ICD-116A01	DEVELOPMENTAL SPEECH OR LANGUAGE DISORDERS Developmental speech or language disorders
ICD-10F80	Specific developmental disorders of speech and language
DSM-5-TRF80.2	Language Disorder

1. Definition and nosology

Developmental speech or language disorders are a group of neurodevelopmental disorders manifesting as persistent and significant difficulties in the acquisition of language and/or speech that are not fully explained by hearing impairment, an intellectual disorder or another neurological cause. In ICD-11, under the 6A01 code, four subtypes are coded:

• 6A01.0 — Developmental speech sound disorder — a deficit in the articulation and phonological formation of speech sounds;
• 6A01.1 — Developmental speech fluency disorder — stuttering;
• 6A01.2 — Developmental language disorder (DLD) — impairment in the development of receptive and/or expressive language (sub-specifiers: 6A01.20 receptive-expressive, 6A01.21 mainly expressive, 6A01.22 mainly pragmatic);
• 6A01.3 — Other specified.

Parallel terminology in DSM-5-TR: Language Disorder (F80.2), Speech Sound Disorder (F80.0), Childhood-Onset Fluency Disorder/Stuttering (F80.81), Social (Pragmatic) Communication Disorder (F80.82).

2. History

• Specific Language Impairment (SLI) — the term used from the 1980s until the 2010s; the word “specific” came to be criticised over time, because language disorder overlaps with numerous cognitive and behavioural domains.
• CATALISE consensus (Bishop D.V.M. et al. PLoS One 2016; J Child Psychol Psychiatry 2017) — a Delphi consensus of 59 international experts: the term “SLI” was replaced with “Developmental Language Disorder” (DLD). The IQ cut-off (≥85) for the diagnosis was abolished, with functional impairment adopted as the primary criterion.
• DSM-5 (2013) and ICD-11 (2019) — the term DLD was adopted; social (pragmatic) communication disorder was recognised as a category separate from autism spectrum disorder (new in DSM-5; as subtype 6A01.22 in ICD-11).
• Stuttering — the biological-genetic conception has been dominant since the 2000s (GNPTAB, GNPTG, NAGPA mutations — Kang C. et al. NEJM 2010).

3. Epidemiology

• DLD (6A01.2): prevalence at 5–6 years of age 7.58% (Norbury C.F. et al. J Child Psychol Psychiatry 2016, population-based study, n=7267, England).
• Speech sound disorder (6A01.0): ~3.8% at 6 years of age (Shriberg L.D. et al. J Speech Lang Hear Res 1999); higher at preschool age.
• Stuttering (6A01.1): cumulative incidence in childhood 5–8% (roughly one in every 20 children stutters at some point); persisting prevalence in adulthood ~1% (Yairi E., Ambrose N. J Fluency Disord 2013).
• Sex: 2–4 times higher in boys across all subtypes.
• Comorbidity: learning disorders 40–60%, ADHD 20–30%, autism spectrum 5–10%, increased risk of anxiety and conduct disorders.

4. Aetiology and pathogenesis

4.1 Genetic factors

• DLD heritability 50–75% in twin studies (Bishop D.V.M. Trends Cogn Sci 2014).
• FOXP2 mutations — rare severe speech and language disorder in the KE family (Lai C.S. et al. Nature 2001); polygenic nature in most cases.
• Stuttering: ~70% heritability (Felsenfeld S. et al. Behav Genet 2000 twin study); mutations in lysosomal pathway genes (GNPTAB, GNPTG, NAGPA) are detected rarely (~9%).
• CNV and GWAS studies — a polygenic risk architecture is also characteristic of DLD.

4.2 Neurobiology

• Atypical patterns in the development of the left perisylvian region (around Broca and Wernicke areas), the arcuate fasciculus, and the basal ganglia.
• In stuttering, dopaminergic dysfunction in the basal ganglia–supplementary motor area connection (Maguire G.A. et al. Curr Med Res Opin 2020 review).
• Early brain asymmetry — in DLD, weakening of the typical dominance of left-hemisphere language areas.

