Autism spectrum disorder, ADHD and developmental delay

• Developmental delay is not a diagnosis: it is a signal that the brain is not yet doing what it should, and it is common. Between 3 and 5 percent of children in North America meet criteria for global developmental delay, and 2 to 3 percent eventually meet criteria for intellectual disability. ^[5]
• The single most useful habit is to look for regression and plateau, not only lateness. A child who loses words, gestures or eye contact at any age needs urgent assessment, because that pattern is a red flag for autism, intellectual disability, epilepsy and other serious conditions. ^[4]
• Autism spectrum disorder (ASD) is defined by two core domains throughout: persistent difficulty with social communication and social interaction across contexts, and restricted, repetitive patterns of behaviour, interests or activities, beginning in the early developmental period and causing significant impairment. ^[4]
• Attention-deficit/hyperactivity disorder (ADHD) is unusually common in childhood (about 7 to 8 percent of children worldwide) and is a chronic condition, not a phase of bad behaviour. ^[3]
• Screening tools (ASQ, PEDS, M-CHAT-R/F, Bayley) improve detection but do not diagnose: a positive screen means "assess, do not label". ^[4]
• Global developmental delay is worked up in three tiers: careful history and examination with hearing and vision tests for everyone; chromosomal microarray plus fragile X as first-tier genetic tests; exome sequencing or a comprehensive gene panel when the first tier is negative. ^[5]

By the end of this page you should be able to:

1. Recognise the red flags for delay in each developmental domain, by age, and know which milestones must be reached on time.
2. Describe the main screening tools used in primary care and what a positive result does and does not mean.
3. Outline the stepwise evaluation of a child with global developmental delay, including when to request neuroimaging and metabolic testing.
4. Paraphrase the psychiatric diagnostic criteria for ASD and ADHD and explain why the two often coexist.
5. Plan the first-line management of ASD, ADHD and global developmental delay by age, including when not to use medication.
6. List the specific, testable points where NICE and AAP guidance agree and where they frame the question differently.

Global developmental delay is not intellectual disability, at least not yet. Intellectual disability is a deficit in intellectual functioning (reasoning, verbal comprehension, abstract thought, comprehending instructions and rules, memory, problem-solving and learning from experience) together with a deficit in adaptive functioning, evident in early childhood. ^[5] Most children first diagnosed with global delay later receive a diagnosis of intellectual disability; the two are stages of the same assessment problem, separated by the child's age. ^{[1] [5]}

The psychiatry cross-check matters here, because all three conditions live in the same family. In psychiatric terms they are neurodevelopmental disorders: brain-based conditions that appear in early childhood and produce deficits in personal, social, academic or occupational functioning. ^[5] ASD, ADHD, intellectual disability, developmental language disorder, developmental coordination disorder and GDD are siblings in this grouping, not separate species. ^{[4] [5]}

GDD and intellectual disability are among the commonest reasons a paediatrician is asked to see a child. In the United States and Canada, 3 to 5 percent of children meet criteria for GDD, and 2 to 3 percent are eventually given a diagnosis of intellectual disability once they are older than 7 years and standardised IQ testing is reliable. ^[5] The prevalence of intellectual disability is higher in regions of low to middle socio-demographic index, largely because of exposure to risk factors such as infections, malnutrition and perinatal complications. ^[5]

ASD is no longer rare. Global prevalence estimates are around 1 in 100. ^[4] In the United States, CDC data from 2025 report 1 in 31 children with ASD, up from 1 in 150 in 2000, driven partly by broader criteria, more screening and greater awareness but also by a genuine increase that is not fully explained. ^[4]

ADHD is one of the commonest childhood disorders. A meta-analysis gives a pooled worldwide prevalence of 7.2 percent in children, with some community samples nearer 8.7 to 15.5 percent. ^[3] In the United States, a 2016 national survey found that 9.4 percent of children aged 2 to 17 years had ever received an ADHD diagnosis (2.4 percent of 2 to 5 year olds), and 8.4 percent currently had the condition, about 5.4 million children. ^[3] ADHD occurs in approximately 7 to 8 percent of children and youth overall, and it is at least twice as likely to have been diagnosed in boys as in girls. ^[3]

No single cause explains most developmental delay. The aetiology is mixed and heterogeneous.

