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Serial Studies (serial + studies)
Selected AbstractsFunctional colonography of Min mice using dark lumen dynamic contrast-enhanced MRIMAGNETIC RESONANCE IN MEDICINE, Issue 3 2008C. Chad Quarles Abstract Dark lumen MRI colonography detects colonic polyps by minimization of the intestinal lumen signal intensity. Here we validate the use of perfluorinated oil as an intestinal-filling agent for dark lumen MRI studies in mice, enabling the physiological characterization of colonic polyps by dynamic contrast-enhanced MRI. In control and Min (multiple intestinal neoplasia) mice with and without pretreatment with oral dextran sodium sulfate (DSS), polyps as small as 0.94 mm diameter were consistently identified using standard 2D gradient echo imaging (voxel size, 0.23 × 0.16 × 0.5 mm). In serial studies, polyp growth rates were heterogeneous with an average ,5% increase in polyp volume per day. In DSS-treated control mice the colon wall contrast agent extravasation rate constant, Ktrans, and extravascular extracellular space volume fraction, ve, values were measured for the first time and found to be 0.10 ± 0.03 min,1 and 0.23 ± 0.09, respectively. In DSS-treated Min mice, polyp Ktrans values (0.09 ± 0.04 min,1) were similar to those in the colon wall but the ve values were substantially lower (0.16 ± 0.03), suggesting increased cellular density. The functional dark-lumen colonography approach described herein provides new opportunities for the noninvasive assessment of gastrointestinal disease pathology and treatment response in mouse models. Magn Reson Med 60:718,726, 2008. © 2008 Wiley-Liss, Inc. [source] Dynamic contrast-enhanced MRI of experimental spinal cord injury: In vivo serial studiesMAGNETIC RESONANCE IN MEDICINE, Issue 4 2001Mehmet Bilgen Abstract The progression of experimental spinal cord injury (SCI) was followed with in vivo dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and neurobehavioral studies on postinjury days 0, 2, 4, 7, 10, 14, 17, 21, 28, 35, and 42. Gadopentate dimeglumine (Gd) was administered IV and postcontrast, T1 -weighted, axial images were acquired repetitively for up to 60 min. Images were analyzed to determine the spatial and temporal evolution of the intensity enhancement. A statistical decision mechanism was developed to objectively detect the enhancement. Strong and rapid enhancement was observed at the epicenter of injury, indicating a significant compromise in blood spinal cord barrier. The enhanced regions in each slice were combined to estimate the area and volume of the lesion. On the day of injury, around 85% of the total cord area at the epicenter showed enhancement within the first 15 min of Gd administration. At the same time, the enhanced volumes attained nearly 40% of the total cord volume and extended axially over 8 mm along the cord. These quantities decreased steadily with time, with a concomitant improvement in the motor functions. The volume of enhancement correlated highly with the neurobehavioral tests (r = ,0.87). DCE-MRIs revealed small hyperintense regions distributed inside white matter about two weeks postinjury. Based on histology, these enhancements appear to represent new vessels with "leaky endothelium." Magn Reson Med 45:614,622, 2001. © 2001 Wiley-Liss, Inc. [source] MOSHER AWARD HONORABLE MENTION,THE LARYNGOSCOPE, Issue 4 2000Natural History of Acoustic Neuromas Abstract Objectives/Hypothesis 1) Develop a computerized technique to accurately compare acoustic neuroma size on routine computed tomography and magnetic resonance imaging (MRI) scans; 2) use this technique to determine the growth pattern in a large series of patients with acoustic neuroma who were conservatively managed; 3) describe the natural history of patients with acoustic neuromas who did not receive surgical intervention and those who underwent subtotal resection; 4) correlate the size and growth rate of acoustic neuromas to clinical presentation and auditory and vestibular testing; and 5) recommend guidelines for the management of patients with acoustic neuromas. Study Design A retrospective study from 1974 to 1999 of patients with unilateral acoustic neuromas who had conservative treatment by serial imaging studies (80 patients) or subtotal resection (49 patients). Methods All patient charts were evaluated for presenting symptoms, reasons for the type of management given, and clinical outcome. Charts were also reviewed with respect to serial audiological assessment, electronystagmography, and brainstem auditory evoked response. Imaging studies were analyzed using a computer technique so that serial studies could be compared to determine growth rates. Results Rigorous computer analysis of tumor size and growth rate was statistically the same as the radiologist's description of the tumor size and growth rate. Of 70 patients who were older than 65 years of age old at the time their tumor was discovered, 4 (5.7%) required intervention and 18 (26%) were dead of unrelated causes. These patients had a mean follow-up of 4.8 years (range, 0.01,17.2 y). Overall, growth rate for nonsurgical patients was 0.91 mm per year. Nonsurgical tumors did not grow or regressed in 42.3%. Overall postoperative growth rate for surgical subtotal resection patients was 0.35 mm per year. Surgical tumors did not grow or regressed after subtotal resection of acoustic neuroma in 68.5% of patients. Three patients (6.1%) required revision surgery because of tumor growth or the development of symptoms. Neither auditory nor vestibular testing was a reliable measure for determining tumor growth. Conclusion Measurement of the maximal tumor diameter on MRI scans is a reliable method for following acoustic neuroma growth. There is no need to perform a rigorous analysis of tumor size to determine whether the tumor is growing significantly. The vast majority of patients older than 65 years with acoustic neuromas do not require intervention. The indications for intervention should be based on a combination of rapid tumor growth with the development of symptoms. [source] Effects of antiepileptic drugs on lipids, homocysteine, and C-reactive protein,ANNALS OF NEUROLOGY, Issue 4 2009Scott Mintzer MD Objective The widely prescribed anticonvulsants phenytoin and carbamazepine are potent inducers of cytochrome P450 enzymes, which are involved in cholesterol synthesis. We sought to determine whether these drugs have an effect on cholesterol and other serological markers of vascular risk. Methods We recruited 34 epilepsy patients taking carbamazepine or phenytoin in monotherapy whose physicians had elected to change treatment to one of the noninducing anticonvulsants lamotrigine or levetiracetam. Fasting blood samples were obtained both before and 6 weeks after the switch to measure serum lipid fractions, lipoprotein(a), C-reactive protein, and homocysteine. A comparator group of 16 healthy subjects underwent the same serial studies. Results In the epilepsy patients, switch from either phenytoin or carbamazepine produced significant declines in total cholesterol (,24.8mg/dl), atherogenic (non,high-density lipoprotein) cholesterol (,19.9mg/dl), triglycerides (,47.1mg/dl) (all p < 0.0001), and C-reactive protein (,31.4%; p = 0.027). Patients who stopped taking carbamazepine also had a 31.2% decline in lipoprotein(a) level (p = 0.0004), whereas those taken off phenytoin had a decrease in homocysteine level (,1.7,mol/L; p = 0.005). All of these changes were significant when compared with those seen in healthy subjects (p < 0.05). Results were similar whether patients were switched to lamotrigine or levetiracetam. Interpretation Switching epilepsy patients from the enzyme-inducers carbamazepine or phenytoin to the noninducing drugs levetiracetam or lamotrigine produces rapid and clinically significant amelioration in several serological markers of vascular risk. These findings suggest that phenytoin and carbamazepine may substantially increase the risk for cardiovascular and cerebrovascular disease. Ann Neurol 2009;65:448,456 [source] | ||||||||||