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Biomedical subjects

C H Tator

Publications and source records attributed to C H Tator.

At least 55 records · Page 3Linked to original sources
PubMed1998

Effect of intrathecal nimodipine on spinal cord blood flow and evoked potentials in the normal or injured cord.

A method was developed for administering intrathecal pharmacotherapy in a rat model of spinal cord injury. The effects of intrathecal administration of nimodipine on spinal cord blood flow (SCBF) and evoked potentials (EPs) were measured in the normal and injured spinal cord. It had previously been shown that systemic nimodipine caused severe hypotension after spinal cord injury. After baseline SCBF and EPs, 15 uninjured rats were blindly allocated to one of three groups: one placebo group (n = 5); and two groups with intrathecal nimodipine, 0.05 mg/kg (n = 5), or 0.2 mg/kg (n = 5). Ten other rats received a 35 g acute clip compression injury of the spinal cord for 1 minute and, were allocated to one of two groups: placebo (n = 5); and intrathecal nimodipine 0.05 mg/kg (n = 5) given 60 min after injury. In the uninjured groups, neither 0.05 nor 0.2 mg/kg of nimodipine increased SCBF during, or 30 min after, intrathecal infusion. However, the mean arterial blood pressure (MABP) decreased significantly to 69.73.1% after the infusion of 0.2 mg/kg nimodipine and did not recover by 98 min. In all three groups of uninjured rats, the amplitude of the cerebellar EP was decreased 30 min after infusion. After spinal cord injury, there were significant decreases in MABP, SCBF and EP amplitude in both placebo and treatment groups, but there was no therapeutic benefit from nimodipine. Thus, intrathecal infusion of nimodipine did not prevent the hypotension encountered with systemic administration and exerted no beneficial effect on SCBF or EPs after acute spinal cord injury.

Animals↗
PubMed1998

Biology of neurological recovery and functional restoration after spinal cord injury.

OBJECTIVE: This article reviews the anatomic and pathophysiological bases for recovery of neurological function after experimental or clinical spinal cord injury (SCI). METHODS: Current knowledge regarding the recovery of neurological function after experimental or clinical SCI was reviewed to determine the biological basis of neurological recovery. RESULTS: There is a great propensity for recovery after clinical or experimental SCI. An examination of the anatomic basis of recovery indicates that there is a potential for both root and cord recovery, with the latter involving recovery of both gray and white matter of the cord. Resolution of acute injury events, such as hemorrhaging, and resolution of secondary pathophysiological processes, such as ischemia and excitotoxicity, can each account for recovery. The third recovery mechanism involves regrowth or regeneration of nervous tissue, resulting from either inherent or induced processes. CONCLUSION: During the Decade of the Brain, there has been a profusion of very promising in vitro and in vivo studies that have shown enhanced neurological recovery after experimental or clinical SCI.

Animals↗
PubMed1998

Prevention of arachnoiditis and postoperative tethering of the spinal cord with Gore-Tex surgical membrane: an experimental study with rats.

OBJECTIVE: Arachnoidal adhesions and inflammation were evaluated in 72 rats after spinal dural repair with one of three materials, i.e., Gore-Tex surgical membrane, collagen-coated Vicryl mesh, or lyophilized spinal dural allograft. METHODS: Laminectomy at L1 was performed, and then a 3- x 4-mm segment of spinal dura mater and arachnoid membrane was excised. After implantation of the dural substitute, the animals were divided into normal and injured groups. In the injured group, a spinal cord injury was produced at the midpoint of the duraplasty site by the clip compression technique, with 25-g force for 1 minute. Neurological performance was assessed by the inclined plane technique, and groups of rats were killed at 8 to 24 weeks after surgery. The spinal column was removed en bloc and processed for histological examination. RESULTS: There were no differences in neurological function among the three dural substitutes in either injured or noninjured rats. However, there were major differences among the groups in the incidence and severity of arachnoid adhesions and tethering. The neural tissue was bound to a thick neomembrane surrounding the lyophilized dural allograft and the collagen-coated Vicryl mesh. In contrast, the Gore-Tex surgical membrane induced only a thin membranous adhesion, which was loose and flexible. The inflammatory and foreign body response was most pronounced in rats treated with collagen-coated Vicryl mesh, at 8 and 24 weeks. CONCLUSION: In the present study, Gore-Tex surgical membrane was a very good material for the surgical repair of spinal dural defects. Additional experimental studies are required to compare Gore-Tex membrane with autologous tissues.

