Biomedical subjects
M A van Buchem
Publications and source records attributed to M A van Buchem.
Correlation of volumetric magnetization transfer imaging with clinical data in MS.
We examined the relations between quantitative volumetric estimates of cerebral lesion load based on magnetization transfer imaging (MTI), clinical data, and measures of neuropsychological function in 44 patients with clinically diagnosed MS. In this population we assessed the correlation between several volumetric MTI measures, measures of neurologic function (Kurtzke Expanded Disability Status Scale and Ambulation Index), and disease duration using Spearman's correlation coefficient. Patients were classified on the basis of neuropsychological test performance as severely impaired, moderately impaired, and normal. We assessed differences between these groups with respect to MTI results using the Kruskal-Wallis test. MTI measures corrected for brain volume were found to correlate with disease duration (p < 0.01) and showed suggestive correlations with measures of neurologic impairment (p < 0.05). Individual neuropsychological tests correlated with MTI measures corrected and not corrected for brain volume (p < 0.001). An MTI measure not corrected for brain volume differed (p < 0.05) between severely impaired, moderately impaired, and normal patients. These preliminary results suggest that volumetric MTI analysis provides new measures that reflect more accurately the global lesion load in the brain of MS patients, and they may serve as a method to study the natural course of the disease and as an outcome measure to evaluate the effect of drugs.
Multiple sclerosis lesion quantification using fuzzy-connectedness principles.
Multiple sclerosis (MS) is a disease of the white matter. Magnetic resonance imaging (MRI) is proven to be a sensitive method of monitoring the progression of this disease and of its changes due to treatment protocols. Quantification of the severity of the disease through estimation of MS lesion volume via MR imaging is vital for understanding and monitoring the disease and its treatment. This paper presents a novel methodology and a system that can be routinely used for segmenting and estimating the volume of MS lesions via dual-echo fast spin-echo MR imagery. A recently developed concept of fuzzy objects forms the basis of this methodology. An operator indicates a few points in the images by pointing to the white matter, the grey matter, and the cerebro-spinal fluid (CSF). Each of these objects is then detected as a fuzzy connected set. The holes in the union of these objects correspond to potential lesion sites which are utilized to detect each potential lesion as a three-dimensional (3-D) fuzzy connected object. These objects are presented to the operator who indicates acceptance/rejection through the click of a mouse button. The number and volume of accepted lesions is then computed and output. Based on several evaluation studies, we conclude that the methodology is highly reliable and consistent, with a coefficient of variation (due to subjective operator actions) of 0.9% (based on 20 patient studies, three operators, and two trials) for volume and a mean false-negative volume fraction of 1.3%, with a 95% confidence interval of 0%-2.8% (based on ten patient studies).
Computer-assisted quantitation of enhancing lesions in multiple sclerosis: correlation with clinical classification.
PURPOSE: To study the utility of a computer-assisted method of quantitating enhancing multiple sclerosis (MS) lesions and to correlate this quantitation with the type and duration of disease. METHODS: Forty untreated patients with MS were studied. The patients had been classified clinically as having either relapsing-remitting (n = 27) or chronic-progressive (n = 13) disease. Postcontrast contiguous 3-mm-thick MR images of the brain were obtained for up to 3 years. The computer program selected potential lesion sites automatically on the basis of the theory of "fuzzy connectedness," which was incorporated into 3DVIEWNIX software. True lesions were selected from these previously detected potential lesions by means of yes/no responses to the program query. The number of enhancing lesions and the enhancing lesions volume were subsequently computed. RESULTS: The enhancing lesion volume in patients with relapsing-remitting disease was statistically significantly higher than that of patients with chronic-progressive disease. There was a strong positive correlation between the number of enhancing lesions and the enhancing lesion volume. No significant correlation was noted between the change in score on the expanded disability status scale (EDSS) and the change in the number of enhancing lesions, or between the change in EDSS score and the change in enhancing lesion volume. A negative correlation was found between enhancing lesion volume and duration of disease, and between the number of enhancing lesions and duration of disease in the patients who had enhancing lesions. CONCLUSIONS: Our data suggest that enhancing lesion volume reflects differences in the classification of clinical MS and in the disease activity over time. Computer-assisted quantitation of enhancing lesion volume is a robust, practical, and objective measure of MS activity.
