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Mid-latency auditory evoked responses in Alzheimer's disease: evaluation of P1 and P3 waves

  [ 4 votes ]   [ Discuss This Article ]
By Cordone A, Bavazzano M, Sismondini A, Mora R, D'An • www.ProHealth.com • April 1, 1999


A great deal of research has revealed a frequent association between hearing impairment and Alzheimer's disease. Many of these studies have, however, been criticized for the lack of statistical significance, for the methodology used and for doubts regarding the diagnostic criteria used. The lack of uniform results prompted the present research.

On the basis of some works in the literature, the authors felt that the study of middle and long-latency auditory evoked potentials, and their expression characterized by the P1 and P3 waves, the appropriate instrument for exploring the cortical and subcortical tracts of the auditory system which are most compromised in Alzheimer's disease. In fact, numerous studies have suggested that wave P1 is generated by peduncle-pontine nucleus cells of the tegmentum and that wave P3 is generated by sites located in the temporal lobes and hippocampus. The present study was conducted on 15 subjects suffering from Alzheimer's disease and 15 controls. Four subjects were excluded from the study because they were affected by Alzheimer's disease with severe dementia and were, thus, unable to cooperate. The 15 controls underwent accurate clinical and instrumental evaluation to rule out any neurological and intellectual disorders.

The results for wave P1 show a statistically significant difference between the subjects affected by Alzheimer's disease and the controls. In fact, there was a difference in the presence of this potential. Moreover there was a statistically significant difference in P1 between those patients with average dementia and the controls but not between those with slight dementia and the controls. Finally, comparison of the abnormalities in P1 potential and P3 latency showed that in Alzheimer's disease alterations in P3 arise earlier and are more constant than alterations in P1. The physiopathological meaning of these results is discussed.

Source: Acta Otorhinolaryngol Ital 1999 Apr;19(2):64-9
PMID: 10434436, UI: 99363280

(Istituto di Clinica Otorinolaringoiatrica, Universita di Genova.)



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