Language delay
Language delay, also known as late language emergence, is a developmental condition in which young children exhibit a slower rate of acquiring speech and language milestones compared to age-matched peers, while following the typical sequence of development and without evident deficits in cognition, motor skills, or other domains.[1][2] It primarily manifests as delayed expressive language, such as limited vocabulary or sentence formation by age 2-3 years, though receptive language (comprehension) is often preserved initially.[3] Prevalence estimates for late language emergence in toddlers range from 10% to 15%, with higher rates observed in males due to sex-linked genetic and maturational factors.[2][4] Distinguishing language delay from persistent developmental language disorder (DLD) remains challenging in early stages, as delays often resolve spontaneously by school age in 70-80% of cases, whereas DLD involves ongoing impairments affecting learning and social integration.[2][5] Risk factors include genetic heritability (e.g., family history of delays), male sex, low socioeconomic verbal input, bilingual exposure (which may transiently mimic delay), and perinatal issues like prematurity, though many cases are idiopathic without clear etiology.[6][7] Environmental contributors, such as reduced parent-child interaction or excessive screen time, correlate with delays but do not imply causation in isolation, emphasizing multifactorial origins over simplistic attributions.[8] Early screening and intervention, including speech therapy focused on naturalistic language stimulation, can mitigate long-term risks like reading difficulties or behavioral issues, though evidence for universal screening efficacy is mixed due to over-identification concerns.[9][10]Overview and Epidemiology
Definition and Terminology
Language delay, also termed late language emergence, describes a condition in which a child's acquisition of spoken language skills occurs at a slower pace than expected for their age, without accompanying impairments in cognition, motor abilities, sensory functions such as hearing, or neurological status.[1] This delay manifests as failure to meet normative milestones, such as producing fewer than 50 words by 24 months or combining words into phrases by 30 months, while the underlying developmental trajectory follows a typical sequence albeit protracted.[11] Unlike transient variations in bilingual or dialectal contexts, language delay implies a quantifiable lag relative to standardized norms, often prompting early screening to differentiate resolvable cases from those requiring intervention.[12] Terminology distinguishes expressive language delay, involving deficits in verbal output such as vocabulary production or sentence formation, from receptive delay, which affects comprehension of spoken input including following directions or identifying objects.[1] Mixed delays combine both domains, while terms like "late talker" specifically denote toddlers with isolated expressive limitations who may catch up by preschool age without therapy.[13] Historical labels such as specific language impairment (SLI) have evolved toward developmental language disorder (DLD) for persistent cases, emphasizing chronicity beyond mere delay; delay connotes potential for spontaneous resolution, whereas disorder indicates atypical patterns persisting into school years with functional impacts.[14] [15] The boundary between delay and disorder hinges on developmental patterning: delays exhibit uniform slowing across skills, akin to a maturational lag, whereas disorders feature uneven or deviant progression, such as preserved articulation amid grammar deficits.[16] This distinction informs prognosis, with approximately 70% of late talkers resolving by age 4, underscoring the need for longitudinal assessment over static diagnosis.[17]Prevalence and Recent Trends
Language delay, encompassing both expressive and receptive deficits without identified biomedical causes, affects approximately 7% of children by school entry, equivalent to about 1 in 14 individuals persisting into later childhood.[18] In the United States, up to 12.5% of children aged 2 to 5 years exhibit speech or language delays, with prevalence estimates for developmental language disorder (DLD) specifically ranging from 5% to 10% among preschoolers.[10] These figures derive from population-based surveys and longitudinal studies, though diagnostic criteria variations—such as excluding transient delays versus persistent DLD—contribute to reported ranges of 3% to 8% globally.[19] Prevalence is higher in certain subgroups: boys show 2-3 times greater risk than girls, and rates elevate to 20-40% among children with low socioeconomic status or multilingual home environments, though the latter often reflects bilingual acquisition patterns rather than true disorder.[18] In clinical settings, such as pediatric outpatient visits, speech and language delays appear in about 2.5% of cases, frequently comorbid with conditions like birth asphyxia or seizures.[6] Recent trends indicate a post-2020 surge linked to COVID-19 disruptions. First-time speech delay diagnoses among U.S. children under 3 years rose from 9.0% on average in 2018 to 11.8% by late 2021 and 16.9% in early 2022, coinciding with lockdowns reducing peer interactions and early interventions.[20] Speech-language pathology referrals increased 70% above 2020 baselines by 2025, with persistent deficits observed in pandemic-era cohorts up to 30 months, attributed to diminished social exposure rather than viral effects.[21][22] Broader developmental disorder prevalence, including language components, climbed from 25.3% in 2016 to 27.7% by 2021, though this encompasses anxiety and behavioral shifts potentially confounding isolated language metrics.[23] Pre-pandemic stability suggests these elevations may normalize with resumed socialization, but longitudinal tracking remains essential.[24]Typical Language Development