Global volumetric estimation of disease burden in multiple sclerosis based on magnetization transfer imaging.
We report a semiautomated postprocessing method based on magnetization transfer MR imaging that can quantify the extent of global disease in patients with multiple sclerosis. The technique combines segmentation and quantitative analysis of imaging data reflecting the structural integrity of white matter. Applications of this technique may include assessment of disease progress and of the efficacy of experimental therapeutic intervention. The height of the histogram peak corresponding to white matter was found to be lowered in patients with multiple sclerosis and the overall distribution of magnetization transfer ratios was shifted to lower values.
White matter lesions and cognitive deterioration in presymptomatic carriers of the amyloid precursor protein gene codon 693 mutation.
OBJECTIVE: To determine early manifestations of hereditary cerebral hemorrhage with amyloidosis (Dutch). DESIGN: Survey. SETTING: Neurologic outpatient department of the University Hospital Leiden in the Netherlands. PARTICIPANTS: Ten presymptomatic carriers of the amyloid precursor protein gene codon 693 mutation. MAIN OUTCOME MEASUREMENTS: Extensive neuropsychological examination and cerebral magnetic resonance imaging. RESULTS: Six subjects older than 40 years showed white matter hyperintensities on magnetic resonance imaging. Three of these six individuals had signs of cognitive deterioration. The four younger subjects (age, < 31 years) showed no abnormalities on magnetic resonance imaging or on neuropsychological examination. CONCLUSIONS: We suggest that white matter hyperintensities in hereditary cerebral hemorrhage with amyloidosis (Dutch) are probably caused by chronic ischemia due to stenosis of the meningocortical arterioles, which becomes visible on magnetic resonance imaging scans in individuals who are between the ages of 30 and 40 years. The finding of cognitive deterioration in three of 10 presymptomatic mutation carriers supports the finding that in hereditary cerebral hemorrhage with amyloidosis (Dutch), deterioration can occur without stroke. A direct relation between cognitive deterioration and white matter hyperintensities is unlikely, because only half of the individuals with white matter hyperintensities showed signs of deterioration.
Quantitative volumetric magnetization transfer analysis in multiple sclerosis: estimation of macroscopic and microscopic disease burden.
Magnetization transfer imaging (MTI) has been shown to be sensitive to both macroscopic and microscopic disease in multiple sclerosis (MS). In this study three-dimensional MTI was used to estimate the global burden of disease in large volumes of brain tissue. MTI was performed in 15 MS patients and 11 normal controls. In seven MS patients MTI was performed on two different occasions. MTI data were displayed as magnetization transfer ratio (MTR) histograms and analyzed. The peak height of the histograms, presumably reflecting the residual amount of normal brain tissue, was lower in MS patients as compared with normal controls (P < 0.001), and was found to correlate with the duration of disease (P < 0.05). A decrease of the MTR histogram peak height was observed in the course of the disease (P < 0.01). These findings suggest that in MS, volumetric MTI provides quantitative information reflecting the global burden of disease.
Calcified meningioma of the skull base simulating chondrosarcoma.
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Reversible neurotoxicity during interleukin-2 therapy for metastatic renal cell carcinoma.
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A case of typhoid fever complicated by unexpected diffuse cerebral edema.
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Endothelial activation antigens in pulmonary leukostasis in leukemia.
Adhesion between leukemic cells and the vascular endothelium has been suggested to play a role in the development of leukostasis in myelocytic leukemia. To define the role of adhesion molecules on the surface of endothelial cells in leukostasis, we used immunohistochemistry to study the expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in lung tissue of 4 patients with pulmonary leukostasis. Lung tissue of 2 patients with myelocytic leukemia without leukostasis and 4 patients with irrelevant nonpulmonary disease was used as a negative control. Positive control tissues included a lymph node with angioimmunoblastic lymphadenopathy and a hyperplastic tonsil. Weak positive staining for ELAM-1 was found in 1 patient in vessels, both with and without leukostasis. Expression of VCAM-1 and ICAM-1 in all patients tested was similar to that in the negative controls. The results of this study suggest that activation of endothelium, with increased expression of the endothelial adhesion molecules under study, is not a prerequisite for the development of pulmonary leukostasis in leukemia.
