The pathophysiological response to spinal cord injury

1974 ◽  
Vol 40 (1) ◽  
pp. 3-33 ◽  
Author(s):  
Jewell L. Osterholm
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Controversial Issues ◽  
Content Type ◽  
Cord Injury ◽  
Injury Research ◽  
Fine Print

✓ In this review of spinal cord injury research, the author has selected contributions which in his opinion best represent modern experimental concepts regarding the mechanism and management of spinal cord injuries. He has placed special emphasis on the controversial issues appropriate to a new, stimulating, and competitive area of research.

Therapeutic trial of hypercarbia and hypocarbia in acute experimental spinal cord injury

1984 ◽  
Vol 61 (5) ◽  
pp. 925-930 ◽  
Author(s):  
Ronald W. J. Ford ◽  
David N. Malm
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Mortality Rates ◽  
Therapeutic Trial ◽  
Tissue Preservation ◽  
Content Type ◽  
Experimental Spinal Cord Injury ◽  
Cord Injury ◽  
Fine Print

✓ Hypocarbia, normocarbia, or hypercarbia was maintained for an 8-hour period beginning 30 minutes after acute threshold spinal cord injuries in cats. No statistically significant differences in neurological recovery or histologically assessed tissue preservation were found among the three groups of animals 6 weeks after injury. No animal recovered the ability to walk. It is concluded that maintenance of hypercarbia or hypocarbia during the early postinjury period is no more therapeutic than maintenance of normocarbia. Mortality rates and tissue preservation data suggest, however, that postinjury hypocarbia may be less damaging than hypercarbia.

Late neurological changes following traumatic spinal cord injury

1988 ◽  
Vol 69 (3) ◽  
pp. 399-402 ◽  
Author(s):  
Joseph M. Piepmeier ◽  
N. Ross Jenkins
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Neurological Status ◽  
Neurological Function ◽  
Traumatic Spinal Cord Injury ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

✓ Sixty-nine patients with traumatic spinal cord injuries were evaluated for changes in their functional neurological status at discharge from the hospital, and at 1 year, 3 years, and 5+ years following injury. The neurological examinations were used to classify patients' spinal cord injury according to the Frankel scale. This analysis revealed that the majority of improvement in neurological function occurred within the 1st year following injury; however, changes in the patients' status continued for many years. Follow-up examinations at an average of 3 years postinjury revealed that 23.3% of the patients continued to improve, whereas 7.1% had deteriorated compared to their status at 1 year. An examination at an average of 5+ years demonstrated further improvement in 12.5%, with 5.0% showing deterioration compared to the examinations at 3 years. These results demonstrate that, in patients with spinal trauma, significant changes in neurological function continue for many years.

The effect of direct-current field on recovery from experimental spinal cord injury

1988 ◽  
Vol 68 (5) ◽  
pp. 781-792 ◽  
Author(s):  
Michael G. Fehlings ◽  
Charles H. Tator ◽  
R. Dean Linden
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Direct Current ◽  
Injury Severity ◽  
Spinal Cord Injuries ◽  
Red Nucleus ◽  
Inclined Plane ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

✓ Recent work has indicated that direct-current (DC) fields may promote recovery after acute spinal cord injury. In the present experiments, the therapeutic value of an applied DC field was studied in 40 rats with clip compression injuries of the cord at C7–T1. The rats were randomly allocated to one of four groups including 10 rats each: two groups received a 17-gm cord injury and two groups a 53-gm injury. One group at each injury severity received implantation of a treatment (14 µA) DC stimulator and the other group a control (0 µA) stimulator. Clinical neurological function was assessed weekly by the inclined-plane technique. At 8 weeks after injury, motor and somatosensory evoked potentials (MEP's and SSEP's) were recorded, and the axonal tracer horseradish peroxidase (HRP) was introduced into the cord at T-6. The total number of HRP-labeled cells was counted in every sixth coronal section through the brain stem and motor cortex. All outcome parameters were assessed blindly. In the 17-gm group, there were no significant differences in any outcome measure between control and treated rats. In contrast, in the 53-gm group, the inclined-plane scores, the amplitude of the MEP's, and the number of labeled cells in the red nucleus, raphé nuclei, and vestibular nuclei were greater in treated than in control rats. These data strongly indicate that an applied DC field can produce functional neurological and anatomical improvement in rats with acute spinal cord injuries.

