Experimental cervical myelopathy

1975 ◽  
Vol 43 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Michael R. Gooding ◽  
Charles B. Wilson ◽  
Julian T. Hoff
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cervical Myelopathy ◽  
Cervical Spondylosis ◽  
Local Deformation ◽  
Cervical Cord ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Adjacent Segments ◽  
Fine Print

✓ The authors report experiments designed to test the effect of regional ischemia induced by selective vascular ligations and anterior compression of the cervical cord at two adjacent segments (C-4, C-5) in the same dog. They conclude that local ischemia of the cervical cord, caused by local deformation, when superimposed on a regional reduction in spinal cord blood flow, accounts for the myelopathy of cervical spondylosis whether produced experimentally in animals or occurring naturally in man.

Effects of laminectomy on spinal cord blood flow

1978 ◽  
Vol 48 (2) ◽  
pp. 232-238 ◽  
Author(s):  
Douglas K. Anderson ◽  
Gregory R. Nicolosi ◽  
Eugene D. Means ◽  
L. Edward Hartley
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cord Blood ◽  
Reference Sample ◽  
Significant Decline ◽  
Entire Length ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Sample Method ◽  
Fine Print

✓ The effect of a one-segment (L-2) laminectomy on spinal cord blood flow (SCBF) was determined by the reference sample method using isotope-labeled microspheres. The SCBF was measured before laminectomy (control) and at 15 minutes postlaminectomy with the dura exposed (Series 1), 1 hour postlaminectomy with the laminectomy site closed (Series 2), 24 hours postlaminectomy with the laminectomy site closed (Series 3), and 24 hours postlaminectomy with the dura exposed (Series 4). With the laminectomy site open, SCBF was significantly depressed (22% to 45%) along the entire length of the spinal cord at 15 minutes postlaminectomy. At 1 hour postlaminectomy (with the laminectomy site closed), SCBF approached control values, although areas with significantly lowered flow were still observed in all portions of the spinal cord. By 24 hours postlaminectomy, SCBF had returned to prelaminectomy levels. However, if within 1 hour preceding the 24-hour SCBF measurement, the laminectomy site was reopened, SCBF tended to fall at and caudad to the laminectomy site. These data indicate that laminectomy can cause a significant decline in SCBF. At the present time, the mechanism(s) for this laminectomy-induced depression of SCBF are unknown, although a temperature-induced vasoconstriction is suspected.

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.

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.

Effect of a calcium channel blocker on posttraumatic spinal cord blood flow

1987 ◽  
Vol 66 (3) ◽  
pp. 423-430 ◽  
Author(s):  
Abhijit Guha ◽  
Charles H. Tator ◽  
Ian Piper
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cord Blood ◽  
Whole Blood ◽  
Channel Blocker ◽  
Rat Spinal Cord ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Pressor Agent ◽  
Fine Print

✓ The normal rat spinal cord blood flow (SCBF) has been shown to increase after administration of nimodipine, a calcium channel blocker. The present study investigates the capability of nimodipine to improve SCBF, as measured by the hydrogen clearance technique, after a 53.0-gm clip compression injury to the T-1 segment of the rat spinal cord. The profound drop in mean systemic arterial blood pressure (MSAP) after cervical cord injury precluded any improvement in posttraumatic SCBF by nimodipine alone. Hence, in a randomized controlled study with five rats per group, pressor agents (whole blood, angiotensin, or adrenaline) were infused to maintain MSAP between 100 and 120 mm Hg after injury. Control animals received only a saline infusion. Nimodipine at the optimal dose found in normal animals (1.5 µg/kg/min) was added to the pressor agents. The MSAP and other physiological parameters were measured in rats receiving the pressor agents only and in those receiving pressor agents combined with nimodipine. In rats receiving whole blood, angiotensin, or adrenaline the posttraumatic MSAP improved to between 100 and 120 mm Hg, but there was no improvement in SCBF compared to the saline group. The addition of nimodipine decreased MSAP and SCBF in all groups except those animals also receiving adrenaline, where the MSAP was maintained at 109 ± 5 mm Hg. In these animals a significant increase in posttraumatic SCBF from 16.5 ± 2.1 to 20.2 ± 2.3 ml/100 gm/min (mean ± standard error of the mean) occurred at the site of injury with the addition of nimodipine. The maintenance of an adequate MSAP by a pressor agent was crucial for nimodipine to improve posttraumatic SCBF by its ability to dilate the spinal vascular bed. Adrenalin was the only pressor agent that could fulfill the above criteria, although other pressor agents need to be investigated. Experiments are underway with the combination of adrenaline and nimodipine to further verify these encouraging results demonstrating an improvement in posttraumatic ischemia of the spinal cord.

