Cognitive profile in cerebral small vessel disease: comparison between cerebral amyloid angiopathy and hypertension-related microangiopathy

Abstract

Cerebral amyloid angiopathy (CAA) is recognized as a cause of cognitive impairment, but its cognitive profile needs to be characterized, also respect to hypertension-related microangiopathy (HA). We aimed at comparing difference or similarity of CAA and HA patients' cognitive profiles, and their associated factors. Participants underwent an extensive clinical, neuropsychological, and neuroimaging protocol. HA patients (n = 39) were more frequently males, with history of vascular risk factors than CAA (n = 32). Compared to HA, CAA patients presented worse performance at MoCA (p = 0.001) and semantic fluency (p = 0.043), and a higher prevalence of amnestic MCI (46% vs. 68%). In univariate analyses, multi-domain MCI was associated with worse performance at MoCA, Rey Auditory Verbal Learning Test (RAVLT), and semantic fluency in CAA patients, and with worse performance at Symbol Digit Modalities Test (SDMT) and phonemic fluency in HA ones. In multivariate models, multi-domain deficit remained as the only factor associated with RAVLT (β = - 0.574) in CAA, while with SDMT (β = - 0.364) and phonemic fluency (β = - 0.351) in HA. Our results highlight different patterns of cognitive deficits in CAA or HA patients. While HA patients' cognitive profile was confirmed as mainly attentional/executive, a complex cognitive profile, characterized also by deficit in semantic memory, seems the hallmark of CAA patients.

Keywords: Arteriolosclerosis; Cerebral amyloid angiopathy; Cerebral small vessel disease; Cognition; Cognitive decline; Cognitive impairment; Cognitive profile; Microangiopathy; Neuropsychological patterns.

Figure 1

Examples of representative brain of HA and CAA patients. (a) Example of a HA patient: Man, 88 years old. History of lacunar stroke three years before; MCI diagnosis according to neuropsychological evaluation. His Brain MRI shows severe subcortical and periventricular WMH (Fazekas 3) in FLAIR sequences. T2* shows one right deep thalamic CMB, with no evidence of lobar CMBs. (b) Example of a CAA patient: Woman, 78 years old. History of lobar ICH two years before (right occipital); CAA diagnosis according to modified Boston criteria. Her Brain MRI shows multiple subcortical WMH spots (Fazekas 2) in FLAIR sequences. T2* shows several lobar CMBs, with no evidence of deep CMBs.

Figure 2

MCI subtypes distributions: comparisons between CAA and HA patients (χ² tests).

Figure 3

Graphical representation of the cognitive domains impaired in patients with CAA and HA. The graph shows the percentages of patients who had obtained PE = 0 (impaired performance) on each neuropsychological test in the CAA and HA cohorts.

Figure 4

Graphical representation of multivariate logistic regression models computed including single/multi-domain MCI, ADL, IADL and GDS as independent variables and adjusting for age, education and sex. Green arrows refer to the CAA cohort, while orange arrows refer to the HA cohort.