Search Results

You are looking at 1 - 10 of 83 items for

  • Author or Editor: Charles H. Tator x
Clear All Modify Search
Restricted access

Charles H. Tator and Izumi Koyanagi

✓ 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.

Full access

Charles H. Tator and Izumi Koyanagi

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.

Restricted access

Charles H. Tator and Willem Wassenaar

✓ The retention and distribution of tritiated methotrexate (MTX-3H) after direct intracerebral or intraneoplastic injection were studied in mice bearing subcutaneous or intracerebral ependymoblastomas. After intracerebral injection of MTX-3H in nontumor-bearing animals, a large amount of the drug was retained in the head, much more than could have been retained after systemic administration, and there was rapid spreading of the drug through the ipsilateral hemisphere. Intraneoplastic injection of subcutaneous and intracerebral tumors produced rapid spreading of the drug through the tumors. Initially, the drug was mainly in the interstitial fluid of the tumors followed by earlier cellular uptake than was seen after intravenous injection. Even though the distribution of the drug in the intracerebral tumors was not uniform, and some intracranial tumor deposits contained less radioactivity than areas closer to the site of injection, intraneoplastic injection may have advantages for brain-tumor chemotherapy. However, further experimental study is necessary before clinical application can be recommended, especially evaluation of neurotoxicity after intracerebral, intraneoplastic injection of MTX or other chemotherapeutic agents.

Restricted access

Willem Wassenaar and Charles H. Tator

✓ Currently available diagnostic tracers for brain tumors are not specific. Tumor-specific tracers would improve the detection of brain tumors by gamma encephalography. Glucose is an important substrate for tumor metabolism and is known to be taken up in large amounts. The authors have studied five labeled carbohydrates in an attempt to find a tumor-specific tracer: three were tritiated (L-galactose-1-3H, L-fucose-3H, and 4,6-dideoxy-xylo-hexose-3H) and two were radioiodinated (methyl-6-125I-6-deoxy-D-glucoside and 6-125I-6-deoxy-D-glucose). The uptake of these tracers by a transplantable mouse ependymoblastoma after intravenous injection was determined by liquid and well scintillation counting. The highest tumor-to-brain ratio was 7.1 to 1 for the tritiated tracers and 6.2 to 1 for the radioiodinated tracers. Although these ratios are not high enough for gamma encephalography, one of the iodinated tracers may be useful for enhancement of contrast in computerized axial tomography.

Restricted access

Eugen J. Dolan and Charles H. Tator

✓ A new method is described for the determination of force-distance curves for aneurysm clips. A dissecting microscope with a goniometer eyepiece was used to determine the angle between the clip blades as various forces were applied to open the clip. The cosine law was then used to calculate the force-distance curves. The method allows accurate characterization of different clips and is especially useful for the early detection of clip weakening.

Restricted access

Charles H. Tator and David W. Rowed

✓ The authors describe a fluoroscopic method of guiding percutaneous needle penetration of the foramen ovale. The advantages are simplicity, speed, accuracy, and comfortable patient positioning. Radiation exposure is minimized.

Restricted access

Abhijit Guha, Charles H. Tator and Ian Piper

✓ The normal rat spinal cord blood flow (SCBF) has been shown to increase after administration of nimodipine, a calcium channel blocker. The present study investigates the capability of nimodipine to improve SCBF, as measured by the hydrogen clearance technique, after a 53.0-gm clip compression injury to the T-1 segment of the rat spinal cord.

The profound drop in mean systemic arterial blood pressure (MSAP) after cervical cord injury precluded any improvement in posttraumatic SCBF by nimodipine alone. Hence, in a randomized controlled study with five rats per group, pressor agents (whole blood, angiotensin, or adrenaline) were infused to maintain MSAP between 100 and 120 mm Hg after injury. Control animals received only a saline infusion. Nimodipine at the optimal dose found in normal animals (1.5 µg/kg/min) was added to the pressor agents. The MSAP and other physiological parameters were measured in rats receiving the pressor agents only and in those receiving pressor agents combined with nimodipine.

In rats receiving whole blood, angiotensin, or adrenaline the posttraumatic MSAP improved to between 100 and 120 mm Hg, but there was no improvement in SCBF compared to the saline group. The addition of nimodipine decreased MSAP and SCBF in all groups except those animals also receiving adrenaline, where the MSAP was maintained at 109 ± 5 mm Hg. In these animals a significant increase in posttraumatic SCBF from 16.5 ± 2.1 to 20.2 ± 2.3 ml/100 gm/min (mean ± standard error of the mean) occurred at the site of injury with the addition of nimodipine.

The maintenance of an adequate MSAP by a pressor agent was crucial for nimodipine to improve posttraumatic SCBF by its ability to dilate the spinal vascular bed. Adrenalin was the only pressor agent that could fulfill the above criteria, although other pressor agents need to be investigated. Experiments are underway with the combination of adrenaline and nimodipine to further verify these encouraging results demonstrating an improvement in posttraumatic ischemia of the spinal cord.

Restricted access

Charles H. Tator and Julian M. Nedzelski

✓ 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.

Restricted access

Ab Guha, Charles H. Tator and Ian Piper

✓ 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.