Infant malnutrition affects cortical auditory evoked potentials.

Auditory evoked potentials (AEPs) to click and name stimuli were recorded for 23 malnourished infants on admission to and 17 on discharge from hospital, together with those from age-matched controls. The number of peaks on the AEPs and the amplitude were examined. The malnourished infants' AEPs to click stimuli differed from the controls' on admission but not on discharge. The malnourished infants had smaller AEP amplitudes to name than to click stimuli on discharge while the controls did not. The data show that cortical AEPs in infants are affected by malnutrition.

Evoked potentials in infant brainstem syndrome associated with Arnold-Chiari malformation.

This study evaluated the contribution of brainstem auditory evoked potentials (BAEPs) and median nerve somatosensory evoked potentials (SEPs) to the assessment of brainstem dysfunction in infants with myelomeningocele and Arnold-Chiari malformation. 16 infants under one year of age were studied. Six had infant brainstem syndrome (IBS). 11 had abnormally prolonged I-V interwave latency (brainstem transmission time, BSTT); BSTT did not differentiate those patients with and without IBS. The cortical 'N20' component of the median-nerve SEPs was absent or had low amplitude and prolonged latency in all six patients with clinical signs of brainstem dysfunction and in four without. Median-nerve SEPs were normal in the patients without IBS. There was a significant difference between patients with and without IBS. Median-nerve SEPs may be a helpful measure of brainstem function in infants with Arnold-Chiari malformation.

Pattern-reversal visual-evoked potentials in the diagnosis of amblyopia in children.

We assessed the potential clinical usefulness of pattern-reversal visual-evoked potentials in the diagnosis of amblyopia. Twenty-seven children with anisometropic amblyopia and four children without amblyopia participated. Estimates of visual acuity for each eye (Snellen visual acuity) were obtained by conventional psychometric methods. Visual-evoked potentials to reversing checks subtending 15 minutes of visual arc were also obtained. Visual-evoked potential testing and interpretation were done in a masked fashion. Ten of the 31 children were retested seven to 21 days after the first test to estimate reliability of the procedures. Of the 27 amblyopic children, 22 were correctly identified by the visual-evoked potential test alone. In four patients initial visual-evoked potential tests failed to identify the disparity in visual acuity between the eyes and retests in two of the four again had false-negative results. In one child initial visual-evoked potential testing incorrectly identified the amblyopic eye but repeat testing did identify it. Of the four children with symmetrically good vision, three were correctly identified as normal by the initial visual-evoked potential test. The other normal child was incorrectly identified by the visual-evoked potential test as having amblyopia.

Abnormal auditory evoked potentials in early infancy malnutrition.

Computer-averaged auditory evoked potentials were found to be abnormal in infants hospitalized because of severe malnutrition (marasmus). They improved as the infants' somatic growth improved during the course of treatment, but were still deviant at the time of discharge from the hospital and at subsequent outpatient follow-up. Abnormalities in evoked potentials may reflect a long-lasting effect of malnutrition on brain function.

Auditory evoked potential development in early childhood: a longitudinal study.

Serial recordings of auditory evoked potentials (AEPs) to clicks were obtained using a vertex-mastoid derivation from 16 normal children during sleep over an age span from near birth to age 3. The AEP components studied were: N0 (38 +/- 10 msec), P1 (79 +/- 24 msec), N1 (109 +/- 39 msec), P2 (186 +/- 35 msec), N2 (409 +/- 97 msec), P3A (554 +/- 116 msec), P3B (757 +/- 121 msec) and P3 (728 +/- 128 msec). Amplitudes and latencies of the components were calculated and regressions of the measures on age were computed for the group as a whole, for each subject and for subsets of the data based on sleep stage, sex, order of stimulus presentation and a rearing/race factor. For the group as a whole the latencies of P1, P2, P3, and P3B decreased with age. The amplitudes of P1N1 and the N2P3 waves increased with age. Most change occurred during the first year of life. In general, the changes with age were also found to hold across all of the factors examined, although individuals varied widely in the degree to which they conformed to the trends found for the data as a whole. The amount contributed by each of the factors mentioned above to the total variance was estimated. The proportions varied for different EP components but, in general, age, sleep state, and subject factors other than rearing/race and sex accounted for most variance. One half to 5/6 of the unexplained variance in AEP latencies and amplitudes (i.e., that not due to age, sleep state, etc.) occurred across rather than within subjects. For both the group as a whole and for individual children, P2 and N2 latencies were found to exhibit the greatest stability across time. The results of the longitudinal study reported here were in good agreement with those of a previous study from this laboratory which utilized a cross-sectional design.

Auditory evoked potentials during sleep in normal children from ten days to three years of age.

Auditory evoked potentials (AEPs) to clicks of moderate intensity were studied in 130 normal sleeping children from 10 days to 3 years of age. Latencies of the principal response components were found to decrease with log age, i.e., change was most rapid during the first year of life. From 15 days of age to 3 years, mean latencies decreased as follows: P2 from 230 to 150, N2 from 535 to 320 and P3 from 785 to 625 msec. Variance was quite high, especially at younger ages. The fact that decreases in the latencies of the various components proceeded at different rates suggest that the components reflect quasi-independent neural substrates. The components of shortest latency displayed the weakest relationship to age. Findings with respect to latency for the subset of data obtained during stage 2 sleep were similar to those for the total population which contained responses recorded during several sleep stages. The amplitude of AEP components increased with age with the exception of N1P2 which decreased. Observations with regard to amplitude held both for the overall data recorded during several sleep stages and stage 2 data for components N0P1, N1P2 and N2P3. The amplitude trends for P1N1 and P2N2 were, however, not significant for the stage 2 subset. The maturation of the morphology of the AEP was characterized by a relative increase in the prominence of long latency components. The most striking change was the development of P3. High amplitude, V shaped P3 waves were also associated with stage 3-4 sleep. The changes which were delineated by this study for infancy and early childhood appear to be continuations of developmental trends reported for premature infants and neonates. AEPs are a reliable elicited measure which correlate well with maturation. They, therefore, can be a useful tool both in the study of central nervous system development and in the diagnosis of sensory and neurologic abnormalities.