ABPN NDD cheat sheet

Cortical neuron migration peaks between gestational weeks 12 and 24; disruption yields heterotopia or lissencephaly patterns.

Myelination begins in the third trimester in brainstem and progresses caudorostrally; adult-like frontal myelination continues into the third decade.

GABA is depolarizing/excitatory in immature neurons due to high intracellular chloride (NKCC1 predominant); KCC2 upregulation shifts it to inhibitory.

Synaptic pruning and experience-dependent plasticity peak in early childhood; excess or failed pruning is implicated in autism and schizophrenia models.

Cerebral blood flow and glucose utilization peak in childhood (roughly ages 3-10) at rates above adult values.

The blood-brain barrier is functionally present by early gestation but is more permeable in the neonate; bilirubin and some drugs cross more readily.

Dopaminergic mesocortical and mesolimbic circuits mature later than sensorimotor circuits, contributing to adolescent risk-taking and executive immaturity.

Standard developmental reflexes (Moro, palmar grasp, asymmetric tonic neck) disappear on a predictable schedule; persistence beyond expected age suggests CNS dysfunction.

Neural tube closes by gestational day 28; failure of anterior closure causes anencephaly, posterior closure causes myelomeningocele.

Primary neurulation forms brain and spinal cord to ~S2; secondary neurulation forms lower sacral cord and is the site of tethered cord and lipomyelomeningocele.

Disorders of prosencephalic cleavage include holoprosencephaly (often SHH pathway, chromosome 13) and septo-optic dysplasia.

Cortical malformations group as proliferation (microcephaly, megalencephaly), migration (lissencephaly, heterotopia), and organization (polymicrogyria, schizencephaly).

Posterior fossa anomalies: Dandy-Walker (cystic fourth ventricle with vermian hypoplasia), Joubert (molar tooth sign), Chiari II (with myelomeningocele).

Head circumference at birth averages ~35 cm and increases ~2 cm/month in the first 3 months, then slows; crossing two major percentile lines warrants evaluation.

Folic acid supplementation before and during early pregnancy reduces neural tube defect risk by roughly 50-70%.

Prematurity and low birth weight increase risk of intraventricular hemorrhage, periventricular leukomalacia, and later cerebral palsy.

DSM-5-TR autism criteria require persistent social communication deficits plus restricted/repetitive behaviors, present in early development and causing impairment.

ASD severity is specified by level of support required (Level 1 requiring support to Level 3 requiring very substantial support).

ADHD requires symptoms before age 12, present in two or more settings, for at least 6 months, with functional impairment.

Intellectual disability requires deficits in intellectual and adaptive functioning with onset during the developmental period; severity is set by adaptive, not IQ, scores.

Global developmental delay applies under age 5 when milestones are not met and standardized assessment is not feasible.

Standardized tools include ADOS-2 and ADI-R for autism, and Conners or Vanderbilt scales for ADHD; diagnosis remains clinical.

Tic disorders are classified by duration (provisional <1 year, persistent >1 year) and presence of both motor and vocal tics (Tourette).

Language disorder is diagnosed when language skills are below age expectations with intact nonverbal ability; differentiate from hearing loss and social communication disorder.

FDA-approved ADHD medications include methylphenidate and amphetamine stimulants, atomoxetine, guanfacine ER, and clonidine ER.

Risperidone and aripiprazole are FDA-approved for irritability/aggression in autism; monitor weight, metabolic panel, and movement side effects.

Early intensive behavioral intervention (ABA-based) has the strongest evidence for improving adaptive behavior in young children with ASD.

Melatonin is commonly used for sleep-onset insomnia in neurodevelopmental disorders; prolonged-release melatonin has trial evidence in ASD.

IDEA Part B guarantees free appropriate public education and individualized education programs for eligible children ages 3-21.

IDEA Part C provides early intervention services for infants and toddlers under age 3 with developmental delay or established risk.

Transition planning under IDEA must begin by age 16 (earlier in some states) and address postsecondary goals.

Coordinated care models (medical home, care coordination) improve access and reduce unmet needs; caregivers should be screened for stress and referred for respite.

The corticospinal tract decussates at the medullary pyramids; upper motor neuron lesions cause spasticity, hyperreflexia, and Babinski sign.

Cranial nerve VI palsy produces impaired abduction; in raised intracranial pressure it is a false-localizing sign.

The cerebellar vermis coordinates midline/gait function; hemispheric lesions cause ipsilateral limb ataxia and intention tremor.

EEG background rhythms mature sequentially: posterior dominant rhythm appears around 3-4 months and reaches adult alpha frequency by ~10 years.