4.3 Risk factors

• Family history of language/speech disorder (the strongest risk factor).
• Preterm birth, low birth weight.
• Chronic otitis media in early childhood — hearing fluctuation may affect language acquisition.
• Low socioeconomic status — cited as a risk factor but not an aetiology; a deprived environment affects the expression of language development.
• Bilingualism — is not a risk factor (expanded topic §10).

4.4 Preventable and treatable causes

• Hearing impairment — the newborn hearing screening programme (UNHS) and timely treatment of otitis media are critical.
• Congenital cleft lip and palate — surgical correction + speech therapy.
• Hypothyroidism — newborn screening.

5. Clinical features

6A01.0 Speech sound disorder

• Age-inappropriate sound omission, substitution, distortion (for example, “r” → “l”, “s” → “t”).
• Unintelligibility — unfamiliar people have difficulty understanding the speech.
• Up to 4 years of age it is considered “mild” within the developmental framework; those persisting beyond 4 years should be reviewed diagnostically.

6A01.1 Speech fluency disorder (stuttering)

• Repetition of sounds and syllables (f-f-f-fish), prolongation (ssshello), blocks (a pause without initiating the sound).
• Secondary behaviours — gaze aversion, head shaking, avoidance.
• Onset typically between 2–5 years of age; ~70–80% of children who stutter recover spontaneously or with intervention within 5 years (Yairi E., Ambrose N. 2013).
• Social and emotional burden — social anxiety, school adjustment problems.

6A01.2 Developmental language disorder (DLD)

• Expressive component: limited vocabulary, short sentences, errors in grammatical morphology (especially tense and case endings), word-finding difficulty.
• Receptive component: difficulty understanding complex sentences, problems responding to behavioural instructions, delayed acquisition of multiple meanings and abstract language.
• Pragmatic component (6A01.22): deficit in the use of social language (turn-taking, context, indirect speech); unlike autism, social interest and non-verbal communication are relatively preserved.

Developmental trajectory

“Late talker” is a category at 2 years of age — 50–70% catch up by 4 years of age; however, the persisting group represents a high risk for DLD. Early identification of this group is based on the features of family history, receptive deficit, and low use of non-verbal gestures.

6. Diagnosis

6.1 Unified diagnostic criteria (DSM-5-TR · ICD-11 · CATALISE 2017 consensus points)

A. Persistent deficit in language or speech acquisition — performance below the age-appropriate normal level in one or more domains (vocabulary, syntax, phonology, fluency, pragmatics).

B. Functional impairment — significant limitation in one or more of academic achievement, social communication, occupational functioning, or daily life (CATALISE: functional impairment is essential for the diagnosis, an IQ cut-off is not).

C. Onset during the developmental period.

D. Exclusions — not fully explained by hearing impairment, a neurological condition, intellectual disability, autism spectrum disorder, or another medical/psychiatric condition. However, when there is comorbid coexistence both diagnoses are made.

6.2 Source-specific clarifications

• CATALISE 2017 (Bishop D.V.M. et al.): the term “specific” is abolished; the IQ cut-off of 85 is abolished (DLD can also be diagnosed against a background of intellectual disability); under the “language disorder” umbrella, co-morbid neurodevelopmental conditions and risk factors are indicated as qualifiers.
• ICD-11 (6A01): separation of subtypes (sound, fluency, language); 3 sub-specifications for language disorder (receptive-expressive, predominantly expressive, predominantly pragmatic).
• DSM-5-TR: Social Communication Disorder as separate category (F80.2); typical onset age for stuttering <6 years.
• ASHA Practice Portal: for diagnosis, standardized assessment by a certified speech-language pathologist (SLP), together with a parent interview and naturalistic observation, is required.
• RCSLT (Royal College of Speech and Language Therapists): the same framework in the United Kingdom; multidisciplinary assessment (hearing + speech-language + development).