Involvement of the complement system in the pathogenesis of pulmonary leukostasis in experimental myelocytic leukemia.
The role of the complement system in the pathogenesis of pulmonary leukostasis in myelocytic leukemia was studied in a rat model. Acute myelocytic leukemia was induced in six Brown-Norway rats, and complement levels were assayed during the course of the disease. Whole complement activity (CH50) and hemolytic activity of C1q, C3, and C4 decreased from day 16 after induction of the leukemia, when the rats developed pulmonary leukostasis. In addition, local complement activation was established in the lung vessels by immunofluorescence microscopy in advanced stages of pulmonary leukostasis. Finally, following systemic activation of the complement system by injection of cobra venom factor (CVF), leukemic rats (n = 6) died of pulmonary leukostasis 4.5 days earlier than did leukemic controls (n = 6). These findings suggest that, in acute myelocytic leukemia in Brown-Norway rats, pulmonary leukostasis is induced by activation of the complement system. This finding could lead to new modes of treatment for a life-threatening complication of leukemia.
Development of pulmonary leukostasis in experimental myelocytic leukemia in the Brown-Norway rat.
The pathogenesis of pulmonary leukostasis in leukemia was studied in a rat model by investigating the course of its development. Leukemia was induced by inoculating rats with leukemic cells. The earliest stage of leukostasis was found from day 14 onward, when leukemic cells appeared in the peripheral blood, and was characterized by accumulation of leukemic cells at the capillary level. Simultaneous with the increase of leukemic cell concentrations in the peripheral blood, accumulation in capillaries increased gradually over a period of several days. This was accompanied by increasing severity of tachypnea. Shortly before death, aggregates consisting almost solely of leukemic cells were found in medium-sized blood vessels. This stage was rapidly followed by the end-stage, characterized by complete obstruction of the lung vasculature--including the largest arteries and veins--by leukemic cell aggregates, giving rise to extensive hemorrhages and edema. The end-stage was considered to be the cause of death, which occurred 18-26 days after the inoculation. The histological and ultrastructural findings in this study suggest that besides the size and stiffness of individual leukemic cells, interactions not only between leukemic cells, but also between leukemic cells and the endothelium play a role in the pathogenesis of pulmonary leukostasis.
Experimental myelocytic leukemia in the Brown-Norway rat as a model for pulmonary leukostasis.
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[A cause of acute dyspnea: leukostasis].
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Leucostasis, an underestimated cause of death in leukaemia.
Massive sludging of leukaemic cells in blood vessels is a frequent and often lethal complication of leukaemia. In a retrospective clinicopathological study on the causes of death in 52 patients with acute myeloid leukaemia and myeloproliferative disease, pulmonary leucostasis was found in 40% of the patients. In many of these patients the vessels of the heart, brain and testes were also involved. In search for signs and symptoms specific for leucostasis, the clinical records of the 21 patients with leucostasis (the study group) were compared to those of 20 patients without leucostasis (the control group). Dysfunction of the organs most affected by leucostasis, namely lungs, heart and brain, was found more often in the study group than in the controls, but the combination of unexplained fever with cardiopulmonary and/or central nervous system failure occurred almost exclusively and in half of the patients with leucostasis. Leucostasis occurs predominantly, but not exclusively, in patients with high leucocyte counts, and especially, but again not exclusively, when the leucocyte counts rise sharply.
Pulmonary leukostasis: radiologic-pathologic study.
The terminal chest radiographs of ten patients with pulmonary leukostasis were correlated with the autopsy findings. In six patients, no abnormalities attributable to leukostasis were seen on chest radiographs. In four patients, diffuse alveolar consolidations were caused by alveolar edema following leukostasis. Leukostasis should be considered in leukemia patients with severe dyspnea who have normal chest radiographs or diffuse alveolar edema.
Septicaemia, meningitis and spondylodiscitis caused by Streptococcus suis type 2.
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