Key Developmental Milestones
Newborns communicate primarily through crying and reflexive vocalizations, which vary in pitch and intensity to signal needs such as hunger or discomfort; by 2-3 months, infants begin cooing and producing pleasure sounds like "oo" and "ah," while recognizing familiar voices and calming to them.[25] These early vocalizations lay the foundation for later language, with most infants babbling consonant-vowel combinations (e.g., "ba," "ma") by 4-6 months and responding to their name.[25] From 7-12 months, babbling becomes more varied and speech-like, incorporating long and short syllable strings (e.g., "tata upup"), and approximately 50% of children produce their first recognizable words like "mama" or "dada" by 12 months, alongside gestures such as pointing and understanding simple directives like "no."[25] [26] Between 1-2 years, expressive vocabulary expands rapidly, with children acquiring new words weekly and forming two-word phrases (e.g., "more milk") by 24 months; by this age, typical children use 50 or more words and follow basic two-step instructions, indicating receptive language outpacing production.[25] [27] In the 2-3 year range, children combine words into short sentences of two to three words, speak in phrases understandable to familiar listeners (50-75% intelligibility), and exhibit a vocabulary spurt to 200-300 words, naming objects and actions while grasping simple questions.[25] [27] By 3-4 years, sentences grow to four or more words with emerging grammar (e.g., plurals, possessives), and children recount events in sequence, answering "who," "what," and "where" queries with 75% intelligibility to strangers.[25] From 4-5 years, language approximates adult complexity, with detailed sentences, full stories, and most speech sounds mastered except perhaps "r," "l," or "s"; vocabulary reaches 1,000-2,000 words, supporting abstract concepts and easy communication.[25] [28] These milestones, derived from normative data on large cohorts, reflect achievements by 75-90% of children, with variations influenced by multilingual exposure but delays warranting evaluation if persistent beyond expected windows.[29]Normal Variations and Predictors of Delay
Children exhibit substantial individual differences in the timing of language milestones, with expressive vocabulary at 24 months ranging from fewer than 50 words in late talkers to over 300 words in advanced talkers, yet many late talkers achieve normal language skills by age 4 without intervention.[2] [1] Late language emergence, often defined as fewer than 50 expressive words by 24 months in the absence of cognitive, sensory, or neurological impairments, affects 13-15% of toddlers and typically resolves spontaneously in the majority, representing a benign variation rather than pathology when isolated.[2] Bilingual exposure introduces temporary delays in lexical acquisition due to divided input, but does not predict persistent impairment if monolingual peers' norms are not rigidly applied; such children often exhibit balanced bilingual proficiency by school entry.[2] Persistent delays beyond transient variations are predicted by multiple risk factors, including male sex, which confers approximately twice the likelihood compared to females across population studies.[3] [30] Familial history of speech-language impairment increases odds by 2-4 fold, reflecting heritable components independent of environmental influences.[3] [31] Prematurity and low birth weight elevate risk through potential neurodevelopmental disruptions, with preterm infants showing 1.5-2 times higher incidence of delays.[3] [32] Lower maternal education and socioeconomic status correlate with delayed trajectories, partly via reduced verbal stimulation, though these effects diminish when controlling for genetic factors.[33] [34] Recurrent otitis media contributes via transient hearing loss, raising delay risk by up to 30% if untreated before 18 months.[30] Early indicators distinguishing normal variations from at-risk trajectories include gestural communication deficits and reduced consonant production by 18-24 months, which forecast poorer outcomes more reliably than vocabulary size alone.[35] Children with isolated late talking but intact nonverbal IQ and pragmatic skills (e.g., joint attention) have over 70% resolution rates, whereas co-occurring factors like sleep disturbances or prenatal exposures (e.g., maternal smoking) compound vulnerability through disrupted neural maturation.[35] [32] Longitudinal tracking reveals that while group-level predictors hold, individual heterogeneity necessitates monitoring rather than presumptive intervention for mild cases.[36]Etiology
