Review of the effect of spinal cord trauma on the vessels and blood flow in the spinal cord

1976 ◽  
Vol 45 (6) ◽  
pp. 638-646 ◽  
Author(s):  
Alan N. Sandler ◽  
Charles H. Tator
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Species Variation ◽  
Spinal Cord Trauma ◽  
Compression Injury ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

✓ The effect of spinal cord trauma on the vasculature and blood flow of the spinal cord is reviewed. Both quantitative and nonquantitative studies are critically discussed and reasons sought for some of the major controversies that have arisen. Differences in methodology, species variation, and variation in the degree and type of cord injury may all be important factors in producing the conflicting results reported in the literature. In general, it can be said that trauma has a profound effect on the vasculature and blood flow in the cord and that severe compression injury of the cord causes marked ischemia in the gray and white matter.

The effect of nimodipine and dextran on axonal function and blood flow following experimental spinal cord injury

1989 ◽  
Vol 71 (3) ◽  
pp. 403-416 ◽  
Author(s):  
Michael G. Fehlings ◽  
Charles H. Tator ◽  
R. Dean Linden
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Compression Injury ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Dextran 40 ◽  
Treatment Groups ◽  
Cord Injury ◽  
Fine Print

✓ There is evidence that posttraumatic ischemia is important in the pathogenesis of acute spinal cord injury (SCI). In the present study spinal cord blood flow (SCBF), measured by the hydrogen clearance technique, and motor and somatosensory evoked potentials (MEP and SSEP) were recorded to evaluate whether the administration of nimodipine and dextran 40, alone or in combination, could increase posttraumatic SCBF and improve axonal function in the cord after acute SCI. Thirty rats received a 53-gm clip compression injury on the cord at T-1 and were then randomly and blindly allocated to one of six treatment groups (five rats in each). Each group was given an intravenous infusion of one of the following over 1 hour, commencing 1 hour after SCI: placebo and saline; placebo and dextran 40; nimodipine 0.02 mg/kg and saline; nimodipine 0.02 mg/kg and dextran 40; nimodipine 0.05 mg/kg and saline; and nimodipine 0.05 mg/kg and dextran 40. The preinjury physiological parameters, including the SCBF at T-1 (mean ± standard error of the mean: 56.84 ± 4.51 ml/100 gm/min), were not significantly different (p > 0.05) among the treatment groups. Following SCI, there was a significant decrease in the SCBF at T-1 (24.55 ± 2.99 ml/100 gm/min; p < 0.0001) as well as significant changes in the MEP recorded from the spinal cord (MEP-C) (p < 0.0001), the MEP recorded from the sciatic nerve (MEP-N) (p < 0.0001), and the SSEP (p < 0.002). Only the combination of nimodipine 0.02 mg/kg and dextran 40 increased the SCBF at T-1 (43.69 ± 6.09 ml/100 gm/min; p < 0.003) and improved the MEP-C (p < 0.0001), MEP-N (p < 0.04), and SSEP (p < 0.002) following SCI. With this combination, the changes in SCBF were significantly related to improvement in axonal function in the motor tracts (p < 0.0001) and somatosensory tracts (p < 0.0001) of the cord. This study provides quantitative evidence that an increase in posttraumatic SCBF can significantly improve the function of injured spinal cord axons, and strongly implicates posttraumatic ischemia in the pathogenesis of acute SCI.

Effect of acute spinal cord compression injury on regional spinal cord blood flow in primates

1976 ◽  
Vol 45 (6) ◽  
pp. 660-676 ◽  
Author(s):  
Alan N. Sandler ◽  
Charles H. Tator
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Cord Blood ◽  
Gray Matter ◽  
Regional Blood Flow ◽  
Compression Injury ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Cord Injury

✓ Spinal cord blood flow (SCBF) was measured in 24 rhesus monkeys after injury to the cord produced by the inflatable circumferential extradural cuff technique. Measurement of regional blood flow in the white and gray matter of the cord in areas of 0.1 sq mm was achieved with the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. After moderate cord injury (400 mm Hg pressure in the cuff maintained for 5 minutes), which produced paraplegia in 50% of animals and moderate to severe paresis in the other 50%, mean white matter SCBF was significantly decreased for up to 1 hour. White matter blood flow then rose to normal levels by 6 hours posttrauma and was significantly increased by 24 hours posttrauma. Gray matter SCBF was significantly decreased for the entire 24-hour period post-trauma. After severe cord injury (150 mm Hg pressure in the cuff maintained for 3 hours), which produced total paraplegia in almost all animals, SCBF in white and gray matter was reduced to extremely low levels for 24 hours posttrauma. In addition, focal decreases in SCBF were seen in white and gray matter for considerable distances proximal and distal to the injury site. It is concluded that acute compression injury of the spinal cord is associated with long-lasting ischemia in the cord that increases in severity with the degree of injury.

