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Biomedical subjects

C H Tator

Publications and source records attributed to C H Tator.

At least 109 records · Page 6Linked to original sources
PubMed1991

Further studies of nimodipine in experimental spinal cord injury in the rat.

Previously in our laboratory, nimodipine was effective in reversing posttraumatic ischemia and promoting electrophysiologic recovery in a rat spinal cord injury (SCI) model. However, these beneficial effects were achieved when nimodipine was combined with adjuvant therapy to reverse posttraumatic hypotension, by either volume expansion or vasopressor therapy. The present experiments determined if nimodipine alone can increase spinal cord blood flow (SCBF) and improve function after SCI. The hydrogen clearance technique was used to measure SCBF, and motor and somatosensory evoked potentials (MEP and SSEP) were used to quantitate electrophysiologic function. SCBF, MEP, and SSEP were recorded before and after a 52 g clip compression injury at the T1 segment and then repeated after a 35 minute infusion of nimodipine. Twenty-five rats were allocated randomly to five equal groups, each of which received 35 minute infusions of one of the following doses of nimodipine: (1) 0 mg/kg, (2) 0.005 mg/kg, (3) 0.01 mg/kg, (4) 0.025 mg/kg, or (5) 0.05 mg/kg. SCBF decreased after injury in all groups, and there was no increase in SCBF after nimodipine infusion in any group. MEP and SSEP were abolished by the injury in all rats, and there was no recovery of the evoked potentials in any group. It is concluded that adjuvant therapy for posttraumatic hypotension may be necessary for nimodipine to improve SCBF and promote recovery of function in the injured spinal cord.

Animals↗
PubMed1991

Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms.

In patients with spinal cord injury, the primary or mechanical trauma seldom causes total transection, even though the functional loss may be complete. In addition, biochemical and pathological changes in the cord may worsen after injury. To explain these phenomena, the concept of the secondary injury has evolved for which numerous pathophysiological mechanisms have been postulated. This paper reviews the concept of secondary injury with special emphasis on vascular mechanisms. Evidence is presented to support the theory of secondary injury and the hypothesis that a key mechanism is posttraumatic ischemia with resultant infarction of the spinal cord. Evidence for the role of vascular mechanisms has been obtained from a variety of models of acute spinal cord injury in several species. Many different angiographic methods have been used for assessing microcirculation of the cord and for measuring spinal cord blood flow after trauma. With these techniques, the major systemic and local vascular effects of acute spinal cord injury have been identified and implicated in the etiology of secondary injury. The systemic effects of acute spinal cord injury include hypotension and reduced cardiac output. The local effects include loss of autoregulation in the injured segment of the spinal cord and a marked reduction of the microcirculation in both gray and white matter, especially in hemorrhagic regions and in adjacent zones. The microcirculatory loss extends for a considerable distance proximal and distal to the site of injury. Many studies have shown a dose-dependent reduction of spinal cord blood flow varying with the severity of injury, and a reduction of spinal cord blood flow which worsens with time after injury. The functional deficits due to acute spinal cord injury have been measured electrophysiologically with techniques such as motor and somatosensory evoked potentials and have been found proportional to the degree of posttraumatic ischemia. The histological effects include early hemorrhagic necrosis leading to major infarction at the injury site. These posttraumatic vascular effects can be treated. Systemic normotension can be restored with volume expansion or vasopressors, and spinal cord blood flow can be improved with dopamine, steroids, nimodipine, or volume expansion. The combination of nimodipine and volume expansion improves posttraumatic spinal cord blood flow and spinal cord function measured by evoked potentials. These results provide strong evidence that posttraumatic ischemia is an important secondary mechanism of injury, and that it can be counteracted.

Animals↗
PubMed1991

Review of experimental spinal cord injury with emphasis on the local and systemic circulatory effects.

