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C H Tator

Publications and source records attributed to C H Tator.

At least 145 records · Page 8Linked to original sources

Motor evoked potentials recorded from normal and spinal cord-injured rats.

A need exists for an accurate neurophysiological technique that monitors the motor tracts of the cord in patients with spinal cord injury or other cord lesions and for the evaluation of experimental models of cord injury. We have recorded and characterized the motor evoked potentials (MEPs) from 10 normal rats and from 10 rats with the following cord lesions at C-8: 4 animals with complete cord transection and 6 with clip compression injury: 2 at 56.0 g, 2 at 20.0 g, and 2 at 1.5 g. MEPs were elicited by applying constant current anodal stimuli to the sensorimotor cortex with the responses recorded from microelectrodes in the spinal cord at T-10. The MEP consisted of an initial D wave (mean latency, 1.22 +/- 0.09 ms) and 4 subsequent I waves, I1 to I4. The D wave was elicited at stimulation frequencies exceeding 100 Hz, consistent with the hypothesis that it results from direct pyramidal cell excitation. The 56.0-g clip compression injuries and the cord transections abolished the MEP distal to the lesion, whereas the 20.0- and 1.5-g injuries resulted in a latency shift and amplitude decrement of the MEP peaks. These experiments suggest that the recording of MEPs will be an extremely useful and accurate method of monitoring the functional integrity of the cord, of value in patients with cord injury.

Animals↗

Successful improvement of blood pressure, cardiac output, and spinal cord blood flow after experimental spinal cord injury.

Thirty-seven rats were anesthetized and ventilated and had continuous monitoring of mean systemic arterial pressure (MSAP) and central venous pressure (CVP). The animals underwent a 60-g clip compression injury at T-1 for 1 minute. Fifteen minutes after injury, microspheres were used to measure cardiac output (CO) and spinal cord blood flow (SCBF). Each animal was then randomized into one of five groups. Four groups received intravenous infusions for 1 hour each of 5% albumin, autologous packed cells, low molecular weight dextran, or autologous whole blood to maintain the MSAP. The fifth group served as a control group and received an infusion of normal saline. Seventy-five minutes after injury, CO and SCBF were measured. The posttraumatic reduction in CO was significantly improved by all four treatment infusions. However, only autologous whole blood and dextran successfully reversed the posttraumatic hypotension. Dextran significantly elevated the CVP (P less than 0.01) and reduced the hematocrit (P less than 0.01). Whole blood improved SCBF in all segments of the spinal cord by nearly 100% (P less than 0.05), and dextran increased SCBF by 200% (P less than 0.01). Thus, the most marked improvements in MSAP, CO, and SCBF were produced by hypervolemia and hemodilution associated with dextran infusion. The therapeutic implications of this reversal of local and systemic changes in acute spinal cord injury are discussed.

Animals↗

Recovery of spinal cord function induced by direct current stimulation of the injured rat spinal cord.

Direct current stimulation has been shown by others to enhance the regeneration of several types of tissues, including nervous tissue in some species. The purpose of the present experiment was to assess the value of direct current stimulation for enhancing the recovery of spinal cord function after clip compression injury of the rat spinal cord. Twenty Wistar rats underwent a 1-minute, 50-g clip compression injury at T-1, after which electrodes were placed epidurally with the anode proximal and the cathode distal to the injury site. These electrodes were attached to a stimulator implanted subcutaneously. Ten animals received stimulators that produced a constant current of 14 microA, and the remainder received stimulators with no electrical output and served as controls. Assignment of stimulators was random, and the treatment group was not identified until sacrifice. Neurological function was tested weekly for 15 weeks by the inclined plane technique, after which the animals were killed and the injured cords were examined for histological evidence of regeneration. The mean inclined plane result for the treatment group (39 +/- 5 degrees) was significantly better than that for the control group (31 +/- 6 degrees) (P less than 0.02), although there was no significant difference in histological findings between the two groups. Thus, direct current stimulation of the injured mammalian spinal cord produced improvement in neurological function and warrants further investigation.

Animals↗

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

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 microgram/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. Adrenaline 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.

Angiotensin II↗

Significance of hemorrhage into brain tumors: clinicopathological study.

A retrospective clinical and pathological review of 905 consecutive brain tumor cases (excluding pituitary adenoma and recurrent tumor) was conducted to identify cases in which intratumoral hemorrhage was confirmed grossly and/or pathologically. There were 132 cases so identified, for an overall tumor hemorrhage rate of 14.6%; of these, 5.4% were classified as macroscopic and 9.2% as microscopic. The presence of hemorrhage was correlated with the neurological presentation. The highest hemorrhage rate (70.0%) was found in patients with prior neurological history who experienced apoplectic deterioration (acute-on-chronic presentation). Only 57.1% of patients with acute deterioration in the absence of prior neurological symptoms had hemorrhages. The highest hemorrhage rate for primary brain tumors was 29.2% for mixed oligodendroglioma/astrocytoma, while the highest hemorrhage rate for any tumor type was 50% for metastatic melanoma. The clinical relevance of tumor hemorrhage is discussed.