Effect of vasodilators and myelotomy on recovery after acute spinal cord injury in rats

1979 ◽  
Vol 50 (3) ◽  
pp. 349-352 ◽  
Author(s):  
Alex S. Rivlin ◽  
Charles H. Tator
Keyword(s):  
Spinal Cord ◽  
Quantitative Method ◽  
Cord Compression ◽  
Central Canal ◽  
Compression Injury ◽  
Dorsal Midline ◽  
Content Type ◽  
Cord Injury ◽  
Spinal Cord Function ◽  
Fine Print

✓ The effect of papaverine, nitroprusside, or myelotomy on the recovery of spinal cord function was studied in rats after acute cord-compression injury. Spinal cord recovery was measured by a quantitative method of clinical assessment previously developed in our laboratory. Neither papaverine nor nitroprusside improved recovery of cord function. Dorsal midline myelotomy extending anteriorly as far as the central canal did not produce significant improvement (p > 0.05). However, when the myelotomy extended completely through the cord in the anteroposterior plane significant improvement (p < 0.01) was obtained.

Pathological findings in acute experimental spinal cord trauma

1971 ◽  
Vol 35 (6) ◽  
pp. 700-708 ◽  
Author(s):  
Thomas B. Ducker ◽  
Glenn W. Kindt ◽  
Ludwig G. Kempe
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Clinical Improvement ◽  
Spinal Cord Trauma ◽  
Pathological Findings ◽  
Pathological Changes ◽  
Content Type ◽  
Acute Trauma ◽  
Central Gray ◽  
Fine Print

✓ This study shows that spinal cord pathology secondary to acute trauma in monkeys evolves with stepwise sequential changes. The acute damage is more central than peripheral. Depending on the amount of trauma, the subacute damage may be limited to central gray necrosis or may progress or evolve to include the neighboring white matter. These pathological changes may be taking place even in the presence of clinical improvement.

Presence and significance of CD-95 (Fas/APO1) expression after spinal cord injury

2001 ◽  
Vol 94 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Mercedes Zurita ◽  
Jesús Vaquero ◽  
Isabel Zurita
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
Spinal Cord Tissue ◽  
Injured Spinal Cord ◽  
Content Type ◽  
Cord Injury ◽  
Positive Immunostaining ◽  
Fine Print

Object. A glycoprotein, CD95 (Fas/APO1) is widely considered to be implicated in the development of apoptosis in a number of tissues. Based on the hypothesis that apoptosis is related to cell death after spinal cord injury (SCI), the authors studied the presence and distribution of CD95 (Fas/APO1)-positive cells in injured spinal cord tissue for the purpose of determining the significance of this protein during the early phases of SCI. Methods. The presence and distribution of cells showing positive immunostaining for CD95 (Fas/APO1) were studied 1, 4, 8, 24, 48, and 72 hours and 1, 2, and 4 weeks after induction of experimental SCI in rats. Studies were conducted using a monoclonal antibody to the CD95 (Fas/APO1) protein. Positivity for CD95 (Fas/APO1) was observed in apoptotic cells, mainly in the gray matter, 1 hour after trauma, and the number of immunostained cells increased for the first 8 hours, at which time the protein was expressed in both gray and white matter. From 24 to 72 hours postinjury, the number of immunostained cells decreased in the gray matter, but increased in the white matter. From then on, there were fewer CD95 (Fas/APO1)-positive cells, but some cells in the white matter still exhibited positive immunostaining 1 and 2 weeks after injury. At 4 weeks, there remained no CD95 (Fas/APO1)-positive cells in injured spinal cord. Conclusions. These findings indicate that CD95 (Fas/APO1) is expressed after SCI, suggesting a role for this protein in the development of apoptosis after trauma and the possibility of a new therapeutic approach to SCI based on blocking the CD95 (Fas/APO1) system.

