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28 - Neuroimaging of cognitive disorders: commentary
- from Section IV - Cognitive Disorders
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- By Mony J. de Leon, Department of Psychiatry New York University School of Medicine New York, NY, USA, Henry Rusinek, Department of Radiology New York University School of Medicine New York, NY, USA, Wai Tsui, Department of Psychiatry New York University School of Medicine New York, NY, USA and Nathan Kline Institute Orangeburg, NY, USA, Thomas Wisniewski, Department of Neurology New York University School of Medicine New York, NY, USA and Department of Developmental Neurobiology Institute for Basic Research Staten Island, NY, USA, Jerzy Wegiel, Department of Developmental Neurobiology Institute for Basic Research Staten Island, NY, USA, Ajax George, Department of Radiology New York University School of Medicine New York, NY, USA
- Edited by Martha E. Shenton, Bruce I. Turetsky, University of Pennsylvania
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- Book:
- Understanding Neuropsychiatric Disorders
- Published online:
- 10 January 2011
- Print publication:
- 09 December 2010, pp 395-402
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Summary
This chapter offers a highly personal view of three-dimensional tomographic imaging related to Alzheimer's disease (AD). The age of structural imaging in AD began with X-ray computed tomography (CT). CT studies introduced the negative angulation acquisition plane to more efficiently reveal and measure temporal horn enlargement and incidentally found evidence for hippocampal atrophy. Structural imaging has been invaluable in anatomically defining the regional tissue vulnerability and atrophy correction as estimated by fluorodeoxyglucose positron emission tomography (FDG-PET) and amyloid imaging and other tracers. Structural imaging owes a great debt to pathology for the contributions made to understanding the lesions and pathologic anatomy of AD. Although magnetic resonance imaging (MRI) imaging has yet to deliver a specific marker of AD pathology, MRI has provided sensitive characterizations of the effects of AD pathology and the promise of new MR contrast agents for identifying amyloid plaque pathology.
Mild cognitive impairment (MCI): a historical perspective
- Barry Reisberg, Steven H. Ferris, Alan Kluger, Emile Franssen, Jerzy Wegiel, Mony J. de Leon
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- Journal:
- International Psychogeriatrics / Volume 20 / Issue 1 / February 2008
- Published online by Cambridge University Press:
- 01 February 2008, pp. 18-31
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Descriptions of dementia can be traced to antiquity. Prichard (1837) described four dementia stages and Kral (1962) described a “benign senescent forgetfulness” condition. The American Psychiatric Association's DSM-III (1980) identified an early dementia stage.
In 1982, the Clinical Dementia Rating (CDR) and the Global Deterioration Scale (GDS) were published, which identified dementia antecedents. The CDR 0.5 “questionable dementia” stage encompasses both mild dementia and earlier antecedents. GDS stage 3 described a predementia condition termed “mild cognitive decline” or, alternatively, beginning in 1988, “mild cognitive impairment” (MCI). This GDS stage 3 MCI condition is differentiated from both a preceding GDS stage 2, “subjective cognitive impairment” (SCI) stage and a subsequent GDS 4 stage of mild dementia.
GDS stage 3 MCI has been well characterized. For example, specific clinical concomitants, mental status and psychological assessment score ranges, behavioral and emotional changes, neuroimaging concomitants, neurological reflex changes, electrophysiological changes, motor and coordination changes, and changes in activities, accompanying GDS stage 3 MCI have been described.
Petersen and associates proposed a definition of MCI in 2001 which has been widely used (hereafter referred to as “Petersen's MCI”). Important differences between GDS stage 3 MCI and Petersen's MCI are that, because of denial, GDS stage 3 MCI does not require memory complaints. Also, GDS stage 3 MCI recognizes the occurrence of executive level functional deficits, which Petersen's MCI did not. Nevertheless, longitudinal and other studies indicate essential compatibility between GDS stage 3 MCI and Petersen's MCI duration and outcomes.