Control of blood flow in the cat spinal cord

1983 ◽  
Vol 58 (5) ◽  
pp. 742-748 ◽  
Author(s):  
Oscar U. Scremin ◽  
Emilio E. Decima
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Ventral Horn ◽  
Hydrogen Gas ◽  
Lumbar Spinal Cord ◽  
Spinal Cord Tissue ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Fine Print

✓ Spinal cord blood flow (SCBF) and the effect of end-tidal CO2 concentration (ETCO2) on SCBF (CO2 reactivity) were studied in the lumbar spinal cord of cats by means of the hydrogen-clearance technique. Hydrogen gas was administered by inhalation, and its level in spinal cord tissue was estimated amperometrically with small (75 µm) platinum electrodes. The average SCBF's at normocapnia (ETCO2 = 4%) of the ventral horn gray matter and of the white matter at several locations were 43.2 and 16.2 ml·100 gm−1·min−1, respectively. For gray and white matter, the values of CO2 reactivity, estimated by the coefficient of the regression of SCBF (ml·100 gm−1·min−1) on ETCO2 (ml·100 ml−1) were 11.6 and 2.1, respectively. No differences in SCBF or CO2 reactivity were observed between intact animals kept under N2O-O2 ventilation and decerebrated animals with no anesthesia. After an acute spinal section, ventral horn SCBF and CO2 reactivity (measured eight segments below the cordotomy) were not altered, in spite of the profound neural depression present (that is, spinal shock). Orthodromic (dorsal root) stimulation of the ventral horn neurons induced an average increase in blood flow of 128% above control values. Antidromic (ventral root) motoneuron activation failed to produce any significant changes in ventral horn blood flow.

Direction of blood flow in the primate cervical spinal cord

1970 ◽  
Vol 33 (3) ◽  
pp. 325-330 ◽  
Author(s):  
Larry C. Fried ◽  
John L. Doppman ◽  
Giovanni Di Chiro
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cervical Spinal Cord ◽  
Cervical Cord ◽  
Content Type ◽  
Vertebral Arteries ◽  
Cast Doubt ◽  
Thoracic Cord ◽  
Cervical Level ◽  
Fine Print

✓ The direction of blood flow in the cervical spinal cord of monkeys was studied by direct cinematic observation of the results of dye injections, plus separate angiographic studies. The studies indicated that in monkeys blood enters the cervical spinal cord mainly from radicular arteries that are usually derived from branches of the costo-cervical trunk. Although some blood entering at the low cervical level flows toward the thoracic cord, the major component flows up to the C-2 level. The findings cast doubt on the established assumption that the vertebral arteries provide the main blood supply of the cervical cord.

Effects of cervical spinal cord stimulation on cerebral blood flow in the rat

2000 ◽  
Vol 93 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Oren Sagher ◽  
Dah-Luen Huang
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Spinal Cord Stimulation ◽  
Cervical Spinal Cord ◽  
Cervical Cord ◽  
Peripheral Vasculature ◽  
Doppler Flowmetry ◽  
Content Type ◽  
Fine Print

