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Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease
G Fein1, V Di Sclafani, J Tanabe
1Neurobehavioral Research, Inc., San Francisco, CA, USA.
Insights
Dementia in subcortical ischemic vascular disease (SIVD) is linked to brain atrophy, not lacunes. Hippocampal and cortical atrophy predict cognitive decline in SIVD, with distinct patterns from Alzheimer's disease.
Area of Science:
- Neurology
- Neuroimaging
- Vascular Dementia Research
Background:
- The etiology of dementia in subcortical ischemic vascular disease (SIVD) remains debated.
- Investigating the relationship between cognitive impairment and brain changes in SIVD is crucial.
Purpose of the Study:
- To determine if cognitive impairment in SIVD correlates with ischemic brain injury or atrophy.
- To assess if cognitive impairment in SIVD is caused by co-occurring Alzheimer's disease (AD).
Main Methods:
- Volumetric MRI was used to assess brain structures in SIVD patients with varying cognitive function, probable AD patients, and controls.
- The study examined correlations between cognitive impairment severity and lacunes, white matter signal hyperintensities (WMSH), and brain atrophy (hippocampal, cortical, CSF volumes).
Main Results:
- Cognitive impairment severity in SIVD correlated with hippocampal and cortical gray matter atrophy, not lacune measures.
- Hippocampal atrophy was the strongest predictor of cognitive impairment, with a secondary atrophic process linked to WMSH and ventricular dilation.
- Autopsied SIVD cases showed mixed ischemic and degenerative pathology in the hippocampus, unlike the localized atrophy in probable AD.
Conclusions:
- Dementia in SIVD, similar to AD, is associated with hippocampal and cortical atrophy.
- SIVD exhibits independent atrophic processes, unlike AD, suggesting mixed pathologies contribute to hippocampal atrophy.
- Diffuse cortical atrophy in SIVD may be linked to white matter signal hyperintensities.
Background:
The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial.
Objectives:
To determine whether cognitive impairment in SIVD 1) correlates with measures of ischemic brain injury or brain atrophy, and/or 2) is due to concomitant AD.
Methods:
Volumetric MRI of the brain was performed in 1) elderly subjects with lacunes (L) and a spectrum of cognitive impairment-normal cognition (NC+L, n = 32), mild cognitive impairment (CI+L, n = 26), and dementia (D+L, n = 29); 2) a comparison group with probable AD (n = 28); and 3) a control group with normal cognition and no lacunes (NC). The authors examined the relationship between the severity of cognitive impairment and 1) volume, number, and location of lacunes; 2) volume of white matter signal hyperintensities (WMSH); and 3) measures of brain atrophy (i. e., hippocampal, cortical gray matter, and CSF volumes).
Results:
Among the three lacune groups, severity of cognitive impairment correlated with atrophy of the hippocampus and cortical gray matter, but not with any lacune measure. Although hippocampal atrophy was the best predictor of severity of cognitive impairment, there was evidence for a second, partially independent, atrophic process associated with ventricular dilation, cortical gray matter atrophy, and increase in WMSH. Eight autopsied SIVD cases showed variable severity of ischemic and neurofibrillary degeneration in the hippocampus, but no significant AD pathology in neocortex. The probable AD group gave evidence of only one atrophic process, reflected in the severity of hippocampal atrophy. Comparison of regional neocortical gray matter volumes showed sparing of the primary motor and visual cortices in the probable AD group, but relatively uniform atrophy in the D+L group.
Conclusions:
Dementia in SIVD, as in AD, correlates best with hippocampal and cortical atrophy, rather than any measure of lacunes. In SIVD, unlike AD, there is evidence for partial independence between these two atrophic processes. Hippocampal atrophy may result from a mixture of ischemic and degenerative pathologies. The cause of diffuse cortical atrophy is not known, but may be partially indexed by the severity of WMSH.