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Anterior-medial thalamic lesions in dementia: frequent, and volume dependently associated with sudden cognitive decline
  1. R H Swartz,
  2. S E Black
  1. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada
  1. Correspondence to:
 R H Swartz
 Room A-421, Sunnybrook Health Sciences Centre, 2075 Bayview Avenue, Toronto, Ontario, Canada M4N 3M5;rick.swartz{at}utoronto.ca

Abstract

Background: The anterior-medial thalamus (AMT), which is associated with memory processing, is severely affected by Alzheimer’s disease pathology and, when damaged, can be the sole cause of dementia.

Objective: To assess the frequency of magnetic resonance imaging (MRI) hyperintensities affecting the AMT, and their relationship with sudden cognitive decline.

Methods: 205 consecutive participants from a university cognitive neurology clinic underwent clinical evaluation, neuropsychological testing and quantitative MRI.

Results: AMT hyperintensities >5 mm3 occurred in 0 of 34 normal controls but were found in 5 of 30 (17%) participants with cognitive impairment with no dementia (CIND), 9 of 109 (8%) patients with probable Alzheimer’s disease, 7 of 17 (41%) with mixed disease and 8 of 15 (53%) with probable vascular dementia (VaD). AMT hyperintensities occurred more often in participants with stepwise decline than in those with slow progression (χ2 = 31.7; p<0.001). Of the 29 people with AMT hyperintensities, those with slow progression had smaller medial temporal width (p<0.001) and smaller anterior-medial thalamic hyperintensities (p<0.001). In a logistic regression model, both variables were significant, and the pattern of decline was correctly classified in 86% of the sample (Cox and Snell R2 = 0.56; p<0.001). Those with AMT hyperintensities >55 mm3 were likely to have stepwise decline in cognitive function regardless of medial temporal lobe width; in contrast, those with smaller AMT hyperintensities showed a stepwise decline only in the absence of medial temporal lobe atrophy. All patients with VaD had left-sided AMT hyperintensities, whereas those with CIND had right-sided AMT hyperintensities.

Conclusions: AMT hyperintensities >55 mm3 probably result in symptomatic decline, whereas smaller lesions may go unrecognised by clinicians and radiologists. Only half of those with AMT hyperintensities had diagnoses of VaD or mixed disease; the other AMT hyperintensities occurred in patients diagnosed with Alzheimer’s disease or CIND. These silent hyperintensities may nevertheless contribute to cognitive dysfunction. AMT hyperintensities may represent a major and under-recognised contributor to cognitive impairment.

  • AMT, anterior-medial thalamus
  • CIND, cognitive impairment, no dementia
  • CVD, cerebrovascular disease
  • MRI, magnetic resonance imaging
  • MTLW, medial temporal lobe width
  • VaD, vascular dementia

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Footnotes

  • Published Online First 25 July 2006

  • Funding: This study was funded by the Canadian Institute of Health Research (CIHR) grant number MT13129 to SEB, and personal support was provided from CIHR with an MD/PhD studentship to RHS.

  • Competing interests: None declared.

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