The role of brain infarcts and hippocampal atrophy in subcortical ischaemic vascular dementia

Gainotti, Guido; Acciarri, Adele; Bizzarro, Alessandra; Marra, Camillo; Masullo, Carlo; Misciagna, Sandro; Tartaglione, Tommaso; Valenza, Alessandro; Colosimo, Carlo

doi:10.1007/s10072-004-0321-5

Cited by 33 publications

(18 citation statements)

References 20 publications

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“…While MTA and Hc volume reductions in SVaD occurred with a comparable frequency to AD, Hc atrophy was significantly less severe than in AD. These findings are comparable with a number of previous studies showing that Hc atrophy commonly occurs in vascular dementia [7,[9][10][11][12][13] and might be milder than in AD [7,9,11] . However, none of these studies strictly focused on SVaD.…”

Section: Discussionsupporting

confidence: 91%

Hippocampal Atrophy in Subcortical Vascular Dementia

et al. 2011

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Background and Purpose: New research criteria for subcortical vascular dementia (SVaD) have been suggested to define a more homogeneous subgroup of vascular dementia. Hippocampal (Hc) atrophy is a hallmark of Alzheimer’s disease (AD), but it also occurs in other dementia disorders including vascular dementias. So far, it is unknown to which extent Hc atrophy is present in SVaD. Methods: From a larger consecutive referral population in a memory clinic, 11 patients fulfilling the research criteria for SVaD were carefully matched with comparison groups of healthy controls and patients with AD. To estimate the extent of Hc atrophy in SVaD, both Hc volumetry and visual rating of medial temporal lobe atrophy (MTA) were applied. Results: In SVaD, significant Hc atrophy occurred. The extent was intermediate between controls and patients with AD both on Hc volumetry and visual MTA ratings. At the same level of global cognition, Hc volumes were reduced by 11.6% in SVaD and 16.6% in AD, relative to controls. Conclusions: Patient groups with AD and SVaD as identified by current research criteria appear to overlap considerably with regard to the feature of Hc atrophy. While contamination with AD is a likely cause, other mechanisms of Hc atrophy in SVaD also deserve consideration. The findings have implications for the design of future clinical trials of SVaD.

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Section: Discussionsupporting

confidence: 91%

Hippocampal Atrophy in Subcortical Vascular Dementia

et al. 2011

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“…Brain infarcts, particularly subcortical ones, are associated primarily with executive dysfunction, whereas hippocampal volume is correlated with memory performance. 9,30,31 Cortical infarcts, in addition to being associated with deficits in processing speed, are also associated with worse episodic memory, but these findings have been interpreted with caution. 7,8 A significant gap has remained in the literature: to our knowledge, ours is the first study to examine whether memory is associated with the presence of prior infarcts independently of hippocampal atrophy.…”

Section: Samplementioning

confidence: 99%

Memory after silent stroke

Blum¹,

Luchsinger²,

Manly³

et al. 2012

Neurology

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Objective: Memory decline commonly occurs among elderly individuals. This observation is often attributed to early neurodegenerative changes in the hippocampus and related brain regions. However, the contribution of vascular lesions, such as brain infarcts, to hippocampal integrity and age-associated memory decline remains unclear. Methods:We studied 658 elderly participants without dementia from a prospective, communitybased study on aging and dementia who received high-resolution structural MRI. Cortical and subcortical infarcts were identified, and hippocampal and relative brain volumes were calculated following standard protocols. Summary scores reflecting performance on tasks of memory, language, processing speed, and visuospatial function were derived from a comprehensive neuropsychological battery. We used multiple regression analyses to relate cortical and subcortical infarcts, hippocampal and relative brain volume, to measures of cognitive performance in domains of memory, language, processing speed, and visuospatial ability.Results: Presence of brain infarcts was associated with a smaller hippocampus. Smaller hippocampus volume was associated with poorer memory specifically. Brain infarcts were associated with poorer memory and cognitive performance in all other domains, which was independent of hippocampus volume. Conclusions:Both hippocampal volume and brain infarcts independently contribute to memory performance in elderly individuals without dementia. Given that age-associated neurodegenerative conditions, such as Alzheimer disease, are defined primarily by impairment in memory, these findings have clinical implications for prevention and for identification of pathogenic factors associated with disease symptomatology. Neurology Memory decline is frequent among the elderly and it is most often attributed to dysfunction and atrophy of the hippocampus and related mesial temporal lobe structures.1-3 Subclinical brain infarcts are present in about one-third of older adults, and are associated with a 2-fold risk of dementia and a steeper decline in age-associated cognitive function. 4 -6 However, the effects of subclinical brain infarcts on hippocampal integrity and age-related memory decline are not well understood. Memory deficits have been described following brain infarcts. Cortical infarcts can result in diverse deficits depending on size and location of lesion and can produce cognitive decline in multiple domains, including perceptual speed and memory. 7,8 Subcortical infarcts can result in executive dysfunction, 9 although strategic thalamic or limbic system infarcts can result in memory loss. 10,11 Clinically, it can be difficult to differentiate between cognitive decline due to

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“…On the other hand, MCI patients with subcortical infarcts were identified using a criterion similar to that adopted in a previous personal work on subcortical vascular dementia (Gainotti et al, 2004). MCI patients were included in this group if they presented three or more small subcortical infarcts or two small infarcts and periventricular white matter hyperintensities.…”

Section: Mri Criteria Used To Identify MCI Patients With Multiple Submentioning

confidence: 99%

Patterns of neuropsychological impairment in MCI patients with small subcortical infarcts or hippocampal atrophy

Gainotti

Ferraccioli

Vita

et al. 2008

J Int Neuropsychol Soc

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We investigated whether MCI patients with hippocampal atrophy or multiple subcortical infarcts demonstrate neuropsychological patterns and markers considered typical of Alzheimer's disease (AD) and of vascular dementia (VD), respectively. An extensive neuropsychological battery, including tests of memory, visual-spatial and executive functions, language, attention, praxis and psychomotor speed, was administered to 36 mild cognitive impairment (MCI) patients with hippocampal atrophy and 41 MCI patients with multiple subcortical infarcts. Both groups of MCI patients were very mildly impaired and well matched in terms of MMSE scores. A clear, disproportionately severe, episodic memory disorder was observed in MCI patients with hippocampal atrophy. A less specific neuropsychological profile, consisting of impairment on an Action Naming task that is sensitive to frontal lobe lesions, was observed in MCI patients with multiple subcortical infarcts. In MCI patients, a disproportionately severe episodic memory impairment strongly points to an Alzheimer's type brain pathology, whereas the prevalence of executive deficits and other frontal lobe symptoms are a much weaker diagnostic marker of small vessel subcortical disease. (JINS, 2008, 14, 611-619.)

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The role of brain infarcts and hippocampal atrophy in subcortical ischaemic vascular dementia

Cited by 33 publications

References 20 publications

Hippocampal Atrophy in Subcortical Vascular Dementia

Hippocampal Atrophy in Subcortical Vascular Dementia

Memory after silent stroke

Patterns of neuropsychological impairment in MCI patients with small subcortical infarcts or hippocampal atrophy

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