Studies of experimental spinal cord injury began approximately 100 years ago, and since then many useful models of acute experimental spinal cord injury have been developed which stimulate many of the common types injuries in man. This review will describe some of these models and the information they have provided about the acute pathophysiological mechanisms in the injured spinal cord. There is good experimental evidence that the spinal cord suffers both a primary or mechanical injury and then a secondary injury which may worsen the prognosis for recovery. This review will emphasize the concept of the secondary injury, especially with respect to the vascular mechanisms. There is evidence from our laboratory and others to support the concept of the secondary injury and that the chief mechanism of the secondary injury is posttraumatic ischemia and infarction of the spinal cord. We have found evidence for the role of vascular mechanisms in three different injury models of acute spinal cord injury (A.S.C.I.) in three species of experimental animals. This review will describe the microangiographic and blood flow methods for assessing the microcirculation of the spinal cord after trauma. In addition, to these local vascular effects, this review will also describe the systemic vascular effects of A.S.C.I. which cause the neurogenic shock in this condition. It is our hypothesis that these local and systemic vascular effects are principal causes of the secondary injury leading to posttraumatic ischemia and infarction of the spinal cord after A.S.C.I. Furthermore, it is our hypothesis that early treatment of these microcirculatory changes and neurogenic shock can lead to improved recovery after A.S.C.I.

Animals↗
PubMed1991

The electrophysiological assessment of the pyramidal and non-pyramidal tracts of the spinal cord of rats.

The present paper summarizes our experience with the use of motor evoked potentials (MEP) and cerebellar evoked potentials (CEP) to assess the physiological integrity of the motor tracts of the spinal cord in a rat model. The MEP elicited by intracortical microstimulation of motor cortex reflected activity only in the pyramidal tracts; in contrast the MEP obtained by extradural cortical stimulation with a macroelectrode also reflected activity in a number of non-pyramidal pathways including the lateral vestibulospinal and rubrospinal tracts. The CEP was principally conducted in ventral spinal cord tracts and may reflect direct activation of brainstem nuclei. Data are presented which correlate the relationship between the MEP and axonal integrity after cord injury.

Animals↗
PubMed1991

Spinal cord distraction: an in vitro study of length, tension, and tissue pressure.

Since the Scoliosis Research Society released a report on cord injury related to Harrington rod instrumentation for scoliosis, little has been published on the pathophysiology of this disorder. Dolan et al. (4) described diminished cord blood flow associated with spinal distraction in a cat model, but failed to demonstrate its cause. In this article, we describe a series of in vitro experiments performed on dog and sheep cadaver spinal cords. Controlled distractive forces were applied to spinal cords while monitoring both cord interstitial pressure and cord elongation. A close (Ravg = 0.986) correlation was noted between applied tensile forces and cord interstitial pressure. At 1,000-g loads, the average tissue pressure obtained was 29.5 cm H2O, ranging from 17 to 47 cm H2O. However, it was noted that the cord demonstrated nonlinear tensile elastic properties that appeared exponential in the range examined. These properties are consistent with those described for collagen-containing compounds. We conclude that spinal cord distraction is capable of generating cord tissue pressures that could cause a spinal cord compartment syndrome and thereby seriously impair spinal cord blood flow causing spinal cord injury.

Animals↗
PubMed1991

Spinal injuries in ice hockey players, 1966-1987.

A registry, established by the Committee on Prevention of Spinal Cord Injuries Due to Hockey, of major injuries to the spine or spinal cord sustained while playing ice hockey contains 117 cases entered between January 1966 and March 1987; 112 of these injuries were sustained in Canada. Between 1981 and 1986 up to 15 hockey related major spinal injuries were reported in Canada each year. Most injuries occurred in teenagers and players under 30 years of age who were playing in supervised games. The most common cause of injury was a push or check from behind, which caused the player to be catapulted head first into the boards. The authors describe the programs currently being implemented to prevent the occurrence of major spinal injuries. Unfortunately, these programs have not decreased the number of injuries reported annually.

Adolescent↗
PubMed1990

Trans oral approach to the nasopharynx and clivus using the Le Fort I osteotomy with midpalatal split.

The Le Fort I level osteotomy is a procedure well known to oral and maxillofacial surgeons, who routinely use it to correct midfacial skeletal deformities and alter the dental occlusion. This osteotomy can also be used as a maxillotomy for access to more superiorly and posteriorly situated structures. The downfracture technique provides the surgeon with a safe approach that allows visualization of the maxillary sinuses, nasal cavity, nasopharynx, base of the skull and upper cervical spine. This approach can also be combined with a midline lip split, mandibulotomy and glossotomy to give access to retropharyngeal structures. By modifying the combined Le Fort I and transmandibular approach utilizing a midline split of the hard and soft palate, the access to the clivus can be improved considerably. The clinical applications of these combined procedures in the treatment of basilar invagination and tumors of the nasopharynx are discussed.

