PubMed Health⌕ Search

Biomedical subjects

C H Tator

Publications and source records attributed to C H Tator.

At least 91 records · Page 5Linked to original sources
PubMed1993

Complications and costs of management of acute spinal cord injury.

This study examined the complications and costs of management of patients with acute spinal cord injury (ASCI) in a regional, multidisciplinary acute spinal cord injury unit (ASCIU). Data were available to compute length of stay (LOS) on 191 of the first 220 consecutive patients managed in this unit from 1974 to 1981. Specific formulae for assessing hospital and medical costs were developed based on a systems analysis approach. The statistical analysis included multiple regression analysis for determining the effect of the principal admission characteristics of ASCI patients, the main types of complications, and the methods of management. The effects of these variables on LOS, costs per day (CPD), and costs per stay (CPS) were determined. Age at admission, sex, and cause of accident had no effect on costs. As expected, increasing severity of injury to the spinal cord and to the vertebral column caused a significant increase in the mean LOS and CPS, and increasing total trauma load resulted in a significant increase in LOS and CPS. The LOS was shorter for patients admitted sooner after trauma. Respiratory, gastrointestinal, thromboembolic and genitourinary complications and decubitus ulceration were all associated with marked increases in LOS and CPS. The annual mean CPS decreased dramatically during the period of the study from 1974-81 due mainly to a decrease in LOS. Multiple regression analysis showed that severity and level of the spinal column and spinal cord injury, and the presence of complications had the most significant effects on duration and cost of care. The study also suggests that a specialized, multidisciplinary regional unit for ASCI patients is associated with a reduction in LOS and cost of care.

Accidents↗
PubMed1993

Sensory evoked potentials for selective monitoring of the rat spinal cord: a cerebellar evoked potential to assess ventral cord integrity.

The purpose of this study was to evaluate two types of ascending sensory evoked potentials (SEPs) in the rat and their capacity for selective monitoring of dorsal versus ventral spinal cord integrity. SEPs were elicited by direct sciatic nerve stimulation. A cerebellar evoked response was recorded over the paramedian lobule of the cerebellar hemisphere (CEPpml) while somatosensory evoked potentials (SSEPs) were simultaneously recorded over the sensorimotor cortex. All components of the CEPpml and SSEP except the longest latency positive waves were present in each animal. At stimulus intensities of 3 to 10 mA, no significant changes in latency of the peaks were observed, but amplitudes of the longer latency responses tended to increase throughout this stimulation range. Unilateral sciatic stimulation resulted in bilateral cortical responses, larger ipsilaterally for the CEPpml, and contralaterally for the SSEP. Selective spinal cord lesions demonstrated N9 and P14 of the CEPpml to be mediated primarily through the ventral spinal cord, while P14 and N19 of the SSEP were conducted primarily through the dorsal columns. Sectioning of the cerebellar peduncles abolished N9 and P14 of the CEPpml despite persistence of the SSEP. This study demonstrates that selective assessment of the ventral and dorsal spinal cord is possible in the rat by monitoring SEPs.

Animals↗
PubMed1993

Silicone rubber microangiography of acute spinal cord injury in the rat.

The purpose of this study was to investigate the acute changes in the large vessels and microvasculature of the spinal cord after acute clip compression injury in the rat. Nineteen female Wistar rats underwent acute compression of the spinal cord at C8-T1 at 53 g for 1 min. Silicone rubber was injected into the ascending aorta at 15 minutes, 1, 4, or 24 hours after injury. An additional nine rats served as normal controls. The perfused spinal cords were cleared by the alcohol-methylsalicylate technique. The results showed that, in the normal rat, the centrifugal arterial system from the sulcal arteries provided the major blood supply to the gray matter and the lateral and ventral white matter extending all the way to the pial surface. In the normal rat, there were large veins in the posterior columns coursing longitudinally in the parasagittal plane at the base of the posterior columns. The injured spinal cords displayed marked ischemia and hemorrhage at the injury site. The hemorrhage predominated in the gray matter and posterior white columns and extended rostrally and caudally for 2 to 7 mm in each direction from the injury site. Remote hemorrhages originated from damage to the large parasagittal veins in the posterior columns. Extravasations of silicone rubber were frequently seen at the earlier posttraumatic times and often originated from the sulcal arteries or their branches at the injury site. Occluded sulcal arteries were identified at the injury site at 4 and 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1993

Spinal cord blood flow and evoked potential responses after treatment with nimodipine or methylprednisolone in spinal cord-injured rats.

