti-oxidative mechanism of action.

Animals↗
PubMed2000

Department of Veterans Affairs Quality Enhancement Research Initiative for spinal cord injury.

Spinal cord injury (SCI) is a lifelong condition, requiring ongoing efforts by multiple disciplines to stabilize, diminish, or prevent impairments; avoid or limit secondary complications; and improve or maintain social role functioning and quality of life for the individual throughout his or her life. There are approximately 200,000 persons with SCI in the United States, of whom roughly 22% are veterans. The estimated national economic impact of SCI is approximately $9.73 billion per year. These figures illustrate why SCI is an important topic for the Department of Veterans Affairs Quality Enhancement Research Initiative (QUERI). The SCI QUERI will identify gaps in knowledge of SCI treatment and management, develop research efforts to address these gaps, identify best practices for care and management of SCI, and assess whether best practices lead to improved outcomes, including health-related quality of life.

Benchmarking↗
PubMed1999

Bioavailability of diclofenac after intramuscular administration to rats with experimental spinal cord injury.

Spinal cord injury (SCI) has been proposed to reduce drug bioavailability after intramuscular administration owing to an impairment in blood flow to paralyzed limbs. To test this hypothesis, we studied diclofenac bioavailability after intramuscular administration in rats with SCI. Female Sprague-Dawley rats were submitted to SCI at the T8 level by contusion and received a 10-mg/kg intramuscular diclofenac dose in the thigh of the right hind limb 24 h after injury. Blood samples were drawn, diclofenac concentration was determined by high-performance liquid chromatography, and whole-blood concentration against time curves were constructed. SCI did not result in a significant change in C(max) and T(max), compared with sham-lesioned controls, suggesting that the rate of drug absorption was not altered. Half-life was prolonged, and therefore area under the curve was greater in SCI than in sham-lesioned animals. Therefore, 24 h after SCI at the T8 level, intramuscular diclofenac bioavailability was not impaired but was actually enhanced. Results suggest that the rate of intramuscular diclofenac absorption is not significantly altered, although its elimination is impaired, during the acute phase of SCI. It then appears that SCI-induced pharmacokinetic alterations are complex, the global bioavailability depending on the sum of SCI effects on absorption, distribution, and elimination. Systematic studies on SCI-induced alterations are thus required to provide information leading to a rational dosing regimen design for SCI patients.

Animals↗
PubMed2003

Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury.

Spinal cord injury (SCI) results in loss of voluntary motor control followed by incomplete recovery, which is partly mediated by the descending corticospinal tract (CST). This system is an important target for therapeutic repair strategies after SCI; however, the question of whether apoptotic cell death occurs in these axotomized neurons remains unanswered. In this study, adult (150-175 g) male Sprague-Dawley rats underwent T9 transection of the dorsal funiculus, which axotomizes the dorsal CST, and introduction of the retrograde tracer Fluoro-Gold into the lesion site. Primary motor cortex (M1) was then examined for evidence of apoptosis weekly for 4 weeks after injury. Axotomized pyramidal cells, identified by retrograde transport of Fluoro-Gold, were found in M1 (57.5 +/- 9.6/median section, 6127 +/- 292 total), and a significant proportion were terminal deoxynucleotidyl transferase (TdT) -mediated deoxyuridine triphosphate (dUTP)-rhodamine nick end labeling (TUNEL) -positive at 1 week after injury (39.3 +/- 5.6%), compared with animals undergoing sham surgery (1.2 +/- 1.4%). At 2-4 weeks, fewer cells were Fluoro-Gold-positive (24.6 +/- 65.06 to 25.3 +/- 6.4/median section, 2338 +/- 233 to 2393 +/- 124 total), of which very few were TUNEL-positive. In TUNEL-positive cells, Hoechst 33342 staining revealed nuclear morphology consistent with apoptosis, chromatin condensation, and formation of apoptotic bodies. Fluoro-Gold-positive cells showed increased caspase-3 and Bax immunoreactivity. Hematoxylin and eosin staining revealed similar nuclear changes and dystrophic cells. Internucleosomal DNA fragmentation was detected by gel electrophoresis at the 1-week time point. Lesioned animals not receiving Fluoro-Gold exhibited the same markers of apoptosis. These results document, for the first time, features of apoptotic cell death in a proportion of axotomized cortical motor neurons after SCI, suggesting that protection from apoptosis may be a prerequisite for regenerative approaches to SCI.

