Abstract

Background and Objectives: The most prevalent dementia are Alzheimer’s disease and vascular dementia. There is evidence that cortical synaptic function may differ in these two conditions. Habituation of cortical responses to repeated stimuli is a well-preserved phenomenon in a normal brain cortex, related to an underlying mechanism of synaptic efficacy regulation. Lack of habituation represents a marker of synaptic dysfunction. The purpose of this study was to assess the habituation of somatosensory evoked potentials (SEPs) in 29 patients affected by mild-to-moderate Alzheimer’s disease (AD-type) or vascular (VD-type) dementia. Materials and Methods: All patients underwent a clinical history interview, neuropsychological evaluation, and neuroimaging examination. SEPs were elicited by electrical stimulation of the right median nerve at the wrist. Six-hundred stimuli were delivered, and cortical responses divided in three blocks of 200. Habituation was calculated by measuring changes of N20 amplitude from block 1 to block 3. SEP variables recorded in patients were compared with those recorded in 15 age- and gender-matched healthy volunteers. Results: SEP recordings showed similar N20 amplitudes in AD-type and VD-type patients in block 1, that were higher than those recorded in controls. N20 amplitude decreased from block 1 to block 3 (habituation) in normal subjects and in VD-type patients, whereas in AD-type patients it remained unchanged (lack of habituation). Conclusions: The findings suggest that neurophysiologic mechanisms of synaptic efficacy that underneath habituation are impaired in patients with AD-type dementia but not in patients with VD-type dementia. SEPs habituation may contribute to early distinction of Alzheimer’s disease vs. vascular dementia.

Highlights

  • This article is an open access articleCognitive disorder refers to the abnormality of cognitive function

  • Using one-way analysis of variance (ANOVA), participants were compared across diagnostic category

  • Complete somatosensory evoked potentials (SEPs) recordings were obtained from all patients and controls participating to the study

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Summary

Introduction

This article is an open access articleCognitive disorder refers to the abnormality of cognitive function. Soluble oligomeric assemblies of amyloidogenic proteins are thought to initiate disease-specific cytopathology and subsequent symptoms. Larger deposits, such as compacted Aβ plaques, seem relatively inert but they might serve as reservoirs of diffusible oligomers [3]. VD refers to a heterogeneous group of cognitive disorders caused by ischemic, hemorrhagic, anoxic, or hypoxic brain damage. Both macrovascular and/or microvascular cerebral disease may induce ischemic cognitive impairment, whereas hypertension is the main cause of hemorrhagic cognitive impairment, by inducing intralobar hemorrhages or multiple petechial hemorrhages [4]

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