20 Degenerative and Metabolic Disorders of the Brain on Magnetic Resonance Imaging

CLINICAL IMAGAGINGAN ATLAS OF DIFFERENTIAL DAIGNOSIS

EISENBERG

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

• Fig SK 20-1 Parkinson's disease. Complete loss bilaterally of the normal hyperintense band between the red nuclei and the pars reticularis of the substantia nigra.30

• Fig SK 20-2 Striatonigral degeneration. Axial T2-weighted image shows striking hypointensity in the putamen.24

• Fig SK 20-3 Olivopontocerebellar atrophy.31

Fig SK 20-4 Progressive supranuclear palsy. Axial T2-weighted scan shows atrophy of the midbrain with prominence of the perimesencephalic cisterns.32

• Fig SK 20-5 Alzheimer's disease. Axial T1-weighted scan shows bilateral temporal horn dilatation, more marked on the right, and a prominent area of decreased signal intensity in the right hippocampal region.24

• Fig SK 20-6 Pick's disease.12

• Fig SK 20-7 Huntington's chorea. (A) Coronal proton-density scan demonstrates atrophy of the caudate nuclei, associated with dilatation of the frontal horns of the lateral ventricles. (B) On an axial scan, the putamen is also small and atrophic bilaterally.32

• Fig SK 20-8 Central pontine myelinolysis. Axial T2-weighted images show (A) extensive increased signal intensity at the level of the midpons (with sparing of a thin band of tissue in the pontine tegmentum) and (B) symmetric hyperintense lesions in the cerebral peduncles (arrows).27

• Fig SK 20-9 Leigh's disease. Axial T2-weighted scan shows characteristic prominent hyperintense signal in the putamen.24

• Fig SK 20-10 Wilson's disease. Axial T2-weighted image shows increased signal intensity in the lenticular nuclei (large arrows) and the posterior aspects of the heads of the caudate nuclei (small arrow).33

• Fig SK 20-11 Hallervorden-Spatz disease. Axial T2-weighted images in a 16-year-old show striking hypointense signal in the globus pallidus (A) and substantia nigra (B) bilaterally.24

• Fig SK 20-12 Adrenoleukodystrophy. Axial T2-weighted scan demonstrates bilaterally symmetric hyperintense signal in the white matter of the occipital and parietal lobes. The posterior temporal lobe is also involved and the abnormality extends into the splenium of the corpus callosum.32