[Surgical wound infection in 4 different surgical departments].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Kucharczyk.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A carotid embolic stroke model in rats was studied with a combination of diffusion- and perfusion-sensitive magnetic resonance (MR) imaging at 4.7 T. Capillary blood deoxygenation changes were monitored during formation of focal ischemia by acquiring multisection magnetic susceptibility-weighted echo-planar images. A signal intensity decrease of 7% +/- 3 in ischemic brain (1% +/- 2 in normal brain) was attributable to a T2* decrease due to increased blood deoxygenation, which correlated well with subsequently measured decreases in the apparent diffusion coefficient. The same multisection methods were used to track the first-pass transit of a bolus of dysprosium-DTPA-BMA [diethylenetriaminepentaacetic acid-bis(methylamide)] to assess relative tissue perfusion before and after stroke and after treatment with a thrombolytic agent. Analysis of contrast agent transit profiles suggested a total perfusion deficit in ischemic tissue and essentially unchanged perfusion in normal brain tissue after stroke.
Explore the source record for details and available documents.
OBJECTIVE: The purpose of this study was to compare white matter maturation as demonstrated with diffusion-weighted MRI and with myelin-sensitive histological staining. MATERIALS AND METHODS: The diffusion-, T1-, and T2-weighted SE MRI at 4.7 T was performed weekly in a total of 16 rat pups, aged from 5 days to 8 weeks, 2 animals evaluated per week. Heavily diffusion-weighted sequences were obtained with the diffusion-sensitizing gradient switched alternately in two orthogonal directions. To enhance signal intensity of anisotropic structures, a synthesized image (referred to as the "anisotropy index map") was constructed from the ratio of pairs of images acquired with diffusion sensitization of identical magnitude but orthogonal direction sensitivity. The anisotropy index maps were used for comparison with T1-weighted and heavily T2-weighted SE sequences and histological sections, respectively. RESULTS: The first evidence of diffusion anisotropy on anisotropy index maps preceded initial myelin as well as neurofibril staining by 5-12 days and T2 shortening by 2 weeks. The T1-weighted sequences did not yield visible changes and were not helpful for the assessment of ongoing white matter maturation in this model. CONCLUSION: Magnetic resonance imaging signal intensity changes based on anisotropic water diffusion were demonstrated in regions of unmyelinated cerebral white matter tracts of albino rat pups before the onset of histologically detectable myelin. The ability of in vivo mapping of premyelinating white matter maturation indicates a new diagnostic use of MRI in evaluating cerebral white matter maturation.
Hyperglycemia is often associated with an increased frequency of cerebrovascular disease and exacerbation of neuronal injury in focal ischemic cerebral infarction. We used a combination of high-field proton MR imaging and 1H and 31P MR spectroscopy to investigate whether hyperglycemia would adversely influence cerebral metabolism and eventual infarct size following unilateral occlusion of the middle cerebral artery (MCA) of cats pretreated with the calcium channel blocker nicardipine. Normoglycemic animals injected with 10 micrograms/kg of nicardipine (8 micrograms.kg-1.hr-1 maintenance dose) manifested only mild disturbances in phosphorus metabolism and cerebral pH regulation compared with untreated controls, and showed a significant reduction in infarct size 7 hr after MCA occlusion. By comparison, hyperglycemic cats (plasma glucose, 200-300 mg/dl) had significantly reduced cerebral high-energy phosphates, elevated lactic acid, and larger ischemic lesions in the occluded MCA territory, irrespective of whether they were treated with nicardipine. These results indicate that moderate hyperglycemia can exaggerate ischemic brain damage by enhancing formation of tissue lactic acid and impairing normal phosphorus metabolism. One implication of this study is that dextrose should not be provided to patients with acute ischemic stroke.
Diabetes insipidus is a clinical syndrome characterized by the excretion of copious volumes of dilute urine combined with persistent intake of abnormally large quantities of fluid. There are two general forms of the disease, central (vasopressin deficient) and nephrogenic (vasopressin resistant). Diabetes insipidus of central origin most often results from lesions in the hypothalamic-neurohypophyseal axis. Twenty-six cases of central diabetes insipidus were evaluated with the use of high-field-strength MR imaging. A wide variety of precipitating conditions were found, including Langerhans cell histiocytosis, neoplasia, trauma, and infection. A thickened pituitary infundibulum was seen in most patients, and an absence of high intensity signal in the posterior pituitary lobe on T1-weighted images was seen in every case. Analysis of stalk morphology; associated brain findings; and correlation with the patient's age, sex, history, and radiographs of other body parts improved diagnostic specificity. When combined with clinical information, MR imaging is able to provide a specific diagnosis in almost all cases of central diabetes insipidus.
