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PubMed1990

[Spinal cord evoked potential in experimental spinal cord injury--the changes in spinal cord evoked potential following impact injury, and effect of mannitol administration on acute experimental spinal cord injury].

The authors reported the changes of spinal cord evoked potential following impact injury by the weight dropping technique in untreated and treated animals. The correlation between the change in amplitude of the spinal cord evoked potential after injury and the prognosis for motor recovery of legs was also discussed. (Materials and Methods) The spinal cord of 57 adult dogs was traumatized by the weight dropping technique at the level of Th10. 37 dogs were not treated. The trauma consisted of 300 gm-cm impact injury, 400 gm-cm impact injury and 500 gm-cm impact injury. The motor function of the dogs was observed by clinical scale for rating hind limb motor function (modified Tarlov score) for one month after trauma. 20 dogs with 300 gm-cm contusion were treated with mannitol. 10 dogs were treated with intravenous continuous infusion of mannitol (1 g/kg/hr) 30 minutes after injury and 10 dogs with intravenous bolus injection of mannitol (2 g/kg) at 30 minutes and 3 hours after injury. The spinal cord evoked potential following direct stimulation of the spinal cord was recorded from the epidural space for 5 hours. The recording electrode was located cephalad to the site of the impact injury. (Results and Conclusion) 1. In each group, the amplitude of I potential decreased remarkably immediately after injury. Subsequently, gradual recovery was obtained. The spinal cord evoked potential following impact injury by the weight dropping technique could be estimated one hour after trauma in 300 gm-cm, 30 minutes after trauma in 400 gm-cm injury and immediately after trauma in 500 gm-cm injury. 2. Spinal cord evoked potential was useful in monitoring the recovery potential of the spinal cord. Recovery of amplitude more than 40% indicated a favorable prognosis. On the other hand, recovery of amplitude less than 19% showed a poor prognosis. However, the precise prognosis for motor recovery could not be accurately estimated in dogs with recovery of amplitude between 39% and 20%. 3. In mannitol-treated group with intravenous continuous infusion, the recovery of the amplitude was superior to that in untreated group at a significance level of p less than 0.05. However, in the group with intravenous bolus injection of mannitol, the recovery was transient.

Animals↗
PubMedDate not supplied

Pushrim biomechanics and injury prevention in spinal cord injury: recommendations based on CULP-SCI investigations.

Over 50 percent of manual wheelchair users with spinal cord injury (SCI) are likely to develop upper-limb pain and injury. The majority of studies related to pain have implicated wheelchair propulsion as a cause. This paper draws from a large multisite trial and a long-standing research program to make specific recommendations related to wheelchair propulsion that may decrease the risk of upper-limb injury. The studies include over 60 subjects over 1 yr after a traumatic SCI below the second thoracic level. Specific aspects of the propulsive stroke that may relate to injury include cadence, magnitude of force, and the pattern of the hand during the nonpropulsive part of the stroke. Lower peak forces, slower cadence, and a circular propulsive stroke in which the hand falls below the pushrim during recovery may help prevent injury. In addition, wheelchair users should use the lightest weight adjustable wheelchair possible. Future work should include interventional trials and larger studies that allow for more complex statistical models that can further detail the relationship between wheelchair propulsion, user characteristics, and upper-limb injuries.

Adult↗
PubMed2002

A novel biodegradable implant for neuronal rescue and regeneration after spinal cord injury.

After spinal cord injury, the severed neuronal pathways fail to regenerate spontaneously. This study describes a biodegradable implant using poly-beta-hydroxybutyrate (PHB) fibers as carrier scaffold for matrix components and cell lines supporting neuronal survival and regeneration after spinal cord injury. After cervical spinal cord injury in adult rats, a graft consisting of PHB fibers coated with alginate hydrogel + fibronectin was implanted in the lesion cavity. In control groups, PHB was omitted and only alginate hydrogel or fibronectin, or their combination, were used for grafting. In addition, comparisons were made with animals treated intrathecally after spinal cord injury with the neurotrophic factors BDNF or NT-3. The neurons of the rubrospinal tract served as experimental model. In untreated animals, 45% of the injured rubrospinal neurons were lost at 8 weeks postoperatively. Implantation of the PHB graft reduced this cell loss by 50%, a rescuing effect similar to that obtained after treatment with BDNF or NT-3. In the absence of PHB support, implants of only alginate hydrogel or fibronectin, or their combination, had no effect on neuronal survival. After addition of neonatal Schwann cells to the PHB graft, regenerating axons were seen to enter the graft from both ends and to extend along its entire length. These results show that implants using PHB as carrier scaffold and containing alginate hydrogel, fibronectin and Schwann cells can support neuronal survival and regeneration after spinal cord injury

Animals↗
PubMed2002

Adrenal gland volume after spinal cord injury.