Genetic and Heritable Factors
Heritability estimates for language delay and related disorders, such as developmental language disorder (DLD) and specific language impairment (SLI), derive primarily from twin and family studies, indicating a moderate to high genetic contribution.[37] A meta-analysis of twin studies reported monozygotic twin concordance rates of 83.6% for spoken language disorders compared to 50.2% for dizygotic twins, supporting genetic influences independent of general cognitive ability in some cases.[38] Recent analyses estimate heritability at 27-52% for DLD traits, with variations depending on diagnostic criteria and measurement methods, such as parental reports versus standardized assessments.[37][39] These figures suggest polygenic inheritance, where multiple genetic variants contribute cumulatively, rather than single-gene dominance, though environmental interactions modulate expression.[40] Rare monogenic forms highlight specific genetic mechanisms, notably mutations in the FOXP2 gene, which disrupt speech motor planning and orofacial coordination, leading to childhood apraxia of speech (CAS) and associated language deficits evident from early childhood.[41] Affected individuals exhibit impaired articulation, grammatical errors, and comprehension difficulties, with pedigree studies tracing transmission in a dosage-dependent manner.[42] However, FOXP2 variants account for only a small fraction of cases, as genome-wide association studies (GWAS) and linkage analyses implicate broader loci without strong FOXP2 involvement in common idiopathic DLD or SLI.[43][44] Candidate genes from targeted and genome-wide research include CMIP, ATP2C2, GRIN2A, ERC1, and downstream targets like CNTNAP2, which influence neuronal connectivity, synaptic function, and cortical development critical for language processing.[44][45] Family aggregation studies further demonstrate elevated risk in relatives, with odds ratios up to 2-4 times higher for language impairments when probands are affected, underscoring heritable polygenic risk shared across neurodevelopmental traits like dyslexia and autism spectrum features.[46] Recent GWAS efforts, though limited by sample sizes, identify novel variants in genes such as ARID4A and PPP2R2C, potentially affecting chromatin regulation and phosphatase signaling in brain regions like the basal ganglia and cerebellum.[47] These findings emphasize multifactorial etiology, where genetic loading interacts with developmental timing to precipitate delays, rather than deterministic causation.[48]Neurobiological and Medical Contributors
Neurobiological contributors to language delay involve structural and functional anomalies in brain regions critical for language processing, independent of overt genetic mutations. A 2024 meta-analysis of structural neuroimaging studies identified consistent abnormalities in the basal ganglia, particularly the anterior neostriatum, among children with developmental language disorder (DLD), a condition encompassing persistent language delays without intellectual disability or other primary causes.[49] These subcortical structures, traditionally linked to motor control, exhibit reduced volume or atypical connectivity, potentially disrupting procedural learning mechanisms essential for grammar and sequencing in speech production.[50] Functional imaging further reveals inefficient activation in perisylvian language networks, including Broca's and Wernicke's areas, during language tasks in affected children, suggesting impaired neural integration rather than isolated regional deficits.[51] Medical conditions contributing to language delay often stem from perinatal insults, recurrent infections, or neurological disorders that impair auditory input or brain maturation. Preterm birth and low birth weight elevate risk for receptive and expressive delays, with a population-based study showing odds ratios up to 2.5 for language impairment at ages 1.5 to 5 years, attributable to white and gray matter disruptions from immature neural development.[52] Chronic otitis media, through fluctuating conductive hearing loss, correlates with phonological and expressive delays; longitudinal evidence indicates that repeated episodes before age 3 years hinder auditory processing maturation, with affected children demonstrating persistent deficits in suprathreshold auditory functions and vocabulary acquisition.[53][54] Epilepsy syndromes frequently manifest with language regression or stagnation, as seizures disrupt cortical networks during sensitive developmental windows. In pediatric cohorts, epilepsy duration exceeding 12 months doubles the likelihood of moderate to severe delays, mediated by epileptiform activity in temporal-parietal regions rather than seizure frequency alone.[55] Central nervous system injuries, including perinatal hypoxia or congenital malformations, further compound risks by altering bilateral language pathway integrity, with outcomes varying by lesion laterality and timing.[56] These contributors underscore the interplay of disrupted sensory-neural cascades, where early intervention targeting underlying physiology—such as tympanostomy for otitis or seizure control—can mitigate but not invariably reverse delays.[57]Environmental and Socioeconomic Influences