This study examined the effect of nimodipine or methylprednisolone on spinal cord blood flow (SCBF) and electrophysiological function after spinal cord injury in rats. Three groups of male rats (n = 10 per group) were injured by compression of the cord at T1 for 1 minute with a 52-g clip. The hydrogen clearance technique was used to measure SCBF at the T1 segment. Motor and somatosensory evoked potentials were recorded. SCBF and evoked potentials were measured before injury and again at approximately 1 and 2.5 hours after injury. The methylprednisolone group received a bolus of methylprednisolone (30 mg/kg) at 5 minutes after injury and then at 15 minutes after injury, the group received an infusion of methylprednisolone at 5.4 mg/kg per hour. The nimodipine group received placebo at 5 minutes and then received an infusion of nimodipine at 0.02 mg/kg per hour at 15 minutes. The placebo group received placebo at both times. Physiological parameters were closely monitored and maintained within the normal range. Albumin was administered after injury to maintain mean arterial blood pressure at or above 80 mm Hg. The infusions were continued for approximately 3 hours after spinal cord injury. SCBF was not significantly different between the experimental groups at either 1 or 2.5 hours postinjury (P = 0.16 and 0.71, respectively), and evoked potential responses did not return in any rat at any time after injury. Thus, this experiment failed to demonstrate an improvement in SCBF or electrophysiological function with either drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Dose-response study of the pathological effects of chronically applied direct current stimulation on the normal rat spinal cord.

Electrical stimulation of the mammalian central nervous system (CNS) can result in extensive destruction of tissue unless applied within specific stimulation parameters. Classically, unbalanced or monopolar currents have been avoided in order to minimize these harmful effects. However, direct current (DC) fields have recently been proposed for the treatment of spinal cord injury. Until now, no rigorous analysis has been made of the safety of these fields in the mammalian CNS. The purpose of this study was to determine the amount of chronically applied DC current that can be tolerated by the normal rodent spinal cord stimulated with metal disc electrodes. Thirty-five normal rats underwent implantation of DC stimulating devices and were allowed to recover for a period of 2 to 12 weeks. The stimulators delivered constant currents of 0 to 50 microA through two disc-shaped platinum/iridium electrodes positioned extradurally at the C-7 and T-3 levels. Following sacrifice of the animals, serial 8-microns cross sections of the spinal cord at the electrode sites were examined microscopically. Evidence of demyelination presumed due to the physical presence of the rostral electrode was seen in animals from most groups including control animals. Pathological changes directly attributable to the applied fields were seen with current as low as 3 microA. It was concluded that DC's of 3 microA or more are harmful to the mammalian CNS with this method of stimulation. In addition, the data suggest that the maximum current density tolerated by the rodent spinal cord is in the order of 75 microA/sq cm. These findings have important implications for the use of chronic DC stimulation in the mammalian CNS.

Animals↗
PubMed1993

Source specificity of early calcium neurotoxicity in cultured embryonic spinal neurons.

To examine the role of Ca2+ in early neuronal death, we studied the impact of free intracellular calcium concentration ([Ca2+]i) on survivability in populations of cultured mouse spinal neurons. We asked whether early neurotoxicity was triggered by Ca2+ influx, whether elevated [Ca2+]i was a predictive indicator of impending neuronal death, and whether factors other than [Ca2+]i increases influenced Ca2+ neurotoxicity. We found that when neurons were lethally challenged with excitatory amino acids or high K+, they experienced a biphasic [Ca2+]i increase characterized by a primary [Ca2+]i transient that decayed within minutes, followed by a secondary, sustained, and irreversible [Ca2+]i rise that indicated imminent cell death. We showed that in the case of glutamate-triggered neurotoxicity, processes triggering eventual cell death required Ca2+ influx, and that neurotoxicity was a function of the transmembrane Ca2+ gradient. Fura-2 Ca2+ imaging revealed a "ceiling" on measurable changes in [Ca2+]i that contributed to the difficulty in relating [Ca2+]i to neurotoxicity. We found, by evoking Ca2+ influx into neurons through different pathways, that the chief determinants of Ca2+ neurotoxicity were the Ca2+ source and the duration of the Ca2+ challenge. When Ca2+ source and challenge duration were taken into account, a statistically significant relationship between measured [Ca2+]i and cell death was uncovered, although the likelihood of neuronal death depended much more on Ca2+ source than on the magnitude of the measured [Ca2+]i increase. Thus, neurotoxicity evoked by glutamate far exceeded that evoked by membrane depolarization with high K+ when [Ca2+]i was made to increase equally in both groups. The neurotoxicity of glutamate was triggered primarily by Ca2+ influx through NMDA receptor channels, and exceeded that triggered by non-NMDA receptors and Ca2+ channels when [Ca2+]i was made to rise equally through these separate pathways. The greater neurotoxicity triggered by NMDA receptors was related to some attribute other than an ability to trigger greater [Ca2+]i increases as compared with other Ca2+ sources. We hypothesize that this represents a physical colocalization of NMDA receptors with Ca(2+)-dependent rate-limiting processes that trigger early neuronal degeneration.

