DISCUSSION 

In the present study, congenitally blind subjects had significantly shorter peak latencies of two middle latency auditory evoked potential components viz., Pa wave (the maximum positive peak between Na and 35 ms) and Nb wave (the maximum negative peak between 38 and 52 ms was described as the Nb wave) compared to age matched subjects with normal vision. In blind subjects there was no difference between the amplitudes of the cortically generated components (i.e., Pa and Nb) recorded over the vertex (Cz) compared to those recorded from the occipital region (Oz). 

Intracerebral recording in man has shown that the neural generator of the Nb wave is relatively localized in the dorsoposterior medial part of the Heschl's gyrs, i.e.. the primary auditory cortex (Liegeois-Chauvel, Musolino, Badier, Marquis and Chauvel, 1994). The pa wave is related to simultaneous activation of both supratemporal auditory cortices (Deiber, Ibanez, Fischer, Perrin and Maugiere, 1988) and changes in Pa wave latency have been regarded as due to modifications in the auditory pathways between the midbrain and cortex (Morlet, Bertrand, Salord, Boulieu, Pernier and Fischer, 1997). Hence in the present study subjects who had no formal rehabilitation with no special programs based on auditory inputs showed similar differences compared to normal

Table 1 Peak latencies and peak amplitudes of AEP-MLRs in congenitally blind (CB) and normal vision (NV) groups, n = 10 each.

sighted subjects, as blind subjects who had undergone a formal rehabilitation program (Naveen et al., 1997). In addition there was a shorter latency of the Pa wave, a possible reason is discussed below. The absence of change in the wave V and Na wave suggests that brainstem and diencephalic areas, which are known generators of these waves (Deiber et al., 1988), appear unchanged.

A previous report comparing AEP-MLR components of congenitally blind and normal sighted subjects, showed that blind subjects had a significantly shorter Nb wave peak latency, similar to the results reported in the present study, though in the earlier study there was no significant difference between the peak latencies of the Pa component, between the two groups. Normal sighted subjects of the two groups had exactly the same peak latencies of wave V and Na waves. The Pa wave peak latency of normal sighted subjects of the present study was 1.2ms longer than that of the normal sighted subjects, studied earlier. In contrast, the Nb wave peak latency of normal sighted subjects of the present study was 2.0 ms shorter than that of the normal sighted subjects, studied earlier. These differences were not significant (t-test for unpaired data). It is possible that the longer peak latency of the normal sighted subjects of the present study compared to the normal sighted subjects studied earlier may have contributed to the present result, viz., the significantly shorter Pa peak latency in the blind subjects. There was another difference between the subjects of the earlier study (Naveen et al., 1997) and those of the present study, viz., they belonged to different age groups: for the earlier study, group average age was 14.3 years with a range of 13 to 16 years, whereas subjects of the present study had a group average age of 22.4 years with a range of 18 to 30 years. AEP MLRs were found to he significantly different between subjects of 20-40 years age range and those with an age range of 60-80 years (Woods and Clayworth, 1986). There are no reports available comparing AEP MLRs for the much smaller age difference between the present and earlier studies. However since the differences in peak latency were not significant, any explanation based on the differences may be misleading.

A previous study (Alho, Kujala, Paavilainen, Summala and Naatanen, 1993), had described a larger processing negativity to attended tones at occipital scalp sites in congenitally blind subjects compared to those with normal vision. In the present study smaller amplitudes of Pa and Nb waves of AEP-MLRs were recorded over Oz compared to Cz, in the congenitally blind and normal sighted subjects. Hence there was no evidence of the occipital cortices contributing to cortically generated AEP-MLRs in the blind.

The results hence suggest that irrespective of early rehabilitation programs, there is facilitation of processing of auditory information at the level of the primary auditory cortex. However, the occipital area does not play a role in auditory information processing at primary cortical areas, in the congenitally blind.