OBJECTIVE: Spinal cord injury in adult men may result in hypothalamic-pituitary-adrenal axis dysfunction. Atrophy of adrenal glands was speculated in these patients. This study was undertaken to clarify the functional-anatomic correlation between adrenal volume and body surface area in subjects with spinal cord injury with impaired adrenal reserve. DESIGN: Twenty male subjects with chronic spinal cord injury with impaired adrenal reserve were identified by adrenocorticotropic hormone stimulation test from a group of 42 subjects. All subjects with spinal cord injury and healthy volunteers underwent computed tomographic imaging with contiguous 3-mm section over adrenal glands for volumetric measurements. Ten pairs of subjects with spinal cord injury and controls with matched height and weight were included in the statistical analysis. RESULTS: Significantly increased relative adrenal volumes were noted among subjects with chronic spinal cord injury and impaired adrenal reserve as compared with the body weight-matched and height-matched control group. CONCLUSIONS: Increased relative adrenal volumes were found after chronic spinal cord injury. Hyperplasia of the zona glomerulosa may be the cause of increased relative adrenal volume after chronic spinal cord injury.

Adrenal Glands↗
PubMed2002

Shoulder biomechanics and muscle plasticity: implications in spinal cord injury.

After spinal cord injury, excessive burden falls on the upper extremity, especially the shoulder. Overall, 51% of persons with spinal cord injury have shoulder problems. Common shoulder problems in persons with spinal cord injury begin with muscle imbalance that can lead to glenohumeral instability, impingement disease, rotator cuff tears, and subsequent degenerative joint disease. These problems can be attributed to the functional demands placed on the shoulder that are specific to patients with spinal cord injury, including overhead activities, wheelchair use, and transfers. Despite preventive exercises, shoulder problems in persons with spinal cord injury remain a significant problem, causing pain and functional limitations. The biomechanics of the shoulder for persons with spinal cord injury resulting from changes in muscle plasticity will be elucidated. Specifically, the effects of scapular protraction that can result from muscle imbalance, the age-dependent properties of the anterior band of the inferior glenohumeral ligament, and the influence of the dynamic restraints around the shoulder will be addressed.

Biomechanical Phenomena↗
PubMed1989

Clinical pharmacokinetics in patients with spinal cord injuries.

Although spinal cord injury is a catastrophic affliction with numerous victims and a variety of physiological manifestations, the associated disarray in physiology has yet to be systematically or comprehensively studied as a probable cause for altered pharmacokinetics. A significant increase in the volume of distribution of drugs such as the aminoglycosides (gentamicin, amikacin, tobramycin), which are highly distributed into the extracellular fluid space and minimally biotransformed, may be anticipated in patients with chronic spinal cord injury. Changes in total body clearance have also been observed for some of these medications. The influence of the pathophysiology of spinal cord injury on gastrointestinal motility appears to be reflected in an impairment in the bioavailability of drugs [theophylline, paracetamol (acetaminophen), doxycycline] which are passively absorbed and which require an intact postprandial gastric emptying to ensure efficient absorption. For theophylline, the impairment in gastrointestinal absorption appears to be directly proportional to both the magnitude of the impairment in gastric emptying and to the neurological level of the injury. Metoclopramide, a gastrointestinal prokinetic drug, has been shown to be extremely effective in normalising the impaired postprandial gastric emptying that characterises spinal cord injury. The systemic absorption of 2 antibiotics (gentamicin and cefotiam) injected into paralysed muscle is also impaired in patients with spinal cord injury, suggesting that a decrease in therapeutic efficacy attributable to this mode of administration may be anticipated. Despite the multiplicity of drugs commonly prescribed for patients with this injury, little is known about the influence of this illness on either bioavailability or postabsorptive pharmacokinetics. For drugs which are biotransformed and which have a relatively small volume of distribution (theophylline, lorazepam, ranitidine), single-dose intravenous pharmacokinetic profiles in patients with spinal cord injury are indistinguishable from the drug disposition profiles characteristic of healthy control populations. It may be inferred, then that the influence of the pathophysiology of spinal cord injury on drug disposition is greatest on those drugs which are the least biotransformed and most likely to be distributed into the increased extracellular fluid volume which is characteristic of patients with this disability.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Semen retrieval by penile vibratory stimulation in men with spinal cord injury.