Animals↗
PubMed1993

Three-dimensional analysis of the vascular system in the rat spinal cord with scanning electron microscopy of vascular corrosion casts. Part 1: Normal spinal cord.

Vascular corrosion casts of polyester resin in the normal spinal cord at C4-C6 and C7-T1 were inspected three-dimensionally by scanning electron microscopy in 13 rats. Arteries and veins were easily differentiated by the impression pattern of endothelial nuclei on the casts. The centrifugal arterial system from the sulcal arteries supplied most of the gray and white matter in the ventral and lateral spinal cord. Each sulcal artery supplied only one side of the cord. The average number of sulcal arteries was 2.6 per mm. The centripetal arterial system from the posterior spinal arteries fed the posterior gray and white matter. In contrast with classical concepts, there was no pial arterial plexus on the ventral and ventrolateral surface except for infrequent transverse branches from the anterior spinal artery. In the posterior columns, two types of large veins were identified: the posterior medial septal veins and the posterior oblique veins that drained the posterior columns, medial posterior gray matter, and posterior gray commissure. The remainder of the gray and white matter was drained by the sulcal veins and the radial veins. This method clearly demonstrates the three-dimensional structure of both the arterial and venous system in the rat spinal cord.

Animals↗
PubMed1993

Three-dimensional analysis of the vascular system in the rat spinal cord with scanning electron microscopy of vascular corrosion casts. Part 2: Acute spinal cord injury.

The purpose of this study was to investigate the vascular mechanisms involved in the pathophysiology of acute spinal cord injury. Vascular corrosion casts of traumatized rat spinal cords at C7-T1 were inspected by scanning electron microscopy. Nineteen rats were subjected to a 51g acute clip compression at C8-T1 and then underwent transcardial perfusion with polyester resin at 15 minutes, 4 hours, or 24 hours after injury. The injured spinal cord appeared almost avascular at the compression site, although the large vessels on the surface of the spinal cord were all intact. The sulcal arteries at the injury site frequently showed constriction, and the impressions of endothelial nuclei were more slender and less distinct in the constricted arterial casts. Extravasation of the injected resin at the injury site was observed most frequently in the 15-minute group. Poorly filled distal branches of the sulcal arteries were seen at the injury site in every group. Indeed, it was concluded that the disruption and occlusion of the sulcal arteries and their branches accounted for a considerable amount of the posttraumatic ischemia of the cord. Occlusion of the sulcal arteries in the anterior median sulcus at the injury site was more frequently observed in the 24-hour group than in earlier groups. This observation suggests that there was a progressive circulatory disturbance of the damaged sulcal arteries at the injury site. The 4- and 24-hour groups showed avascular areas extending longitudinally from the injury site in the posterior columns, probably the result of hemorrhage and venous obstruction.

Aneurysm↗
PubMed1992

The effect of direct current field polarity on recovery after acute experimental spinal cord injury.

Recent evidence indicates that direct current (DC) fields promote recovery of acutely injured central and peripheral nervous system axons. The polarity of the applied DC field may play an important role in modulating these effects. In the present study, the effect of DC field polarity on recovery of injured spinal cord axons was examined anatomically, electrophysiologically and behaviourly in a rat model. After a 53 g clip compression injury of the cord at T1, 30 adult rats were randomly and blindly allocated to one of three groups (n = 10 each): one group received implantation of a DC stimulator (14 microA) with the cathode caudal to the injury site; the second group received implantation of a similar stimulator with the cathode rostral to the injury site; and the third group received a sham (O microA) stimulator. Clinical neurological function was assessed by the inclined plane technique and axonal function was assessed by motor- and somatosensory-evoked potentials (MEP and SSEP). A quantitative assessment of axonal integrity was performed by counting neurons in the brain retrogradely labelled by the axonal tracer horseradish peroxidase (HRP) and by counting axons at the injury site. The inclined plane scores (P less than 0.0001), MEP amplitude (P less than 0.02), counts of neurons retrogradely labelled by HRP (P less than 0.0001), and axon counts at the injury site (P less than 0.01) were significantly greater in the group treated with a DC field with the cathode caudal to the lesion than in the other two groups. Conversely, the cathode rostral DC field caused a decrease in the number of neurons retrogradely labelled by HRP (P less than 0.05) compared to the sham and cathode caudal groups. These data confirm our previous finding that DC fields promote recovery of acutely injured spinal cord axons. Furthermore, the polarity of the applied field is of critical importance to this effect.

