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PubMedDate not supplied

Spinal cord injury with a narrow spinal canal: utilizing Torg's ratio method of analyzing cervical spine radiographs.

A 65-year-old inebriated man crashed his car and presented with spinal shock and neurogenic shock from a cervical spinal cord injury without cervical spine fracture or dislocation. The lateral cervical spine radiography was initially read as normal, except for degenerative disk disease; however, Torg's ratio method of analyzing cervical spinal canal sagittal width indicated the spinal canal was congenitally narrow. Magnetic resonance imaging confirmed this and showed bulging and herniation of multiple invertebral disks between C2 and C7. This case illustrates the value of using Torg's ratio method of analyzing lateral cervical spine radiographs. Although Torg's method has not been prospectively validated, it may be useful to identify patients at risk for cervical spinal cord injuries without fractures or dislocations. An abnormal Torg's ratio may be the only clue to the fact that the patient is at higher risk of spinal cord injury when the patient's history or examination is questionable because of head injury, drug intoxication, or therapeutic sedation and paralysis.

Accidents, Traffic↗
PubMed1986

Proteolytic enzymes in experimental spinal cord injury.

Experimental spinal cord injury was produced in rats by dropping a 10 g weight from 30 cm upon dura-invested exposed spinal cord. Proteolytic activities at neutral (pH 7.6) and acid (pH 5.5 and 3.6) pH were determined in whole homogenate and the cytosolic fraction of the lesion (lumbar) and cervical control segments. The enzyme activity was monitored by SDS-PAGE analysis of the extent of substrate myelin basic protein (MBP) degradation. Activities (neutral and cathepsin B-like) in the sham-operated spinal cord were lower than those of cervical autologous control at 24 h after injury. The increase in neutral proteinase activity was progressive and greater in the lesion than the autologous control. A 61.5% +/- 3.5 loss of MBP was observed at 2 h following injury and increased at 24 h (78.2% +/- 3.4). The loss of MBP coincided with the appearance of several low molecular weight peptides. The cathepsin B-like and cathepsin D activities were also increased in the lesion but to a lesser extent than the neutral proteinase. The neutral proteinase and cathepsin B-like activity were inhibited by leupeptin and not by pepstatin while the converse obtained for cathepsin D activity. The release of neutral proteolytic activity which is nonlysosomal in origin suggests a novel hypothesis for the mechanism of traumatic axon-myelin injury.

Animals↗
PubMed2000

Neuroanatomical substrates of functional recovery after experimental spinal cord injury: implications of basic science research for human spinal cord injury.

Human spinal cord injury (SCI) is a devastating condition that results in persistent motor deficits. Considerable basic and clinical research is directed at attenuating these deficits. Many basic scientists use animal models of SCI to (1) characterize lesion development, (2) determine the role of spared axons in recovery, and (3) develop therapeutic interventions based on these findings. In this article, current research is reviewed that indicates: (1) most individuals with SCI will have some sparing of white matter at the lesion epicenter even when the lesion appears clinically complete, (2) even minimal tissue sparing has a profound impact on segmental systems and recovery of function, and (3) facilitatory intervention such as weight bearing and locomotor training after SCI may be more effective than compensatory strategies at inducing neuroplasticity and motor recovery. Body weight supported treadmill step training is discussed as an example of new facilitatory interventions based on basic science research using animal models.

Animals↗
PubMed1992

Spinal cord injury models.

Spinal cord injury models continue to be used to learn more about the pathophysiology of injury as well as potential therapeutic interventions. Most researchers now rely on rat models of injury with injury produced by impact, compression, or even photochemical techniques. A number of laboratories have confirmed that reproducible and graded injury can be produced in the rat with outcome monitored by behavioral, neurophysiologic, and morphologic analyses. Biochemical, physiologic, and pharmacologic studies with these models are being used to further define factors that contribute to chronic injury and thus may be the subject of therapeutic intervention. In addition, a new approach to therapy is being explored via implantation of cells into the injured spinal cord. Cell suspensions can be implanted in clinically relevant injury models without exacerbating the effects of injury and with some indications of beneficial effect. The potential usefulness of such an approach is just beginning to be evaluated.