Low socioeconomic status (SES) constitutes a prominent environmental risk factor for language delay, primarily through reduced quantity and quality of linguistic input during critical early periods. Children from low-SES households experience disparities in vocabulary acquisition and syntactic development as early as 18 months, with effect sizes indicating 4-6 months of delay in expressive language by age two compared to higher-SES peers.[58] These gaps arise from fewer parent-child verbal interactions, averaging 30 million fewer words heard by age three—a finding from observational studies replicated across diverse cohorts despite variations in measurement.[59] Parental education, as a SES proxy, correlates strongly with delay incidence; a 2019 cross-sectional study of 1,658 Indian children aged 1-12 found low maternal education in 81% of cases with delay versus 28.6% without (p<0.001), and low paternal education in 71.4% versus 42.9% (p=0.008).[6] Similarly, inadequate home stimulation—encompassing limited reading, play, or conversation—was present in 61.9% of delayed children versus 0% of controls (p<0.001), underscoring how resource scarcity impairs responsive caregiving.[6] Multilingual or bilingual home environments, often intersecting with low SES, elevate risk when input lacks depth or consistency; the same study reported multilingualism in 73.8% of delayed cases versus 7.1% of typical developers (p<0.001), though this reflects insufficient monolingual reinforcement rather than bilingualism inherently causing impairment.[6] In deprived minority-ethnic communities, such as those studied in UK cohorts, poverty amplifies these effects, with children facing 1.5-2 times higher odds of delay due to compounded stressors like housing instability and reduced access to early enrichment.[60] Broader environmental mediators include chronic parental stress from economic hardship, which diminishes interactive parenting quality and correlates with slower lexical growth rates in toddlers.[58] Neuroimaging data further reveal poverty-linked alterations in brain regions for language processing, such as reduced activation in left-hemisphere areas during comprehension tasks, persisting into preschool without intervention.[61] These influences operate independently of genetic factors, as twin studies disentangle SES effects via differential input, emphasizing causal pathways amenable to environmental modification.[62]Classification
Expressive Language Delay
Expressive language delay refers to a developmental condition in which a child's ability to produce spoken language, including vocabulary, grammar, and sentence structure, lags significantly behind age expectations, while receptive language skills—such as understanding words and instructions—remain relatively intact or develop appropriately.[63][57] This discrepancy distinguishes it from global language delays, where both expressive and receptive domains are impaired.[64] In clinical classification, expressive language delay is often identified through standardized assessments showing expressive scores at least 1.25 to 2 standard deviations below the mean, with receptive scores within normal limits and no primary deficits in nonverbal cognition, hearing, or oral-motor function.[65] For instance, late language emergence, a common precursor, is defined by fewer than 70 expressive words or absence of word combinations by 24 months of age.[65] Historical diagnostic manuals, such as DSM-IV, categorized it under expressive language disorder (code 315.31), requiring symptoms like limited vocabulary, tense errors, word-finding difficulties, or impaired discourse that interfere with academic or social functioning, excluding causes like intellectual disability or sensory impairment.[66] Contemporary frameworks, including those from the American Speech-Language-Hearing Association (ASHA), emphasize functional communication impacts rather than rigid subtypes, though expressive-predominant profiles persist in differential diagnosis.[1] Key manifestations include delayed onset of first words (often beyond 18 months), slow vocabulary growth (e.g., fewer than 50 words by 24 months), simplified grammar with omissions of function words or morphemes, and challenges in narrative formation or conversational turn-taking, despite adequate comprehension of similar complexity.[57][67] Unlike receptive delays, which involve core comprehension deficits, expressive delays may stem from motor planning issues, lexical retrieval problems, or syntactic formulation challenges, but classification requires ruling out autism spectrum disorder, where social-pragmatic deficits often compound expressive issues.[64] Longitudinal studies indicate that approximately 50% of children with isolated expressive delay at toddlerhood resolve spontaneously by school age, supporting its classification as a potentially transient subtype within the broader spectrum of developmental language disorders.[68] Classification also considers etiological exclusions: delays must not primarily arise from neurological conditions (e.g., cerebral palsy), environmental deprivation, or bilingualism, which can mimic expressive lags but resolve with targeted support.[69] Peer-reviewed reviews highlight that specific expressive language impairment, characterized by normal nonverbal IQ and receptive skills, affects 3-7% of preschoolers and warrants early monitoring to differentiate persistent cases from normative variation.[67][70]Receptive Language Delay