Brain Neoplasms↗

Neck injuries in ice hockey: a recent, unsolved problem with many contributing factors.

Previously unrecognized, major neck injuries in hockey have become a common problem in Canada and they have increased markedly in the 1980s. At the present time, the incidence remains high and has shown no sign of diminishing. The etiology of the problem appears to be multifactorial. Several epidemiologic factors have been identified and a reporting system established so that prevention programs can be monitored. It is hoped that greater awareness of the risk factors among players, coaches, leagues, referees, and parents will be an effective prophylactic measure in itself. Prevention must involve several approaches by hockey organizations and leagues, players, equipment manufacturers, and health care professionals and researchers.

Adolescent↗

Is no treatment good treatment in the management of acoustic neuromas in the elderly?

Two hundred twenty-eight patients with acoustic neuromas were seen between 1974 and 1985. Twenty-eight received no surgical treatment. Five patients who had undergone previous partial excision were excluded. The mean age was 71 years. The mean expected survival was 14.3 years. The mean follow-up interval was 51 months (range 12 to 120 months). All patients underwent at least two CAT scans (mean = 4). Tumor size ranged from 4 mm to 30 mm. Three patients underwent insertion of ventricular-peritoneal shunt for hydrocephalus (mean 16 months after presentation) and two patients partial tumor removal (mean 30 months after presentation). Tumor growth was measured in each patient using CAT scanning. Monitoring by clinical examination and regular CAT scanning is possible, but in this study 20% of patients required surgical treatment within one third of their expected survival time. This suggests that an expectant attitude for this group of patients may be a debatable form of management.

Age Factors↗

Spinal cord blood flow measured with microspheres following spinal cord injury in the rat.

A decrease in spinal cord blood flow (SCBF) is a known sequela of spinal cord injury. The radioactive microsphere technique permits repeated measurement of spinal cord blood flow (SCBF) and cardiac output (CO) in the same experimental animal. The purpose of this study was to adapt the radioactive microsphere technique for use in the rat extradural clip compression injury model used in our laboratory. Thirteen adult Wistar rats were anaesthetized and ventilated. Mean systemic arterial pressure (MSAP) was recorded continuously. Control animals (n = 8) did not have a surgical procedure whereas the injured animals (n = 5) underwent a C7-T1 laminectomy followed by a one minute, 50 gram extradural clip compression injury at T1. Radioactive microspheres were used for two blood flow and CO determinations in both groups. MSAP fell 59% in the injured animals (p less than 0.01), but this was not accompanied by significant changes in heart rate or CO. There was a 50% reduction in SCBF in the injured cord (p less than 0.02), and there were significant reductions in cerebral blood flow (p less than 0.05) and cerebellar blood flow (p less than 0.02) following spinal cord injury.

Animals↗

Failure of naloxone to improve spinal cord blood flow and cardiac output after spinal cord injury.

It has been reported that the narcotic antagonist, naloxone, can improve spinal cord blood flow (SCBF) and clinical recovery after experimental spinal cord injury produced by the weight-dropping technique. The purpose of the present study was to determine the effect of naloxone on SCBF, cardiac output (CO) and blood flow to other organs following clip compression injury. Rats were anesthetized, paralyzed and ventilated, with mean systemic arterial pressure (MSAP) recorded continuously. After a C-7-T-1 laminectomy and a 1-minute acute compression injury with a 50-g clip at T-1, rats were given injections of radioactive microspheres for measurement of SCBF, CO, and blood flow to other organs. The first determination was made 15 minutes after injury and a second was made after a 1-hour treatment with naloxone. Treated animals each received an intravenous bolus injection of naloxone (10 mg/kg) followed by a 1-hour intravenous infusion (2 mg/kg/hour). Naloxone failed to improve posttraumatic SCBF in the injured spinal cord. In addition, naloxone did not prevent posttraumatic hypotension or the progressive decline in CO seen between 15 and 75 minutes after injury. Thus, this study does not support the previous claims of a beneficial effect of naloxone on posttraumatic SCBF and MSAP.

Animals↗

Relationship between posttraumatic ischemia and hemorrhage in the injured rat spinal cord as shown by colloidal carbon angiography.