Animals↗
PubMed2005

FAS deficiency reduces apoptosis, spares axons and improves function after spinal cord injury.

After spinal cord injury (SCI), apoptosis of neurons and oligodendrocytes is associated with axonal degeneration and loss of neurological function. Recent data have suggested a potential role for FAS death receptor-mediated apoptosis in the pathophysiology of SCI. In this study, we examined the effect of FAS deficiency on SCI in vitro and in vivo. FAS(Lpr/lpr) mutant mice and wildtype background-matched mice were subjected to a T5-6 clip compression SCI, and complementary studies were done in an organotypic slice culture model of SCI. Post-traumatic apoptosis in the spinal cord, which was seen in neurons and oligodendrocytes, was decreased in the FAS-deficient mice both in vivo and in vitro particularly in oligodendrocytes. FAS deficiency was also associated with improved locomotor recovery, axonal sparing and preservation of oligodendrocytes and myelin. However, FAS deficiency did not result in a significant increase in surviving neurons in the spinal cord at 6 weeks after injury, likely reflecting the importance of other cell death mechanisms for neurons. We conclude that inhibition of the FAS pathway may be a clinically attractive neuroprotective strategy directed towards oligodendroglial and axonal preservation in the treatment of SCI and neurotrauma.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1989

Continuous monitoring of detrusor pressure in patients with a reflex urinary bladder after spinal cord injury.

In spinal cord injury, the detrusor pressure, as a parameter of urinary bladder dysfunction, is related to incontinence and renal complications. In order to determine the intraindividual variation of maximum pressure and duration of detrusor contractions, in patients with a spinal reflex bladder, the detrusor pressure was registered during 24 hours of physiological filling in 16 patients. Between the bladder contractions the detrusor pressure was low in all patients, indicating high bladder complicance. During contractions the maximum detrusor pressure and its duration varied both inter- and intraindividually. In individual patients, however, mean values during the initial 12 hours correlated with mean values during the final 12 hours. Thus, mean values of a series of contractions appear to be characteristic of each patient and useful in describing the voiding pressure in spinal reflex bladder.

Adult↗
PubMed2005

Cell proliferation and replacement following contusive spinal cord injury.

After spinal cord injury (SCI), about 50% of the oligodendrocytes and astrocytes in the residual white matter at the injury site are lost by 24 h. However, chronically after SCI, the density of oligodendrocytes is normal. Previous studies have shown that the adult rat spinal cord contains a pool of proliferating glial progenitors whose progeny could help restore cell density after injury. To study proliferation in response to injury, we performed SCI on adult female rats at the T8 level, using a standardized contusion model. Animals received bromodeoxyuridine (BrdU) injections during the first week after SCI, and were perfused within 2 h for acute studies, and at 6 weeks for chronic studies. The tissue was analyzed using immunohistochemical detection of BrdU and cell marker antigens. We demonstrate that cell proliferation in the residual white matter is increased at 1-7 days after SCI, peaking on day 3. Dividing cells include oligodendrocytes, astrocytes, microglia/macrophages, and a high proportion of NG2(+) glial precursors. By 6 weeks, some cells that had been labeled 2-4 days after SCI were still present. Double immunohistochemistry showed that while very few of these cells expressed NG2 or the microglia/macrophage marker OX42, about 50% expressed CC1 or glial fibrillary acidic protein (GFAP), markers of mature oligodendrocytes and astrocytes, respectively. The post-injury environment represented by residual white matter is thus permissive to the differentiation of glial precursors. Cells that are stimulated to divide during the first week after SCI develop chronically into mature phenotypes that replace macroglia lost after injury.

Animals↗
PubMed1999

C-fos expression in the spinal cord of rats exhibiting allodynia following contusive spinal cord injury.

