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G R Wayne Moore

Publications and source records attributed to G R Wayne Moore.

4 recordsLinked to original sources
PubMed2006

Three-tesla magnetic resonance imaging of the ventrolateral thalamus: a correlative anatomical description.

OBJECT: Surgery for tremor targets the ventrolateral nuclei of the thalamus. An initial radiological estimation of this target can be further refined through intraoperative physiological confirmation. Direct visualization of these nuclei has not yet been described. The improved signal-to-noise ratio associated with 3-tesla (3T) magnetic resonance (MR) imaging makes increased spatial resolution possible, which may aid in the identification of subtle morphological features. This study was conducted to describe the anatomy of the nuclei and fiber projections within the ventral thalamus by using 3T MR imaging. METHODS: Using a commercially available 3T MR unit, the authors obtained images of a formalin-fixed, paraffin-embedded brain. Slices with a 2-mm thickness and 0.2-mm gap were obtained parallel to the anterior commissure-posterior commissure (AC-PC) line. The brain was then sectioned through the cerebral hemispheres to obtain tissue slices encompassing the same levels. Adjacent 10-microm paraffin sections from the middle of each level were stained with Luxol fast blue and cresyl violet. The MR image and histological sections at the level of the AC-PC line were then compared in detail. In a separate study, the human thalamus was scanned in vivo using 3T and 1.5T MR imaging for anatomical comparison. CONCLUSIONS: The anatomy of the nuclei and fiber projections within the ventrolateral thalamus in humans can be described using 3T MR imaging. The findings were reproducible in vivo with 3T but not 1.5T MR imaging. Additional studies are needed to confirm the accuracy of this observation for clinical purposes.

Artifacts↗
PubMed2003

MRI-clinical correlations: more than inflammation alone-what can MRI contribute to improve the understanding of pathological processes in MS?

Magnetic resonance imaging (MRI) is a sensitive technique in the detection and follow-up of multiple sclerosis (MS) lesions. However, the pathologic basis of these changes is poorly understood. It is becoming increasingly apparent that routine MRI techniques do not represent specific histopathologic changes but reflect a variety of pathological changes in tissue. This review will outline the findings in MRI-pathology correlation in MS to date, and the current understanding of the evolution of pathologic changes in the MS lesion and non-lesional white matter as reflected by MRI. Possible future contributions of MRI to unveiling the dynamic pathology of MS will also be discussed.

Brain↗
PubMed2003

Dendritic and synaptic pathology in experimental autoimmune encephalomyelitis.

Evidence has shown that excitotoxicity may contribute to the loss of central nervous system axons and oligodendrocytes in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). Because dendrites and synapses are vulnerable to excitotoxicity, we examined these structures in acute and chronic models of EAE. Immunostaining for microtubule-associated protein-2 showed that extensive dendritic beading occurred in the white matter of the lumbosacral spinal cord (LSSC) during acute EAE episodes and EAE relapses. Retrograde labeling confirmed that most motoneuron dendrites were beaded in the white matter of the LSSC in acute EAE. In contrast, only mild swelling was observed in the gray matter of the LSSC. Dendritic beading showed marked recovery during EAE remission and after EAE recovery. In addition, synaptophysin, synapsin I, and PSD-95 immunoreactivities were significantly reduced in both the gray and white matter of the LSSC during acute EAE episodes and EAE relapses, but showed partial recovery during EAE remission and after EAE recovery. Pathologically, both dendritic beading and the reduction in synaptic protein immunoreactivity were well correlated with inflammatory cell infiltration in the LSSC at different EAE stages. We propose that dendritic and synaptic damage in the spinal cord may contribute to the neurological deficits in EAE.

Acute Disease↗