HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by O'Mahony, D. Articles by Coakley, D. Search for Related Content PubMed PubMed Citation Articles by O'Mahony, D. Articles by Coakley, D.

Primary auditory pathway and reticular activating system dysfunction in Alzheimer's disease

Mercer's Institute for Research on Ageing (Drs. O'Mahony, Walsh, and Coakley), St. James's Hospital, and the Department of Pharmacology and Therapeutics (Drs. Rowan and Feely), Trinity College, Dublin, Ireland.

Patients with Alzheimer's disease (AD) have pathologic involvement of several important components of the primary auditory pathway, including the inferior colliculus, medial geniculate body, primary auditory cortex, and secondary auditory cortex. The main components of the brainstem auditory evoked response (BAER) and middle latency response (MLR) reflect the function of portions of the primary auditory pathway, including those affected pathologically in AD. The amplitude of the P1 component of the MLR reflects the degree of neuronal activity of midbrain portions of the ascending reticular activating system (ARAS) with cortical cholinergic projections. To determine whether there is dysfunction of the primary auditory pathway and ARAS in AD, we compared simultaneous BAER and MLR component latency and amplitude measurements in patients with mild-moderate AD (n = 35) and age-matched healthy elderly controls (n = 34). There were significant latency delays in brainstem transmission time (BAER I-V interpeak latency; p < 0.05) and in primary auditory cortex evoked potential generation (MLR Pa latency; p < 0.05) in the AD group compared with controls. In addition, there was a significant reduction in the PI component amplitude of the MLR in the AD group (p < 0.01). These results indicate dysfunction of the primary auditory pathway and ARAS in patients with mild-moderate AD and support the hypothesis that impairment of auditory function and of arousal are intrinsic features of AD.

Address correspondence and reprint requests to Dr. D. O'Mahony, Clinical Geratology Division, Radcliffe Infirmary, Woodstock Rd., Oxford, OX2 6HE, United Kingdom.

Supported by The Mercer's Fund, The Alzheimer Society of Ireland, and The Health Research Board of Ireland.

Received December 2, 1993. Accepted in final form April 30, 1994.