Contusive spinal cord injury (SCI) may result in central neuropathic pain marked by allodynia-like features in the dermatomes close to the level of injury. The aim of this study was to compare the laminar distribution of activated neurons (as determined by c-fos immediate early gene expression) in the spinal cord immediately above the level of a SCI in rats with or without allodynia-like features. Non-noxious mechanical stimulation was applied to half the animals in the dermatomes corresponding to the level of injury prior to perfusion. Stimulation resulted in a significant increase in c-fos labelling in all laminae of the spinal dorsal horn in the segment immediately above the level of injury only in allodynia animals. Animals that had allodynia also demonstrated a significant increase in the level of c-fos labelling in lamina III, IV and V of the dorsal horn without stimulation. Thus, allodynia following SCI is associated with significant increases in basal and evoked c-fos expression ("neuronal activity") in response to non-noxious mechanical stimulation. The data also suggest that allodynia-like behaviour following SCI cannot be accounted for solely by changes occurring at a spinal level.

Animals↗
PubMed1993

Occupational spinal cord injury: demographic and etiologic differences from non-occupational injuries.

Most spinal cord injuries (SCIs) are the result of motor vehicle accidents (MVAs). There are no published reports specifically addressing SCIs that occur in the workplace. We report a cohort survey study examining the frequency and etiology of SCI in the workplace. Through a cooperative program, an evaluation of all SCIs seen in Colorado during a 5 1/2-year period (January 1, 1986 through June 6, 1991) is presented. We report a detailed analysis of specific data of all SCIs occurring in the workplace. There were a total of 566, with 74 (13.1%) due to injuries that occurred during the course of employment. The most common cause of occupational SCI was falls, which occurred in 37 (50%), as compared with only 15.9% of non-occupational SCIs. Only 14 (18.9%) occupational SCIs resulted from MVAs, compared with 59.3% of non-occupational SCIs. Other major etiologies for occupational SCI included being hit by a falling object in 14 individuals (18.9%), gunshot wound in three (4%), skiing in one (1.4%), stabbing in one (1.4%), and other causes in four (5.4%). Construction occupations were over-represented in occupational SCIs with 41.9% of cases as compared with only 6.3% for the non-occupational group. Because of the large percentage of occupational SCIs, efforts should be aimed at educating workers in at-risk occupations to prevent this serious injury.

Accidents, Occupational↗
PubMed2005

Cervical spinal cord injury upregulates ventral spinal 5-HT2A receptors.

Following chronic C2 spinal hemisection (C2HS), crossed spinal pathways to phrenic motoneurons exhibit a slow, spontaneous increase in efficacy by a serotonin (5-HT)-dependent mechanism associated with 5-HT2A receptor activation. Further, the spontaneous appearance of cross-phrenic activity following C2HS is accelerated and enhanced by exposure to chronic intermittent hypoxia (CIH). We hypothesized that chronic C2HS would increase 5-HT and 5-HT2A receptor expression in ventral cervical spinal segments containing phrenic motoneurons. In addition, we hypothesized that CIH exposure would further increase 5-HT and 5-HT2A receptor density in this region. Control, sham-operated, and C2HS Sprague-Dawley rats were studied following normoxia or CIH (11% O2-air; 5-min intervals; nights 7-14 post-surgery). At 2 weeks post-surgery, ventral spinal gray matter extending from C4 and C5 was isolated ipsilateral and contralateral to C2HS. Neither C2HS nor CIH altered 5-HT concentration measured with an ELISA on either side of the spinal cord. However, 5-HT2A receptor expression assessed with immunoblots increased in ipsilateral gray matter following C2HS, an effect independent of CIH. Immunocytochemistry revealed increased 5-HT2A receptor expression on identified phrenic motoneurons (p<0.05), as well as in the surrounding gray matter. Contralateral to injury, 5-HT2A receptor expression was elevated in CIH, but not normoxic C2HS rats (p<0.05). Our data are consistent with the hypothesis that spontaneous increase in 5-HT2A receptor expression on or near phrenic motoneurons contributes to strengthened crossed-spinal synaptic pathways to phrenic motoneurons following C2HS.