Adolescent↗
PubMed1990

Comparisons of the clinical and radiological features and surgical management of posterior fossa meningiomas and acoustic neuromas.

Next to acoustic neuromas, meningiomas are the most common benign tumour of the posterior fossa. This paper reviews the personal experience of one of the authors with the management of 26 posterior fossa meningiomas and 212 acoustic neuromas. The aim was to compare the clinical and radiological features of these two types of posterior fossa tumours to determine whether they can be differentiated preoperatively. The study also aimed at analysing the surgical treatment of posterior fossa meningiomas. The results showed that posterior fossa meningiomas can usually be differentiated from acoustic neuromas on the basis of clinical and radiological features. Preoperative differentiation aids surgical management, especially for selection of surgical approach. In most instances, posterior fossa meningiomas can be totally resected with minimal morbidity and mortality.

Adult↗
PubMed1990

Cervical myelopathy in diffuse idiopathic skeletal hyperostosis. Case report.

The case of a rapidly progressive cervical myelopathy in a 64-year-old man is presented. Radiological studies revealed a partial extradural block, which at surgery was found to be a focal fibrous, calcified mass associated with the ligamentum flavum. On the basis of the underlying disorder of diffuse idiopathic skeletal hyperostosis (DISH), the etiology of this compression was concluded to be focal fibrous proliferation and dystrophic calcification. The neurological complications of DISH are reviewed. The authors are not aware of any other reports of this cause of myelopathy associated with DISH.

Calcinosis↗
PubMed1989

Improvement in post-traumatic spinal cord blood flow with a combination of a calcium channel blocker and a vasopressor.

We have recently shown that nimodipine, a calcium channel blocker, can increase spinal cord blood flow (SCBF) in normal rats and can improve SCBF after spinal cord trauma if the mean systemic arterial pressure (mSAP) is restored to normal levels by the vasopressor, adrenalin. The present study is a further analysis of the improvement in post-traumatic SCBF (measured with the hydrogen clearance technique) with the combination of adrenalin and nimodipine. In addition, image analysis was used to study the potential risk of this combination for exacerbating intramedullary hemorrhage in the injured spinal cord. SCBF, mSAP, and other physiologic parameters were measured preinjury, postinjury, and post-treatment. A 53.0-gram clip compression injury at the T1 spinal segment was delivered for 1 minute to three treatment groups (saline, adrenalin, and adrenalin plus nimodipine) comprised of five rats each. Injury caused a marked decline in SCBF and mSAP. Treatment with adrenalin alone or combined with nimodipine (1.5 micrograms/kg/min IV) improved mSAP to 100-125 mm Hg. However, adrenalin alone failed to improve SCBF, whereas nimodipine plus adrenalin produced a marked improvement of approximately 60% in post-traumatic SCBF. Morphometric analysis showed no significant difference between per cent area or volume of hemorrhage between the three treatment groups, although there was a trend for increased hemorrhage in the adrenalin-alone group perhaps due to the higher post-traumatic mSAP in this group. Further studies are required to find the minimal elevation in mSAP produced by a vasopressor that would still cause an improvement in post-traumatic SCBF by nimodipine, and to determine whether this combination improves function after spinal cord injury.

Animals↗
PubMed1989

Spinal cord blood flow and systemic blood pressure after experimental spinal cord injury in rats.