Animals↗
PubMed1992

Changes in thyroid hormones, thyroid stimulating hormone and cortisol in acute spinal cord injury.

To determine the hormonal response to acute spinal cord injury, serial serum samples were collected from 18 patients with acute spinal cord injury and from 14 control patients with spinal fractures without cord injury. The first sample was taken within 24 hours of injury, the second at 24-48 hours; and the third at 7 days for determination of thyroxine (T4), free T4 (FT4), triiodothyronine (T3), reverse T3 (rT3), T3 uptake (T3U), thyroid stimulating hormone (TSH), thyroxine binding globulin (TBG), growth hormone (GH), cortisol, and insulin. Significant increases were observed in rT3 levels and transient changes were observed in the T4 and T3 levels in the spinal cord injured group but not in the group with spinal fractures alone. The changes in the spinal cord injured patients are consistent with the 'low T3 syndrome'. However, the persisting rise of rT3 at 7 days was an unexpected finding. In addition to the cord injury, these changes may also be related to dexamthasone administration and nutritional factors.

Acute Disease↗
PubMed1992

Elevated gene expression in the red nucleus after spinal cord compression injury.

Since the mechanism of injury in the majority of human traumatic spinal cord injuries involves rapid cord compression due to bone displacement or fracture-dislocation, we have used a compression injury model to examine the response of adult rat rubrospinal neurons to traumatic spinal cord injury. We have applied in situ hybridization techniques to examine levels of mRNA for cytoskeletal and growth-associated proteins. We report a population of magnocellular red nucleus neurons with elevated levels of T alpha 1 tubulin and GAP-43 up to four weeks post-lesion. In control animals, both probes had very low hybridization signals indistinguishable from background. These and other findings suggest that kinetic compression injuries of the adult spinal cord can result in regeneration-associated gene expression in intrinsic CNS neurons.

Animals↗
PubMed1992

High-resolution magnetic resonance imaging of experimental spinal cord injury in the rat.

The ability of magnetic resonance imaging (MRI) to display the anatomic changes after spinal cord injury in the rat were examined in postmortem specimens. With the clip compression technique, acute spinal cord injuries of three grades of severity were produced in adult male rats. One hour after injury, during which time physiological parameters were measured and maintained within the normal range, the rats were killed by transcardiac perfusion of formalin. The vertebral column containing the cervical and upper thoracic segments was excised and, after further formalin fixation, 20 contiguous MRI scans centered on the injury site were obtained using a spin-echo imaging sequence. The volume of signal acquisition for each image was 15 x 15 x 1.0 mm thick. The spinal cords were then removed from the vertebral column, sectioned, and stained for histological examination. Ten-micrometer serial sections of each cord were examined microscopically. MRI scans and microscopic sections at comparable levels were examined to determine the quality of anatomical detail and spatial resolution of the MRI scans. MRI scans with resolution of about 75 microns per pixel edge were obtained. At the site of injury, there was disruption of the normally well demarcated gray-white interface and variable areas of low signal intensity. Because of the resolution achieved, it was possible to determine that these low signal intensity areas were post-traumatic hemorrhages. Indeed, hemorrhages with dimensions of the order of 100 microns were detected on the MRI scans. Furthermore, by examining the serial sections of the cord, the extent of the injury along the cord could be determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Evoked potentials from direct cerebellar stimulation for monitoring of the rodent spinal cord.

