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Nils Bodammer

Publications and source records attributed to Nils Bodammer.

5 recordsLinked to original sources
PubMed2006

Age-related water diffusion changes in human brain: a voxel-based approach.

The aim of the present study is to investigate age-related changes in water self-diffusion in cerebral white matter by analysing diffusion-weighted MRI from a sample of 54 healthy volunteers. A voxel-based analysis of the relative anisotropy and the apparent diffusion coefficients was performed by applying an optimized normalization protocol. Linear regression analysis revealed significant correlations with age in the corpus callosum, prefrontal regions, the internal capsule, the hippocampal complex, and the putamen. However, in other regions, such as those surrounding the ventricles, the insula, or the inferior frontal plane, significant correlations between age and ADC were observed, presumably as a result of morphological age-related variations. A mask procedure was carried out in order to distinguish between morphological involvement and real age-related white matter changes. Our results indicate that in interpreting the changes in each significant region it is necessary to proceed with precaution because the voxel-based statistical analysis might yield a mixture of two effects: (i) morphological changes that remain after the normalization procedure and (ii) actual diffusivity parameter changes. Anatomically defined regions of interest may help us to minimize morphologic involvement and draw comparisons with findings previously published.

Adult↗
PubMed2004

Eddy current correction in diffusion-weighted imaging using pairs of images acquired with opposite diffusion gradient polarity.

In echo-planar-based diffusion-weighted imaging (DWI) and diffusion tensor imaging (DTI), the evaluation of diffusion parameters such as apparent diffusion coefficients and anisotropy indices is affected by image distortions that arise from residual eddy currents produced by the diffusion-sensitizing gradients. Correction methods that coregister diffusion-weighted and non-diffusion-weighted images suffer from the different contrast properties inherent in these image types. Here, a postprocessing correction scheme is introduced that makes use of the inverse characteristics of distortions generated by gradients with reversed polarity. In this approach, only diffusion-weighted images with identical contrast are included for correction. That is, non-diffusion-weighted images are not needed as a reference for registration. Furthermore, the acquisition of an additional dataset with moderate diffusion-weighting as suggested by Haselgrove and Moore (Magn Reson Med 1996;36:960-964) is not required. With phantom data it is shown that the theoretically expected symmetry of distortions is preserved in the images to a very high degree, demonstrating the practicality of the new method. Results from human brain images are also presented.

Algorithms↗
PubMed2004

Differentiation of idiopathic Parkinson's disease, multiple system atrophy, progressive supranuclear palsy, and healthy controls using magnetization transfer imaging.

The differentiation of multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) from idiopathic Parkinson's disease (IPD) is difficult. Magnetization transfer imaging (MTI), a measure that correlates with myelination and axonal density, was employed in this study in the attempt to distinguish between these disorders. Measurements were carried out in 15 patients with IPD, 12 patients with MSA, 10 patients with PSP, and in 20 aged-matched healthy control subjects. The main finding was a change in the magnetization transfer ratio in the globus pallidus, putamen, caudate nucleus, substantia nigra, and white matter in IPD, MSA, and PSP patients, matching the pathological features of the underlying disorder. Furthermore, stepwise linear discriminant analysis provided a good classification of the individual patients into the different disease groups. All IPD patients and control subjects were correctly separated from the MSA and PSP cohort, and all PSP patients and 11 of 12 MSA patients were correctly separated from the IPD and control cohort. There was also a fairly good discrimination of IPD patients from control subjects and of MSA from PSP patients. In conclusion, MTI revealed degenerative changes in patients with different parkinsonian syndromes matching the underlying pathological features of the different diseases, underlining the high potential of this method in distinguishing MSA and PSP from IPD.

Aged↗
PubMed2003

Focal thinning of the cerebral cortex in multiple sclerosis.

Brain atrophy as determined by quantitative MRI can be used to characterize disease progression in multiple sclerosis. Many studies have addressed white matter (WM) alterations leading to atrophy, while changes of the cerebral cortex have been studied to a lesser extent. In vivo, the cerebral cortex has been difficult to study due to its complex structure and regional variability. Measurement of cerebral cortex thickness at different disease stages may provide new insights into grey matter (GM) pathology. In the present investigation, we evaluated in vivo cortical thickness and its relationship to disability, disease duration, WM T2 hyper-intense and T1 hypo-intense lesion volumes. High-resolution MRI brain scans were obtained in 20 patients with clinically definite multiple sclerosis and 15 age-matched normal subjects. A novel method of automated surface reconstruction yielded measurements of the cortical thickness for each subject's entire brain and computed cross-subject statistics based on the cortical anatomy. Statistical thickness difference maps were generated by performing t-tests between patient and control groups and individual thickness measures were submitted to analyses of variance to investigate the relationship between cortical thickness and clinical variables. The mean overall thickness of the cortical ribbon was reduced in multiple sclerosis patients compared with controls [2.30 mm (SD 0.14) versus 2.48 mm (SD 0.11)], showing a significant main effect of group (controls versus patients). In patients, we found significant main effects for disability, disease duration, T2 and T1 lesion volumes. The visualization of statistical difference maps of the cortical GM thickness on inflated brains across the cortical surface revealed a distinct distribution of significant focal thinning of the cerebral cortex in addition to the diffuse cortical atrophy. Focal cortical thinning in frontal [2.37 mm (SD 0.17) versus 2.73 mm (SD 0.25)] and in temporal [2.65 mm (SD 0.15) versus 2.95 mm (SD 0.11)] brain regions was observed, even early in the course of the disease or in patients with mild disability. Patients with longstanding disease or severe disability, however, presented additionally with focal thinning of the motor cortex area [2.35 mm (SD 0.19) versus 2.74 mm (SD 0.15)]. We conclude that in vivo measurement of cortical thickness is feasible in patients suffering from multiple sclerosis. The data provide new insight into the cortical pathology in multiple sclerosis patients, revealing focal cortical thinning beside an overall reduction of the cortical thickness with disease progression.

Adult↗