Animals↗
PubMed2004

Mechanically engineered hydrogel scaffolds for axonal growth and angiogenesis after transplantation in spinal cord injury.

OBJECT: Spinal cord injury (SCI) is a complex pathological entity, the treatment of which requires a multipronged approach. One way to integrate different therapeutic strategies for SCI is to develop implantable scaffolds that can deliver therapies in a synergistic manner. Many investigators have developed implantable "bridges," but an important property of such scaffolds--that is, mechanical compatibility with host tissues--has been neglected. In this study, the authors evaluated the results of implanting a mechanically matched hydrogel-based scaffold to treat SCI. METHODS: A nonbiodegradable hydrogel, poly(2-hydroxyethylmethacrylate) (PHEMA), was engineered using thermally initiated free radical solution polymerization. Two groups of 12 adult Sprague-Dawley rats underwent partial cervical hemisection injury followed by implantation of either PHEMA or PHEMA soaked in 1 microg of brain-derived neurotrophic factor (BDNF). Four rats from each group were killed 1, 2, or 4 weeks after induction of the injury. Immunofluorescence staining was performed to determine the presence of scarring, cellular inflammatory responses, gliosis, angiogenesis, and axonal growth in and around the implanted scaffolds. CONCLUSIONS: The implanted PHEMA with 85% water content had a compressive modulus of 3 to 4 kPa, which matched the spinal cord. Implanted PHEMA elicited modest cellular inflammatory responses that disappeared by 4 weeks and minimal scarring was noted around the matrix. Considerable angiogenesis was observed in PHEMA, and PHEMA soaked in BDNF promoted axonal penetration into the gel. The authors conclude that mechanically engineered PHEMA is well accepted by host tissues and might be used as a platform for sustained drug delivery to promote axonal growth and functional recovery after SCI.

Animals↗
PubMed1994

Operant conditioning of spinal stretch reflexes in patients with spinal cord injuries.

Hyperactive spinal stretch reflexes (SSRs) often occur with spinal cord injuries (SCI). These altered SSRs may impair movement. Recent studies in monkeys and human subjects have indicated that the magnitude of SSRs can be modulated using operant conditioning. The purpose of this study was to determine whether hyperactive biceps brachii SSRs could be operantly conditioned downward. Seventeen chronic (> 1 year postlesion) spinal cord-injured patients participated. Subjects were trained to keep biceps background (prestretch) electromyographic (EMG) activity and elbow angle at predetermined levels prior to having the elbow rapidly extended by a torque motor to elicit the biceps SSR. All subjects participated in six baseline sessions over a 2-week period. Then, subjects were randomly assigned to either control or training groups for the next 24 sessions over an 8-week period. By the end of the study, training subjects had significantly reduced biceps SSRs (t test, P < 0.001), while control subjects SSRs were not significantly reduced (t test, P > 0.05). The reduced SSRs persisted for up to 4 months following cessation of training. The results of this study support the hypothesis that hyperactive SSRs can be operantly conditioned downward in SCI patients.

Adolescent↗
PubMed1994

Changes in choline acetyltransferase distribution in the cervical spinal cord after reversible cervical spinal cord injury.

Reversible spinal cord injury (SCI) at C6 level in rats, produced by the weight-placed method, resulted in a severe motor functional deficit initially, followed by a gradual recovery. During the recovery, choline acetyltransferase (CAT) distribution in the cervical spinal cord was investigated at 2, 4, 7, 14 and 28 days after the injury by quantitative immunohistochemistry with a fluorescence microphotometry system. At C6 level, the fluorescence intensity of the ventrolateral anterior horn (VLAH), which reflected the concentration of CAT, decreased to approximately 50% of that of the sham-operated group at 2 days. It then recovered to 60% at 4 days after the injury, and remained unchanged thereafter. Fluorescence intensities in VLAH at C4-5 and C7-8 levels decreased to approximately 60-70% at 2 days after the injury, but it recovered and increased to 110-130% thereafter.