Acquired causes (hypoxia, infections, perinatal brain injury, exposure to alcohol, illicit drugs or heavy metals in pregnancy, severe neglect) are a major and preventable contributor to GDD and intellectual disability. ^[5] Genetic causes are identified in up to 47 percent, and include chromosomal abnormalities, copy number variants and single-gene disorders. ^[5] In one large cohort from an outbred population, de novo (not inherited) pathogenic variants explained 42 to 48 percent of cases, while recessive causes accounted for only 3.6 percent. ^[5] Where consanguinity is common, recessive causes rise to 51 to 80 percent. ^[5]

Risk factors that should raise suspicion in any child include:

• prematurity (especially before 35 weeks' gestation), low birth weight and neonatal encephalopathy;
• a family history of ADHD, ASD, intellectual disability, epilepsy or consanguinity;
• maternal illness in pregnancy, teratogen exposure (alcohol, valproate, topiramate) and perinatal complications;
• looked-after children, children known to youth justice, and children with acquired brain injury;
• advanced maternal age, low parental education, socio-economic adversity and consanguineous marriage. ^{[1] [2] [5]}

The mechanisms are shared across the three conditions more than is often appreciated. All are disorders of early brain construction: synaptic signalling, protein homeostasis, epigenetic control of gene expression and the assembly of the circuits that carry attention, language and social behaviour. ^[5] The same set of genes (for example SHANK, NLGN, SYNGAP1) has been implicated in isolated intellectual disability, ASD and epilepsy, depending on the variant and the genetic background. ^[5] This is why a child rarely presents with "only" one condition, and why a developmental assessment always looks for the others.

The table below condenses the most consistent warning signs agreed across a systematic review of 54 studies, grouped by the neurodevelopmental domain. ^[4] They are grouped on purpose by what is missing and when it should have appeared, rather than by diagnosis, because delay is seen before the diagnosis is possible.

By age, the clues look like this. ^[4]

Birth to 6 months. Absent or fading social smile, little interest in faces, persistent hypotonia, poor head control, an atypical cry, and feeding or sleep difficulties. An accelerating head circumference after 3 to 4 months can be an early biological marker in ASD, although it is not specific on its own. ^[4]

6 to 12 months. No babbling by 9 to 12 months, reduced sustained eye contact, failure to respond to name, clenched fists, asymmetry of movement or early handedness, and difficulty sitting. Absent or reduced back-and-forth sharing of attention and emotion is the strongest early red flag for autism. ^[4]

12 to 18 months. No single words by 15 to 16 months, no declarative pointing or showing at 12 to 18 months, absence of gestures such as "bye-bye", no independent walking by 18 months, and poor imitation or exploration of objects. ^[4]

18 to 24 months. Still not combining two words at 24 months, no pretend play, severe food selectivity, sensory hypo- or hypersensitivity, and excessive insistence on routines. ^[4]

Preschool (3 to 5 years). Slurred or restricted speech, difficulty with simple social rules and games, excessive dependence on adults for self-care, and a gap between fluent-sounding language and actual social understanding. ^[4]

A screen is a sieve, not a diagnosis. It exists to triage large numbers of well children cheaply. The validated tools below have established age ranges and domains. ^{[4] [5]}

The aim of the work-up is to answer three questions: is there an acquired cause, is there a specific syndrome, and can a specific aetiology be found that changes management or recurrence risk. ^[5]

Every child with GDD, irrespective of outcome, should have vision and hearing formally assessed, because sensory impairment is both common and treatable. ^[5]

Step 1: history and examination. Take a three-generation family history, prenatal and perinatal history and a full neurodevelopmental history. Look for an acquired cause (perinatal asphyxia, infection, prematurity) and for features of a known syndrome. If a clear acquired cause is present, no genetic testing is needed. If a specific syndrome is recognised clinically (for example Rett syndrome), order the targeted test first. ^[5]

