Auditory processing disorder (APD) is a poorly understood, heterogenous and surprisingly common condition. It manifests as a perceptual difficulty in centrally processing auditory information. Diagnosis is usually based on a variety of behavioural tests involving verbal and non-verbal assessments. In this study, the authors investigated the central pathways that may be involved in the aetiology of APD. Cortical evoked auditory potentials assess auditory responses in the auditory cortex. They occur between 50 and 400ms after sound stimulation and, similarly to other auditory potentials, have different components. The components P1 and N1 are early components, and are considered purely responsive to acoustic spectral characteristics, and unaffected by neurodevelopmental conditions that can, and often do, co-exist with APD. P1 is thought to arise from the medial part of Heschl’s gyri, and N1 from the planum temporale. Children with APD have already been shown to have differing P1/N1 responses to speech stimuli. The aim of this study was to compare the P1 and N1 responses directly between verbal and non-verbal stimuli in children with and without APD. They enrolled 21 children with APD, and a group of 16 age-matched controls. The APD group had a longer P1 and N1 latency for both verbal and non-verbal stimuli, but physiological increases in latency with speech stimulus seen in the control group were absent in the APD group. The APD group had a greater amplitude in P1 responses to speech rather than non-verbal stimuli, and the inverse was seen in N1 amplitudes. These results give some insight into mechanisms that may underly APD, specifically the patterns in which neurones in the central nervous system may be recruited in response to verbal and non-verbal stimuli. However, there remains a major limitation to our understanding of the aetiology due to the disparity between the immense complexity of central processing, and our ability to observe this at the required level of detail. More importantly at the moment, is whether such data can help formulate objective tests for APD and allow earlier, more robust diagnosis. As our interventions for APD improve, this will become even more important.