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Research Article| Volume 29, ISSUE 1, P68-81, January 01, 1991

Cerebral structure on MRI, part II: Specific changes in Alzheimer's and Huntington's diseases

  • Terry L. Jernigan
    Correspondence
    Address requests to Dr. Terry L. Jernigan, Department of Psychiatry, University of California, San Diego, 0631, 9500 Gilman Drive, La Jolla CA 92093-0631, USA
    Affiliations
    From the VA Medical Center, the University of California, San Diego, CA, USA

    Department of Psychiatry, the University of California, San Diego, CA, USA

    Department of Radiology, the University of California, San Diego, CA, USA
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  • David P. Salmon
    Affiliations
    The Alzheimer's Disease Research Center, the University of California, San Diego, CA, USA

    Neurosciences, the University of California, San Diego, CA, USA
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  • Nelson Butters
    Affiliations
    From the VA Medical Center, the University of California, San Diego, CA, USA

    Department of Psychiatry, the University of California, San Diego, CA, USA
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  • John R. Hesselink
    Affiliations
    Department of Radiology, the University of California, San Diego, CA, USA

    Neurosciences, the University of California, San Diego, CA, USA
    Search for articles by this author
DOI:https://doi.org/10.1016/0006-3223(91)90211-4
Cerebral structure on MRI, part II: Specific changes in Alzheimer's and Huntington's diseases
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      Abstract

      Using magnetic resonance (MR) imaging and morphometric techniques, groups of patients with Alzheimer's disease (AD) and Huntington's disease (HD) were compared with a large group of normal control subjects. Measures of volume loss in specific subcortical nuclei and eight cortical regions as well as an index of white matter abnormality were obtained. Results indicated expected widespread cortical volume reductions in AD, which were especially severe in mesial cortices; but comparable reductions were present in subcortical structures, particularly the thalamus. In HD, the greatest reductions were present in striatal structures, but significant abnormalities were also detected in the thalamus and inferior cortical areas, especially in mesial temporal lobe structures. Significant degeneration in white matter was present in both groups, but was more dramatic in the HD patients. The significant diencephalic reduction in AD may make an important contribution to early memory deficits in the disorder, which are usually attributed to hippocampal damage. Similarly, damage to both the thalamus and mesial temporal lobe structures may play a role in the memory deficits of HD.
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      Article info

      Publication history

      Received in revised form: July 5, 1990
      Received: April 26, 1990

      Footnotes

      ☆This investigation was supported by funds from the Medical Research Service of the Veterans Administration to Dr. Terry Jernigan and Dr. Nelson Butters, and by NIA grants AG 08204 and AG 05131 to the University of California. Special thanks are due to the staff of the UCSD Alzheimer's Disease Research Center for their assistance. Some of the results reported here were presented at the meeting of the American Academy of Neurology in Chicago in 1989.

      Identification

      DOI: https://doi.org/10.1016/0006-3223(91)90211-4

      Copyright

      © 1991 Published by Elsevier Inc.

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