Neurologia/Neurociências

Os pacientes realizaram um questionário codificado visual durante a RNMf e foram testados para reconhecimento do estímulo posteriormente. As regiões do LTM de interesse foram identificadas em cada RNM estrutural individual e a ativação foi quantificada em cada região.

Grandes extensões de ativação dentro da formação hipocampal e giro para-hipocampal (PHG) foram correlacionadas com melhor performance mnemônica. Houve, entretanto, uma relação paradoxal entre a extensão da ativação e o estado clínico tanto do basal quanto das avaliações no acompanhamento. Os pacientes com maior déficit clínico, baseados na Avaliação de Demência Clínica Soma de Caixas (Clinical Dementia Rating Sum of Boxes), recrutaram uma maior extensão do PHG direito durante a codificação, mesmo após contagem para atrofia.   Além disso, aqueles que subseqüentemente declinaram durante os 2,5 anos de acompanhamento clínico (44% dos pacientes) ativaram uma extensão significativamente maior do PHG direito durante a codificação, apesar da performance de memória equivalente.

 Medial temporal lobe function and structure in mild cognitive impairment - Annals of Neurology; 2004; 56(1): 27-35

Original Article

Medial temporal lobe function and structure in mild cognitive impairment

Bradford C. Dickerson, MD 1 2 3 4 *, David H. Salat, PhD 2 4 5, Julianna F. Bates, PhD 2 4 6, Monika Atiya, MD 6 7, Ronald J. Killiany, PhD 8, Douglas N. Greve, PhD 2 4 5, Anders M. Dale, PhD 2 4 5, Chantal E. Stern, PhD 2 9, Deborah Blacker, MD 2 4 6, Marilyn S. Albert, PhD 1 2 4 6 10, Reisa A. Sperling, MD 1 2 3 4

1Department of Neurology, Massachusetts General Hospital 2Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA 3Department of Neurology, Brigham and Women's Hospital 4Harvard Medical School, Boston, MA 5Department of Radiology, Massachusetts General Hospital, Charlestown, MA 6Department of Psychiatry, Massachusetts General Hospital, Charlestown, MA 7Max Planck Institute for Psychiatry, Munich, Germany 8Departments of Anatomy and Neurobiology, Boston University of Medicine 9Center for Memory and Brain, Boston University, Boston, MA 10Department of Neurology, Division of Cognitive Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD

email: Bradford C. Dickerson (bradd@nmr.mgh.harvard.edu)

^*Correspondence to Bradford C. Dickerson, Gerontology Research Unit, MGH-East (149-2691) 149 13th Street, Charlestown, MA 02129

Funded by:
 NIH (National Institute on Aging); Grant Number: PO1-AG04953, K23-AG22509
 National Institute of Neurological Disorders and Stroke; Grant Number: K23-NS02189
 Clinical Investigator Training Program (Harvard/MIT Health Sciences and Technology-Beth Israel Deaconess Medical Center)
 NCRR; Grant Number: P41-RR14075
 Mental Illness and Neuroscience Discovery (MIND) Institute

Abstract

Functional magnetic resonance imaging (fMRI) was used to study memory-associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). Subjects performed a visual encoding task during fMRI scanning and were tested for recognition of stimuli afterward. MTL regions of interest were identified from each individual's structural MRI, and activation was quantified within each region. Greater extent of activation within the hippocampal formation and parahippocampal gyrus (PHG) was correlated with better memory performance. There was, however, a paradoxical relationship between extent of activation and clinical status at both baseline and follow-up evaluations. Subjects with greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a larger extent of the right PHG during encoding, even after accounting for atrophy. Moreover, those who subsequently declined over the 2.5 years of clinical follow-up (44% of the subjects) activated a significantly greater extent of the right PHG during encoding, despite equivalent memory performance. We hypothesize that increased activation in MTL regions reflects a compensatory response to accumulating AD pathology and may serve as a marker for impending clinical decline. Ann Neurol 2004;56:27-35