Animals↗
PubMed2004

A global perspective on spinal cord injury epidemiology.

Spinal cord injury (SCI) is a devastating condition often affecting young and healthy individuals around the world. This debilitating condition not only creates enormous physical and emotional cost to individuals but also is a significant financial burden to society at large. This review was undertaken to understand the global impact of SCI on society. We also attempted to summarize the worldwide demographics and preventative strategies for SCI in varying economic and climatic environments and to evaluate how cultural and economic differences affect the etiology of SCI. A PUBMED database search was performed in order to identify clinical epidemiological studies of SCI within the last decade. In addition, World Bank and World Health Organization websites were used to obtain demographics, economics, and health statistics of countries of interest. A total of 20 manuscripts were selected from 17 countries. We found that SCI varies in etiology, male-to-female ratios, age distributions, and complications in different countries. Nations with similar economies tend to have similar features and incidences in all the above categories. However, diverse methods of classifying SCI were found, making comparisons difficult. Based upon these findings, it is clear that the categorization and evaluation of SCI must be standardized. The authors suggest improved methods of reporting in the areas of etiology, neurological classification, and incidence of SCI so that, in the future, more useful global comprehensive studies and comparisons can be undertaken. Unified injury prevention programs should be implemented through methods involving the Internet and international organizations, targeting the different etiologies of SCI found in different countries.

Adult↗
PubMed1985

Vascular permeability in experimental spinal cord injury.

Following spinal cord injury in rats there was a time-dependent change of vascular permeability as reflected by extravasation of 125I-labelled serum albumin. The change of vascular permeability correlated with tissue calcium and water accumulation suggesting that cord exposure to plasma calcium as a consequence of vascular injury may contribute to the progressive post-traumatic cord necrosis.

Animals↗
PubMed1989

Effect of 4-aminopyridine on axonal conduction-block in chronic spinal cord injury.

The spinal cords of 18 anesthetized cats were injured by standardized contusion. The animals were maintained for 4-16 months, then the thoracic spinal cord was isolated in vitro at 25 degrees C. Microelectrode recordings were made from single axons conducting through the lesion in ventral and lateral tracts. On warming the tissue, action potential conduction was found to block at temperatures below 36 degrees C in 29% of 129 axons tested. Of 17 axons in which it was possible to demonstrate a block below physiological temperature, apply 0.1-1 mM 4-AP, wait for 10 min and test conduction again, 7 showed increases in blocking temperature and 4 of these restored to conduction above 37 degrees C. The other 10 fibers showed no improvement in blocking temperature. 4-AP also increased the spontaneous activity of axons. It was concluded that 4-AP may eventually be useful in chronic spinal cord injuries, because it improves safety factor in some axons and increases excitability in others, which may compensate to some extent for the reduction in density of projections through the lesion.

4-Aminopyridine↗
PubMed2002

First-ever guidelines for spinal cord injuries.

How spinal cord injuries (SCI) are managed--especially in the critical early stages--has a profound effect on a patient's outcome. The publication of the first comprehensive SCI treatment guidelines is an important step in standardizing evidence-based care.

Humans↗
PubMed1993

Development of a methylprednisolone protocol for use in acute spinal cord injuries.

Acute spinal cord injury is a serious medical condition that results in 10,000 new cases of paralysis each year. Initial physical damage to the spinal cord is followed by chemical damage, resulting in cell death and scar tissue formation. Methylprednisolone therapy has proven effective in suppressing the chemical damage, particularly when started within 8 hours of injury. A protocol developed by the Pharmacy Department at Methodist Medical Center in Dallas, Texas, is described. This protocol facilitates accurate, efficient preparation and administration of this emergency therapy. The protocol takes advantage of the pharmacist's unique expertise to lessen the risk of calculation errors and mistakes in preparation, by providing a tailored drug admixture for administration at a fixed flow rate. The protocol and a sample of the pharmacy work sheet are presented.

Clinical Protocols↗