Traumatic spinal cord injury resulting from car accidents, falls, violence or sport-related activities is a common occurrence throughout the world. Spinal cord injuries occur most often to young men in their parenting years. Among the medical challenges facing many of these men is the inability to ejaculate via sexual intercourse. To achieve biological fatherhood, their semen may be retrieved by methods of assisted ejaculation. This paper discusses the use of penile vibratory stimulation in men with spinal cord injury, and includes the topics: patient selection and management; proper placement and timing of stimulation; appropriate use of low-amplitude, high-amplitude or dual vibrators; and factors influencing ejaculatory success rate. Also summarized are recent data on semen quality in men with spinal cord injury. When performed properly, penile vibratory stimulation is a safe and easy method of obtaining semen from anejaculatory men with spinal cord injury. Semen quality is better when obtained by penile vibratory stimulation compared with electroejaculation, an alternative method of semen retrieval. For these reasons, and because of the low investment of time and money, it is recommended that penile vibratory stimulation be used as the first line of treatment for anejaculation in men with spinal cord injury.

Ejaculation↗
PubMed2006

Part 1: recognizing neonatal spinal cord injury.

Neonatal spinal cord injury can occur in utero, as well as after either a difficult delivery or a nontraumatic delivery. Spinal cord injury can also be related to invasive nursery procedures or underlying neonatal pathology. Early clinical signs of spinal cord injury that has occurred in utero or at delivery includes severe respiratory compromise and profound hypotonia. Knowledge of risk factors and awareness of symptoms is required for early recognition and appropriate treatment. This article reviews the embryological development of the spinal column highlighting mechanisms of injury and identifying underlying factors that increase the risk of spinal cord injury in newborns. Signs and symptoms of injury, cervical spine immobilization, and the differential diagnosis are discussed. Nursing implications, general prognosis, and research in spinal cord injury are provided.

Birth Injuries↗
PubMed1995

Early surgery for thoracolumbar spinal cord injury: initial experience from a developing spinal cord injury centre in India.

The spinal cord injury centre of Nizam's Institute of Medical Sciences, Andhra Pradesh, India has been functioning now for 8 months and offers its services to the population of 80 million in the state. To date, 92 patients with a spinal cord injury have been treated; 51 had a thoracolumbar spinal injury. This report presents the results of the management of these 51 patients. Preoperatively both CT and MRI were performed and the radiological findings were correlated with outcome. Twenty five had a thoracic and 26 a lumber location. Twenty nine patients underwent surgical treatment (15 thoracic and 14 lumbar) and the others were treated conservatively (10 thoracic and 12 lumbar). All these operations were carried out within 2 weeks following trauma, and methylprednisolone therapy was instituted in those who reached the hospital early. Contraindications for surgery included a delay in admission of more than 3 weeks following trauma, a focus of sepsis, bedsores, a generalised bone disorder such as osteopenia, and medical illnesses. Transpedicular screw-plate fixation was performed in 27 patients, and two patients underwent decompressive laminectomy and interlaminar bone and wire fixation. Delayed spinal decompression was offered to one patient to relieve radiculopathy. Fracture-dislocation spinal injury and those with transection of the spinal cord had the worst outcome, whilst patients with a wedge compression fracture and cord oedema fared better. Operated cases had a shorter hospital stay, and complications of immobilisation were limited. Positive psychological influence of mobilisation and early acclimatisation to the altered style of living with their disability were the most significant outcomes following surgery.

Female↗
PubMed2004

Neutralization of the chemokine CXCL10 enhances tissue sparing and angiogenesis following spinal cord injury.

After spinal cord injury, there is a chemoattractant-mediated inflammatory response that is associated with secondary degeneration. The chemoattractant CXCL10 recruits CD4 Th1 cells via the CXCR3A receptor and inhibits growth and chemotaxis of endothelial cells via the CXCR3B receptor. To test the hypothesis that CXCL10 inhibits angiogenesis following spinal cord injury, we assayed the brainstems and spinal cords of spinal cord-injured mice treated with anti-CXCL10 antibodies for expression of angiogenesis-associated genes and quantified blood vessels within their spinal cords. Brainstem microarray analysis indicated eight angiogenesis-associated genes that had significantly higher expression levels in the treated mice than in the untreated mice. Ribonuclease protection assays of the spinal cords showed a significant increase in eight angiogenesis-associated genes in treated animals compared with untreated animals. Histological analysis of the spinal cords of treated and untreated mice showed a significant increase in the number of blood vessels in treated animals. We conclude that CXCL10 plays a critical role in vasculature remodeling following spinal cord injury and that angiogenesis is enhanced following anti-CXCL10 treatment of spinal cord injuries. Improved blood flow and oxygen supply to the injury site may contribute to the functional improvement associated with this treatment.