Although the assessment of spinal cord function by electrophysiological techniques has become important in both clinical and research environments, current monitoring methods do not completely evaluate all tracts in the spinal cord. Somatosensory and motor evoked potentials primarily reflect dorsal column and pyramidal tract integrity, respectively, but do not directly assess the status of the ventral funiculus. The present study was undertaken to evaluate the use of evoked potentials, elicited by direct cerebellar stimulation, in monitoring the ventral component of the rodent spinal cord. Twenty-nine rats underwent epidural anodal stimulation directly over the cerebellar cortex, with recording of evoked responses from the lower thoracic spinal cord, both sciatic nerves, and/or both gastrocnemius muscles. Stimulation parameters were varied to establish normative characteristics. The pathways conducting these "posterior fossa evoked potentials" were determined after creation of various lesions of the cervical spinal cord. The evoked potential recorded from the thoracic spinal cord consisted of five positive (P1 to P5) and five negative (N1 to N5) peaks. The average conduction velocity (+/- standard deviation) of the earliest wave (P1) was 53 +/- 4 m/sec, with a latency of 1.24 +/- 0.10 msec. The other components followed within 4 msec from stimulus onset. Unilateral cerebellar stimulation resulted in bilateral sciatic nerve and gastrocnemius muscle responses; there were no significant differences (p greater than 0.05) in the thresholds, amplitudes, or latencies of these responses elicited by right- versus left-sided stimulation. Recordings performed following creation of selective lesions of the cervical cord indicated that the thoracic response was carried primarily in the ventral funiculus while the sciatic and gastrocnemius responses were mediated through the dorsal half of the spinal cord. It is concluded that the posterior fossa evoked potential has research value as a method of monitoring pathways within the ventral spinal cord of the rat, and should be useful in the study of spinal cord injury.

Animals↗
PubMed1992

Hypoglossal-facial nerve anastomosis for facial nerve palsy following surgery for cerebellopontine angle tumors.

Hypoglossal-facial nerve anastomosis is one of the procedures frequently performed to restore function after facial palsy secondary to surgery for removal of cerebellopontine angle tumors. The published results of hypoglossal-facial nerve anastomosis have been variable, and there are still questions about the indications, timing, and surgical techniques for this procedure. The goals of the present retrospective analysis of 22 cases of hypoglossal-facial nerve anastomosis were to assess the extent of the functional recovery and to analyze the factors affecting this recovery. The 22 cases of complete facial palsy were gleaned from a series of 245 cases of cerebellopontine angle tumors treated surgically by one of the authors. Twenty patients had an acoustic neuroma (average size 3.5 cm), one patient had a petrous meningioma, and one patient had a facial neuroma. The average age of the patients was 47.3 years (range 19 to 69 years). The average interval from tumor surgery to hypoglossal-facial nerve anastomosis was 6.4 months (range 12 days to 17 months), and the average follow-up period after the procedure was 65 months. The results were graded as good, fair, poor, or failure according to a new method of classifying facial nerve function after hypoglossal-facial nerve anastomosis. The results were good in 14 cases (63.6%), fair in three (13.6%), and poor in four (18.2%); one (4.5%) was a failure. Good and fair results occurred with higher frequency in younger patients who were operated on within shorter intervals, although these relationships were not statistically significant. There were no surgical complications. Good or fair results were achieved in 17 (77.3%) of the 22 cases, and thus hypoglossal-facial nerve anastomosis is considered an effective procedure for most patients with facial palsy after surgery for cerebellopontine angle tumors.

Adult↗
PubMed1991

Effect of continuous versus intermittent turning on nursing and non-nursing care time for acute spinal cord injuries.

The present study was conducted to determine whether automated, continuous turning beds would reduce the nursing care time for spinal cord injured (SCI) patients by freeing hospital staff from manual turning of patients every 2 hours. Seventeen patients were randomly assigned to continuous or intermittent turning and were observed during the 8 hour shift for 1 to 18 days following injury. Trained observers recorded the time taken for patient contact activities performed by the nursing staff (direct nursing care) and other hospital staff. The mean direct nursing care time per dayshift per patient was 130 +/- 22 (mean +/- SD) minutes for 9 patients managed with continuous turning and 115 +/- 41 (mean +/- SD) minutes for 8 patients managed with intermittent turning. The observed difference in care time between the two treatment groups was not significant (p greater than 0.05). Numerous factors including neurological level, time following injury, and medical complications appeared to affect the direct nursing care time. Although continuous turning did not reduce nursing care time it offered major advantages for the treatment of selected cases of acute SCI. Some major advantages of continuous turning treatment were observed. Spinal alignment was easier to maintain during continuous turning in patients with injuries of the cervical spine. Continuous turning allowed radiological procedures on the spine, chest and abdomen to be more easily performed without having to alter the patients' position in bed. Therapy and nursing staff indicated that the continuous turning bed facilitated patient positioning for such activities as chest physiotherapy. With continuous turning, one nurse was sufficient to provide care for an individual SCI patient without having to rely on the assistance of other nurses on the ward for patient turning every 2 hours.

Acute Disease↗