Step 2: deciding on neuroimaging. Brain imaging is indicated when there is an abnormal or rapidly changing head circumference, focal neurological findings or focal epilepsy. When imaging is chosen selectively, abnormalities are found more often than when everyone is screened; MRI is preferred over CT. ^[5]

Step 3: inherited metabolic disorders. Screen biochemically for inherited metabolic disorders if there are clinical red flags (plateau or regression in skills, altered consciousness, movement disorders such as chorea, dystonia, ataxia or myoclonus, hepatomegaly, splenomegaly, drug-resistant seizures, coarse facial features, multisystem involvement), or if newborn metabolic screening was not performed. Routine metabolic screening in children with non-syndromic GDD in a non-consanguineous population has a yield of only 0.25 to 0.42 percent; paediatric and child-neurology bodies (Canadian Paediatric Society, AAP) recommend testing everyone, while others reserve it for when features suggest it. Be honest with parents about that uncertainty. ^[5]

Step 4: genetic testing. All children in whom the initial assessment does not yield a cause should undergo chromosomal microarray (CMA) and fragile X testing as first-tier tests. CMA detects chromosomal copy number variants and has a yield of 10 to 20 percent in the wider neurodevelopmental group, and about 10.9 percent specifically in non-syndromic GDD. Exome sequencing is the next-tier, standard step: it yields a diagnosis in about 36 percent of individuals with neurodevelopmental delay (54 percent in syndromic, 31 percent in isolated presentations), and most current guidance strongly recommends it as a first- or second-line test. Trio sequencing (child plus both parents) improves yield and interpretation. Re-analysis of an unrevealing exome every 1 to 3 years picks up an additional 10 to 16 percent of diagnoses. ^[5]

Fragile X syndrome is one of the commonest monogenic causes of GDD and intellectual disability, with a prevalence of about 1.4 in 10,000 males and 0.9 in 10,000 females. Fragile X testing has a yield of about 1.2 percent in unselected cohorts with neurodevelopmental disorder, and 9.5 to 17 percent when targeted at males with suggestive features or a family history. Fragile X cannot be diagnosed by CMA, exome sequencing or gene panels, so it must be requested specifically. ^[5]

Table 3 below summarises the tiered approach.

NICE frames autism assessment as a recognition, referral and diagnosis pathway, with a local autism multi-agency strategy group and a designated autism team. ^[1]

Recognition. Autism may be under-recognised in girls, and a "negative" feature set does not exclude it: good eye contact, smiling at family, apparently normal language, and settling after a supportive intervention are explicitly listed as reasons not to rule it out. ^[1]

Referral thresholds. Children younger than 3 years with regression in language or social skills should be referred directly to the autism team. Those older than 3 years with regression in language, or any child with regression in motor skills, should be referred first to a paediatrician or paediatric neurologist, who can then refer on. Box 1 of the guideline lists factors that increase the chance of autism and should be applied at referral: gestational age under 35 weeks, a sibling with autism, birth defects involving the central nervous system, parental schizophrenia-like psychosis or affective disorder, learning or intellectual disability, ADHD, neonatal encephalopathy or epileptic encephalopathy including infantile spasms, chromosomal disorders (for example Down syndrome), fragile X, muscular dystrophy, neurofibromatosis, tuberous sclerosis, and exposure to valproate or topiramate (pregnancy or, for valproate, paternal use in the 3 months before conception). ^[1]

Diagnosis. The autism diagnostic assessment starts within 3 months of referral and is a multidisciplinary process. It must include a developmental history focused on features consistent with ICD-11 or DSM-5 criteria, structured observation of social and communication skills, a medical history, physical examination, consideration of differential diagnoses, and an assessment of coexisting conditions. Physical examination specifically looks for neurofibromatosis or tuberous sclerosis skin stigmata (Wood's light), dysmorphic features and macro- or microcephaly, and signs of injury or maltreatment. The diagnosis itself is made against ICD-11 or DSM-5 criteria, using clinical judgement across all sources, never on a single tool. ^[1]