Object. Spinal cord stimulation (SCS) is frequently used for the treatment of chronic pain. Although the mechanisms by which SCS alleviates pain are unclear, they are believed to involve changes within the dorsal horn of the spinal cord. Spinal cord stimulation has also been found to cause significant vasodilation in the peripheral vasculature. The mechanisms underlying this effect are thought to involve sympathetic blockade. A rostral vasodilatory effect has also been described, but changes in cerebral blood flow (CBF) have been poorly delineated. Using laser Doppler flowmetry (LDF), the authors examined the effects of cervical SCS on CBF in rats. Methods. Cervical SCS was found to result in a significant increase in cortical LDF values (83 ± 11% [mean ± standard error of the mean]). The increase in cortical LDF values was not accompanied by a significant increase in systemic blood pressure. Stimulation of the upper cervical spinal cord was more effective in inducing LDF changes than was that of the lower cervical cord. Changes in SDS-induced LDF values were significantly attenuated after spinal cord transection at the cervicomedullary junction and by the administration of the sympathetic blocker hexamethonium. Conclusions. These results indicate that cervical SCS may induce cerebral vasodilation and that this effect may involve indirect effects on vasomotor centers in the brainstem as well as an alteration in sympathetic tone.

Effect of laminectomy and anesthesia upon spinal cord blood flow

1984 ◽  
Vol 61 (3) ◽  
pp. 545-549 ◽  
Author(s):  
Patrick W. Hitchon ◽  
Jeffrey M. Lobosky ◽  
Thoru Yamada ◽  
James C. Torner
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cord Blood ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Radioactive Microsphere ◽  
Radioactive Microsphere Technique ◽  
And Control ◽  
Over Time ◽  
Fine Print

✓ Spinal cord blood flow (SCBF) in 10 sheep subjected to laminectomy at L6–7, T6–7, and C7–T1 was compared to that of 10 control sheep subjected to anesthesia alone. Blood flow was measured using the radioactive microsphere technique, with the PaCO2 maintained at 40 ± 2 mm Hg. Both laminectomy and control animals showed a decrease in SCBF at a rate of 7% to 16%/hr for the 3 hours following the first blood flow determination. When prelaminectomy and postlaminectomy SCBF values were compared to their counterparts in the control animals, there were no significant differences. Laminectomy does not appear to alter SCBF from control values. Spinal evoked potentials (SEP's) were elicited in the laminectomy group by direct cord stimulation at C-7 and L-7. No changes were noted in amplitude or latency of SEP's over time in either caudal or rostral conduction.

Experimental chronic compressive cervical myelopathy: effects of decompression

1995 ◽  
Vol 83 (2) ◽  
pp. 336-341 ◽  
Author(s):  
H. Louis Harkey ◽  
Ossama Al-Mefty ◽  
Isam Marawi ◽  
Dudley F. Peeler ◽  
Duane E. Haines ◽  
...  
Keyword(s):  
Cervical Myelopathy ◽  
Disease Process ◽  
Cord Compression ◽  
Magnetic Resonance Images ◽  
Pathological Examination ◽  
Cervical Cord ◽  
Spinal Cord Blood Flow ◽  
Flow Measurements ◽  
Content Type ◽  
Fine Print

✓ Twelve dogs developed a delayed onset of neurological abnormalities from chronic cervical cord compression that was characteristic of myelopathy. The animals were divided into two groups and matched according to degree of neurological deficit. Six animals underwent decompression through removal of the anteriorly placed compressive device. Throughout the experiment, serial neurological examinations and somatosensory evoked potential studies were performed on each animal. Spinal cord blood flow measurements were obtained during each surgical procedure and at sacrifice. Magnetic resonance images were obtained after compression and before sacrifice. All animals in the decompressed group showed significant neurological improvement after decompression; no spontaneous improvement in neurological function was seen in the compressed group. On pathological examination, irreversible changes including large motor neuron loss, necrosis, and cavitation were seen in four of the animals in the decompressed group and five in the compressed group. Cervical spondylotic myelopathy in humans is known to respond to decompression; this study provides further evidence that this animal model for chronic compressive cervical myelopathy accurately reflects the disease process seen in humans.

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.

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