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Fig. 8. Serial axial FLAIR MR images in a patient with features of frontotemporal dementia at age 79 (A), which then evolves to include nonfluent aphasia at age 81 (B) and corticobasal syndrome findings at age 82 (C).

matter, most often in superior frontal gyrus, superior parietal gyrus, pre- and postcentral gyri, and striatum (Fig. 17). Tau+ oligodendroglial coiled bodies are also common (Fig. 18). While achromatic, ballooned neurons that are immunoreactive to phosphorylated neurofilament or aB-crystallin are typically present in CBD (Fig. 19), their absence does not preclude the diagnosis of CBD if the appropriate tau+ lesions are present. These criteria have been validated (Litvan et al., in preparation).

These pathological features are indistinguishable from those in frontotemporal dementia and par-kinsonism linked to chromosome 17 (FTDP-17) (46). Thus, knowledge about the family history and molecular genetics is necessary to adequately classify cases with CBD-type pathology.

Fig. 9. Sagittal T1-weighted (A), axial FLAIR (B), and coronal T1-weighted (C) MR images in a patient who presented with the posterior cortical atrophy syndrome (i.e., Balint's syndrome, Gerstmann's syndrome, etc.) and subsequently developed classic corticobasal syndrome features.
Fig. 10. Axial FLAIR MR images in a patient with the corticobasal syndrome, showing focal increased signal in the left posterior frontal white matter. Autopsy revealed corticobasal degeneration with significant tau-positive glial pathology in this region.
Fig. 11. Axial FLAIR MR images in a patient with the corticobasal syndrome, showing focal increased signal in the right frontal > parietal white matter. Autopsy revealed corticobasal degeneration with significant tau-positive glial pathology in this region.

Age 71 Age 72 Age 73

Fig. 12. Serial axial FLAIR MR images in a patient with the corticobasal syndrome, showing progressive focal increased signal evolving in the periventricular and subcortical white matter of the left parietal region.

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