Medical investigations are not part of the autism assessment by default. Genetic testing is considered if there are dysmorphic features, congenital anomalies or evidence of learning disability; EEG is considered only if there is suspicion of epilepsy. ^[1]

A diagnosis of uncertainty is acknowledged in young children (under 24 months, developmental age under 18 months), in older teenagers, and in children with complex coexisting conditions (ADHD, sensory or motor impairment). In those cases, consider keeping the child under review or obtaining a second opinion. ^[1]

NICE NG87 and the American Academy of Pediatrics 2019 guideline (the Wolraich guideline, which updates the 2011 version) are the two standard references used here, and they agree more than they differ. ^{[2] [3]}

Recognition. NICE lists groups with increased prevalence: preterm birth, looked-after children, conduct and oppositional defiant difficulties, mood and anxiety disorders, a close family member with ADHD, epilepsy, other neurodevelopmental disorders (ASD, tic disorders, intellectual disability, specific learning difficulties), substance misuse, a criminal-justice history, and acquired brain injury. ^[2] Both NICE and AAP state that ADHD is under-recognised in girls and women, and that an incorrect alternative mental-health diagnosis is common. ^{[2] [3]}

Diagnosis. For both NICE and AAP, ADHD requires symptoms meeting DSM-5 criteria: onset before age 12, impairment in more than one setting, and a significant level of impairment, established through a full clinical, developmental and psychiatric history with observer reports from home and school. ^{[2] [3]} NICE sets a higher bar verbally: "at least moderate" impairment, with symptoms in 2 or more settings. AAP frames it as meeting DSM-5 criteria with involvement of more than one major setting. Neither guideline allows a diagnosis based on a rating scale alone, though scales (Conners, ADHD Rating Scale, SDQ, Vanderbilt) are helpful additions. ^{[2] [3]}

AAP advises that evaluation can be initiated in primary care for any child or adolescent aged 4 years to the 18th birthday presenting with academic or behavioural problems and symptoms of inattention, hyperactivity or impulsivity; AAP also recommends screening for comorbid conditions (anxiety, depression, oppositional defiant and conduct disorder, substance use, learning and language disorders, ASD, tics, sleep apnoea). ^[3]

NICE is more conservative about timing in younger children: if a child or young person presents with suggestive problems, the practitioner should first judge severity and pervasiveness, then consider up to 10 weeks of watchful waiting and group-based ADHD-focused support for parents, and refer to secondary care if problems persist with at least moderate impairment, or directly if severe. Primary care practitioners should not make the initial diagnosis or start medication. ^[2]

Management by age (both sources agree on the ladder, expressed differently):

• Under 5 years. First-line is a structured, ADHD-focused parent-training programme (parent management training). Medication should not be offered without a second specialist opinion; ADHD cannot be the explanation in a very young child without careful differential diagnosis. NICE offers medication only after environmental modifications have been tried and reviewed, with specialist input. AAP likewise recommends parent training (PTBM) and/or behavioural classroom interventions as first line for 4 to 5 year olds, allowing methylphenidate only if interventions fail and disturbance is moderate to severe. ^{[2] [3]}
• 5 to 11 years. All major guidelines put medication together with behavioural and educational interventions. AAP makes FDA-approved medication plus parent training and classroom intervention a standard (grade A). NICE offers medication only where symptoms still cause persistent significant impairment in at least one domain after environmental modifications have been tried, with a baseline physical assessment, and titration against symptoms and side effects. First-line pharmacological treatment under NICE is methylphenidate (short or long acting) for children 5 years and over, with lisdexamfetamine and then atomoxetine or guanfacine as alternatives. AAP does not prescribe a specific first drug in the same way but titrates to maximal benefit with tolerable side effects. ^{[2] [3]}
• 12 to 18 years. Medication with the adolescent's assent, plus behavioural or training interventions and educational supports. Adolescents should be assessed for substance use, anxiety, depression and learning difficulties, which are common comorbidities. ^{[2] [3]}
• Adults. Fall outside the paediatric remit of this page in detail, but for completeness: ADHD continues into adult life in many, and NICE recommends lisdexamfetamine or methylphenidate first line for adults, with non-pharmacological treatment for those who decline or do not tolerate medication. ^[2]