Retrograde degeneration of corticospinal axons following transection of the spinal cord in rats

1988 ◽  
Vol 68 (1) ◽  
pp. 124-128 ◽  
Author(s):  
Roberto Pallini ◽  
Eduardo Fernandez ◽  
Alessandro Sbriccoli
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Standard Deviation ◽  
Objective Assessment ◽  
Content Type ◽  
Retrograde Degeneration ◽  
Therapeutic Modalities ◽  
Cord Injury ◽  
Injury Research ◽  
Fine Print

✓ The extent of the retrograde degeneration of corticospinal axons following transection of the spinal cord was studied in rats by labeling corticospinal axons with anterogradely transported horseradish peroxidase injected in the sensorimotor cortex. Axotomized corticospinal axons underwent progressive and continuing retrograde degeneration. In specimens examined 5, 14, 28, and 56 days after trauma, the tips of the transected corticospinal axons were seen to terminate at 181 ± 80 µm, 977 ± 203 µm, 1751 ± 344 µm, and 2559 ± 466 µm (mean ± standard deviation), respectively, from the site of transection. The rate of retrograde degeneration varied according to the interval after spinal cord transection, as follows: 36.2 µm/day during the first 5 days; 88.4 µm/day between 5 and 14 days; 55.3 µm/day between 14 and 28 days; and 28.8 µm/day between 28 and 56 days. These findings may serve as useful parameters for the objective assessment of therapeutic modalities in spinal cord injury research.

Federal programs for the care and study of spinal cord injuries

1972 ◽  
Vol 36 (4) ◽  
pp. 379-385 ◽  
Author(s):  
Henry L. Heyl
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Federal Programs ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

✓ This report summarizes in one document the four federal programs devoted specifically to the care and study of spinal cord injuries. The accompanying editorial emphasizes the need for coordination between these agencies in the optimal use of specific capabilities and separate federal budgets, particularly in the planning for regional spinal cord injury centers.

The effect of spinal distraction on regional spinal cord blood flow in cats

1980 ◽  
Vol 53 (6) ◽  
pp. 756-764 ◽  
Author(s):  
Eugen J. Dolan ◽  
Ensor E. Transfeldt ◽  
Charles H. Tator ◽  
Edward H. Simmons ◽  
Kenneth F. Hughes
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Cord Blood ◽  
Spinal Cord Injuries ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Cord Injury ◽  
Autoradiographic Technique ◽  
Fine Print

✓ Distraction is considered to be a factor in many spinal cord injuries. With a specially designed distraction apparatus and the 14C-antipyrine autoradiographic technique, the effect of distraction on spinal cord blood flow (SCBF) in cats was studied. Distraction was performed at L2–3 at a rate of 0.25 cm/10 min, and the spinal evoked response (SER) was monitored by stimulating the sciatic nerve and recording at T-13. The SCBF was assessed in five control animals, four animals in whom the SER was markedly altered by distraction, and five animals after the SER had been abolished and an additional 0.5 cm distraction applied. Control cats had gray- and white-matter flows of 44.5 ± 1.4 (SEM) and 10.5 ± 0.4 ml/100 gm/min, respectively. Distraction to the point of marked SER alteration caused a 50% loss of SCBF at and caudal to the distraction site. An additional 0.5 cm distraction produced total abolition of SCBF at the distraction site and for a considerable distance rostral and caudal to it. Thus, it is shown that spinal distraction causes cord ischemia similar to that seen with other types of spinal cord injury. In addition, distraction severe enough to cause loss of the SER has already produced severe cord ischemia.

Microangiographic study of experimental spinal cord injuries

1971 ◽  
Vol 35 (3) ◽  
pp. 277-286 ◽  
Author(s):  
David J. Fairholm ◽  
Ian M. Turnbull
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axonal Degeneration ◽  
Spinal Cord Injuries ◽  
Spinal Injury ◽  
Degenerative Changes ◽  
Injured Spinal Cord ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

✓ The pathology of spinal cord injury has been studied in 34 rabbits and 5 dogs with attention focused on the condition of the microvasculature during the evolution of neuronal and axonal degeneration and necrosis. The animals were killed and perfused arterially with colloidal barium from 10 min to 14 days after a controlled spinal injury. Microradiographs of the injured tissues were obtained and compared with corresponding histological sections. Microangiography at 7 to 14 days defines two zones in the injured spinal cord. Zone 1 is located in the posterocentral part of the cord. Capillaries in this region progressively lose their ability to conduct blood and perfusate over the first 4 hours. Degenerative changes in neurons are visible by 1 hour after injury. Necrosis of all elements including capillaries ensues. Zone 2 surrounds Zone 1. Microvascular patterns are normal in Zone 2 although neuronal and axonal degeneration is severe. Pericapillary hemorrhages which occur as early as 10 min after injury in Zone 1 and become progressively larger over the first 4 hours seldom are seen in Zone 2. The evidence indicates that at all times in the pathogenesis of spinal cord injury the microvasculature in Zone 2 is capable of perfusion. Degeneration of neural structures either precedes microvascular breakdown (Zone 1) or occurs in the absence of microvascular disruption (Zone 2). Recovery of damaged neurons and axons depends upon a preserved microcirculation.