6.3 Diagnostic algorithm

1. Parent and teacher interview (developmental history, language milestones).
2. Hearing test (audiometry — mandatory in all cases).
3. Standardized speech and language assessment (CELF-5, PLS-5, GFTA-3, DELV).
4. Naturalistic speech sample (in a play or conversation setting).
5. Non-verbal IQ measure (for the exclusion of ASD and intellectual disability).
6. Autism spectrum screening (M-CHAT-R/F < 30 months; SCQ preschool).
7. Social-emotional and behavioural screening.
8. Medical examination — neurological, cleft lip and palate examination, motor examination.

6.4 Differential diagnosis

7. Examination and assessment

7.1 Standardized tests

• Language: CELF-5 (Clinical Evaluation of Language Fundamentals, 5–21 years), PLS-5 (Preschool Language Scales, <7 years), CASL-2, Reynell Developmental Language Scales.
• Vocabulary: PPVT-5 (Peabody Picture Vocabulary Test), EVT-3, MacArthur-Bates CDI (up to 24 months).
• Speech sound: GFTA-3 (Goldman-Fristoe Test of Articulation), DEAP.
• Pragmatic language: CCC-2 (Children's Communication Checklist), Test of Pragmatic Language (TOPL-2).
• Non-verbal IQ: Leiter-3, RIAS-2 (independent of the verbal component).

7.2 Laboratory investigations

Not mandatory; based on specific suspicion:

• Hearing test — mandatory in all cases (audiometry, tympanometry, otoacoustic emissions).
• Fragile X (FMR1) — in cases of severe DLD + comorbid intellectual disability.
• Thyroid function (TSH, T4) — if congenital hypothyroidism has not been detected.
• Lead level — if risk factors are present.

7.3 Instrumental investigations

• Brain MRI — when there are focal neurological signs, regression, macro/microcephaly, or seizures. Not indicated in routine DLD.
• EEG — when a seizure is suspected, for the exclusion of Landau-Kleffner syndrome.

8. Treatment

8.1 General principles (ASHA · RCSLT · CATALISE · NICE consensus)

1. Individual speech-language therapy by a certified speech-language pathologist (SLP) is the first-line intervention for all disorders.
2. Early intervention — intervention between 2–4 years of age shows a greater effect; a “wait and see” approach is harmful when certain risk factors (family history, receptive deficit) are present.
3. Parent-coached interventions at a young age — the Hanen “It Takes Two to Talk” programme has shown effect in RCTs.
4. Intensity and duration — 1–3 sessions per week, 6–18 months, individualized according to behavioural and academic components.
5. Multidisciplinary approach — SLP + teacher + paediatrician + audiologist, occupational therapist, psychologist as needed.
6. School support — individual education plan (IEP / EHCP), classroom modifications, one-to-one support as needed.
7. Bilingualism is preserved — support maintaining the child's two languages; “abandoning” one language is not recommended (ASHA Position 2004).
8. Pharmacotherapy is not approved for the speech-language disorder itself. Separate intervention for comorbid ADHD, anxiety, or autism.

8.2 Intervention in speech sound disorder (6A01.0)

• Articulation therapy — a phoneme-by-phoneme approach (van Riper); minimal pair training (comparison of contrastive pairs of similar sounds).
• Reduction of phonological processes — systematic process-based therapy (Bowen C., Cupples L. 1999).
• In complex and severe cases — PROMPT, a multisensory approach.

8.3 Intervention in stuttering (6A01.1)

• The Lidcombe Program (Onslow M., Australian Stuttering Research Centre) — first-line at 3–6 years of age; a parent-coached, home-administered operant programme based on positive reinforcement. Evidence: Jones M. et al. BMJ 2005 RCT, n=54 — at 9 months the proportion of syllables stuttered was 1.5% (SD 1.4) in the treatment arm and 3.9% (SD 3.5) in the control arm; difference 2.3 percentage points (95% CI 0.8–3.9; p=0.003). Cochrane 2021 rates the evidence as very low certainty.
• Demands and Capacities Model (DCM) — Starkweather C.W. — adaptation of communicative demands to the child's current capacity.
• Older children/adults — Stuttering Modification (Van Riper), Fluency Shaping (Webster); family and group support.
• Pharmacotherapy: There is no drug officially approved by the FDA for stuttering. Off-label dopamine antagonists (risperidone, olanzapine) and SSRIs (paroxetine) have been studied in selected adult cases, but the effect is modest and the side-effect profile is significant (Maguire G.A. et al. 2020 review).