Medication safety points that are easy to forget and commonly examined:

• No ADHD medication is started in primary care in the UK model; baseline assessment includes medical history, current medication, height and weight plotted against the normal range for age, sex and height, pulse and blood pressure, and a cardiovascular assessment. An ECG is not required routinely before stimulants, atomoxetine or guanfacine unless specified cardiac risk factors are present. ^[2]
• children under 5 need a second specialist opinion before any drug; ^[2]
• dose titration should be slower and monitoring more frequent in children with coexisting neurodevelopmental, mental health or physical conditions; ^[2]
• the same medicines are offered to children with coexisting ASD, anxiety or tic disorder as to any child with ADHD; ^[2]
• ECG not routinely needed before stimulants, atomoxetine, guanfacine unless specified risk factors; ^[2]
• stimulant and non-stimulant therapy in ADHD is titrated slowly with frequent monitoring where coexisting conditions are present. ^{[2] [3]}

Monitoring. Once stable, height is measured every 6 months in children and young people, weight every 3 months in children 10 years and under, weight at 3 and 6 months and then 6-monthly in those older than 10 years, and weight every 6 months in adults, plotted on a growth chart. ^[2]

Because ASD and ADHD are psychiatric diagnostic categories, the DSM-5-TR and ICD-11 criteria underpin every paediatric guideline on this page. The DSM-5 wording itself is copyrighted and is not quoted here; the paraphrase below follows the international literature, which summarises them. ^{[4] [5]}

ASD (paraphrased). Persistent deficits in social communication and interaction in multiple contexts (social-emotional reciprocity, nonverbal communication, relationship development) and restricted, repetitive patterns of behaviour, interests or activities (stereotyped movements, insistence on sameness, fixed interests, atypical sensory responsivity). Onset in the early developmental period; significant functional impairment; not better explained by intellectual disability or GDD alone. ^{[4] [5]}

ADHD (paraphrased). A persistent pattern of inattention and/or hyperactivity-impulsivity occurring often, in two or more settings, beginning in childhood, and causing impairment. NICE anchors this at "at least moderate" impairment; AAP confirms DSM-5 onset before the 12th birthday. Preschool children (4 to 6 years) are diagnosed more cautiously, with early onset of features compared with peers. ^{[2] [3]}

Overlap. ASD and ADHD coexist frequently: ADHD is one of the most common comorbidities in ASD and vice versa. NICE CG128 lists ADHD in the differential diagnosis of autism and again among conditions that must be considered as coexisting; both NICE and AAP say the same medicines are offered to children with ADHD and ASD as to any other child. ^{[1] [2]} Always assess both, and never treat a label as an excluding diagnosis.

General principles. A family-centred, multidisciplinary model: paediatrician or paediatric neurologist, speech and language therapist, occupational and physiotherapist, special educator, psychologist, and social worker, with parents as partners rather than observers. ^[5] The challenges change with age, so the plan is reviewed, not written once. ^[5] Common comorbid medical issues in children with GDD and intellectual disability are epilepsy, behavioural challenges, sleep disturbance, movement disorders and orthopaedic deformity. ^[5]

Autism spectrum disorder. Management is psychosocial, developmental and educational rather than pharmacological, and starts as soon as the diagnosis (or the strong suspicion) is formed. ^{[1] [4]}

