Elsevier

Clinical Neurophysiology

Volume 110, Issue 11, 1 November 1999, Pages 1942-1947
Clinical Neurophysiology

Impaired preconscious auditory processing and cognitive functions in Alzheimer's disease

https://doi.org/10.1016/S1388-2457(99)00153-4Get rights and content

Abstract

Objective: To study whether preconscious auditory processing is deteriorated in patients with Alzheimer's disease (AD) having mild to moderate cognitive symptoms. To investigate whether auditory processing correlates with the impairment of the higher cortical functions.

Methods: P50m and N100m responses elicited by a sequence of repetitive tones were recorded with a whole-head magnetometer from 22 patients with probable AD and from 18 healthy age-matched controls. In addition, an extensive neuropsychological test battery assessing main cognitive domains was administered to all subjects.

Results: The patients with AD had significantly delayed N100m responses in the left hemisphere that correlated with the impairment of the language functions.

Conclusions: N100m auditory responses measured with magnetoencephalography may be useful in evaluating the severity and progression of the cortical dysfunction in dementia.

Introduction

Magnetoencephalography (MEG) is a non-invasive method to study cerebral function with millisecond time resolution (Hämäläinen et al., 1993). Previous MEG studies with normal subjects have demonstrated functional asymmetry in parallel auditory processing, that is, auditory responses peaked slightly earlier in the contralateral than in the ipsilateral auditory cortex with respect to the ear stimulated (Rinne et al., 1999, Pantev et al., 1998, Mäkelä et al., 1993, Pantev et al., 1986, Nakasato et al., 1995). Recent MEG findings have shown that aging and especially Alzheimer's disease (AD) impair parallel preconscious auditory processing between the hemispheres and that this is mainly caused by the delayed cortical processing in the hemisphere ipsilateral to the ear stimulated (Pekkonen et al., 1996, Perret, 1974). In AD, a massive neuronal loss mainly involves hippocampal formation and cortical association areas, the primary auditory cortices being less damaged (Davies et al., 1992, Wechsler, 1978). It has not been studied thoroughly with MEG, however, whether the preconscious auditory processing is abnormal already in AD patients with mild to moderate cognitive symptoms. The second aim of the present study was to investigate whether the damaged preconscious auditory processing correlates with the deterioration of higher cognitive functions in patients with AD.

Section snippets

Material and methods

Eighteen healthy, right-handed subjects (mean age 68 years, range 59–76 years; 8 males) and 22 outpatients with probable AD (mean age 64 years, range 51–80 years; 8 males, one left-handed) participated in the study. After a complete description of the study to the subjects, written informed consent was obtained from each subject or his/her near relative. The study was accepted by the Ethics Committee of the Department of Neurology, the Helsinki University Central Hospital, in compliance with

Results

Fig. 1 demonstrates the magnetic responses of one AD patient and one control subject to the standard tones with the ISI of 2.5 s. Each subject elicited clear P50m and N100m responses, the maximal amplitudes being over the temporal lobes. The patient had larger latency difference between the ipsilateral and contralateral N100m responses than the healthy subject.

The interhemispheric latency differences of the AEFs, which were first calculated and then subjected to group by ISI analysis (repeated

Discussion

Our results provided MEG-evidence for a significant correlation between the delayed preattentive auditory processing in the left hemisphere and impaired language functions in patients with AD. The left hemisphere usually contributes to the language functions when subjects are right-handed as most subjects were in this study (Mayeux and Chun, 1995). Thus both the delayed ipsilateral N100m response and the deteriorated language functions probably reflect functional changes caused by the loss of

Acknowledgements

This work was supported by the Academy of Finland and the EU grant BMH4-CT96-08 19 (COBRAIN) and by the Helsinki University Central Hospital Research Funds.

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    Resubmitted to Clinical Neurophysiology, June 3, 1999.

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