Animals↗
PubMed1990

[Beneficial effect of a selective TXA2 synthetase inhibitor, OKY-046, both on thromboxane B2 production and vascular damage after spinal cord injury in rat spinal cord].

Thromboxane A2 (TXA2) is an eicosanoid with potent platelet aggregation and vasoconstricting activity, while prostaglandin I2 (PGI2) antagonizes its activity. But these eicosanoids are so labile that the stable degradation products, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), are determined in biological materials. In a rat spinal cord compression injury model, a production of TXB2 reached a peak (133.6 +/- 13.8 pmol/g cord) 5 minutes after compression injury, while that of 6-keto-PGF1 alpha slightly increased (26.2 +/- 11.7 pmol/g cord). And the magnitude of the increase in TXB2 and the extent of post-traumatic vascular damage as determined by fluorescein uptake were both dependent on the degree of spinal cord compression injury. We also studied the effect of a selective TXA2 synthetase inhibitor, OKY-046 [E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid), both on TXB2 production in the injured spinal cord and post-traumatic vascular damage. When OKY-046 was administered intravenously 10 minutes prior to compression injury at a dose of 500 micrograms/kg body weight, the increased production of TXB2 was inhibited by about 80% and uptake of sodium fluorescein was reduced by a maximum of 40%. When the compression injury was induced before OKY-046 was administered, the inhibitory effect of OKY-046 on TXB2 production decreased depending on the duration before administration. In contrast, the 6-keto-PGF1 alpha level was not affected in the presence of OKY-046.

6-Ketoprostaglandin F1 alpha↗
PubMed2001

Upregulation of the HLH Id gene family in neural progenitors and glial cells of the rat spinal cord following contusion injury.

Spinal cord injury (SCI) leads to a complex sequence of cellular responses, including astrocyte activation, oligodendrocyte death, and ependymal cell proliferation. Inhibitors of DNA binding (Id1, Id2, Id3) belong to a helix-loop-helix (HLH) gene family. Id genes have been implicated in playing a vital role in the proliferation of many cell types, including astrocytes and myoblasts. In the present study, the expression of Id family members in spinal cord after contusion injury was investigated by in situ hybridization. Id1, Id2, and Id3 mRNA expression was upregulated 5 mm rostral and caudal to the lesion center, and reached maximal levels 3 days after SCI. In addition, cell populations expressing Id1, Id2, and Id3 mRNA were maximally increased 3 days after SCI. The increase in Id2 and Id3 mRNA expression and Id2 and Id3 mRNA+ cells was still observed at 8 days. The Id mRNA expressing cells were phenotyped by combining immunostaining of cell-specific markers with in situ hybridization. Glial fibrillary acidic protein (GFAP)+ astrocytes were found to express all three Id mRNA, whereas S-100alpha+ astrocytes only expressed high levels of Id2 and Id3 mRNA. Cells having a neural progenitor morphology and the marker nestin appeared after SCI and they expressed Id1, Id2, and Id3 mRNA. Interestingly, some Rip+ oligodendrocytes located in the areas close to the central canal expressed Id3 mRNA after injury. In conclusion, Id genes are upregulated in a time-dependent manner in astrocytes, oligodendrocytes, and neural progenitor subpopulations after SCI, suggesting that they play major roles in cellular responses following SCI.

Animals↗
PubMed1999

Neurologic recovery after traumatic spinal cord injury: data from the Model Spinal Cord Injury Systems.

OBJECTIVE: To present data on neurologic recovery gathered by the Model Spinal Cord Injury (SCI) Systems over a 10-year period. DESIGN: Case series. SETTING: Twenty-one Model SCI Systems. PATIENTS: A total of 3,585 individuals with traumatic SCI admitted between January 1, 1988 and December 31, 1997. MAIN OUTCOME MEASURES: Neurologic impairment category; Frankel grade; American Spinal Injury Association (ASIA) Impairment Scale (AIS) grade; motor score. RESULTS: SCI caused by violence is more likely than SCI from nonviolent etiologies to result in a complete injury. Changes in severity of injury were similar using the older Frankel scale and the newer ASIA Impairment Scale. Individuals who were motor-complete with extended zones of sensory preservation but without sacral sparing were less likely to convert to motor-incomplete status than those with sacral sparing (13.3% vs 53.6%; p < .001). Motor score improvements at 1 year were related to severity of injury, with greater increases for better AIS grades except grade D, because of ceiling effects. Individuals with AIS grade B injuries have a mixed prognosis. CONCLUSION: Neurologic recovery after SCI is influenced by etiology and severity of injury. Multicenter studies on prognostic features such as preserved pin sensation in grade B injuries may identify subgroups with similar recovery patterns. Identification of such groups would facilitate clinical trials for neurologic recovery in acute SCI.