Animals↗
PubMed1997

Animal assisted therapy and the individual with spinal cord injury.

Spinal cord injury (SCI) is a devastating event that results in significant adjustments during the acute and rehabilitation phase. During this period, it is imperative to maintain the patient's self-esteem, reduce stress levels, encourage the expression of feelings, and provide sensory stimulation. Animal Assisted Therapy (AAT) involves the use of animals as a complement to more traditional forms of therapy. The program is based on the knowledge that animals have a positive influence on people who are ill in the healthcare setting. The Animals Heal Hearts Program (TM) has two components, pet visitation and pet therapy. Pet visitation consists of allowing a patient to have his/her own personal dog for a visit, provided there are no medical contraindications. Pet therapy is a structured program using a dog that has completed behavioral and health screening. Dogs are used in the hospital to reduce patients' stress, increase their self-esteem, and help them express feelings. The dogs provide sensory stimulation as patients view and handle the animals and learn about animals and pets. A carefully planned and evaluated program ensures that it is safe and effective.

Adaptation, Psychological↗
PubMed1992

Postoperative wound infections following myocutaneous flap surgery in spinal injury patients.

Severe pressure ulcers in patients with spinal cord injury are frequently treated by using musculocutaneous (m-c) flap surgery. There have been few studies of the use of perioperative antibiotics to prevent postoperative infection in this setting. We reviewed 74 m-c flap surgeries in 53 patients (41 male and 12 female) from October 1989 for one year. The sites involved were ischial (31), sacral (24), trochanteric (18), deltoid (2), olecranon (1) and posterior thigh (1). An antibiotic was usually administered perioperatively for 5 days. Patients were followed for a median of 30 (8-96) weeks. Postoperative infections occurred at a median of 12 (4-25) days in 6 of 74 (8%) surgeries. The organisms cultured from the 6 infected wounds were: Bacteroides sp. (4), Proteus mirabilis (2), E. coli (2), MRSA (2), and others (6--each isolated once). These results indicate that antibiotics did not prevent postoperative infection in approximately 8% of patients undergoing m-c surgery. The frequency of isolation of Bacteroides sp. from these infections suggests that anaerobic bacteria may persist in healing pressure ulcers and perioperative antibiotics might include coverage for anaerobic bacteria.

Adolescent↗
PubMed2005

Exercise as a health-promoting activity following spinal cord injury.

Spinal cord injury is a catastrophic event that immeasurably alters activity and health. Depending on the level and severity of injury, functional and homeostatic decline of many body systems can be anticipated in a large segment of the paralyzed population. The level of physical inactivity and deconditioning imposed by SCI profoundly contrasts the preinjury state in which most individuals are relatively young and physically active. Involvement in sports, recreation, and therapeutic exercise is commonly restricted after SCI by loss of voluntary motor control, as well as autonomic dysfunction, altered fuel homeostasis, inefficient temperature regulation, and early-onset muscle fatigue. Participation in exercise activities also may require special adaptive equipment and, in some instances, the use of electrical current either with or without computerized control. Notwithstanding these limitations, considerable evidence supports the belief that recreational and therapeutic exercise improves the physical and emotional well-being of participants with SCI. This article will examine multisystem decline and the need for exercise after SCI. It will further examine how exercise might be used as a tool to enhance health by slowing multisystem medical complications unique to those with SCI. As imprudent exercise recommendations may pose avoidable risks of incipient disability, orthopedic deterioration, or pain, the special risks of exercise misuse in those with SCI will be discussed.

