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Edward Weinberger

Publications and source records attributed to Edward Weinberger.

5 recordsLinked to original sources
PubMed2004

Supplemental oxygen causes increased signal intensity in subarachnoid cerebrospinal fluid on brain FLAIR MR images obtained in children during general anesthesia.

PURPOSE: To prospectively test the hypothesis that high levels of the fraction of inspired oxygen (Fio(2)) during general anesthesia cause subarachnoid cerebrospinal fluid (CSF) hyperintensity during fluid-attenuated inversion-recovery (FLAIR) magnetic resonance (MR) imaging. MATERIALS AND METHODS: At brain MR imaging during general anesthesia with propofol, two FLAIR sequences were performed in 20 children with American Society of Anesthesiologists physical status classification system grades of 3 or lower. The first FLAIR sequence was performed with the child breathing 100% oxygen; the second was performed with the child breathing 30% oxygen. CSF signal intensity was quantified on a three-point ordinal scale (0 = hypointense to brain parenchyma, 1 = isointense to brain parenchyma, 2 = hyperintense to brain parenchyma) by a pediatric neuroradiologist who was blinded to the Fio(2) level. The Wilcoxon signed rank test was used to determine if CSF hyperintensity was correlated with Fio(2). RESULTS: CSF hyperintensity was present in all 20 children (age range, 1.9-16.7 years; 12 children were boys) when the Fio(2) was 100%. The hyperintensity partially or completely disappeared in the basilar cisterns (P <.001) and cerebral sulcal subarachnoid space (P <.001) after Fio(2) was reduced from 100% to 30%. CONCLUSION: These findings are consistent with the hypothesis that increased arterial oxygen tension and consequently increased CSF Po(2) resulting from administration of high Fio(2) during general anesthesia are responsible for the increased CSF signal intensity noted on brain FLAIR MR images.

Adolescent↗
PubMed2002

Effects of aging on vasopressin production in a kindred with autosomal dominant neurohypophyseal diabetes insipidus due to the DeltaE47 neurophysin mutation.

Postmortem examinations of the hypothalamus of patients with autosomal dominant neurohypophyseal diabetes insipidus (adNDI), which have been reported only on persons dying between the ages of 37-87 yr, reveal the presence of the arginine vasopressin (AVP)-producing parvocellular neurons but the absence of 95% of the expected AVP-producing magnocellular neurons. To determine whether the clinical course of adNDI is compatible with the hypothesis that the neuropathologic findings are attributable to a progressive loss of magnocellular neurons beginning in early life, we performed posterior pituitary magnetic resonance imaging and water deprivation tests, including plasma ACTH measurements, on 17 affected members of a kindred with the deltaE47 neurophysin mutation whose ages ranged from 3 months to 54 yr. Nine adult nonaffected members (ages, 20-56 yr) underwent these tests as controls. All six children undergoing magnetic resonance imaging demonstrated a posterior pituitary hyperintense signal (PPHS). Eight of nine affected adults showed an absent or barely visible PPHS, whereas eight of nine age-matched nonaffected adults produced a normal size PPHS. During water deprivation tests, infants concentrated their urine normally, and a 3-month-old infant produced a high plasma AVP level of 15.7 pmol/liter. By school age, affected children were no longer able to concentrate their urine or prevent hypernatremia. Affected adults became dehydrated; their median plasma AVP level was less than 1.0 pmol/liter, but their median fasting plasma ACTH was 2-fold greater than the level of nonaffected adults (10.0 vs. 5.0 pmol/liter; P = 0.008). These results suggest that adNDI is a progressive disease associated with chronic loss of the magnocellular neurons that supply AVP to the posterior pituitary but preservation of the parvocellular neurons that supply AVP and CRH to the median eminence and stimulate ACTH production during hypernatremia.

Adult↗
PubMed2002

MyPACS.net: a Web-based teaching file authoring tool.

OBJECTIVE: We sought to develop a Web service that would easily allow radiologists to create their own online teaching file cases from any Web browser. CONCLUSION: We created MyPACS, a hosted teaching file authoring tool that allows easy uploading of images and descriptive information from any computer with Web access. Radiologists may designate their cases to be public or private (viewable only by the case author), and cases may be retrieved on searching for multiple parameters.

Authorship↗
PubMedDate not supplied

Interactive digital MR atlas of the pediatric brain.

The interpretation of magnetic resonance (MR) images of the pediatric brain may require consultation of an atlas to determine if a perceived finding represents an abnormality. However, most hard-copy atlases show only a few levels of the brain at selected points of time in myelination, and therefore a simultaneous comparison of different age groups is difficult with a hard-copy approach. The authors believe that a digital atlas of the normal pediatric brain may be a more efficient way to present this information and that correct interpretation of potential abnormalities may be facilitated by the online atlas they have created (available for free download from http://radiology.seattlechildrens.org/teaching/pediatricbrainatlas). Images for the atlas were derived from Digital Imaging and Communications in Medicine-compliant data sets from brain MR imaging in patients younger than 4 years. The images were interpreted as normal with respect to the appearance of the brain parenchyma. The software program used for viewing the atlas, written in C#, incorporates many features of a picture archiving and communication system viewer, such as linked scrolling and resizing. Simultaneous comparison of cases also is possible. The digital atlas facilitates learning about normal changes in the MR appearance of the pediatric brain, and it may be used during online interpretation of cases on a picture archiving and communication system.

Brain↗