Contribution of Structural Neuroimaging to the Early Diagnosis of Alzheimer's Disease
- Mony J. de Leon, Antonio Convit, Susan DeSanti, Maciej Bobinski, Ajax E. George, Henryk M. Wisniewski, Henry Rusinek, Roberta Carroll, L. A. Saint Louis
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- Journal:
- International Psychogeriatrics / Volume 9 / Issue S1 / December 1997
- Published online by Cambridge University Press:
- 10 January 2005, pp. 183-190
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There is compelling evidence for the early involvement of the hippocampal formation in the natural history of Alzheimer's disease (AD). The evidence comes from recent neuropathology, neuropsychology, and neuroimaging studies. AD-type histopathologic changes limited to the hippocampus have been described and may be seen in normal aging subjects. The sites of maximal neuronal loss in the hippocampal formation are in the CA1, subiculum, and entorhinal cortex. Minimally cognitively impaired (MCI) individuals (defined by ratings of functional capacity and psychiatric symptomatology) exhibit a neuropsychological profile that is distinct from that of the unimpaired elderly. Pathologic evidence suggests that most of these cases already have AD brain changes accentuated in the hippocampal region, and our own longitudinal studies reveal that 70% of this group develop dementia within a 4-year period. We have developed a negative-angle axial view designed to cut parallel to the anterior-posterior plane of the hippocampus. Using this modified axial plane of section in conjunction with computed tomography (CT) and magnetic resonance imaging (MRI), we estimated the prevalence of hippocampal atrophy in normal aging and across severity levels of cognitively impaired elderly patients. Longitudinal study shows that hippocompal atrophy is a sensitive and specific predictor of future AD for patients with MCI. MRI volume study of AD patients, controls, and MCI patients shows specific hippocampal volume loss in MCI. We conclude that the atrophic changes associated with early AD can be visualized using qualitative techniques and are readily quantifiable with volumetry. This article is not intended to be comprehensive, but to provide an overview of some of the structural neuroimaging data from our laboratory.
Mortality and Temporal Course of Probable Alzheimer's Disease: A 5-Year Prospective Study
- Barry Reisberg, Steven H. Ferris, Emile H. Franssen, Emma Shulman, Isabel Monteiro, Steven G. Sclan, Gertrude Steinberg, Alan Kluger, Carol Torossian, Mony J. de Leon, Eugene Laska
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- Journal:
- International Psychogeriatrics / Volume 8 / Issue 2 / June 1996
- Published online by Cambridge University Press:
- 07 January 2005, pp. 291-311
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Alzheimer's disease (AD) is asociated with an increased mortality in comparison with aged control populations. The relationship between the clinical and the temporal course of AD has not been well studied over significant intervals. Community residing patients with probable AD (N = 103, 42 men, mean age = 70.2 ± 8.0 years) were studied at baseline on demographic and clinical variables, including measures of global deterioration (Global Deterioration Scale; GDS), mental status and cognition (e.g., Mini-Mental State Examination; MMSE), and functional impairment (Functional Assessment Staging; FAST). Baseline characteristics included a GDS range of Stage 4, 5, or 6 (38.8%, 39.8%, and 21.4% respectively) and a mean MMSE score of 15.4 ± 5.6. The mean follow-up interval was 4.6 ± 1.4 year. Follow-ups were done blind to baseline measures and when necessary were conducted in residential and nursing home settings. Of locatable subjects (n = 95, 92%), 30 (31.6%) were deceased. Survivors (n = 65) had a mean GDS stage of 6.2 ± 0.9 and a mean MMSE score of 5.1 ± 6.9; 51% had MMSE scores of 0. Increased age and male gender, but not baseline clinical dementia variables, increased the risk of death (ps < .01). Change in clinical variables correlated significantly with time elapsed (r = .32, p < .05, for MMSE change, to r = .48, p < .001, for GDS change). Significant variance in temporal change (i.e., time elapsed) was accounted for by change in two of the five clinical measures studied (i.e., GDS and FAST; multiple r = .53). The results support previous estimates of mean duration of the GDS and FAST stages. For subjects with probable AD followed over approximately 5 years, clinical variables changed significantly over time in survivors. However, the majority of temporal variance in the course of AD remains unexplained.