Receptive language delay is defined as a child's impaired ability to comprehend spoken or signed language, including difficulties processing vocabulary, syntax, and semantics, relative to chronological age and nonverbal cognitive abilities.[64] This contrasts with typical development, where receptive skills precede expressive ones, such that delays in comprehension often signal more profound impairments than isolated expressive delays.[1] Key characteristics include failure to follow age-appropriate directions (e.g., a 2-year-old not responding to "point to the ball"), limited recognition of common objects or body parts, and challenges understanding questions or narratives, without primary deficits in hearing or motor skills.[25] Isolated receptive delays are uncommon in otherwise typically developing children and frequently co-occur with expressive impairments, autism spectrum disorder, or global developmental delays, necessitating exclusion of sensory or neurological causes.[71] Diagnosis requires standardized assessments, such as the Peabody Picture Vocabulary Test (PPVT) or Clinical Evaluation of Language Fundamentals (CELF) receptive subtests, showing scores at least 1.5–2 standard deviations below the mean, alongside parent/teacher reports and observation.[3] Unlike expressive delay, which may resolve spontaneously in up to 70–80% of late talkers by age 3, receptive-predominant profiles demand earlier referral due to higher persistence rates; for instance, in cohorts with severe receptive impairment at preschool age, approximately one-third exhibit ongoing deficits into school age.[71] Familial aggregation is evident, with siblings of affected children showing elevated risk (up to 30% outside normal ranges), pointing to heritable components over purely environmental factors.[71] Prognosis for receptive language delay is generally poorer than for expressive-only cases, with untreated children facing heightened risks of academic underachievement, including reading comprehension deficits persisting into adulthood, and social-emotional challenges from misinterpreted interactions.[72] Early identification before age 3 correlates with better outcomes via targeted interventions, but severe cases rarely resolve without support, underscoring the need for multidisciplinary evaluation to rule out comorbidities like intellectual disability or specific language impairment transitioning to developmental language disorder (DLD).[10][64]Developmental Language Disorder and Mixed Types
Developmental Language Disorder (DLD) refers to a persistent neurodevelopmental impairment in language acquisition and use, characterized by deficits that significantly affect comprehension, expression, or both, unexplained by intellectual disability, hearing loss, autism spectrum disorder, or acquired brain injury.[5] Unlike transient language delays, DLD manifests in early childhood and endures into school age or beyond, with language abilities typically falling more than 1.25 standard deviations below age-matched norms on standardized assessments.[73] Prevalence estimates indicate DLD affects about 7% of kindergarten-aged children, or roughly 1 in 14, positioning it as a common yet underrecognized condition with lifelong implications for communication and learning.[5][74] In classification, DLD encompasses profiles where receptive and expressive domains are both compromised, often termed mixed receptive-expressive presentations, distinguishing it from isolated expressive or receptive delays that may resolve spontaneously.[75] Children with mixed DLD exhibit combined difficulties, such as limited vocabulary comprehension alongside grammatical errors in speech production, leading to challenges in following multi-step instructions, narrating events coherently, and participating in conversations.[76] This mixed subtype correlates with heightened risks for co-occurring issues, including attention deficits and behavioral problems, compared to unimpaired profiles.[75] Diagnostic criteria emphasize exclusionary factors through multidisciplinary evaluation, including cognitive testing to confirm non-verbal IQ within normal limits and absence of environmental deprivation.[77] Subtypes within DLD, including mixed forms, arise from heterogeneous underlying mechanisms, with empirical studies highlighting genetic heritability rates of 50-70% in familial cases, though environmental modulators like low socioeconomic status exacerbate severity.[77] Longitudinal data reveal that mixed DLD profiles predict poorer academic outcomes, with affected individuals showing persistent deficits in reading comprehension and written language by adolescence.[78] Early identification relies on milestones such as failure to combine words by age 2 or comprehend basic questions by age 3, prompting referral for comprehensive language testing.[79] While DLD terminology standardizes diagnosis across clinical and research contexts—superseding older labels like specific language impairment—its application requires caution to avoid overpathologizing normal variations, prioritizing evidence from norm-referenced tools over subjective checklists.[73][80]Clinical Presentation and Diagnosis