Adult female Wistar rats underwent extradural clip compression injury of the spinal cord at T-1. A force of 40 g was applied for 1 minute; this moderately severe injury renders animals paraparetic. We performed colloidal carbon angiography with Aquablak on four animals at 15 minutes, 2 hours, and 24 hours after injury. The entire spinal cord was then removed, frozen, and sectioned serially at 250 micron. The sections were examined microscopically for patterns of ischemia and hemorrhage at the site of compression injury and at adjacent and remote sites in the spinal cord. There was a marked lack of filling of the arterioles, capillaries, and venules at the injury site. In addition, there was a specific anatomical distribution of the ischemic areas in that ischemia of the white matter occurred in areas supplied by arteries that traversed adjacent hemorrhagic gray matter. For example, ischemia of the ventral funiculus was consistently seen adjacent to hemorrhage in the ventral gray matter. Similarly, ischemia of the dorsal white columns was related to hemorrhagic lesions surrounding the feeding vessels in the dorsal gray matter. This study also demonstrates the usefulness of a new colloidal carbon suspension (Aquablak) for documenting the pathophysiology of posttraumatic ischemia of the spinal cord. The results suggest that ischemic lesions in the white matter are anatomically related to hemorrhagic lesions in the gray matter. The pathophysiology of this relationship is unknown, but may include thrombosis, vasospasm, or direct injury of the feeding vessels.

Angiography↗

Failure of blood transfusion or naloxone to improve clinical recovery after experimental spinal cord injury.

Thirty adult Wistar rats underwent an extradural clip compression injury of 50 g of force for 1 minute at T-1. After injury, the animals were randomly separated into three groups: the control group received a saline infusion for the 2-hour treatment period; the second group was given a blood transfusion over 2 hours titrated to maintain mean systemic arterial pressure (MSAP) at preinjury levels; and the third group received an intravenous bolus dose of naloxone (10 mg/kg), followed by a 2-hour infusion of intravenous naloxone (2 mg/kg/minute). The rats were observed postoperatively for 15 weeks, during which their clinical recovery was measured weekly by the inclined plane technique. At 15 weeks, the spinal cords were removed and prepared for histological assessment. The blood pressure before, during, and immediately after injury did not differ statistically among the three groups. During the initial 2 hours after injury, blood transfusion produced a significant increase in MSAP (P less than 0.02) and hematocrit (P less than 0.001), but naloxone infusion did not result in a significant change in MSAP. Performance on the inclined plane at 15 weeks was 35.6 +/- 6 degrees, 32.7 +/- 4 degrees, and 36.1 +/- 6 degrees for the control, transfusion, and naloxone groups, respectively, and no significant differences were found (P greater than 0.05). Histological examination confirmed a consistent injury of moderate severity in all three groups with no major differences among groups. Thus, this study demonstrates no significant clinical benefit either from a blood transfusion to maintain MSAP or from naloxone given by bolus and infusion after an extradural clip compression injury of the rat spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Epidermoid tumor: an unusual cause of ossification within the spinal canal.

Epidermoid tumors of the spinal canal are rare. We report two patients with intraspinal lesions and radiographically evident calcification. One proved to have an epidermoid tumor. Although the tissue diagnosis in the second was not definitive, it suggested an epidermoid tumor as well. Radiographically visible ossification or calcification has not been reported before in intraspinal epidermoids.

Calcinosis↗

Ocular complications following excision of cerebellopontine angle tumours.

The incidence of ocular complications in 91 patients who underwent excision of cerebellopontine angle tumours was reviewed. Facial nerve paralysis occurred postoperatively in 40 of 88 patients (45.5%). Sixty-four percent of these patients recovered; thus the final count was 86% of patients with facial nerve function following tumour removal. Patients who sustained a delayed facial paralysis recovered well. In patients who sustained an immediate paralysis when the nerve was left anatomically intact postoperatively, recovery was again excellent if paralysis was incomplete, and varied if the paralysis was complete. Not surprisingly, postoperative facial paralysis was more common in patients who had had large tumours. Corneal hypoesthesia and a poor Bell's phenomenon were the most important factors in predicting corneal complications as a result of facial nerve paralysis. Eye complications in 45% of the patients who suffered facial nerve paralysis were managed conservatively with ocular lubricants and an eye shield only; the others received some form of eyelid surgery.

Cerebellar Neoplasms↗

Acoustic neuromas: management of 204 cases.

This paper reviews the author's personal experience with the management of 204 patients with the clinical diagnosis of acoustic neuroma. Craniotomy was performed in 181 of these cases, all of whom were proven to have acoustic neuromas. The remaining 23 cases with the clinical diagnosis of acoustic neuroma did not have tumour surgery, mainly because of advanced age or concurrent disease, although some required shunts for hydrocephalus. The management of acoustic neuromas including the selection of surgical approach depends upon the patient's age and general health, the size and growth direction of the tumour, previous surgical attempts at removal, and the presence of hydrocephalus, a contralateral tumour, and serviceable hearing. Twenty-nine other cases with the clinical diagnosis of acoustic neuroma underwent craniotomy: 20 had petrous or tentorial meningiomas encroaching on the porus acousticus or growing in the internal auditory canal, six had neuromas of the seventh cranial nerve and three had arachnoiditis occluding the internal auditory canal.

