Abstract
Cognitive dysfunction and emotional–behavioral changes are symptoms with increasing clinical relevance during progression of the disease. They cannot be explained by demyelination of white matter alone but clearly indicate cortical dysfunction. Positron emission tomography (PET) provides methods to assess cortical dysfunction quantitatively by measuring cerebral glucose metabolism using the tracer 18F-2-fluoro-2-deoxy- d-glucose (FDG). The technique has been employed to study fatigue and disease progression. Microglial activation was studied by 11C-PK-11195 PET. It was found not only in active plaques but also in degenerating fibre tracks. Other tracers offer a broad spectrum of measuring local physiological functions and pathophysiological processes, but some of them are still limited to experimental animal research.
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