Signs, Symptoms, and Early Indicators
Language delay in children is characterized by a failure to achieve expected milestones in speech production (expressive language) or comprehension (receptive language), often evident as early as infancy through observable absences in vocalization, gesturing, or response to auditory stimuli.[25] Early indicators include reduced babbling, limited imitation of sounds, and lack of response to one's name or simple directives, which deviate from typical development where infants begin cooing by 2-3 months and progress to meaningful words by 12 months.[81] These signs must be assessed against population norms, as isolated delays may resolve spontaneously in up to 70-80% of late talkers by age 3, though persistent absence signals potential disorder.[2] In infants under 12 months, key early indicators encompass:- Absence of cooing or vowel-like sounds by 4-6 months, contrasting with typical reactive vocal play to caregiver interaction.[25]
- No consonant-vowel babbling (e.g., "ba-ba") or varied intonation by 7-9 months, often accompanied by failure to respond to name or familiar sounds.[81]
- Limited gesturing, such as not pointing to desired objects or waving by 10-12 months, which correlates with delayed joint attention foundational to language acquisition.[10]
- Fewer than 6-10 first words by 18 months, versus the norm of 20-50 words, indicating expressive delay.[64]
- No two-word combinations (e.g., "more milk") by 24 months, alongside vocabulary stagnation below 50 words.[25]
- Receptive deficits, such as not following simple one-step directions (e.g., "give me the ball") or identifying body parts/objects by 18-24 months.[81]
Screening and Diagnostic Tools
Screening for language delay typically involves parent- or caregiver-completed questionnaires or brief clinician-administered measures to identify children at potential risk, often during well-child visits between 18 and 36 months of age.[82] These tools aim to detect delays in expressive or receptive language skills but exhibit variable accuracy, with systematic reviews indicating median sensitivities of 81% (range 50-100%) and specificities of 78% (range 50-100%) for parent-reported screeners detecting true speech and language delays.[83] Factors influencing performance include child age, tool format (e.g., checklist vs. structured questions), and domain specificity, with communication subscales often underperforming compared to comprehensive assessments.[84] The Ages and Stages Questionnaires, Third Edition (ASQ-3), a widely used developmental screening instrument, includes a communication subscale relying on parent reports of milestones like word production and comprehension.[10] It demonstrates high specificity (72-99%) and negative predictive value (69-98%) across domains but lower sensitivity (19-74%) and positive predictive value (11-59%), potentially missing over one-third of children with low language ability.[85][86] Validity studies confirm moderate utility for predicting severe delays when scores exceed 2 standard deviations below the mean, though it is less reliable for isolated language concerns without broader developmental risks.[87] The MacArthur-Bates Communicative Development Inventories (MB-CDI) assess early vocabulary size, gestures, and sentence complexity through parent checklists for children aged 8-37 months.[88] Short forms and adaptive versions like CDI-CAT enhance feasibility for screening, showing reliability in normative samples, but evidence for diagnostic validity in identifying language difficulties remains insufficient, with limited sensitivity and specificity data for clinical cutoffs.[89][90] Diagnostic evaluation follows positive screening or clinical concern, involving speech-language pathologists (SLPs) in comprehensive assessments that include standardized tests, observation, and exclusion of confounding factors like hearing loss via audiometry.[74] The Clinical Evaluation of Language Fundamentals, Fifth Edition (CELF-5), a norm-referenced battery for ages 5-21, evaluates receptive, expressive, and pragmatic language through subtests like sentence repetition and word structure, with optimal cutoffs at -1.33 standard deviations (standard score of 80) balancing sensitivity and specificity for disorder severity.[91] Its screening version yields high sensitivity (0.90) and acceptable specificity (0.87) in some cohorts, though sensitivity drops to 35.6% for receptive deficits specifically.[92][93] Sentence repetition tasks within such tools show promise for distinguishing developmental language disorder, with meta-analyses supporting their discriminative power against typically developing peers.[94]| Tool | Type | Key Metrics (Sensitivity/Specificity) | Age Range | Source |
|---|---|---|---|---|
| ASQ-3 Communication | Screening (parent-report) | 19-74% / 72-99% | 1-60 months | [86] |
| MB-CDI | Screening (parent-report) | Insufficient evidence for clinical validity | 8-37 months | [89] |
| CELF-5 Screener | Screening/Diagnostic | 0.90 / 0.87 (overall); 35.6% / 95.3% (receptive) | 5-21 years | [92] [93] |