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Chronic Progressive External Ophthalmoplegia: MR Spectroscopy and MR Diffusion Studies in the Brain

Jens O. Heidenreich1,2, Thomas Klopstock3, Timo Schirmer2, Philipp Saemann2, Wolfgang Mueller-Felber4 and Dorothee P. Auer2

1 Department of Radiology and Nuclear Medicine, Charité Campus Benjamin Franklin, Hindenburgdamm 30, Berlin, Germany 12200.
2 Department of Radiology, Max-Planck-Institute of Psychiatry, AG NMR, Munich, Germany
3 Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilians-University, Munich, Germany.
4 Friedrich-Baur-Institute, Munich, Germany.


Figure 1
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  		Fig. 1A —Axial FLAIR images of patient 4, 26-year-old man with chronic progressive external ophthalmoplegia plus. Arrows show signal hyperintensities in pyramidal tract.

 

Figure 2
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  		Fig. 1B —Axial FLAIR images of patient 4, 26-year-old man with chronic progressive external ophthalmoplegia plus. Arrows show signal hyperintensities in subcortical white matter that can be traced through pyramidal tract.

 

Figure 3
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  		Fig. 2A —Axial T2-weighted images of patient 9, 20-year-old woman with Kearns-Sayre syndrome. Arrows show signal hyperintensities in cerebellar peduncles.

 

Figure 4
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  		Fig. 2B —Axial T2-weighted images of patient 9, 20-year-old woman with Kearns-Sayre syndrome. Arrows show signal hyperintensities in thalamus.

 

Figure 5
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  		Fig. 3 —Box plots showing N-acetylaspartate (NAA) normalized to creatine (CR) in three different brain regions (cortex and right and left white matter [WM]) for patients with chronic progressive external ophthalmoplegia (gray boxes) and age-matched controls (white boxes). O = outliers.

 

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