Cranial Nerve Neoplasms↗

Preservation of hearing in patients undergoing excision of acoustic neuromas and other cerebellopontine angle tumors.

Microsurgical techniques have made it possible to identify and preserve the cochlear nerve from its origin at the brain stem and along its course through the internal auditory canal in patients undergoing removal of small or medium-sized acoustic neuromas or other cerebellopontine angle (CPA) tumors. In a consecutive series of 100 patients with such tumors operated on between 1975 and 1981, an attempt was made to preserve the cochlear nerve in 23. The decision to attempt to preserve hearing was based on tumor size and the degree of associated hearing loss. In cases of unilateral acoustic neuroma, the criteria for attempted preservation of hearing were tumor size (2.5 cm or less), speech reception threshold (50 dB or less), and speech discrimination score (60% or greater). In patients with bilateral acoustic neuromas or tumors of other types, the size and hearing criteria were significantly broadened. All patients were operated on through a suboccipital approach. Hearing was preserved postoperatively in six (31.6%) of the 19 patients with unilateral acoustic neuromas, although the cochlear nerve was preserved in 16. Of the six patients with postoperative hearing, three retained excellent hearing, and the other three had only sound awareness and poor discrimination. Hearing was preserved in three cases with other CPA tumors, including an epidermoid cyst and small petrous meningiomas in the internal auditory canal. Of the two cases with bilateral tumors, hearing was preserved in one. Of the 23 patients in whom hearing preservation was attempted, nine (39.1%) had some postoperative hearing, which in six was equal to or better than the preoperative level. Thus, it is worthwhile to attempt hearing preservation in selected patients with CPA tumors.

Brain Neoplasms↗

Increase in rat spinal cord blood flow with the calcium channel blocker, nimodipine.

Nimodipine, a calcium channel blocker, is known to increase cerebral blood flow. In the present study, the authors investigated the effect of nimodipine on spinal cord blood flow in normal rats. Cardiovascular parameters, including mean systemic arterial blood pressure, cardiac output, and heart rate, were recorded during infusion of nimodipine in a dose-response fashion. The experiment was a randomized blind study in which four groups of five rats received different doses of nimodipine (0.001, 0.01, 0.05, and 0.10 mg/kg) intravenously over 30 minutes, and a control group of five rats received only the diluent. The hydrogen clearance and thermodilution techniques were used to measure spinal cord blood flow and cardiac output, respectively. The 0.05-mg/kg dose of nimodipine caused the largest increase in spinal cord blood flow, with a 40% increase over the preinfusion level, although there was a 25% reduction in mean arterial pressure. The 0.10-mg/kg dose did not increase spinal cord blood flow more than the 0.05-mg/kg dose, most likely due to the concomitant 37% reduction in mean arterial pressure. Cardiac output was significantly increased by the 0.05- and 0.10-mg/kg doses secondary to the drop in total peripheral resistance. The increase in spinal cord blood flow produced by nimodipine lasted approximately 20 minutes after the termination of the infusion. Thus, nimodipine at a dose of 0.05 mg/kg markedly increased blood flow in the normal spinal cord even though there were major changes in mean systemic arterial pressure and cardiac output. Further research is required to determine whether this drug might be beneficial in treating ischemic states of the spinal cord, such as posttraumatic ischemia.

Analysis of Variance↗

Spinal cord injury in the work force.

Of 144 patients with spinal cord injury admitted to the Sunnybrook Medical Centre from 1974 to 1979, 25 (24 men) (17.4%) had sustained their injuries at work. The 25 patients ranged in age from 20 to 56 years, with more than half being in their third decade of life. Work-related spinal cord injury was more frequent in the thoracic region than spinal injuries from other causes. The injuries were generally severe, 24% of them being complete cord injuries (i.e., no sensory or motor function below the level of injury). The mean neurologic grade of these patients did not change substantially between the time of admission and discharge. The mortality was 8%. The pattern of spinal cord injury in this series was compared to that in the period 1948 to 1973, when 105 (29.3%) of 358 spinal cord injuries occurred at work, constituting the second most frequent cause of acute spinal cord injury, after traffic accidents. In the current series, only 17.4% sustained their injuries at work. This was the third most common cause of spinal injuries in this period after traffic accidents and sports-recreational injuries. Falls in industry were the most frequent mode of work injury from 1974 to 1979, compared with construction accidents in the earlier period. The number of work-related spinal cord injuries is still too high. Furthermore, the severe neurologic damage suffered and the lack of substantial improvement emphasize the importance of preventive efforts, especially in industry. The fact that work injuries now rank third as a relative cause of spinal injury may indicate an absolute decline in this type of injury, especially among construction workers.

Accidents, Occupational↗