Cognition and Early Thalamic Atrophy

Friday, May 29, 2015
Griffin Hall
Robert T Naismith, MD , Department of Neurology, Division of Neuroimmunology, Washington University School of Medicine in St. Louis, St. Louis, MO
Vaishak A Amblee, M.D. Candidate 2017 , University of Illinois at Chicago College of Medicine, Chicago, IL
Samantha Lancia, MS , Department of Neurology, Division of Neuroimmunology, Washington University School of Medicine in St. Louis, St. Louis, MO


Cognitive deficits are seen in about 20% of all relapsing-remitting multiple sclerosis patients. Studies indicate that in addition to cortical lesions, gray matter atrophy, specifically atrophy of deep brain structures like the thalamus, may be involved in cognitive impairment.  


This study attempted to determine the relationships between neurocognitive testing and changes in thalamic volume in MS patients over a 2 year disease period.


75 MS patients underwent a comprehensive cognitive battery at month 0, 6, 12, and 24. Brain MRI with contrast was performed monthly. Cognitive domains assessed included information processing speed, visual-spatial/executive function, and verbal memory/attention. A single trained observer (IRR = 0.988) manually outlined thalamic volumes on axial MRI scans using the T2- and proton density-weighted images to determine the percent volume change over two years.  The percent change in thalamic volumes were evaluated for relationships with neurocognitive testing. 


For up to two years, 65 subjects experienced a decrease in thalamic volume, 5 demonstrated stability in thalamic volume, and 5 subjects were stable.  For those with thalamic atrophy, mean change from baseline to last scan was -8.4%. Changes in each cognitive test over 2 years did not correspond to rates of thalamic atrophy. For those with early decreases in processing speed as assessed by the WAIS Symbol Search over the first 12 month, there was a relationship between worsening processing scores and atrophy (r=0.38, p=0.003). However, between 12 through 24 months, processing speed stabilized or improved with treatment, whereas thalamic volumes continued to decline.


For subjects recently diagnosed with active MS, initiation of disease modifying therapy can be associated with stabilization or improvement in cognitive testing over the first 6-12 months. However, thalamic atrophy may continue over the first two years. This may suggest a lag period from when cognition improves and thalamic volumes stabilize, possibly due to continued neurodegeneration. Long-term data past 2 years would help determine when rates of thalamic atrophy stabilize with treatment.