• Parent-mediated and naturalistic developmental behavioural interventions (early intensive behavioural intervention, JASPER-type joint-attention interventions) are the evidence-based mainstay in the preschool years. Early intervention is associated with better cognitive and adaptive outcomes. ^[4]
• Speech and language therapy targets communication, including augmentative and alternative communication for non-verbal children.
• Educational support, a needs-based plan, occupational therapy and sensory strategies for atypical reactivity.
• Pharmacology is reserved for comorbid problems, not for autism itself: risperidone or aripiprazole for severe irritability or self-injury in ASD where behavioural programmes are insufficient; attention and anxiety addressed with the ADHD and mental-health approaches in their own sections; sleep with sleep hygiene and melatonin. ^[2]
• Families need prognostic honesty, information about sibling and recurrence risk, and a named key worker. NICE recommends that a follow-up appointment with the autism team takes place within 6 weeks of the end of the assessment to discuss conclusions and implications. ^[1]

ADHD. See the age-graded ladder above. Non-pharmacological first: parent training, classroom behavioural programmes, reasonable educational adjustments (individualised education programmes, rehabilitation plans), structured environment, sleep and exercise. Medication only after those and only while they continue. ^{[2] [3]} CBT is considered for adolescents who have benefited from medication but retain significant impairment. ^[2] Titrate medication to maximum benefit with tolerable side effects, more slowly and with closer monitoring where comorbid or physical conditions exist. ^{[2] [3]}

GDD and intellectual disability. The specific intervention depends on the profile, but the components are predictable:

• hearing and vision support and correction, which can be the entire explanation and the entire treatment;
• early intervention services (physiotherapy, occupational therapy, speech therapy) for the preschool brain's critical windows;
• behavioural intervention for problem behaviour, with atypical antipsychotics reserved for severe aggression or self-injury after psychosocial approaches;
• sleep management with hygiene, then melatonin and, if needed, gabapentin, clonidine or trazodone;
• seizure control with careful avoidance of sedating or cognition-worsening antiepileptics;
• family support, respite, and help with navigating services and benefits.

ADHD medication: what to tell parents briefly. NICE first-line pharmacological treatment in children aged 5 and over is methylphenidate; lisdexamfetamine (also first line in adults) and then dexamfetamine, atomoxetine or guanfacine follow. Stimulants improve core symptoms within days; they are not sedatives and do not teach skills, which is why behavioural and educational supports must continue. ^{[2] [3]}

Untreated ADHD in children is associated with poorer educational attainment, higher rates of injury, substance use and self-harm in adolescence and adulthood, and an increased risk of death from all causes including suicide; discontinuing treatment raises the risk of car crashes, criminality and depression. ^[3] These are the reasons continuation of care matters as much as starting it. ^{[2] [3]}

ASD outcomes vary enormously with cognitive ability, language, the presence of epilepsy (which affects a substantial minority of autistic people over the lifespan), and the quality and timing of early support. Global delay resolves fully in some children, stabilises in many, and progresses to intellectual disability in others; the more severe the delay, the earlier it is evident, often in the first year of life. ^{[4] [5]}

No screening programme finds every case, but a rational schedule catches most. The AAP recommends developmental surveillance at every well-child visit, formal developmental screening through infancy and toddlerhood, and autism screening with a validated tool such as the M-CHAT-R/F at 18 and 24 months. ^{[4] [6]} The "no safe blood lead level" and iron "screen late in infancy" points belong to the wider well-child topic, and hearing (newborn OAE or AABR) and vision (red reflex, then instrument-based screening) complete the picture. ^[4]

• Girls. ADHD and ASD are both under-recognised in girls, who present more often with inattention, anxiety or depression rather than disruptive behaviour, and are more likely to receive a wrong diagnosis first. ^{[2] [3]} Both guidelines say so explicitly. Screening and diagnostic criteria need to be applied without the stereotype of the disruptive boy. ^{[1] [2]}
• Children under 4. There is insufficient evidence to diagnose ADHD below age 4 (other than behavioural parent training, which does not need a diagnosis to help). ^[3] For very young children, developmental and sensory assessment and parent training come first. ^[3]
• Adolescents. In ASD, higher-functioning individuals may present for the first time in adolescence when social demands outstrip coping; in ADHD, onset must be shown to predate age 12. ^{[1] [2]}
• Pregnancy and heredity. In Carney-type familial syndromes the genetic perspective applies to parents; for ASD, the recurrence risk for siblings is increased and family planning discussions are part of the 6-week follow-up. ^[1]
• Low birth weight and prematurity. Both raise the risk of neurodevelopmental disorder; preterm children benefit from structured developmental follow-up. ^[5]