The normal neurohypophysis is hyperintense relative to brain and adenohypophysis on T1-weighted MR images, but the signal is not chemically shifted with respect to water. The source of the hyperintense MR signal in the normal neurohypophysis has been the subject of recent controversy. To date, an adequate biophysical explanation for the unusual imaging properties of the neurohypophysis has not been found. The purpose of this study was to investigate the effect of two chemical components of the neurohypophysis, phospholipids and vasopressin, on the MR signal. We synthesized phospholipid vesicles of the same size as those found in the neurohypophysis (100-200 nm) and quantitatively measured T1, T2, and chemical shift in a spectrometer at concentrations of 0-250 mg/ml of phospholipid. Imaging of the test materials was performed on a 1.5-T whole-body MR system using T1-weighted images, T2-weighted images, reduced bandwidth, and fat suppression techniques. The experiment was also performed with saline buffer, mineral oil, vasopressin, and vasopressin incorporated into the core of the phospholipid vesicles. We found that a solution containing phospholipid vesicles has T1 and T2 characteristics analogous to the neurohypophysis and that this solution exhibits a single peak that is not chemically shifted with respect to water. Vasopressin had no effect on the signal, neither in solution nor in the vesicles. We conclude that phospholipid acts as a relaxation enhancer of water protons and that the MR characteristics of the phospholipid vesicles can account for the observed MR properties of the neurohypophysis.
The MR images of four female patients with acute onset of central diabetes insipidus and pathologically confirmed Langerhans cell histiocytosis were evaluated retrospectively for evidence of lesions in the hypothalamic-pituitary axis. The examinations were conducted on a 1.5-T MR system with thin-section sagittal and coronal T1-weighted (short TR/short TE) and T2-weighted (long TR/long TE) images. Three patients underwent T1-weighted MR after IV administration of gadopentetate dimeglumine. Compared with 20 normal subjects who were evaluated with the same MR protocol, three of the four patients had a symmetrically thickened pituitary stalk that demonstrated homogeneous signal enhancement following contrast administration. The high signal intensity of the posterior lobe, which was seen in normal subjects on T1-weighted sagittal images, was absent in all four patients. Two patients had associated abnormalities on either chest films or imaging studies of the temporal bone and two patients had isolated CNS Langerhans cell histiocytosis. The combination of a thickened pituitary stalk and absent posterior pituitary hyperintensity, while nonspecific for Langerhans cell histiocytosis, should nevertheless prompt further studies, such as chest films, bone scanning, or temporal bone CT, to attempt to narrow the differential diagnosis. Gadopentetate dimeglumine, in particular, may be a useful adjunct in the MR examination of the patient with diabetes insipidus.
Explore the source record for details and available documents.
Using high-field-strength, 1.5-T, high-resolution MR, we identified the following complex of neurohypophyseal abnormalities in each of five pituitary dwarfs: (1) severe hypoplasia or total absence of the infundibulum; (2) absence of the posterior pituitary bright spot in its normal location; and (3) a 3-8-mm tissue nodule at the median eminence exhibiting lipidlike signal on T1-weighted images. On the basis of its signal features and the clinical absence of diabetes insipidus in these patients, the median eminence nodule appears to represent an ectopic and functional posterior pituitary gland. We propose that this anatomic derangement is the end result of a localized defect of developmental origin, possibly ischemic in nature, and involving principally the infundibular stem. Thus, human growth hormone deficiency could result from perinatal disruption of the peri-infundibular hypophyseal portal system, which in turn impairs anterior pituitary function through deprivation of direct delivery of crucial hypothalamic-releasing factors. Finally, we suggest that the trophic influence of continued axonal neurosecretion at the median eminence engages proliferation of rest cell pituicytes; a process that induces formation of an ectopic and functional posterior pituitary gland, complete with its characteristic bright spot.
PURPOSE: To compare the efficacy of two nonionic T2*-shortening contrast agents, DyDTPA-BMA dysprodiamide injection and GdDTPA-BMA gadodiamide injection, as perfusion-sensitive MR imaging agents in normal and acutely ischemic brain. METHODS: The magnetic susceptibility effects of intravenous injections of 0.10-0.50 mmol/kg of each contrast agent were quantified on T2-weighted spin-echo images of cat brain before and after unilateral occlusion of the middle cerebral artery by measuring signal intensity changes in the same regions-of-interest in parietal cortex. RESULTS: In normal brain, DyDTPA-BMA produced a significantly greater loss of signal intensity than equimolar doses of GdDTPA-BMA. The magnitude of the signal intensity attenuation was dosage-dependent and proportional to the square of the magnetic moments of the two contrast agents. Restoration of baseline image signal intensity was observed within 30 min after each injection. However, injection of GdDTPA-BMA also produced a delayed, persistent hyperintensity on T2-weighted images, presumably due to its underlying T1-shortening effect. Following unilateral occlusion of the middle cerebral artery, unenhanced T2-weighted images failed to show evidence of cerebral injury for 1.5-3 hours. Administration of 0.10-1.0 mmol/kg DyDTPA-BMA shortened the time for detection of perfusion deficits (residual hyperintensity) in 22 of 36 (61%) treated cats, often to within 30 min after arterial occlusion. DyDTPA-BMA enhancement also improved lesion conspicuity in 26 of 36 (72%) cases, and disclosed very small infarcts that were not visible on T2-weighted precontrast images. Perfusion deficits in areas of partial ischemia were seen more clearly on DyDTPA-BMA-enhanced images than after equimolar injections of GdDTPA-BMA. CONCLUSIONS: Magnetic susceptibility contrast-enhanced MR imaging enables detection of perfusion deficits associated with acute cerebral ischemia well in advance of conventional T2-weighted spin-echo MR imaging without contrast. DyDTPA-BMA appears to delineate regions of ischemic damage better than GdDTPA-BMA.