Between the ages of three and six years, children can understand spoken language effortlessly. However, preschoolers do not perceive speech as efficiently as adults do, and there may also be differences between children of the same age who have different language skills, for example, children with typical language development (TLD) versus those with Developmental Language Disorder (DLD). DLD, previously referred to as Specific Language Impairment (SLI), affects around 7% of children and is characterised by a range of language deficits, especially in morphosyntactic and phonological processing, without an identifiable medical cause [1]. The underlying causes of DLD are still largely unknown, but many studies suggest that children with language difficulties process speech differently from their typically developing peers [2,3].

However, the neural mechanisms underlying speech processing in young children are not well understood. Despite plenty of behavioural and brain imaging research, scholars do not know yet what cortical patterns of speech perception are typical at preschool age or whether these patterns vary between children and adults or between children with TLD and DLD [4]. Understanding this is important because early childhood is a period of significant language growth, and spoken language perception is critical for children’s later communication and literacy development. It is also during early childhood when many children with language disorders are first diagnosed, suggesting that some language symptoms could become more apparent at this age. Therefore, identifying neural patterns associated with typical and atypical speech processing in children could aid the development of objective clinical measures, fostering the earlier detection of and intervention in language disorders. Importantly, this would require determining adult reference values first, representing the neurotypical, mature cortical speech-processing patterns against which to compare children’s responses.

As for the role of speech perception deficits in DLD, different hypotheses have pointed out that specific problems with processing speech sounds could be an underlying marker of this disorder [5,6]. However, there is no clarity about the nature of these difficulties. Some early theories of DLD state that low-level speech perception deficits are a hallmark of DLD. For example, difficulties in detecting rapid acoustic changes within speech sounds or extracting distinctive acoustic cues from the speech stream could lead to unstable phonological representations, which then manifest as phonological deficits, such as difficulties in repeating non-words (see [7] for a review). Other accounts have proposed that speech perception deficits in DLD could be a consequence and not a cause of language difficulties [8], where less efficient speech processing in DLD derives from limited language skills, and not vice versa. For example, poorer phonological processing skills in DLD than in TLD may affect children’s ability to detect subtle acoustic changes in speech sounds but not in other sound contrasts [9]. Notably, several studies have failed to detect any evidence of atypical speech processing in DLD [10], suggesting that either these deficits do not exist or they cannot be detected with the current methods. So far, neurobiological findings are contradictory, making it difficult to identify any neural markers of speech perception deficits in DLD.

An advantageous method to investigate the brain processing of complex, rapidly changing acoustic signals, such as speech, is the electroencephalogram (EEG) because of its high temporal resolution. From the EEG, it is possible to extract event-related potential (ERP) components, such as the Mismatch Negativity (MMN), which has been extensively used across a wide range of ages and populations [11,12], and the less-studied Late Discriminative Negativity (LDN). Unlike early auditory detection responses, such as the P50/P1/N1 components, the MMN and LDN reflect cortical sound discrimination, a process that occurs later in the brain, at fixed latencies (time-locked), after a change in auditory stimulation. In adults, the auditory MMN is a negative deflection of about 0.5–5 µV that occurs 100–250 ms after a discriminable change in any acoustic feature [12]. The LDN appears later (250–400 ms) and seems to be more pronounced in children than in adults [13] and for auditory contrasts involving speech rather than nonspeech sounds [14], for which some studies consider it a signature of sound processing complexity [15]. In infants and young children, the MMN and LDN may present an immature form, so mismatch response (MMR) is a generic term to refer to these responses deviating from the adult-like pattern [16]. Like the adult MMN/LDN, the MMR reflects the brain’s sensitivity to physical and abstract changes (“deviants”) in a sequence of regular sounds (“standards”) in many acoustic contrasts, including speech. The MMR/MMN/LDN can be elicited during unattended listening, making it a valuable measure when behavioural responses are not possible or are less reliable, as in young children or clinical groups [12].

In speech perception research, the MMR/MMN/LDN is used as a pre-attentive discrimination index of general auditory processing elicited by low-level, physical changes (i.e., in pitch, duration, or intensity) but also of speech-specific processing elicited by changes in higher-level, abstract linguistic representations (e.g., phonemic categories, lexical status, or word classes). Thus, the MMR/MMN/LDN not only depends on the bottom-up (afferent) processing of the speech acoustic features but is also influenced in a top-down manner by psycholinguistic factors, such as the listener’s knowledge of phonological categories and structures, as well as the words’ grammatical function, distributional frequency, and meaning [17]. Evidence from adults indicates that language-specific top-down mechanisms selectively facilitate the processing of speech [18], developing gradually during childhood from around the age of 7 years [19]. However, there is little evidence about how top-down modulations of speech perception operate at different stages of language development or whether they are impaired in children with language difficulties. Considering several studies indicating reduced or slower MMR/MMN/LDN in DLD (see [20] for a review), it is possible that the MMR/MMN/LDN response could serve as a neural marker of speech-specific difficulties in DLD.

One potential factor contributing to this gap in knowledge about the underlying nature and cause of DLD is the methodological complexity of conducting MMR research in young children (especially in clinical populations) and comparing groups of children and adults [21]. Children are less able to tolerate long, repetitive testing sessions and may become fussy, introducing movement-related artefacts in the EEG. There are also neuroanatomical differences between adults and children (e.g., in head size, skull and cortical thickness, cortical fibre density) that complicate a direct comparison of their ERP responses [22]. In general, adults’ ERPs are intrinsically smaller and more consistent in timing than those of children, which are larger and much more variable [23]. Thus, when studying speech perception development across broad age ranges, it would be appropriate to complement conventional time-domain measures (e.g., amplitude and latency) with time–frequency measures (e.g., changes in spectral power or phase coherence over time). This would allow the measurement of important cortical oscillatory activity that is not consistently time-locked to the stimulus and would be otherwise lost in ERP averaging [24].

2. MMR/MMN/LDN in Speech Perception Development

3. MMR Time–Frequency Analysis and Speech Perception Development