Animals↗
PubMed1998

Failure of topical DMSO to improve blood flow or evoked potentials in rat spinal cord injury.

Dimethyl sulfoxide (DMSO) is a well-known hydroxyl radical scavenger, which is readily absorbed through biological membranes. We studied the effects of locally applied DMSO on acute spinal cord injury. Either 10% DMSO in saline (n=8) or saline alone (n=7) was applied directly to the exposed cervical spinal cord of rats 1 hour after clip compression injury of 26 g force for 1 minute. The outcomes measured were spinal cord blood flow and evoked potentials. Spinal cord blood flow was not significantly different between these two groups. Although the evoked potentials showed spontaneous recovery after injury, there was no significant difference between the groups. In this study we failed to show any beneficial effects from topical application of high-dose DMSO on spinal cord blood flow or evoked potentials after acute spinal cord injury.

Administration, Topical↗
PubMed1998

Surgical research in Canada: synopsis of a consensus conference.

Canadian surgical research requires careful nurturing if it is to flourish in tomorrow's environment. A consensus conference organized by the Research Development Committee of the Canadian Association of Surgical Chairs has addressed a number of issues to promote Canadian surgical research. This synopsis is a summary of the proceedings of that conference. It reflects on the meaning of surgical science, elements of establishing a successful research program, leadership in surgical science, identification of talented trainees, and the means to make the most of opportunities for funding. The information contained in the synopsis should not only assist departments of surgery and surgical specialty societies but should challenge them to set goals and innovative approaches to plan for strong surgical research in a changing environment.

Canada↗
PubMed1997

Effect of a single huge dose of methylprednisolone on blood flow, evoked potentials, and histology after acute spinal cord injury in the rat.

Effects of a single, huge dose of methylprednisolone on post-traumatic spinal cord blood flow (SCBF), evoked potentials and histological changes were studied in a rat model of spinal cord injury. The purpose of this study was to assess the optimal dose of methylprednisolone for the treatment of rat spinal cord injury. Twenty-five male Wistar rats were subjected to an acute clip compression injury at 51 g for 1 min at C8-T1, and then received an intravenous bolus injection of one of the following 30 min after injury: vehicle, 30, 60, 120 or 240 mg kg-1 methylprednisolone. SCBF was measured at the injury site and an adjacent area with the hydrogen clearance technique. Sensory evoked potentials following sciatic stimulation were recorded from the somatosensory and cerebellar cortices. Descending volleys were recorded from T9-10 spinal cord following cerebellar stimulation. SCBF and evoked potential recordings were repeated until perfusion-fixation at 4 h after injury. After injury, SCBF at both levels significantly dropped, and all evoked potentials disappeared in all animals. None of the doses of methylprednisolone improved post-traumatic SCBF, or evoked potentials. Quantitative histological assessment of the injured cords revealed no significant differences in hemorrhages or cavitation in the spinal cord among the treatment groups. This study showed that a single huge dose of methylprednisolone from 30 to 240 mg kg-1 had no beneficial effects on the traumatized rat spinal cord in the acute stage.

Acute Disease↗
PubMed1997

Serial recording of somatosensory and myoelectric motor evoked potentials: role in assessing functional recovery after graded spinal cord injury in the rat.