Databases, Factual↗
PubMed1990

Endogenous peroxidatic activity in astrocytes after spinal cord injury.

After spinal cord injury, endogenous peroxidatic-like activity develops along the axis of the cord. At 2 weeks postinjury, this activity appears in cells whose processes are intimately associated with microvessels. The objectives of this study were to further characterize this response and to identify the cellular localization of endogenous peroxidatic-like activity. After traumatic injury to the rat spinal cord, adjacent sections of spinal cord were processed in medium to visualize antiglial fibrillary acidic protein, endogenous peroxidatic activity, or cytochrome oxidase activity. In addition, certain sections, stained for endogenous peroxidatic-like activity, were prepared for electron microscopy. To identify the nature of the activity, some sections were exposed to an incubation medium that included inhibitors of either catalase or heme protein activity. The distribution of prominent glial fibrillary acidic protein immunoreactivity in the dorsal columns corresponded to that of marked staining for endogenous peroxidatic-like activity and cytochrome oxidase. At the ultrastructural level, endogenous peroxidatic-like activity was identified in the cytoplasmic compartment of the astrocyte. This activity was abolished when potassium cyanide (an inhibitor of heme protein) was added to the incubation medium. Spinal cord injury elicited a pronounced cellular response along the axis of the cord that was characterized by enhanced staining for antiglial fibrillary acidic protein, cytochrome oxidase activity, and endogenous peroxidatic-like activity. It is not clear whether pronounced cytochrome oxidase activity corresponded to astrocytes that also expressed prominent endogenous peroxidatic-like activity. However, according to both light and ultrastructural findings, endogenous peroxidatic-like activity was prominently associated with the astrocytic cytoplasm. The biochemical nature of the peroxidatic activity is unknown, but these results suggest that it is related to a heme-containing protein.

Animals↗
PubMed1990

[Effect of mannitol administration and myelotomy on acute experimental spinal cord injury: investigation by spinal cord evoked potential].

The authors reported the changes in spinal cord evoked potential following impact injury by the weight-dropping technique in untreated and treated animals. The effect of mannitol and myelotomy therapy on spinal cord evoked potential in experimental spinal cord injury was discussed. (Materials and Methods) 32 adult dogs, ranging in weight from 9 to 13 kg, were used. 28 dogs received 300 gm-cm contusion of the T10 spinal cord. Eight dogs were not treated and twenty dogs were treated with mannitol. Ten dogs were treated with intravenous continuous infusion of mannitol (1g/kg/hr) 30 minutes after the injury, and ten dogs with intravenous bolus injection of mannitol (2 g/kg) at 30 minutes and 3 hours after the injury. At one hour after the injury, five dogs with 400 gm-cm contusion were treated with posterior midline myelotomy. The spinal cord evoked potential following direct stimulation of the spinal cord was recorded from the epidural space for 5 hours. The recording electrode was located cephalad to the site of the impact injury. (Results and Discussion) In each group, the amplitude of I potential decreased remarkably immediately after the injury. Subsequently, gradual recovery was obtained. In the untreated 300 gm-cm contusion group, no apparent improvement was seen from one hour after injury. On the other hand, in the mannitol-treated group, the recovery of the amplitude was superior to that found in the untreated group at a significant level of P less than 0.05. However, in the group with intravenous bolus injection of mannitol, the recovery was transient.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Orthostatic hypotension and paroxysmal hypertension in humans with high spinal cord injury.

The spinal cord is essential for normal autonomic nervous system regulation of the cardiovascular system as the preganglionic neurons controlling the heart and blood vessels originate in the thoracolumbar spinal segments. The site and extent of a spinal cord injury determine the degree of autonomic involvement in cardiovascular dysfunction after the injury. After complete cervical cord lesions the entire sympathetic outflow is separated from cerebral control; this may cause orthostatic hypotension. Commonly after traumatic injuries to the spinal cord, one or more segments are totally destroyed. However, the distal portion of the spinal cord often retains function and activation of spinal cord reflexes working independently of the brain can result in paroxysmal hypertension. This chapter will focus on orthostatic hypotension and paroxysmal hypertension in cord-injured people with lesions affecting the cervical and upper thoracic spinal cord. Conditions promoting these abnormalities in blood pressure will be elaborated. Possible mechanisms for the hypo- and hypertension will be discussed, as will strategies for managing these problems.

Autonomic Dysreflexia↗