Adequate sensory experience is critical to the developing nervous system – for the expression as well as maintenance of sensory functions even when such functions are innately determined [1
]. Development and maintenance of auditory sense is no exception. In other words, reduced auditory input, early in life, may affect auditory processing later in life. Otitis media (OM) is a common condition that results in hearing loss in early years of life. Sandeep and Jayaram [2
] have reported that OM occurring early in life may lead to subtle difficulties in speech identification, particularly under adverse listening conditions. Furthermore, such negative effects may persist for 4 years or even more after an attack of OM.
OM is the most prevalent disease during childhood, next only to common cold. It is estimated that chronic OM affects 65 million to 330 million people worldwide, and 60% of them (39 million to 200 million) show clinically significant hearing impairment [3
]. Incidence of OM is known to be higher in the first 3 years of life [4
]. Jayaram [5
], in an Indian population, reported that OM was the cause of conductive hearing loss in nearly 71% of the 1505 persons ranging in age from 1 – 80 years. Similar results have been reported also by Parsram and Jalvi [6
Past research has demonstrated that early OM in children influences auditory brainstem physiology [7
]. Webster and Webster [7
] reported a reduction in both the size and number of neurons in the auditory brainstem in subjects with OM. Past research has documented prolonged latencies for wave III and wave V [8
], delayed wave III and prolonged III–V wave intervals [8
], prolonged wave III–V interval [9
] and, prolonged wave III–V and I–V intervals [10
]. Anteby et al. [12
] and Hafner, Anteby, Pratt et al. [14
] reported significant increase in the III–V and I–V interwave intervals for several OM groups (separated by clinical state and history of treatment) compared with a control group. Persistence of delayed waves has been thought to be a reflection of the slowly recovering system than structural damage per se [9
Delayed wave III and V, and prolonged interpeak intervals I–III and III–V are the most common findings reported in past research on children with early onset OM. However, there seems to be very little common in the operational definition of early onset OM in the studies referred to above. Early OM was OM occurring before 18 months in Gunnarson and Finitzo [10
], in infancy [9
], before 12 months of age [13
], before 5.8 years of age at the least [11
], and before 2 years 4 months at the least in Chambers et al. [8
There is evidence to show that major changes in brain organization take place in the first year of life though changes continue into adolescence [15
]. The sensori motor region witnesses the earliest myelogenesis [16
]. Waves I, II and V of auditory brainstem responses are readily discernible at birth [17
], while the inter-peak intervals II–III and IV–V continue to shorten during the first 2 years of life [18
]. These intervals reflect trans-synaptic transmission. Matschke, Stenzel, Plath, and Zilles [19
], in a study of 39 human brains ranging in age from 29 weeks of gestation to 70 years, demonstrated that myelination takes place in the first year of life which is necessary for functional maturation. It appears that normal auditory development is dependent on adequate stimulation during this sensitive period of life. There is also evidence to say that inter-peak intervals and central conduction time of the auditory brainstem responses shorten between 3rd
trimester of pregnancy and first 2 years of life [20
]. Maturation of nerve cells in the upper nuclei as well as myelinization of small and large fibers in the auditory pathway was the reason for the reduction in central conduction time.
Synchronized encoding of transient acoustic information at the brainstem level leads to robust processing of auditory signals at the cortical level in the normal auditory system. Dys-synchronized activity at the brainstem may result in temporally degraded responses. Degraded auditory signals will not obviously result in the accurate encoding of the temporal features of the signal at the auditory cortex. Wible, Nicol and Kraus [21
] recorded ABR and LLR for speech sound/da/in children with language-based learning problems and reported a good positive correlation between the results of ABR and LLR. Prolonged duration of brainstem encoding of speech sound onset, suggesting less precise timing of generation and/or transmission at inferior colliculus, was associated with weaker cortical activity. Wible et al reported 2 distinct group of subjects in whom auditory processing was different. The first group of subjects demonstrated measures of auditory signal processing at brainstem and cortical levels that were proportionate to each other. The abnormal processing of auditory signals in these subjects at the cortical level may primarily have been a result of corrupt 'input' to the thalamo-cortical circuitry which, in turn, was perhaps because of possibly degraded processing and/or transmission at the lateral lemniscus and/or inferior colliculus. A second group of children showed degraded processing at the brainstem level, but robust processing of signals at the cortical level. However, as changes in LLRs are determined, among other factors, by the integrity of underlying neural substrates at the peripheral, brainstem, and cortical levels, it is logical to say that LLRs are influenced also by the maturation and/or pathological status of the lower-level auditory processors.
Thus, cortical potentials are reported to be more sensitive than brainstem potentials in detecting subtle auditory processing deficits [22
]. However, there are no studies which have recorded cortical potentials in children to study the effects of early onset OM. As there is some evidence to suggest that auditory processing is affected at the level of brainstem as a consequence of OM, it can be assumed that auditory cortex receives abnormal input from the brainstem which, in turn, results in abnormal auditory processing at the cortical level also. Such effects would be more pronounced if OM, and thus the reduced auditory input, occurs before 2 years of chronological age as auditory brainstem and cortical structures show greater development in the first year of a child's life.
Therefore, the purpose of this study was to determine the effect of early onset OM (occurring in the first year of life) on auditory brainstem and cortical potentials in an Indian population. A second purpose was to see the persisting nature of the effects of early onset OM. The high probability of OM, in Indian population, as a cause of conductive hearing loss [5
] necessitates such studies in the Indian context.