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J Neurol Neurosurg Psychiatry doi:10.1136/jnnp.2008.158881

White matter hyperintensities and medial temporal lobe atrophy in clinical subtypes of mild cognitive impairment: the DESCRIPA study

  1. laura van de pol (l.vandepol{at}vumc.nl)
  1. vumc, Netherlands
    1. Frans Verhey (f.verhey{at}np.unimaas.nl)
    1. Department of Psychiatry and Neuropsychology, University of Maastricht, Netherlands
      1. Giovanni Frisoni (gfrisoni{at}oh-fbf.it)
      1. IRCCS San Giovanni, Laboratory of Epidemiology and Neuroimaging, Brescia, Italy
        1. magda tsolaki (tsolakim{at}hellasnet.gr)
        1. Aristotle University of Thessaloniki, Memory and Dementia Centre, 3rd Department of Neurology, G. Pa, Greece
          1. Panagiota Papapostoulou (papapostoula{at}hotmail.com)
          1. Papageorgiou Hospital, Department of Radiology, Thessaloniki, Greece
            1. Flavio Nobili (flaviomariano.nobili{at}hsanmartino.liguria.it)
            1. Clinical Neurophysiology Service, Dept of Endocrinological and Metabolic Sciences, University of Ge, Italy
              1. Lars-Olof Wahlund (lars-olof.wahlund{at}neurotec.ki.se)
              1. NVS Department, Karolinska Institutet, Karolinska University Hospital, Huddinge, Sweden
                1. Lennart Minthon (lennart.minthon{at}skane.se)
                1. Clinical Memory Research Unit, Dept of Clinical Sciences, Malmö, Lund University, United Kingdom
                  1. Lutz Frolich (froelich{at}zi-mannheim.de)
                  1. Dept of Geriatric Psychiatry, Zentralinstitut für Seelische Gesundheit, University of Heidelberg, Ma, Germany
                    1. Harald Hampel (hampel{at}med.uni-muenchen.de)
                    1. Alzheimer Memorial Centre and Geriatric Psychiatry Branch, Dementia and Neuroimaging Section Departm, Germany
                      1. Hilkka Soininen (hilkka.soininen{at}uku.fi)
                      1. University of Kuopio, Department of Neurology, Kuopio University Hospital, Kuopio, Finland
                        1. dirk knol (d.knol{at}vumc.nl)
                        1. Department of Clinical Epidemiology and Biostatistics, VU Medical Centre, Amsterdam, Netherlands
                          1. Frederik Barkhof (f.barkhof{at}vumc.nl)
                          1. Department of Radiology, Alzheimer Centre, VU Medical Centre, Amsterdam, Netherlands
                            1. philip scheltens (p.scheltens{at}vumc.nl)
                            1. Department of Neurology, Alzheimer Centre, VU Medical Centre, Amsterdam, Netherlands
                              1. Pieter Jelle Verhey (pj.visser{at}np.unimaas.nl)
                              1. Department of Psychiatry and Neuropsychology, University of Maastricht, Netherlands
                                • Published Online First 18 June 2009

                                Abstract

                                Clinical subtypes of mild cognitive impairment (MCI) may represent different underlying aetiologies. In a European, multi-center, memory-clinic based study (DESCRIPA) of non-demented subjects we investigated whether MCI subtypes have different brain correlates on MRI and whether the relation between subtypes and brain pathology is modified by age. Using visual rating scales medial temporal lobe atrophy (MTA) (0-4) and white matter hyperintensities (WMH) (0-30) were assessed. Severity of MTA differed between MCI subtypes (p<0.001), increasing from (mean±standard deviation) 0.8±0.7 in subjective complaints (n=77), to 1.3±0.8 in non-amnestic MCI (n=93), 1.4±0.9 in single-domain amnestic MCI (n=70) and 1.7±0.9 in multiple-domain amnestic MCI (n=89). The association between MCI subtype and MTA was modified by age, and mainly present in subjects >70 years. Severity of WMH didn’t differ between MCI subtypes (p=0.21), However, the combination of MTA and WMH differed between MCI subtypes (p=0.02) We conclude that MCI subtypes may have different brain substrates, especially in older subjects. Isolated MTA was mainly associated with amnestic MCI subtypes, suggesting AD as underlying cause. In non-amnestic MCI the relatively higher prevalence of MTA in combination with WMH may suggest a different pathophysiological origin.

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