title: Imaging correlates of pathology in corticobasal syndrome.
abstract: BACKGROUND
  Corticobasal syndrome (CBS) can be associated with different underlying pathologies that are difficult to predict based on clinical presentation. The aim of this study was to determine whether patterns of atrophy on imaging could be useful to help predict underlying pathology in CBS.
  
  
  METHODS
  This was a case-control study of 24 patients with CBS who had undergone MRI during life and came to autopsy. Pathologic diagnoses included frontotemporal lobar degeneration (FTLD) with TDP-43 immunoreactivity in 5 (CBS-TDP), Alzheimer disease (AD) in 6 (CBS-AD), corticobasal degeneration in 7 (CBS-CBD), and progressive supranuclear palsy in 6 (CBS-PSP). Voxel-based morphometry and atlas-based parcellation were used to assess atrophy across the CBS groups and compared to 24 age- and gender-matched controls.
  
  
  RESULTS
  All CBS pathologic groups showed gray matter loss in premotor cortices, supplemental motor area, and insula on imaging. However, CBS-TDP and CBS-AD showed more widespread patterns of loss, with frontotemporal loss observed in CBS-TDP and temporoparietal loss observed in CBS-AD. CBS-TDP showed significantly greater loss in prefrontal cortex than the other groups, whereas CBS-AD showed significantly greater loss in parietal lobe than the other groups. The focus of loss was similar in CBS-CBD and CBS-PSP, although more severe in CBS-CBD.
  
  
  CONCLUSIONS
  Imaging patterns of atrophy in CBS vary according to pathologic diagnosis. Widespread atrophy points toward a pathologic diagnosis of FTLD-TDP or AD, with frontotemporal loss suggesting FTLD-TDP and temporoparietal loss suggesting AD. On the contrary, more focal atrophy predominantly involving the premotor and supplemental motor area suggests CBD or PSP pathology.
authors.affiliation: Department of Radiology, Mayo Clinic, 200 1st Street SW, Rochester, MN 55905, USA. whitwell.jennifer@mayo.edu
authors.forename: J L
authors.initials: JL
authors.lastname: Whitwell
authors.forename: C R
authors.initials: CR
authors.lastname: Jack
authors.forename: B F
authors.initials: BF
authors.lastname: Boeve
authors.forename: J E
authors.initials: JE
authors.lastname: Parisi
authors.forename: J E
authors.initials: JE
authors.lastname: Ahlskog
authors.forename: D A
authors.initials: DA
authors.lastname: Drubach
authors.forename: M L
authors.initials: ML
authors.lastname: Senjem
authors.forename: D S
authors.initials: DS
authors.lastname: Knopman
authors.forename: R C
authors.initials: RC
authors.lastname: Petersen
authors.forename: D W
authors.initials: DW
authors.lastname: Dickson
authors.forename: K A
authors.initials: KA
authors.lastname: Josephs
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000150:complications / Q000473:pathology; D001284:Atrophy; D001479:Basal Ganglia / Q000473:pathology*; D001927:Brain Diseases / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism; D002102:Cadaver; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000473:pathology*; D004268:DNA-Binding Proteins / Q000378:metabolism; D005260:Female; D005625:Frontal Lobe / Q000473:pathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000473:pathology; D010296:Parietal Lobe / Q000473:pathology; D010487:Periaqueductal Gray / Q000473:pathology; D017397:Prefrontal Cortex / Q000473:pathology; D013494:Supranuclear Palsy, Progressive / Q000150:complications / Q000473:pathology; D013577:Syndrome; D013702:Temporal Lobe / Q000473:pathology
chemical_list: D004268:DNA-Binding Proteins