Most of the yield comes from free or cheap actions: a careful history and three-generation family history (free), a watchful neurological examination and Hammersmith Infant Neurological Examination (free), hearing tested by distraction and observation, a red reflex with any ophthalmoscope, and the ASQ or PEDS questionnaires, which need only paper. ^{[4] [5]}

Where M-CHAT-R/F and ASQ are unavailable, systematic observation of joint attention, eye contact, babbling, gestures and play against the red flags above carries most of the screening weight. ^[4] Motor assessment techniques such as the General Movements Assessment can be learned at low cost. ^[4]

MRI, CMA and exome sequencing are simply not available in many settings, and that is where the door should be explained, not pretended open: brain imaging is prioritised for abnormal head size, focal signs or epilepsy; genetic testing is justified only where it changes management or recurrence counselling; hearing aids and community-based early intervention programmes usually matter more than a diagnosis label. Inherited metabolic screening may be the one test worth pursuing where there is an affected family, consanguinity, or regression, because a handful of these conditions are treatable and the yield is higher than 0.4 percent when red flags are present. ^[5]

• Global delay is common and is not a diagnosis; two-thirds of children with mild to moderate impairment and one-third with severe to profound impairment go on to receive an intellectual disability label, so begin evaluation early. ^[5]
• GDD is a delay of two standard deviations in two or more domains in children under 5; ID is a deficit in intellect and adaptive functioning evident in early childhood. ^[5]
• Around 3 to 5 percent of North American children meet criteria for GDD, 2 to 3 percent for ID, about 7 to 8 percent for ADHD, and roughly 1 in 100 worldwide for ASD (1 in 31 in the United States in 2025). ^{[3] [4] [5]}
• Red flags by domain are the most useful clinical tool; loss of any acquired skill at any age is an emergency red flag. ^[4]
• Every child with GDD needs hearing and vision tested before any label is accepted. ^[5]
• NICE CG128 autism: multidisciplinary autism team, referral on regression of language, social skills or motor skills, diagnostic assessment within 3 months, diagnosis against ICD-11 or DSM-5 criteria, no routine medical investigations but genetics if dysmorphic and EEG if seizing. ^[1]
• NICE NG87 and AAP 2019 agree that ADHD is a chronic condition with childhood onset before age 12 and impairment in more than one setting, that rating scales support but do not make the diagnosis, and that parent training comes first in preschool children. ^{[2] [3]}
• First-line parent management training for children under 5; ADHD medication for children aged 5 and over where impairment persists after environmental modification, with methylphenidate first line in the NICE framework. Titrate slowly in children with comorbid conditions. ^{[2] [3]}
• GDD work-up is tiered: history and sensory tests everyone; chromosomal microarray plus fragile X first tier (10 to 20 percent and 1.2 percent yield); exome sequencing next (around 36 percent); imaging only when indicated (higher yield when selective); metabolic testing only when red flags or no newborn screen. ^[5]
• Fragile X cannot be picked up by CMA or exome sequencing and must be requested specifically. ^[5]
• Re-analysis of an exome every 1 to 3 years adds a further 10 to 16 percent of diagnoses. ^[5]
• Share the plan, not just the label: a 6-week follow-up after an autism assessment, family support, and a named key worker change outcomes more than any single test. ^[1]

• anticipatory guidance and screening in childhood
• child abuse and neglect
• faltering growth
• neonatal seizures and hypoxic-ischaemic encephalopathy
• prematurity and its complications
• childhood asthma and wheeze
• infectious diarrhoea
• type 1 diabetes mellitus in children
• epilepsy (not yet written)
• genetic counselling and chromosomal microarray (not yet written)
• intellectual disability and cerebral palsy (not yet written)