We looked at the relation between systemic arterial blood pressure and recovery from spinal cord injury by inducing both hypertension and hypotension in 25 rats randomly allocated to five equal groups. The rats received no injury, a mild (2.3-g), or a severe (53.0-g) spinal cord injury lasting 1 minute. We used the hydrogen clearance technique to measure spinal cord blood flow at the injury site (T1) and at an adjacent site (C6). Mean systemic arterial blood pressure was either increased with adrenaline or decreased by phlebotomy in 20-mm-Hg intervals except for the severe-injury group, in which the posttraumatic pressure could only be increased with adrenaline. Spinal cord blood flow remained constant in the no-injury group between 81 and 180 mm Hg. After a mild injury, induced moderate hypertension (121-140 mm Hg) improved spinal cord blood flow significantly, whereas hypotension decreased it in a linear fashion. Severe injury caused a marked decrease in spinal cord blood flow and mean systemic arterial blood pressure. Even extreme hypertension (161-180 mm Hg) induced by adrenaline did not significantly increase spinal cord blood flow at T1 but caused hyperemia at C6 due to loss of autoregulation. In conclusion, normotension should be attempted, irrespective of the severity of spinal cord injury. Induced hypertension after severe spinal cord injury was not beneficial in improving spinal cord blood flow at the injury site while potentially increasing hemorrhage and edema.

Animals↗
PubMed1989

Effect of blood transfusion, dopamine, or normal saline on neurogenic shock secondary to acutely raised intracranial pressure.

An experimental model to simulate acutely raised intracranial pressure due to a rapidly expanding intracranial space-occupying lesion was used to produce neurogenic shock. Forty-one rats in neurogenic shock (defined as a mean systemic arterial pressure (SAP) of less than 60 mm Hg) were subjected to various treatments to increase the mean SAP to a level of more than 80 mm Hg. The control group with neurogenic shock received no treatment, and the six treatment groups received infusions of: whole blood, packed cells, plasma, normal saline, dopamine, or a combination of dopamine and saline. Detrimental effects were observed after transfusion of packed cells or whole blood, which caused further deterioration of mean SAP. Although dopamine or the combination of dopamine and saline were both effective (p = 0.0001) for reversing hypotension, the combination was the most effective. If this rat paradigm correlates with human disease, these results indicate that, in the absence of hypovolemia, neurogenic shock due to acute intracranial hypertension should be treated with a combined transfusion of dopamine and normal saline, but not blood since the latter could have a detrimental effect.

Animals↗
PubMed1989

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

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 greater than 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 less than 0.0001) as well as significant changes in the MEP recorded from the spinal cord (MEP-C) (p less than 0.0001), the MEP recorded from the sciatic nerve (MEP-N) (p less than 0.0001), and the SSEP (p less than 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 less than 0.003) and improved the MEP-C (p less than 0.0001), MEP-N (p less than 0.04), and SSEP (p less than 0.002) following SCI. With this combination, the changes in SCBF were significantly related to improvement in axonal function in the motor tracts (p less than 0.0001) and somatosensory tracts (p less than 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.

Animals↗
PubMed1989

Subependymoma of the thoracolumbar cord. Case report.

Subependymomas are benign, usually asymptomatic, intraventricular tumors, the origin of which remains controversial. Spinal cord subependymomas are rare: a literature review yields 10 previous cases which are critically appraised in this report. A case of thoracolumbar intramedullary subependymoma is reported, and the histology, ultrastructure, and pre- and postoperative management are reviewed. Awareness that subependymomas may occur as a separate entity in the spinal cord should lead to increased frequency of diagnosis and a better understanding of the biological behavior of these tumors.

Adult↗
PubMed1989

Effect of a direct current field on axons after experimental spinal cord injury.

There is evidence that direct current (DC) stimulation promotes neurologic recovery in spinal cord injury. The authors conducted a morphometric analysis of axons at the site of spinal cord injury in adult rats treated with a DC field. Ten rats received a 17-g and 15 rats a 53-g clip compression injury and were treated with either a sham (control) or a functioning DC stimulator for 8 weeks. Five normal rats were also assessed. There was a significant relation (p less than 0.0001) between the severity of injury and the number of axons at the injury site. After the 17-g injury, there was no significant difference in the number of axons between control and treated rats. However, after the 53-g injury, there were significantly (p less than 0.05) more axons in treated than control rats. Both degrees of injury caused preferential destruction of large-calibre axons. Subsequent analysis showed that the axon diameter of treated rats with 17-g or 53-g injury was significantly greater (p less than 0.05) than that of control rats with 17-g or 53-g injury. These data, for the first time, show that the application of a DC field increases the number and calibre of axons at the site of a spinal cord injury and enhances the survival or regrowth of axons following spinal cord injury in the rat.

Animals↗