Children who have listening difficulties (LiD) despite having normal audiometry are often diagnosed as having an auditory processing disorder (APD). A lack of evidence regarding involvement of specific auditory mechanisms has limited development of effective treatments for these children. Here, we examined brainstem pathway mechanisms in children with and without defined LiD. We undertook a prospective controlled study of 132 children aged 6-14 years with normal pure tone audiometry, grouped into LiD (n=63) or Typically Developing (TD; n=69) based on scores on the Evaluation of Childrens Listening and Processing Skills (ECLiPS), a validated caregiver report. The groups were matched on age at test, sex, race, and ethnicity. Neither group had diagnoses of major neurologic disorder, intellectual disability, or brain injuries. Both groups received a test battery designed to measure receptive speech perception against distractor speech, Listening in Spatialized Noise - Sentences (LiSN-S), along with multiple neurophysiologic measures that tap afferent and efferent auditory subcortical pathways. Group analysis showed that participants with LiD performed significantly more poorly on all subtests of the LiSN-S. The LiD group had significantly steeper wideband middle ear muscle reflex (MEMR) growth functions and shorter Wave III, Wave V, and I-V interpeak latencies in their auditory brainstem responses (ABR). Across individual participants, shorter latency ABR Wave V correlated significantly with poorer parent report of LiD (ECLiPS composite). Steeper MEMR growth functions also correlated with poorer ECLiPS scores and reduced LiSN-S talker advantage. The LiD and TD groups had equivalent summating potentials, compound action potentials, envelope-following responses (EFR), and binaurally activated medial olivocochlear reflexes (MOCR). In conclusion, there was no evidence for auditory synaptopathy or lower brainstem dysfunction for LiD. Evidence for higher brainstem differences between groups showed that the LiD group had increased efferent control or central gain, with shorter ABR Wave III and V latencies and steeper MEMR growth curves. These differences were related to poorer parent report and speech perception ability.