8.4 Intervention in developmental language disorder (6A01.2)

• Hanen “It Takes Two to Talk” — a parent-coached group programme at 2–4 years of age; following the child's lead, expanding dialogue. Evidence: Roberts M.Y., Kaiser A.P. Am J Speech Lang Pathol 2011 meta-analysis — a moderate effect on expressive and receptive language measures.
• Naturalistic language intervention (enhanced milieu teaching, focused stimulation) — presenting language models in the context of the child's interests.
• Structured morpho-syntactic therapy — targeted training of grammatical forms (for example, past tense, plural).
• Pragmatic language interventions (6A01.22) — Social Stories (Carol Gray), video-modelling, group training.
• Academic support at school age — a Structured Literacy approach due to the high comorbidity of reading difficulties; assessment for learning disorder.

8.5 Source-specific clarifications

• ASHA Practice Portal: an evidence-based practice framework — the triad of clinician judgement + evidence + family values; certification and continuing education requirements.
• RCSLT (2017 Position Paper on DLD): proposes early identification and service accessibility; the “Bercow” report (2008, 2018) shaped the service structure in England.
• NICE NG (a separate full guideline for child speech and language is still under development; existing guidance is directed at the coordination of education and health services).
• WHO mhGAP IG v2.0: assessment at the primary care level in low- and middle-income countries; parent training and community-based rehabilitation are emphasized.

Treatment methods

1. Hanen “It Takes Two to Talk” — a parent training programme developed by the Hanen Centre in Canada for late talkers and children at risk of DLD aged 2–4 years. 8 group sessions + 3 individual home visits; the principles of “OWL” (Observe, Wait, Listen) and following the child's lead. Evidence: Roberts M.Y., Kaiser A.P. Am J Speech Lang Pathol 2011 meta-analysis. hanen.org.
2. The Lidcombe Program — a behaviourally based, parent-coached programme for preschool-age stuttering developed by Onslow M. in Australia. The parent reinforces the child's fluent speech in a daily 10–15 min structured play session. Evidence: Jones M. et al. BMJ 2005 RCT n=54, 9 months; Onslow M. et al. reviews. lidcombeprogram.org.
3. Enhanced Milieu Teaching (EMT) — Naturalistic language intervention — the presentation and expansion of consistent language models in the context of the child's play and daily routine. Evidence: Kaiser A.P., Roberts M.Y. Am J Speech Lang Pathol 2013.
4. PROMPT method (Prompts for Restructuring Oral Muscular Phonetic Targets) — a tactile-kinaesthetic speech motor intervention — indicating the correct place of articulation with a physical sensory cue to the child's oral muscles. Used in complex speech sound disorder and childhood apraxia of speech. The evidence base is developing; Rogers S.J. et al. 2006 (against a background of autism) and other pilot studies.
5. Social Stories — Carol Gray — training appropriate behaviour in a social context in a short, individualized story format. In building pragmatic skills in pragmatic language disorder and the autism spectrum. carolgraysocialstories.com.
6. Clinical Evaluation of Language Fundamentals (CELF-5) — a standardized comprehensive assessment of language for ages 5–21 — receptive, expressive, language memory, word-sentence structure.
7. Preschool Language Scales (PLS-5) — language assessment from birth to 7 years — auditory comprehension and expressive communication scales.
8. Children's Communication Checklist (CCC-2) — parent/teacher assessment of pragmatic language and general communicative function; assists in the sub-typing of DLD.

9. Prognosis

Good prognostic factors

• Mild-to-moderate severity, expressive component only.
• Early identification (<3 years) and intervention.
• High non-verbal IQ.
• Absence of comorbid disorders (ASD, intellectual disability).
• Parental involvement and a language-rich environment at home.

Poor prognostic factors

• Severity of the receptive component (poorer prognosis than expressive only).
• Comorbid intellectual disability or ASD.
• Late identification (>5 years).
• Persistent DLD in the family history.
• Low socioeconomic support, limited service accessibility.