Electric Stimulation Therapy↗
PubMed2000

Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury.

Spinal cord injury (SCI) with resultant quadriplegia or high paraplegia is associated with significant dysfunction of the sympathetic nervous system. This alteration of sympathetic nervous system activity occurs as a consequence of loss of supraspinal control of the sympathetic nervous system and is further complicated by at least three subsequent phenomena that occur below the level of SCI: reduced overall sympathetic activity, morphologic changes in sympathetic preganglionic neurons, and peripheral alpha-adrenoceptor hyperresponsiveness. Reduced sympathetic activity below the level of SCI appears to result in orthostatic hypotension, low resting blood pressure, loss of diurnal fluctuation of blood pressure, reflex bradycardia, and, rarely, cardiac arrest. Peripheral alpha-adrenoceptor hyperresponsiveness likely accounts for some, if not the majority, of the excessive pressor response in autonomic dysreflexia and may also contribute to decreased blood flow in the peripheral microcirculation, potentially increasing susceptibility to pressure sores. What has yet to be established is whether this alpha-adrenoceptor hyperresponsiveness is a consequence of receptor hypersensitivity or a failure of presynaptic reuptake of noradrenaline at the receptor level. Better understanding of the pathophysiology of sympathetic nervous system dysfunction after high-level SCI should allow development of more effective measures to manage clinical complications.

Autonomic Dysreflexia↗
PubMed2005

High seminal platelet-activating factor acetylhydrolase activity in men with spinal cord injury.

Spinal cord injury (SCI) causes male infertility, with low sperm motility the major long-term cause. It has been suggested in previous studies that some seminal components may be responsible for the pathological asthenozoospermia. It is hypothesized that platelet-activating factor (PAF) acetylhydrolase (PAFah), which originates in the epididymis and other accessory sexual glands, may be a causative factor. This enzyme catalyzes PAF to acetate and biologically inactive lyso-PAF. PAF is well recognized to be an important phospholipid mediator that stimulates sperm motility and enhances sperm capacitation and fertilization. The present study was designed to analyze differences in PAFah activity in semen of men with SCI and age-matched healthy men. PAFah assay reagent kits were used to measure enzymatic activity by monitoring the production rates of 4-nitrophenol on a spectrophotometer during a given interval. The results showed that subjects with SCI had a higher concentration of PAFah than men in the control group (P < .001). A statistically significant negative correlation was found between enzymatic activity and sperm motility (r(2) = 0.8449; P < .001). Further studies will determine whether seminal vesicle dysfunction in men with SCI leads to abnormal PAFah activity, resulting in low sperm motility.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2006

Overexpression of SOD1 in transgenic rats attenuates nuclear translocation of endonuclease G and apoptosis after spinal cord injury.

Spinal motor neurons are selectively vulnerable after spinal cord injury (SCI). Recent studies suggest they undergo apoptosis after caspase activation through a mitochondria-dependent apoptosis pathway, and that oxidative stress after SCI is likely to play a role. However, other signaling pathways of apoptosis that involve mitochondria have not been thoroughly studied after SCI. Apoptosis-inducing factor (AIF) and endonuclease G (EndoG) are mitochondrial apoptogenic proteins that are capable of inducing neuronal apoptosis when translocated from mitochondria to nuclei through a caspase-independent pathway. In this study, we examined translocation of these proteins and apoptotic cell death of motor neurons. The role of oxidative stress was also studied using transgenic (Tg) rats that overexpress the intrinsic antioxidant copper/zinc-superoxide dismutase (SOD1). Western blots and an activity assay demonstrated that a greater amount of SOD1 and higher activity of SOD presented in mitochondria of Tg rats compared with wild-type (Wt) rats. Immunohistochemistry and Western blots showed translocation of EndoG and AIF from mitochondria to nuclei in motor neurons 1 day after SCI in both groups of rats. However, there was significantly less translocation of EndoG in the Tg rats compared with the Wt rats. Less apoptotic cell death was detected in the Tg rats than in the Wt rats 3 days after SCI. These results suggest that translocation of EndoG and AIF from mitochondria to nuclei may initiate a caspase-independent pathway of apoptosis. An increased level of SOD1 in mitochondria conceivably reduces oxidative stress, thereby attenuating EndoG translocation, and resulting in reduction of caspase-independent apoptosis.