Effect of aminophylline and isoproterenol on spinal cord blood flow after impact injury

1980 ◽  
Vol 53 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Diana Dow-Edwards ◽  
Vincent DeCrescito ◽  
John J. Tomasula ◽  
Eugene S. Flamm
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Cord Blood ◽  
Gray Matter ◽  
Adenosine Monophosphate ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Cord Injury ◽  
Matter Flow

✓ A study of the effects of spinal cord injury upon spinal cord blood flow was carried out in cats. A 400 gm-cm impact produced an overall reduction in spinal cord blood flow of 24% in the white matter and 30% in the gray matter, as determined by 14C-antipyrine autoradiography. At the level of the injury, white-matter flow was 8.1 ml/100 gm/min, a reduction of 49%, and in the gray matter, 12.5 ml/100 gm/min, a reduction of 76%. Treatment with aminophylline and isoproterenol improved the overall blood flow in the spinal cord. At the level of the injury, white-matter flow after this treatment was no longer significantly different from control values. The gray-matter flow remained decreased to 26.2 ml/100 gm/min, a reduction of only 47%. It is proposed that aminophylline and isoproterenol may increase cyclic adenosine monophosphate (AMP) and prevent platelet aggregation along the endothelial surfaces of the microcirculation, and may thereby help to maintain improved perfusion of the injured spinal cord.

Spinal blood flow in 24-hour megadose glucocorticoid treatment in awake pigs

2003 ◽  
Vol 99 (3) ◽  
pp. 286-290
Author(s):  
Wolf R. Drescher ◽  
Karen P. Weigert ◽  
Mathias H. Bünger ◽  
Ebbe S. Hansen ◽  
Cody E. Bünger
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Body Weight ◽  
High Dose ◽  
Content Type ◽  
Significant Difference ◽  
Cord Injury ◽  
Methylprednisolone Treatment ◽  
Fine Print

Object. Because of the controversy regarding the benefits of 24-hour administration of methylprednisolone in patients with spinal cord injury (SCI), it is important to investigate its mechanism of action and side effects. This study was conducted to determine if high-dose methylprednisolone modulates neural and vertebral blood flow in an awake large-sized animal model without SCI. Methods. From a group of 18 immature female domestic pigs born to nine different litters, nine animals were randomly allocated to receive methylprednisolone treatment, whereas their nine female siblings served as controls. Drug or placebo was applied in a blinded fashion by a third person not involved in the study. The following treatment for SCI, as suggested by the North American Spinal Cord Injury Study, was administered to the awake pig: methylprednisolone (30 mg/kg of body weight) was infused into the jugular vein during a 15-minute period, followed by a 45-minute pause, and the infusion was maintained over a 23-hour period at a dose of 5.4 mg/kg body weight/hour. By means of the radioactive tracer microsphere technique, spinal cord blood flow (SCBF) was measured in the awake standing pig in the cerebrum, and in spinal gray and white matter, nerve roots, endplates, cancellous bone, cortical shell, and T12—L2 discs. Blood flow was measured before, 1 hour after initiation of infusion, and 24 hours postinfusion. Examination of blood flow in the neural and vertebral tissue samples, as well as of central hemodynamics, revealed no significant difference between the experimental and control groups, and this parity was maintained throughout the experimental phases. Conclusions. In the awake pig model, 24-hour methylprednisolone treatment does not modulate cerebral or SCBF, nor does it increase the risk for vertebral osteonecrosis by producing vertebral ischemia.

Regional spinal cord blood flow in rats after severe cord trauma

1978 ◽  
Vol 49 (6) ◽  
pp. 844-853 ◽  
Author(s):  
Alex S. Rivlin ◽  
Charles H. Tator
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cord Blood ◽  
Gray Matter ◽  
Albino Rats ◽  
Compression Injury ◽  
Spinal Cord Blood Flow ◽  
Compression Technique ◽  
Content Type ◽  
Cord Injury

✓ Spinal cord blood flow (SCBF) was measured in 12 albino rats following acute cord injury produced by the extradural clip compression technique. Severe injury was produced with the clip compressing the cord with a force of 180 gm for 5 minutes, an injury previously shown to produce a severe functional deficit. Regional SCBF was measured 15 minutes, 2 hours, and 24 hours after injury by the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. At 15 minutes and 2 hours, white and gray matter blood flow was severely diminished, and, at 24 hours, there was only minimal improvement. Focal decreases in blood flow were seen in white and gray matter for a considerable distance proximal and distal to the site of cord trauma. Thus, it has been confirmed in this model that severe cord compression injury produces severe posttraumatic ischemia in the cord which lasts for at least 24 hours.