Follow-up targets

• High comorbidity of reading and writing difficulties in children with DLD (40–60%) — phonological awareness training at preschool age; then Structured Literacy.
• Social-emotional health — increased risk of anxiety and depression in adolescents with DLD (Conti-Ramsden G., Botting N. J Child Psychol Psychiatry 2008).
• Screening for conduct disorder and ADHD.
• Vocational and academic support planning in adolescence.
• After stuttering has reached remission, monitoring for relapse (during stressful periods).

10. Myths and misconceptions

10.1 Aetiology myths

Myth 1: “Bilingualism (speaking two languages) causes a child to develop a language disorder”

Why it is widespread: it is instilled by families and sometimes paediatricians as “mixing languages” “confuses the child”; in late-talking bilingual children the vocabulary in each language separately may appear small compared with monolingual children (but total conceptual vocabulary is equivalent).

Clinical and biological rationale: The human brain is adapted from birth to develop in several languages; bilingualism has a superior effect on executive function and cognitive flexibility (Bialystok E. et al. Trends Cogn Sci 2012 review). Bilingual children with DLD show impairment in the same pattern in both languages — this is related not to the number of languages but to the neurodevelopmental disorder.

Evidence: Paradis J., Genesee F., Crago M.B. (2011) — in bilingual children, language acquisition develops in parallel with monolingual patterns; DLD arises not from bilingualism but on a neurodevelopmental basis.

Real clinical step: a DLD diagnosis in a bilingual child can be made only when impairment in both languages is documented. Cutting off the family's mother tongue is not recommended — social-emotional harm and disruption of the family bond.

Myth 2: “Stuttering arises from the parent's improper behaviour (impatience, harshness)”

Why it is widespread: Wendell Johnson's “Diagnosogenic Theory” in the 1940s–1950s — the claim that stuttering arises as a result of the parent drawing attention to the child's normal disfluency; subsequently refuted, but it has remained in popular belief.

Biological logic and evidence: Stuttering is genetically and neurobiologically based — heritability ~70% (Felsenfeld 2000); GNPTAB and related lysosomal pathway mutations in rare forms (Kang C. NEJM 2010); fMRI studies show functional impairment in the basal ganglia-supplementary motor area circuit (Maguire 2020). The parent's reaction may affect the persistence of stuttering (increase in a stress context), but is not the cause of the onset of stuttering.

Real clinical step: support for the family — creating a calm, listening environment; an evidence-based parent-coached intervention such as the Lidcombe Program.

Myth 3: “If a child does not talk, it is because they are ‘lazy’ or 'too young, let's wait'”

Evidence: The “wait and see” approach is appropriate only for a late talker WITHOUT risk factors — 70–80% of this group catch up by 4 years of age. However, when risk factors are present (family history, receptive deficit, low use of non-verbal gestures, hearing suspicion), waiting loses the critical intervention window — Roos E.M., Weismer S.E. Top Lang Disord 2008.

Real clinical step: screening at 18–24 months (CDI, ASQ); SLP assessment if risk factors are present.

10.2 Harmful methods or those that delay the primary intervention

Myth 4: “Tongue-tie (ankyloglossia) surgery will solve the speech problem”

Why it is widespread: the commercial popularity of “frenotomy” and “frenuloplasty” procedures; the existence of some indications in breastfeeding problems.

Evidence: Only severe anatomical restriction (Coryllos III–IV) with a breastfeeding problem makes frenotomy effective (AAP, ABM 2020 protocols). There is no systematic evidence for speech sound disorder — Webb A.N. et al. Int J Pediatr Otorhinolaryngol 2013 review. Erroneous surgery — bleeding, infection, formation of a double frenulum, difficulty with normal breastfeeding.

Real clinical step: first-line for speech sound disorder — SLP assessment and articulation therapy, not frenotomy.

Myth 5: “Auditory Integration Training (AIT) — the Berard or Tomatis method”

Why it is widespread: alternative-clinic marketing; the claim of “reprogramming the auditory system”.

Evidence: ASHA Position Statement 2004 — no evidence of effect in auditory-language disorders or autism; experimental status. AAP 1998 Statement — does not recommend AIT.

