Biomedical subjects

George C Newman

Publications and source records attributed to George C Newman.

6 recordsLinked to original sources

PubMed2006

Experimental estimates of the constants relating signal change to contrast concentration for cerebral blood volume by T2* MRI.

Estimates of cerebral blood volume (CBV) obtained from dynamic contrast T2(*)-weighted magnetic resonance imaging (MRI) tend to be significantly higher than values obtained by other methods. This may relate to the common assumption that the proportionality constants relating signal change to contrast concentration are equal in tissue and artery. To test this hypothesis and provide estimates for the ratio of those proportionality constants, the authors compared measurements of CBV by both MRI and computed tomography (CT) scans in nine healthy volunteers obtained using identical kinetic paradigms for the two imaging modalities. Both boluses and infusions of contrast were studied. Measurements were made in nine anatomic regions of interest of the cerebral hemispheres bilaterally. Cerebral blood volume values obtained by CT were generally lower than those obtained by MRI, especially in the cerebral cortex. As a result, the calculated values of the ratios of proportionality constants relating signal change to concentration in tissue and artery after bolus injections were significantly less than 1 in cortex (0.69) and white matter (0.76), although not in deep gray matter structures (0.87). Values of the ratios based on infusion measurements were closer to 1. In addition, CBV measurement errors with bolus MRI were significantly larger than those observed with infusion MRI or by CT. The reasons that the constants differ from 1 and for the larger variance of bolus MRI are discussed in terms of the T2* signal mechanisms. These studies help define the magnitude by which CBV is overestimated with typical T2*-weighted perfusion imaging. Infusion measurements of CBV can reduce the variance intrinsic to T2* MRI and lessen the likelihood of type II error.

Adult↗

PubMed2005

Effects of carotid or vertebrobasilar stent placement on cerebral perfusion and cognition.

INTRODUCTION: There are no well-established physiologic or neuropsychological criteria for identifying which patients with stenosis of the cervicocerebral vessels are at high risk of stroke or cognitive impairment. Our purpose was to evaluate changes in cognitive performance and cerebral perfusion associated with endovascular stent placement of the cervicocerebral vessels. METHODS: A consecutive series of 20 patients, 31-88 years of age, who underwent 21 stent procedures for arterial stenosis (10 extracranial carotid stents [ECS], four intracranial carotid stents [ICS], and seven extra- or intracranial vertebrobasilar stents [VBS]) was investigated retrospectively. All patients were evaluated with CT or MR perfusion studies both before and after stent placement. Cognitive response after stent placement was evaluated by using an informant questionnaire. RESULTS: In patients with anterior circulation stenoses (ECS and ICS group), 11 of 14 (79%) had a baseline perfusion abnormality and all 11 patients showed improved perfusion after stent placement. Four of seven (57%) patients with posterior circulation stenoses (VBS group) had a baseline perfusion abnormality and two of the four patients showed improved perfusion after stent placement. Degree of stenosis was the strongest predictor of the presence of a baseline perfusion abnormality (P = .03). Fifteen of 19 (79%) of the patients showed improved cognitive scores after stent placement. Among patients with improvement in perfusion after stent placement, 11 of 13 (85%) had improved cognitive scores. Improved perfusion after stent placement was a significant predictor of cognitive improvement (P = .04). Patients who were stented on an elective basis demonstrated greater improvement in cognition as compared with patients stented urgently (P = .01). CONCLUSION: Endovascular stent placement of the cervicocerebral vessels can safely and effectively resolve cerebral perfusion abnormalities. Improvement in perfusion parameters is associated with cognitive improvement. Larger, blinded, prospective studies are needed to confirm these preliminary observations.

Adult↗

PubMed2003

Edema after intracerebral hemorrhage: correlations with coagulation parameters and treatment.

OBJECT: Development of edema is known to contribute to poor outcome after spontaneous intracerebral hemorrhage (ICH). Recent research has identified thrombin as a key mediator in the development of edema in animal models; however, little has been published correlating the coagulation cascade and edema in humans. METHODS: In this retrospective clinical study of 80 patients with spontaneous supratentorial ICH, the authors sought to identify factors associated with edema development and outcome, including lesion imaging parameters, anticoagulant use, international normalized ratio and platelet count on hospital admission, and treatment with mannitol and steroid medications. A multivariate model was used to identify edema volume, use of mannitol, elevated blood glucose, and the presence of intraventricular hemorrhage as predictors of poor outcome at the time patients were discharged from the hospital. The authors developed a quadratic model for predicting edema volume against time by using a random coefficients model, and found that edema peaks between Days 5 and 6 after onset of ICH. The volume of the hemorrhage and the platelet count correlated significantly with edema volume within the first 24 hours post-ICH in the multiple regression analysis (p < 0.0001, r2 = 0.75). Edema growth during the first 5 days post-ICH also correlated with the platelet count, with an increasing platelet count associated with an increasing growth of edema (p = 0.0013). CONCLUSIONS: The authors propose that factors released from activated platelets at the site of hemorrhage, for example vascular endothelial growth factor, may interact with thrombin to increase vascular permeability and contribute to the development of edema.

