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Biomedical subjects

R von Hanwehr

Publications and source records attributed to R von Hanwehr.

8 recordsLinked to original sources
PubMed1995

Optimization of dose distribution for LINAC based radiosurgery using elliptical collimators.

The use of non-circular collimators is considered on all or some of the arcs used for radiosurgery on a linear accelerator in order to obtain conformal dose distribution for non-spherical lesions using a single isocenter. An extension of software to allow for use of non-circular collimators and a mathematical optimization based on prescribed doses on the lesion surface and on points in normal tissue (critical structures) are presented. Tests of the optimization method on simulated cases indicate that several boosts from selected positions along the arcs, superimposed on an optimized arc configuration allows one to obtain a highly conformal dose distribution with simple elliptical inserts. The optimization method can be applied to any type of collimation and is particularly effective with variable dose-rate machines.

Brain Neoplasms↗
PubMed1995

Interventional telemedicine for noninvasive neuroradiosurgery: remote-site high-performance computing, mathematical optimization, and virtual scenario simulation.

Interventional Telemedicine may have potential utility in providing connectivity and access to specialized high performance computing and advanced software resources in support of clinical procedures in the field of Minimally-Invasive Surgery and Stereotactic Linear Accelerator (LINAC) Radiosurgery. Such interventions may benefit from application of nonlinear quadratic inverse solution methods designed to provide the capability to reverse optimize a 'best case' treatment plan. The formidable decision-making challenges posed by increasingly complex optimized data and progressively versatile LINAC delivery systems require volume visualization of projected treatment data and imaging anatomy via photorealistic rendering and virtual scenario simulation techniques. Both these new directions are heavily dependent on access to specialized high performance computing platforms solely accessible via broad-bandwidth network connectivity. This pilot project presents resimulation of retrospective radiosurgical case data using inverse solution optimization models running on workstation clusters and then volume rendered and simulated on the Princeton Graphics Engine Supercomputer. Evidence for effective utilization of such optimization and virtual simulation methods running on remotely accessed, distant high performance computing resources is discussed in view of the potential for long-term clinical investigation and eventual development of Interventional Telemedicine as a clinically practical approach for providing support to remote or non-urban radiosurgery centers in the industrialized and developing world.

Algorithms↗
PubMed1995

Correlating angiograms with CT/MRI scans for radiosurgery.

A mathematical solution is described to reconstruct 3-D objects in the stereotactic space from angiographic, not necessarily perpendicular 2-D projections. The mathematical calculation requires 6 markers, whose coordinates should be known within the stereotactic frame reference system. This method was developed to improve the planning in stereotactic radiosurgery of AVM. An AVM nidus can be geometrically described as delineated on plane film angiography. This approach provides a more accurate determination of the lesion shape, size, angulation and position when using information from stereotactic planar angiograms. Further more this technique supports a stereotactically accurate projection of the surface volume model of the AVM nidus on to the corresponding CT and MRI scans images.

Arteriovenous Malformations↗
PubMed1986

Changes in extra- and intracellular pH in the brain during and following ischemia in hyperglycemic and in moderately hypoglycemic rats.

Incomplete forebrain ischemia of 15-min duration was induced in rats made hyperglycemic or moderately hypoglycemic prior to ischemia. Tissue CO2 tension, CO2 content, labile tissue metabolites, and extracellular pH (pHe) were measured, and intracellular pH (pHi) was derived by calculation on the assumption that cerebral intracellular fluids can be lumped into one space. In hypoglycemic animals, mean tissue lactate content increased from 2 to 10 mumol g-1. Tissue CO2 content was virtually unchanged and the CO2 tension increased from approximately 50 to approximately 145 mm Hg. In hyperglycemic animals, tissue lactate content rose to 20 mumol g-1, and the CO2 content decreased by 25%, demonstrating that some CO2 was lost to the blood supplied by the remaining perfusion. Accordingly, tissue CO2 tension did not rise above 200 mm Hg. pHe was reduced in proportion to the amount of lactate accumulated, the values obtained in hypo- and hyperglycemic animals showing relatively little scatter (6.76 +/- 0.03 and 6.25 +/- 0.04, respectively). In hypoglycemic animals the extracellular HCO-3 concentration was virtually unchanged, demonstrating that any influx of lactic acid from the cells must have been accompanied by H+ efflux and/or HCO-3 influx via independent routes. In hyperglycemic animals [HCO-3]e fell by greater than 10 mumol ml-1. In both groups [HCO-3]e was reduced during the first 5 min of recovery. Recovery of pHe was slower in hyper- than in hypoglycemic animals. During ischemia calculated pHi fell to 6.37 +/- 0.04 and 5.95 +/- 0.06 in hypo- and hyperglycemic animals, respectively. Differences in pHi were maintained for the first 15 min of recovery, but in both hypo- and hyperglycemic animals pHi had normalized after 30 min. It is concluded that preischemic hyperglycemia leads to a more pronounced intra- and extracellular acidosis than normo- and hypoglycemia, an acidosis that also resolves more slowly during recirculation.

