Fetal Alcohol Spectrum Disorders and Their Persisting Sequelae in Adult Life: Maturation of the Auditory Pathway

Abstract

Neonates are screened for auditory function. Congenital hypacusis is found in 1/1000 neonates; the fetal alcohol spectrum disorders (FASD) are more common. The oto-acoustic emissions measured in neonates only reflect the contractility of the outer hair cells in the cochlea; a positive test result does not provide any information on central defects. Further, in children with FASD, acoustic evoked potentials should be measured and the maturation of the auditory pathway should be controlled, as was stipulated by the Mayo Clinic as early as in 1981 (1). The central transmission time from the potential of the acoustic (vestibulocochlear or auditory) nerve to the thalamus serves as the benchmark. In normal babies aged 18 months, the time is about 4 milliseconds, and the maturation time is notably prolonged in FASD. There are children whose auditory pathways never completely mature. The result is deficient maturation; the development may stall at age 1 year. If in FASD the auditory pathway has not matured when a child has reached the age of 4 years, no improvements are to be expected. In a serious case in our practice, a neglected infant died and was buried by his father at a motorway car park; neither of the two siblings spoke a word and their diet consisted of non-alcoholic malt beer. If the auditory pathway has not matured and further central disorders are present, parents willing to adopt are merely informed about the problems that are already present; one cannot help feeling that that state and the youth welfare offices are trying to pass the risk to adoptive families without further regard of the potentially serious sequelae.