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. 2008;3(1):187-99.
doi: 10.2147/cia.s2537.

Classifying late-onset dementia with MRI: is arteriosclerotic brain degeneration the most common cause of Alzheimer's syndrome?

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Classifying late-onset dementia with MRI: is arteriosclerotic brain degeneration the most common cause of Alzheimer's syndrome?

Marie Cécile Henry-Feugeas et al. Clin Interv Aging. 2008.

Abstract

Our aim was to use early magnetic resonance imaging (MRI) to investigate the causes of cognitive decline in elderly people with mild cognitive impairment (MCI). Baseline structural and flow quantification MR sequences, and clinical and neuropsychological follow-up for at least two years, were performed on 62 elderly subjects with MCI. Of these subjects, 17 progressed to dementia, and 15 of these progressed to dementia of the Alzheimer type (DAT). Conversion to clinically diagnosed DAT was related to six distinct MR profiles, including one profile suggesting severe AD (20% of these converters) and five profiles suggesting severe cerebrovascular dysfunction. Two profiles suggested arteriosclerotic brain degeneration, one profile suggested severe venous windkessel dysfunction, and two suggested marked cerebral hypoperfusion associated with very low craniospinal compliance or marked brain atrophy. As compared with vascular MR type converters, AD MR type converters showed high executive and mobility predementia performances. Severe whole anteromesial temporal atrophy and predominantly left brain atrophy on visual MR analysis was only observed in AD MR type converters. In conclusion, these observations enhance the pathogenic complexity of the Alzheimer syndrome, and suggest that the role of arteriosclerotic brain degeneration in late life dementia is underestimated.

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Conflict of interest statement

Disclosure Grants: from the French Ministry of Health (Programme Hospitalier de Recherche Clinique AOM98053 “Apport de technologies récentes d’exploration cérébrale par résonance magnétique dans le diagnostic précoce de la maladie d’Alzheimer”, principal investigator MC Henry-Feugeas). There are no conflicts of interest to report.

Figures

Figure 1
Figure 1
Mesiotemporal atrophy in the AD MR class of converters to dementia of the Alzheimer type. These oblique coronal reformatted T1-weighted images at the level of the anterior parahippocampal gyri are from a nonconverter (A) and three AD MR type converters (B, C and D), respectively 41 (B), 17 (C) and 11 (D) months before diagnosis of dementia. Compared with the nonconverter, these converters showed predominantly left mesial temporal atrophy and ventricular enlargement and marked atrophy of the AD type; there was a marked dilatation of the left rhinal sulcus (long arrows) and concave superior border of the anterior amygdala region (short arrows).
Figure 2
Figure 2
Mesiotemporal atrophy in the vascular MR class of converters to dementia of the Alzheimer type. These oblique coronal reformatted T1-weighted images at the level of the anterior parahippocampal gyri are from five vascular type converters; one with arterial windkessel dysfunction and cerebral microangiopathy 9 months before diagnosis of dementia (A), one with arterial windkessel dysfunction and marked cortical atrophy 33 months before diagnosis of dementia (B), one with venous windkessel dysfunction 12 months before the diagnosis of dementia (C), one with resistive MR subtype 24 months before diagnosis of dementia (D), and the last one with a MR pattern of global cerebral hypoperfusion 13 months before diagnosis of dementia (E). There is no disproportionate enlargement of the left rhinal sulcus (long arrows), no marked concavity of the upper limit of the left amygdala region (short arrows), nor marked evidence of left predominance of brain atrophy.

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References

    1. Bateman GA, Levi CR, Schofield P, et al. The pathophysiology of the aqueduct stroke volume in normal pressure hydrocephalus: can co-morbidity with other forms of dementia be excluded? Neuroradiol. 2005;47:741–8. - PubMed
    1. Bateman GA, Levi CR, Schofield P, et al. Quantitative measurements of cerebral haemodynamics in early vascular dementia and Alzheimer’s disease. J ClinNeurosci. 2006;13:563–8. - PubMed
    1. Bateman GA, Loiselle AM. Can MR measurement of intracranial hydrodynamics and compliance differentiate which patient with idiopathic normal pressure hydrocephalus will improve following shunt insertion? Acta Neurochir (Wien) 2007;149:455–62. - PubMed
    1. Baumbach GL. Effects of increased pulse pressure on cerebral arterioles. Hypertension. 1996;27:159–67. - PubMed
    1. Bell-McGinty S, Lopez OL, Cidis-Meltzer C, et al. Differential cortical atrophy in subgroups of mild cognitive impairment. Arch Neurol. 2005;62:1393–97. - PubMed

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