Accurate functional outcome measures are essential in assessing therapeutic interventions after experimental spinal cord injury (SCI). We examined the hypothesis that serial recording of somatosensory (SSEP) and myoelectric motor evoked potentials (mMEPs) would provide complementary information to standard methods of behavioral analysis in a rat model of SCI and would allow objective discrimination of functional recovery in sensory and motor tracts. Clip compression injury of varying severity (sham, 23 g, 34 g, 56 g) and transections were performed at T1 in adult rats. SSEPs were recorded from the right sensorimotor cortex (SMC) after stimulation of the contralateral hind paw; mMEPs were recorded from the paraspinal, quadriceps, and the tibialis anterior muscles after anodal stimulation of the SMC. The inclined plane and Tarlov techniques were used to assess clinical neurological function. All outcome measures were assessed weekly prior to and up to 6 weeks following injury. Changes in clinical neurological function as assessed by the inclined plane and Tarlov methods varied with increasing injury severity (R = -0.72 and R = -0.73, respectively). SSEP latency was strongly correlated with injury severity (R = 0.92) and with clinical behavioral scores (R = -0.93 for inclined plane). The tibialis anterior mMEP correlated significantly, though weakly, with changes in inclined plane (R = 0.49) and Tarlov scores (R = 0.41). Although the mMEPs were sensitive to the presence of SCI, these recordings did not discriminate between severities of injury. We conclude that serial recording of SSEPs but not myoelectric MEPs correlates closely with the extent and temporal course of clinical neurological recovery after graded SCI in the rat.

Animals↗
PubMed1997

Occipital condyle fractures.

OBJECTIVE: Occipital condyle fractures (OCFs) are infrequently recognized. Three recent cases of OCF in our center prompted a review of the incidence, clinical presentation, diagnosis, and treatment of this entity. METHODS: A retrospective review of medical records and radiographic results was performed for 93 of 316 consecutive patients who were victims of trauma, who presented at the Toronto Hospital during a 13-month period, and who had undergone computed tomography of the occiput. RESULTS: A review of the literature regarding OCF revealed that cranial nerve deficits occurred in 31% of the patients with OCFs; of those, the deficits were delayed in 38%. Three new cases of OCF, with neck pain but without cranial nerve deficits, have been reported. The cervical spine x-rays revealed nothing abnormal in 96% of the reported cases. In our retrospective review, asymptomatic OCF was revealed by computed tomography for 1 of the 93 patients. CONCLUSION: OCF is a diagnostic challenge. We suggest that computed tomographic scans of O-C2 be obtained in the following circumstances: presence of lower cranial nerve deficits, associated head injury or basal cranial fracture, or persistent severe neck pain despite normal radiographic results. We propose a new classification system for the management and treatment of OCF based on the stability of the O-C1-C2 joint complex reflected by the presence of displacement of the condyle, computed tomographic or radiographic evidence of O-C1-C2 instability, and magnetic resonance evidence of ligamentous injury. OCFs are divided into the following types: Type 1 (stable), undisplaced fracture; Type 2A (stable), displaced fracture with no ligamentous instability; and Type 2B (unstable), displaced fracture with ligamentous instability.

Aged↗
PubMed1997

New spinal injuries in hockey.

OBJECTIVES: In this study, we wished to examine the nature and incidence of major spinal injuries sustained by ice hockey players and to add reported cases to a permanent registry. DESIGN: The study was a retrospective review of questionnaires returned by physicians reporting spinal injuries due to ice hockey. SETTING: Canada primarily, with reported cases from other nations. PATIENTS: Two hundred forty-one cases of fracture or dislocation of the spine have been reported. MAIN OUTCOME MEASURES: The registry includes annual incidence and mortality incidence as well as documentation of sex, age, mechanism of injury, vertebral level of injury, neurologic deficit, type of event, and type of fracture for most cases. RESULTS: Between 1982 and 1993, an average of 16.8 ice hockey related major spinal injuries were reported each year. Many of these injuries occurred to the cervical spine of players aged 16-20 years who were playing in supervised games. CONCLUSIONS: Prevention programs are beginning to become effective in decreasing the number of severe injuries and the number of injuries caused by a check from behind, although there has not been a significant decrease in the total number of injuries reported annually.

Adolescent↗
PubMed1997

Vascular mechanisms in the pathophysiology of human spinal cord injury.

Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3-5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was no evidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3-9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins by the initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

Acute Disease↗
PubMed1997

Multilevel anterior cervical corpectomy and fibular allograft fusion for cervical myelopathy.

This study was conducted to determine the safety and efficacy of multilevel anterior cervical corpectomy and stabilization using fibular allograft in patients with cervical myelopathy. Thirty-six patients underwent this procedure for cervical myelopathy caused by spondylosis (20 patients), ossified posterior longitudinal ligament (four patients), trauma (one patient), or a combination of lesions (11 patients). The mean age (+/- standard deviation) of the patients was 58 +/- 10 years and 30 of the patients were men. The mean duration of symptoms before surgery was 30 +/- 6 months and 11 patients had undergone previous surgery. Prior to surgery, the mean Nurick grade of the myelopathy was 3.1 +/- 1.4. Seventeen patients also had cervicobrachial pain. Four vertebrae were removed in six patients, three in 19, and two in 11 patients. Instrumentation was used in 15 cases. The operative mortality rate was 3% (one patient) and two patients died 2 months postoperatively. Postoperative complications included early graft displacement requiring reoperation (three patients), transient dysphagia (two patients), cerebrospinal fluid leak treated by lumbar drainage (three patients), myocardial infarction (two patients), and late graft fracture (one patient). One patient developed transient worsening of myelopathy and three developed new, temporary radiculopathies. All patients achieved stable bone union and the mean Nurick grade at an average of 31 +/- 20 months (range 0-79 months) postoperatively was 2.4 +/- 1.6 (p < 0.05, t-test). Cervicobrachial pain improved in 10 (59%) of the 17 patients who had preoperative pain and myelopathy improved at least one grade in 17 patients (47%; p < 0.05). Twenty-six surviving patients (72%) were followed for more than 24 months and stable, osseous union occurred in 97%. These results show that extensive, multilevel anterior decompression and stabilization using fibular allograft can be achieved with a perioperative mortality and major morbidity rate of 22% and with significant improvement in pain and myelopathy.

Aged↗
PubMed1996

Voltage-sensitive calcium channels mediate calcium entry into cultured mammalian sympathetic neurons following neurite transection.

Calcium ion entry following mechanical neurite transection was examined in cultured sympathetic neurons loaded with the Ca2+ indicator fluo-3. Neurite transection produced a rapid [Ca2+]i rise in the cell soma which preceded any [Ca2+]i rise in the neurite (n = 30). Blocking sodium channels with tetrodotoxin had no effect on the Ca2+ rise, but inactivating voltage-sensitive Ca2+ channels by bath-applying 140 mM potassium prior to the transection, and the simultaneous application of nimodipine and omega-conotoxin GVIA, blockers of L-type and N-type Ca2+ channels, respectively, considerably attenuated the Ca2+ rise in the soma and neurites. These data contradict the intuitive hypothesis that Ca2+ entry following mechanical neurite transection occurs via non-specific influx pathways produced by cell-membrane disruption and provide direct evidence in mammalian neurons that immediate, traumatically-induced, increases in neuronal [Ca2+]i are amenable to pharmacological manipulation.

Animals↗
PubMed1996

The effects of cortical stimulation, anesthesia and recording site on somatosensory evoked potentials in the rat.

The purpose of this study was to standardize the method of spinal cord monitoring with evoked potentials in the rat. Seventeen male Wistar rats were anesthetized with alpha-chloralose and urethane. Somatosensory evoked potential (SEP) and cerebellar evoked potential (CEP) following sciatic nerve stimulation were mapped at different time points after induction of anesthesia. SEP peaks at latencies of 13-18 ms (P13, N18) were localized to an extremely small area over the sensory cortex. In contrasts, a negative peak of the SEP at 11 ms (N11) and the CEP were widely distributed over the cerebral or cerebellar surface. Anesthesia significantly influenced the cortical components of the SEP. In 10 rats, MEP or posterior fossa evoked potential (PFEP) following stimulation of the sensorimotor or cerebellar cortices respectively, were recorded at T9. Stimulation of different points produced little change on the waveforms of the MEP or PFEP. Successive recordings of MEP and SEP revealed that the P13-N18 complex of the SEP was markedly suppressed after MEP recordings were made. In conclusion, this study identified several factors which alter SEP waveforms in the rat including location of recording, anesthesia and sequence with respect to MEP recording. MEP by stimulation of the same sensory cortex as SEP recordings should not be used for concurrent monitoring, since cortical stimulation will change the waveforms of the SEP.