Acidosis↗
PubMed1986

Extra- and intracellular pH during near-complete forebrain ischemia in the rat.

The objective of the present study was to estimate extracellular pH (pHe) and intracellular pH (pHi) during near-complete forebrain ischemia in the rat, and to evaluate the relative importance of lactic acidosis and rise in tissue Pco2 (Ptco2) in causing pHe and pHi to fall. The animals, which were ventilated, normoxic, normocapnic, and normothermic, were subjected to 15 min of ischemia, either without or with 30-60 min of recirculation. Ptco2 was measured with a tissue electrode, pHe with a double-barrel liquid ion-exchanger microelectrode, changes in extracellular fluid (ECF) volume by impedance measurements, tissue CO2 content by a microdiffusion technique, and labile tissue metabolites by enzymatic fluorometric methods. Ischemia caused Ptco2 to rise to between 95 and 190 mm Hg (mean 149 mm Hg), and pHe to fall by 0.45-1.05 units (mean 0.70 units). During recovery, Ptco2 normalized within 5 min and pHe after 15-30 min. During ischemia, high-energy phosphates were depleted and tissue lactate content increased to 15 mumol X g-1. The total CO2 content (Tco2) was minimally or moderately reduced (normal, 11.9 mumol X g-1; range of ischemic values, 7.9-12.1 mumol X g-1), this range probably reflecting variable amounts of remaining blood flow. Impedance measurements demonstrated that ECF volume during ischemia was reduced to 55% of control, with gradual normalization during the first 15-30 min of recirculation. From values for Ptco2, Tco2, [HCO3-]e, and ECF volume, [HCO3-]i and pHi could be calculated. These values pertain to an idealized homogeneous intracellular compartment, and the methods used cannot detect whether different intracellular compartments diverge in their acid-base responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1985

Extra- and intracellular pH in the brain during seizures and in the recovery period following the arrest of seizure activity.

The objective of the study was to estimate changes in extracellular pH (pHe) and intracellular pH (pHi) during seizures and in the recovery period following the arrest of seizure activity. Seizures of 5- and 20-min duration were induced in rats by fluorothyl added to the insufflated gas mixture, and recovery for 5, 15, and 45 min was instituted by withdrawal of the fluorothyl supply following 20 min of continuous seizures. Changes in pHe were measured by double-barreled, liquid ion-exchange pH microelectrodes, and in pHi by the CO2 method, following estimation of tissue PCO2 and extracellular fluid (ECF) volume. The animals were either normoxic or rendered moderately hypoxic (arterial PO2 40-50 mm Hg). Upon induction of seizures in normoxic animals, pHe decreased by a mean of 0.36 unit, the values being identical at 5 and 20 min. In moderate hypoxia, seizures sustained for 20 min were accompanied by a further fall in pHe (mean decrease 0.51 unit). The changes in pHe seemed mainly to reflect the nonionic diffusion of lactic acid from cells to the ECF (tissue lactate levels approximately 10 and 15 mumol g-1 during seizures in normoxic and hypoxic animals, respectively). However, the gradual fall in pHe attributable able to lactic acid production was preceded by rapid acidification, sometimes exceeding the steady-state values subsequently attained. This acidification was interpreted to reflect spreading depression and fast transcellular Na+/H+ exchange. Following cessation of seizure discharge, pHe normalized at a surprisingly slow rate, with some acidosis persisting even after 45 min. The difference between cerebrovenous and arterial PCO2 was reduced during seizures and increased in the recovery period, probably reflecting alterations in the blood flow/metabolic rate coupling. Impedance changes were slight, indicating only minor changes in ECF volume. Changes in pHi after 5 min of seizures ranged from 0.20 (normoxic animals) to 0.32 (hypoxic animals) unit, the pHi values after 20 min being 0.07-0.08 unit higher. The results suggest the regulation of pHi during ongoing seizures. Upon arrest of seizure activity, pHi rapidly increased to normal and subsequently to supranormal values. Postepileptic intracellular alkalosis occurred at a time when pHe was still reduced and in spite of the fact that tissue lactate values had not normalized. It is concluded that the rapid normalization of pHi and overt alkalosis were caused by the simultaneously occurring oxidation of lactate, with the removal of a stoichiometrical amount of H+, and the extrusion of H+ from cells, possibly via a Na+/H+ exchanger, the latter probably delaying normalization of pHe.

Acid-Base Equilibrium↗
PubMed1985

Thoracic spinal angiomyolipoma: case report and literature review.

A rare case of thoracic spinal angiomyolipoma presenting with evidence of vertebral body infiltration and concurrent epidural spinal cord compression is described. Clinicopathological correlates, aspects of radiological diagnosis, considerations for surgical management, and histopathological features denoting possible unique attributes of biological behavior for this entity are discussed in conjunction with a review of the previous literature on angiolipomas in general.

Adult↗