title: T2 hypointensity in the deep gray matter of patients with multiple sclerosis: a quantitative magnetic resonance imaging study.
abstract: BACKGROUND
  While gray matter T2 hypointensity in multiple sclerosis (MS) has been associated with physical disability and clinical course, previous studies have relied on visual magnetic resonance imaging (MRI) assessments.
  
  
  OBJECTIVE
  To quantitatively determine if T2 hypointensity is associated with conventional MRI and clinical findings in MS.
  
  
  METHODS
  Case-control study.
  
  
  METHODS
  University-affiliated community-based hospital.
  
  
  METHODS
  Sixty patients with MS and 50 controls.
  
  
  METHODS
  T2 intensities of the substantia nigra, red nucleus, thalamus, putamen, globus pallidus, and caudate; third ventricular width; total brain T1 (hypointense) and T2 (hyperintense) lesion volumes; Expanded Disability Status Scale (physical disability) score; and disease course.
  
  
  RESULTS
  Deep gray matter T2 hypointensity was present in patients with MS in all structures (P<.005) except for the substantia nigra. T2 hypointensity was associated with third ventricle enlargement and higher T2 but not T1 plaque load. The regression model predicting third ventricle width included caudate T2 hypointensity (P =.006). The model predicting T2 lesion load included globus pallidus T2 hypointensity (P =.001). Caudate T2 hypointensity was the only variable associated with disability score in regression modeling (P =.03). All T2 hypointensities differentiated the secondary progressive from the relapsing-remitting clinical courses. The final model (P<.001) predicting clinical course retained T2 hypointensity of the thalamus, caudate, and putamen but not MRI plaques or atrophy.
  
  
  CONCLUSIONS
  Gray matter T2 hypointensity in MS is associated with brain atrophy and is a stronger predictor of disability and clinical course than are conventional MRI findings. While longitudinal studies are warranted, these results suggest that pathologic iron deposition is a surrogate marker of the destructive disease process.
authors.affiliation: Department of Neurology, University at Buffalo, State University of New York, USA. rbakshi@buffalo.edu
authors.forename: Rohit
authors.initials: R
authors.lastname: Bakshi
authors.forename: Ralph H B
authors.initials: RH
authors.lastname: Benedict
authors.forename: Robert A
authors.initials: RA
authors.lastname: Bermel
authors.forename: Shelton D
authors.initials: SD
authors.lastname: Caruthers
authors.forename: Srinivas R
authors.initials: SR
authors.lastname: Puli
authors.forename: Christopher W
authors.initials: CW
authors.lastname: Tjoa
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Fabiano
authors.forename: Lawrence
authors.initials: L
authors.lastname: Jacobs
mesh_terms: D000328:Adult; D001284:Atrophy; D001479:Basal Ganglia / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D020528:Multiple Sclerosis, Chronic Progressive / Q000473:pathology*; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000473:pathology*; D012012:Red Nucleus / Q000473:pathology; D013378:Substantia Nigra / Q000473:pathology; D013788:Thalamus / Q000473:pathology; D020542:Third Ventricle / Q000473:pathology