Adrenal Cortex Hormones↗

PubMed2002

Cerebral blood volume measurements by rapid contrast infusion and T2*-weighted echo planar MRI.

Cerebral blood volume (CBV) provides information complementary to that of cerebral blood flow in cerebral ischemia, tumors, and other conditions. We have developed an alternative theory and method for measuring CBV based on dynamic imaging by MRI or CT during a short contrast infusion. This method avoids several limitations of traditional approaches that involve waiting for steady state or measuring the area under the curve (AUC) during bolus contrast injection. Anesthetized dogs were studied by T2*-weighted echo planar imaging during gadolinium-DTPA infusions lasting 30-60 sec. CBV was calculated from the ratio of the signal changes in tissue and artery. Method responsiveness was compared to AUC measurements using the vasodilator acepromazine. The ratio of signal change in tissue to that in artery rapidly approached an asymptotic value even while the amount of contrast in artery continued to increase. Using 30-sec infusions, the mean (+/- SD) of CBV for control animals was 3.6 +/- 0.9 ml blood/100 g tissue in gray matter and 2.3 +/- 0.8 ml blood/100 g tissue in white matter (ratio = 1.6). Acepromazine increased CBV to 5.7 +/- 1.5 ml blood/100 g tissue in gray matter and 3.1 +/- 0.8 ml blood/100 g tissue in white matter (ratio = 2.0). AUC measurements after bolus injection yielded similar values for control animals but failed to demonstrate any change after acepromazine. It is possible to measure CBV using dynamic MRI or CT during 30-60-sec contrast infusions. This method may be more sensitive to changes in CBV than traditional AUC methods.

Acepromazine↗

PubMed2002

Calcium compartments in brain.

Excellent progress has been made toward understanding the physiology and pharmacology of specific calcium-related cellular processes of the brain, but few studies have provided an integrated view of brain calcium kinetics. To further the knowledge of the size and binding properties of brain calcium compartments, the authors have conducted a series of experiments in hippocampal brain slices exposed to high and low extracellular calcium. Slices were incubated in buffers containing 0.001 to 4.5 mmol/L calcium for up to 75 minutes. Slice calcium content was analyzed by three methods: exchange equilibrium with 45Ca, synchrotron-radiation-induced x-ray emission, and inductively coupled plasma. Data were analyzed using a model based on a Langmuir isotherm for two independent sites, with additional extracellular and bound compartments. In parallel experiments, altered low calcium had no effect on slice histology and only mild effects on slice adenylates. When combined with prior 45Ca and fluorescent probe binding experiments, these results suggest that there are at least five kinetically distinct calcium compartments: (1) free extracellular (approximately 10%); (2) loosely associated extracellular plasma membrane (approximately 55%); (3) intracellular compartment with moderate avidity (approximately 17%); (4) tightly bound, nonexchangeable intracellular compartment ( approximately 15%); and (5) free cytoplasmic (<0.01%). If only the third compartment is considered a potential calcium buffer, then the buffering ratio is calculated to be approximately 2,700:1, but if the second compartment is also included, then the buffering ratio would be approximately 13,000:1. This may explain the wide range of estimates observed by fluorescent probe studies.

Animals↗

PubMed2002

Changes in plasma homocyst(e)ine in the acute phase after stroke.

BACKGROUND AND PURPOSE: Elevated plasma homocyst(e)ine [H(e)] concentration has been associated with an increased risk of stroke. Although the literature suggests that H(e) increases from the acute to the convalescent phase after a stroke, it is not known whether H(e) changes within the acute period. METHODS: A prospective, multicenter study was conducted to examine changes in H(e) during the 2 weeks after an incident stroke. Blood samples were collected at days 1, 3, 5, 7, and between 10 and 14 days after the stroke. RESULTS: Seventy-six participants (51 men) were enrolled from 9 sites from February 1997 through June 1998. Mean age was 65.6 years, and subjects had at least two H(e) measurements. The estimated mean H(e) level at baseline was 11.3+/-0.5 micromol/L, which increased consistently to a mean of 12.0+/-0.05, 12.4+/-0.5, 13.3+/-0.5, and 13.7+/-0.7 micromol/L at days 3, 5, 7, and 10 to 14, respectively. The magnitude of the change in H(e) was not affected by age, sex, smoking status, alcohol use, history of hypertension or diabetes, or Rankin Scale Score. CONCLUSIONS: ; These data suggest that the clinical interpretation of H(e) after stroke and the eligibility for clinical trials assessing treatment for elevated H(e) levels require an adjustment in time since stroke to properly interpret the observed H(e) levels.

Acute Disease↗