Anesthesia↗
PubMed1996

Clinical syndromes associated with disproportionate weakness of the upper versus the lower extremities after cervical spinal cord injury.

Patients with cervical spinal cord injuries who present with weakness or paralysis of the hands and arms with relative preservation of lower extremity strengths are often categorized as having two clinical syndromes, cruciate paralysis and acute central cervical spinal cord injury. The explanation for the pathophysiological findings of the dissociated strength in the upper versus the lower extremities has relied on the assumption that there is a localized injury within a somatotopically organized corticospinal tract. This article summarizes the evidence that there is no somatotopic organization within the corticospinal tract in the medulla or cervical spinal cord in primates. An alternative hypothesis for these two syndromes is presented and is based on evidence that has demonstrated that the corticospinal tract in primates is critical for hand function but not for locomotion. Other prevailing theories are reviewed. Thus, we propose that a syndrome consisting of relatively greater hand and arm weakness compared with leg weakness can occur after an injury to the corticospinal tracts in the medulla or the cervical cord. The proposed mechanism, based on the function of the corticospinal tract, unifies a spectrum of injuries of the lower medulla and cervical spinal cord, which produce similar clinical syndromes (cruciate paralysis and acute central cervical spinal cord injury).

Animals↗
PubMed1996

Normal and abnormal calcium homeostasis in neurons: a basis for the pathophysiology of traumatic and ischemic central nervous system injury.

Clinical recovery after central nervous system (CNS) trauma or ischemia may be limited by a neural injury process that is triggered and perpetuated at the cellular level, rather than by a lesion amenable to surgical repair. It is widely thought that one such process, a fundamental pathological mechanism initiated by CNS injury, is a disruption of cellular Ca2+ homeostasis. Because of the critical role of Ca2+ ions in regulating innumerable cellular functions, this major homeostatic disturbance is thought to trigger neuronal and axonal degeneration and produce clinical disability. We review those aspects of normal and pathological Ca2+ homeostasis in neurons that relate to neurodegeneration and to the application of neuroprotective strategies for the treatment of CNS injury. In particular, we examine the contribution of Ca(2+)-permeable ionic channels, Ca2+ pumps, intracellular Ca2+ stores, intracellular Ca2+ buffering systems, and the roles of secondary, Ca(2+)-dependent processes in neurodegeneration. A number of hypotheses linking Ca2+ ions and Ca2+ permeable channels to neurotoxicity are discussed with an emphasis on strategies for lessening Ca(2+)-related damage. A number of these strategies may have a future role in the treatment of traumatic and ischemic CNS injury.

Animals↗
PubMed1996

Ultrastructural evidence for arteriolar vasospasm after spinal cord trauma.

OBJECTIVE: The primary objective of this study was to investigate the potential contribution of vasospasm to the cascade of secondary injury process after traumatic spinal cord injury. Although ischemic factors have been implicated, in that vessel rupture, compression, and intravascular thrombosis are readily identifiable, vasospasm has been more difficult to detect. METHODS: The sulcal arterioles in the ventral median fissure of the cervical spinal cord from adult rats were quantitatively examined at the ultrastructural level up to 24 hours after compression injury. RESULTS: There were statistically significant changes in the luminal cross-sectional area of sulcal arterioles after spinal cord injury, correlating directly with decreases in length and increases in width of medial smooth muscle cells. A simple mathematical model of postinjury blood flow is presented, suggesting an 80% decrease caused by vasospasm alone. CONCLUSION: Our results clearly implicate vasospasm as a contributing factor to secondary injury processes after traumatic spinal cord injury.

Animals↗