Why the study?
Very few studies have evaluated autonomic function in MCI, and none have evaluated MCI subtypes or the relationship of HRV indices with cognitive domains and structural brain damage.
Does autonomic function, assessed by heart rate variability during orthostatic challenge, differ between amnestic and non-amnestic mild cognitive impairment subtypes?
Does autonomic function, assessed by heart rate variability during orthostatic challenge, differ between amnestic and non-amnestic mild cognitive impairment subtypes?
Autonomic nervous system function is differentially impaired in amnestic versus non-amnestic mild cognitive impairment, reflecting their distinct neuroanatomic substrates.
Findings support subtype-specific autonomic impairment in MCI; leaves open diagnostic or prognostic utility pending longitudinal studies.
Mild cognitive impairment (MCI) is a heterogeneous syndrome with two main clinical subtypes, amnestic (aMCI) and non-amnestic (naMCI). The analysis of heart rate variability (HRV) is a tool to assess autonomic function. Cognitive and autonomic processes are linked via the central autonomic network. Autonomic dysfunction entails several adverse outcomes. However, very few studies have investigated autonomic function in MCI and none have considered MCI subtypes or the relationship of HRV indices with different cognitive domains and structural brain damage. We assessed autonomic function during an active orthostatic challenge in 253 oupatients aged ≥ 65, [n = 82 aMCI, n = 93 naMCI, n = 78 cognitively normal (CN), neuropsychologically tested] with power spectral analysis of HRV. We used visual rating scales to grade cerebrovascular burden and hippocampal/insular atrophy (HA/IA) on neuroimaging. Only aMCI showed a blunted response to orthostasis. Postural changes in normalised low frequency (LF) power and in the LF to high frequency ratio correlated with a memory test (positively) and HA/IA (negatively) in aMCI, and with attention/executive function tests (negatively) and cerebrovascular burden (positively) in naMCI. These results substantiate the view that the ANS is differentially impaired in aMCI and naMCI, consistently with the neuroanatomic substrate of Alzheimer's and small-vessel subcortical ischaemic disease.
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Nicolini et al. (2020) studied this question.
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