Effect of aluminum on neurological recovery in rats following spinal cord injury

2000 ◽  
Vol 93 (2) ◽  
pp. 276-282 ◽  
Author(s):  
Khalaf Al Moutaery ◽  
Saleh Al Deeb ◽  
Nabil Biary ◽  
Christudas Morais ◽  
Haseeb Ahmad Khan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Motor Deficit ◽  
Sprague Dawley ◽  
Compression Injury ◽  
Content Type ◽  
Sensory Score ◽  
Cord Injury ◽  
Histopathological Studies ◽  
Fine Print

Object. This investigation was undertaken to study the effect of aluminum on neurobehavioral, electrophysiological, structural, and biochemical changes in rats following spinal cord injury (SCI). Methods. Adult male Sprague—Dawley rats classified into different groups were given aluminum sulfate—dosed drinking water in the concentrations of 0%, 0.25%, 0.5% and 1%, respectively. After 30 days of aluminum treatment, the animals were subjected to spinal cord trauma. Laminectomy was performed at T7–8 in anesthetized rats, followed by placement of a compression plate (2.2 × 5 mm) loaded with a 35-g weight over the exposed spinal cord for 5 minutes. Control animals underwent the same surgical procedure, but the compression injury was not induced (sham). Postoperative neurological function was assessed using the inclined-plane test and by obtaining a modified Tarlov score and vocal/sensory score daily for 10 days. Electrophysiological changes were assessed using corticomotor evoked potentials, whereas pathological changes were assessed by light microscopy. The level of vitamin E in the spinal cord was measured as an index of antioxidant defense. The behavioral, biochemical, and histological analyses were performed in a blinded fashion. Conclusions. Analysis of results obtained in the behavioral studies revealed that the compression of spinal cord produced transient paraparesis in which a maximum motor deficit occurred at Day 1 following SCI and resolved over a period of 10 days. Administration of aluminum significantly impaired the recovery following SCI. Analysis of the results of the biochemical, electrophysiological, and histopathological studies also confirmed the deleterious effects of aluminum on recovery from SCI in rats.

Spinal Cord Blood Flow in Experimental Transient Traumatic Paraplegia

1980 ◽  
Vol 52 (3) ◽  
pp. 335-345 ◽  
Author(s):  
Dean C. Lohse ◽  
Howard J. Senter ◽  
John S. Kauer ◽  
Richard Wohns
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Cord Blood ◽  
Spinal Cord Blood Flow ◽  
Flow Measurements ◽  
Content Type ◽  
The Mean ◽  
Blood Flow Measurements ◽  
Fine Print

✓ Blood flow in the lateral funiculus of the thoracic spinal cord was measured in 24 anesthetized cats using the hydrogen clearance method. In a control series of eight nontraumatized animals, blood flow measurements were taken from the T-5 and T-6 segments for 6 consecutive hours. The mean spinal cord blood flow (SCBF) in the control group was 12.8 ± 3.51 (SD) ml/min/100 gm on the basis of 107 measurements over 6 hours. In the experimental groups, 16 animals were similarly prepared. The spinal cords of these animals were then traumatized by dropping a 20-gm weight 5 cm (100 gm-cm trauma) or 13 cm (260 gm-cm trauma) onto the T-5 segment. Previous experiments have shown that these trauma levels lead to a transient paraplegia of less than 10 and 30 days' duration, respectively. Two hundred blood flow measurements from T-5 and T-6 were taken over the 6 hours following trauma. In the seven animals of the 100 gm-cm group, mean SCBF after trauma from the T-5 segment was 12.6 ± 3.45 (SD) ml/min/100 gm on the basis of 50 measurements taken over 6 hours; not significantly different from the controls (p > 0.70). In the 260 gm-cm group, mean SCBF from T-5 for 6 hours after trauma was 17.3 ± 6.60 (SD) ml/min/100 gm; significantly higher than controls (p < 0.001). Mean SCBF 3 to 6 hours after trauma was significantly elevated over controls (p < 0.05). The mean hyperemia in the 260 gm-cm group was found to be due to marked hyperemia in only four animals of the series, while five animals maintained blood flows in the normal range. This experiment provides quantitative evidence that white matter ischemia does not occur in spinal cord injuries that can be expected to produce only transient paraplegia. The data support the concept that white matter ischemia in the acute phase of severe spinal cord trauma may be related to secondary injury and subsequent permanent paraplegia.

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