The effects of methylprednisolone and the ganglioside GM1 on acute spinal cord injury in rats

1994 ◽  
Vol 80 (1) ◽  
pp. 97-111 ◽  
Author(s):  
Shlomo Constantini ◽  
Wise Young
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Body Weight Loss ◽  
Ganglioside Gm1 ◽  
Rat Spinal Cord ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Fine Print

✓ Recent clinical trials have reported that methylprednisolone sodium succinate (MP) or the monosialic ganglioside GM1 improves neurological recovery in human spinal cord injury. Because GM1 may have additive or synergistic effects when used with MP, the authors compared MP, GM1, and MP+GM1 treatments in a graded rat spinal cord contusion model. Spinal cord injury was caused by dropping a rod weighing 10 gm from a height of 1.25, 2.5, or 5.0 cm onto the rat spinal cord at T-10, which had been exposed via laminectomy. The lesion volumes were quantified from spinal cord Na and K shifts at 24 hours after injury and the results were verified histologically in separate experiments. A single dose of MP (30 mg/kg), given 5 minutes after injury, reduced 24-hour spinal cord lesion volumes by 56% (p = 0.0052), 28% (p = 0.0065), and 13% (p > 0.05) in the three injury-severity groups, respectively, compared to similarly injured control groups treated with vehicle only. Methylprednisolone also prevented injury-induced hyponatremia and increased body weight loss in the spine-injured rats. When used alone, GM1 (10 to 30 mg/kg) had little or no effect on any measured variable compared to vehicle controls; when given concomitantly with MP, GM1 blocked the neuroprotective effects of MP. At a dose of 3 mg/kg, GM1 partially prevented MP-induced reductions in lesion volumes, while 10 to 30 mg/kg of GM1 completely blocked these effects of MP. The effects of MP on injury-induced hyponatremia and body weight loss were also blocked by GM1. Thus, GM1 antagonized both central and peripheral effects of MP in spine-injured rats. Until this interaction is clarified, the authors recommend that MP and GM1 not be used concomitantly to treat acute human spinal cord injury. Because GM1 modulates protein kinase activity, protein kinases inhibit lipocortins, and lipocortins mediate anti-inflammatory effects of glucocorticoids, it is proposed that the neuroprotective effects of MP are partially due to anti-inflammatory effects and that GM1 antagonizes the effects of MP by inhibiting lipocortin. Possible beneficial effects of GM1 reported in central nervous system injury may be related to the effects on neural recovery rather than acute injury processes.

Ultrastructural scoring of graded acute spinal cord injury in the rat

2002 ◽  
Vol 97 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Erkan Kaptanoglu ◽  
Selcuk Palaoglu ◽  
H. Selcuk Surucu ◽  
Mutlu Hayran ◽  
Etem Beskonakli
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Behavioral Assessment ◽  
Traumatic Injury ◽  
Significant Negative Correlation ◽  
Content Type ◽  
Cord Injury ◽  
Contusion Injury ◽  
Weight Drop ◽  
Fine Print

Object. There is a need for an accurate quantitative histological technique that also provides information on neurons, axons, vascular endothelium, and subcellular organelles after spinal cord injury (SCI). In this paper the authors describe an objective, quantifiable technique for determining the severity of SCI. The usefulness of ultrastructural scoring of acute SCI was assessed in a rat model of contusion injury. Methods. Spinal cords underwent acute contusion injury by using varying weights to produce graded SCI. Adult Wistar rats were divided into five groups. In the first group control animals underwent laminectomy only, after which nontraumatized spinal cord samples were obtained 8 hours postsurgery. The weight-drop technique was used to produce 10-, 25-, 50-, and 100-g/cm injuries. Spinal cord samples were also obtained in the different trauma groups 8 hours after injury. Behavioral assessment and ultrastructural evaluation were performed in all groups. When the intensity of the traumatic injury was increased, behavioral responses showed a decreasing trend. A similar significant negative correlation was observed between trauma-related intensity and ultrastructural scores. Conclusions. In the present study the authors characterize quantitative ultrastructural scoring of SCI in the acute, early postinjury period. Analysis of these results suggests that this method is useful in evaluating the degree of trauma and the effectiveness of pharmacotherapy in neuroprotection studies.

A reproducible spinal cord injury model in the cat

1983 ◽  
Vol 59 (2) ◽  
pp. 268-275 ◽  
Author(s):  
Ronald W. J. Ford
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Sharp Transition ◽  
Content Type ◽  
Spinal Cord Injury Model ◽  
Injury Model ◽  
Cord Injury ◽  
Weight Drop ◽  
Future Evaluation

✓ Allen's weight-drop method for producing experimental spinal cord injuries was improved by placing a curved stainless steel plate anterior to the spinal cord to provide a smooth, hard surface for the receipt of posterior cord impact. In addition, an electronic circuit was used to ensure that cord injury was produced by a single impact, thereby enhancing the reproducibility of the injury mechanism. Using a spinal cord injury model with these modifications, the author found that the recovery of hindlimb function and the histopathological appearance of the injured cord 6 weeks after upper lumbar injury were closely related to injury magnitude. The curve of functional recovery versus injury magnitude has a sharp transition centered at 10 gm × 15 cm, and indicates that an injury of 10 gm × 20 cm produces a “threshold” lesion suitable for the future evaluation of spinal cord treatment methods.

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