Animals↗
PubMed2005

Deteriorated geometric structure and strength of the midfemur in men with complete spinal cord injury.

Spinal cord injury (SCI) results in a dramatic loss of bone mineral and a marked increase in fracture incidence in the femur; however, its effect on the femur's geometric structure and strength is poorly studied. The primary purpose of the present study was to assess the geometric structure, composition, and strength of the midfemur in men with long-term (>2 years), complete SCI (C6-L1 level; n=7) relative to men without SCI (n=8). T1-weighted axial images of the thigh were collected on a GE 1.5-T magnetic resonance imager and geometric, structure, composition, and strength measurements of the midfemur and skeletal muscle volume of the midthigh were determined. Areal bone mineral density (aBMD), bone mineral content (BMC), and bone area of the midthird of the femur and arms were determined using dual-energy X-ray absorptiometry. There were no differences in age, height, weight, femur length, arm BMC, arm aBMD, or arm bone area between the SCI group and controls. While the volume of the midfemur was not different in the two groups, the medullary cavity had 53% more volume and was 21-25% wider in the SCI group (P<0.05). In contrast, the cortical wall in the SCI group had a 24% lower volume and was 27-47% thinner (P<0.05). The cortical wall was particularly thin in the posterior section of the bone. The SCI group also had lower BMC and aBMD in the midfemur (21% and 25%, respectively, P<0.05). Calculated cross-sectional moment of inertia (CSMI), section modulus (Z), and polar moment of inertia (J) were lower in the SCI group (13-19%, P<0.05). A higher ratio of cortical bone volume to muscle volume and BMC to muscle volume in the SCI group (P<0.05) suggests that there was a greater loss of muscle than cortical bone after SCI; however, muscle volume was strongly correlated with cortical bone volume and BMC in the SCI and control groups (r=0.71 to 0.90, P<0.05). Muscle volume was also moderately to strongly correlated with CSMI and Z in the anterior-posterior direction and J. Muscle volume was weakly correlated or not correlated with bone strength measures in the control group (P>0.05). These findings suggest that after SCI, the midfemur erodes on the endosteal surface, resulting in a decreased resistance to bending and torsion. Although midthigh muscle volume appears to decline to a greater degree than midfemur cortical bone volume and BMC, their relationships remain strong.

Adult↗
PubMed2004

Polyethylene glycol improves function and reduces oxidative stress in synaptosomal preparations following spinal cord injury.

Spinal cord injury (SCI) results in rapid and significant oxidative stress. We have previously demonstrated that administration of polyethylene glycol (PEG) inhibits oxidative stress using an in vitro model of SCI. In this study we tested the effects of PEG in vivo, to elucidate the mechanism of PEG-mediated neuroprotection. We show that a compression injury at T10-11 induced diffusive oxidative stress in crude synaptosomal preparations, correlated with synaptosomal dysfunction and increased intrasynaptosomal calcium. Administration of PEG immediately post-injury produced a marked decrease in synaptosomal oxidative stress and calcium, associated with an increase in synaptosomal function. Confocal microscopy using fluorescein conjugated PEG revealed that PEG entered the cells of the injured spinal cord, placing the polymer in a position to directly interact with cellular organelles. PEG attenuates calcium-induced functional compromise of normal spinal cord synaptosomes and mitochondria in vitro. These results indicate that PEG may exert its neuroprotective effect through direct interaction with mitochondria, besides its known ability to rescue neurons and their axons by repairing the plasma membranes. We submit that PEG is likely to interfere with the cascade of secondary injury by several mechanisms of action that in concert reduce oxidative stress.

Animals↗