Myth 6: “Complete cure of stuttering with hypnotherapy or ear devices (DAF — delayed auditory feedback)”

Evidence: Hypnotherapy — no evidence of effect for stuttering (Bothe A.K. et al. Am J Speech Lang Pathol 2006 review). DAF devices (SpeechEasy and similar) may provide a short-term increase in fluency in some adults, but the long-term effect is limited and superiority over behavioural therapy has not been confirmed (Lincoln M., Packman A. J Fluency Disord 2007).

10.3 Ineffective or scientifically unfounded methods

Myth 7: “Non-Speech Oral Motor Exercises (NSOME) — tongue, lip, and jaw exercises correct speech sounds”

Why it is widespread: an intuitive basis — “if a muscle is exercised, it works better”; still applied by some therapists.

Evidence: ASHA 2009 and update — there is no evidence of effect of non-speech oral motor exercises in speech sound disorder; speech and non-speech oral movements are separate neuromotor programmes (McCauley R.J., Strand E., Lof G.L. Am J Speech Lang Pathol 2009 systematic review). The use of NSOME diverts therapy time from evidence-based speech-based intervention.

Real clinical step: for speech sound disorder — direct articulation therapy (phoneme-by-phoneme or phonological processes); NSOME is avoided.

Myth 8: “Brain Gym / Edu-K — brain coordination exercises cure language disorder”

Evidence: Reviews (Hyatt K.J. Remedial Spec Educ 2007) — “Brain Gym” claims do not conform to neurobiology; no effect on learning outcomes. Criticized as a commercial programme.

Myth 9: “Hyperbaric oxygen chamber (HBOT) and stem cell injections cure language disorder”

Evidence: Cochrane (Xiong T. 2016 — autism; a similar position for DLD) — no evidence of effect; risks of pneumothorax and barotrauma with HBOT; deaths in unregulated stem cell clinics (Berkowitz NEJM 2016).

Myth 10: “A special diet (gluten-free, casein-free) cures language disorder”

Evidence: ASHA, AAP, AACAP — the effect of special diets on speech and language disorders has not been proven. If coeliac disease or a confirmed food allergy is present, a diet is a medical indication, but it has no effect on language-speech development.

11. Sources

1. Bishop D.V.M., Snowling M.J., Thompson P.A., Greenhalgh T., CATALISE consortium. CATALISE: a multinational and multidisciplinary Delphi consensus study of problems with language development: Terminology. J Child Psychol Psychiatry 2017;58(10):1068–1080.
2. WHO. ICD-11 for Mortality and Morbidity Statistics. 6A01 Developmental speech or language disorders. 2024.
3. American Psychiatric Association. DSM-5-TR. Washington DC: APA Publishing; 2022.
4. ASHA Practice Portal — Language Disorders, Speech Sound Disorders, Fluency Disorders. American Speech-Language-Hearing Association. asha.org/practice-portal.
5. RCSLT — Developmental Language Disorder. Royal College of Speech and Language Therapists. rcslt.org.
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9. Roberts M.Y., Kaiser A.P. The effectiveness of parent-implemented language interventions: a meta-analysis. Am J Speech Lang Pathol 2011;20(3):180–199.
10. McCauley R.J., Strand E., Lof G.L. et al. Evidence-based systematic review: effects of nonspeech oral motor exercises on speech. Am J Speech Lang Pathol 2009;18(4):343–360.
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13. Kang C., Riazuddin S., Mundorff J. et al. Mutations in the lysosomal enzyme-targeting pathway and persistent stuttering. NEJM 2010;362(8):677–685.
14. Maguire G.A., Yeh C.Y., Ito B.S. Overview of the diagnosis and treatment of stuttering. Curr Med Res Opin 2020;36(8):1399–1407.
15. Paradis J., Genesee F., Crago M.B. Dual Language Development and Disorders: A Handbook on Bilingualism and Second Language Learning. 2nd ed. Brookes Publishing; 2011.
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18. Starkweather C.W. Fluency and Stuttering. Englewood Cliffs: Prentice-Hall, 1987.