Central auditory processing deficits and central auditory processing disorder (CAPD) has been linked to a number of different etiological bases. Reports document CAPD in children stemming from neurological abnormalities, including seizure disorders, neoplasms, degenerative processes, traumatic brain injury, cerebrovascular accidents, metabolic disorders, and genetic disorders across a variety of sites of lesion at all levels of the central auditory nervous system (CANS). Also documented is the efficiency of central auditory behavioral tests and electrophysiological procedures in evaluating pediatric patients with known or suspected neurological involvement. All regions of the CANS can be assessed using auditory evoked potentials, electoacoustic procedures, and central auditory behavioral tests after a careful assessment of the peripheral auditory system. Multidisciplinary evaluation is crucial to both diagnosis and intervention given the potential for multiple system involvement, complex clinical profiles, and frequent co-morbidities in children with neurological problems. The patterns of performance deficits seen in children with documented CANS lesions are comparable to those patterns seen in adult patients with documented CANS lesions. Moreover, central auditory test battery deficit patterns seen in children with auditory-related complaints but with no identifiable lesions of the CANS mirror those patterns seen in pediatric and adult populations with circumscribed disorders of the CANS, and these deficit patterns correlate with neuroimaging results. These common patterns indicate that lesion studies of adult (or pediatric) patients can serve to approximate a ‘ gold standard’ for CAPD in children with no identifiable CANS lesion. Whether the source of CANS dysfunction is benign or the result of neurological lesion or compromise, the underlying source of the resulting CAPD is neurobiological, originating in the central nervous system.