Neurotransmitter systems relevant to neurodevelopment include dopamine (attention, reward), serotonin (mood, gut), and GABA (inhibition).

A normal newborn EEG is discontinuous and slow; absence of expected maturational patterns can indicate encephalopathy.

Gross motor milestones: head control ~3 months, sitting ~6-8 months, walking ~12-15 months; regression is always abnormal.

Synaptogenesis peaks in the first 2 years; myelination of the frontal lobes continues into early adulthood.

Microcephaly is head circumference more than 2-3 SD below the mean; causes include genetic, teratogenic (alcohol, Zika), and perinatal injury.

Chiari I malformation involves cerebellar tonsillar herniation >5 mm below the foramen magnum; often asymptomatic or presents with headache.

Syndromic causes of developmental delay include Down syndrome (trisomy 21), fragile X (FMR1), and Rett (MECP2).

Autism screening tools include the M-CHAT-R/F for toddlers; a positive screen requires diagnostic evaluation, not diagnosis.

Hearing evaluation is mandatory in any child with language delay before assigning a primary language disorder.

Adaptive behavior is measured with tools such as the Vineland-3; IQ testing alone is insufficient for intellectual disability severity.

Comorbidity screening in ASD should cover epilepsy, sleep disorders, GI symptoms, and anxiety.

Differential for ADHD includes anxiety, depression, sleep apnea, hearing/vision problems, and absence seizures.

Tourette syndrome requires motor and vocal tics for >1 year with onset before age 18.

Genetic testing yield in ASD with intellectual disability is higher than in ASD without; chromosomal microarray is first-tier.

Behavioral parent training is first-line for preschool ADHD; stimulants are first-line for school-age children.

Monitor growth, blood pressure, and heart rate with stimulants; screen for cardiac risk before starting.

SSRIs are used for anxiety/OCD in ASD but carry activation risk; start low and monitor.

Epilepsy in neurodevelopmental disorders is managed with standard antiseizure medications; avoid valproate in females of childbearing potential.

School accommodations (504 plan) provide supports without specialized instruction; IEP provides specialized instruction and related services.

Caregiver training and respite are system-level supports that reduce family burden and improve outcomes.

Transition to adult care should begin in adolescence and address guardianship, vocational training, and insurance continuity.

Neural induction and patterning depend on signaling gradients (SHH ventral, BMP/Wnt dorsal) that establish dorsoventral identity.

The ventricular zone is the source of radial glia, which guide neuronal migration along radial fibers.

Apoptosis and pruning refine circuits; failure of programmed cell death can cause cortical dysplasia.

The limbic system (amygdala, hippocampus) matures earlier than prefrontal cortex, contributing to adolescent emotional reactivity.

Mitochondrial and metabolic disorders can present as developmental regression, seizures, or encephalopathy in early childhood.

Neural tube defects are screened with maternal serum alpha-fetoprotein and fetal ultrasound; elevated AFP suggests open defects.

Holoprosencephaly presents with midline facial anomalies (cyclopia, proboscis) and is often associated with chromosome 13.

Lissencephaly (smooth brain) results from defective migration and presents with seizures and severe delay.

Periventricular leukomalacia is a white matter injury of prematurity and a leading cause of spastic diplegic cerebral palsy.

Fetal alcohol spectrum disorder causes microcephaly, facial dysmorphism, and cognitive/behavioral deficits.

DSM-5-TR ADHD presentations: predominantly inattentive, predominantly hyperactive/impulsive, and combined.

Social communication disorder involves pragmatic language deficits without restricted/repetitive behaviors.

Developmental coordination disorder involves motor skill deficits affecting daily activities, not due to intellectual disability.

Specific learning disorder is diagnosed when academic skills are substantially below age expectations despite adequate instruction.

Autism evaluation should include developmental history, direct observation, and collateral information from caregivers and teachers.

Regression in language or social skills warrants urgent evaluation for autism, epilepsy (Landau-Kleffner), or neurodegenerative disease.

Applied behavior analysis targets socially significant behaviors with data-driven, individualized goals.

Speech-language therapy addresses communication; occupational therapy addresses sensory, motor, and daily living skills.

Physical therapy targets gross motor function and mobility; orthotics may support gait in cerebral palsy.

Medication for irritability in ASD should follow behavioral intervention and target specific symptoms.

Systems of care emphasize family-centered, community-based, coordinated services across health, education, and social sectors.

Insurance coverage for autism services varies; early intervention is often funded through state programs.

Cranial nerve XII (hypoglossal) controls tongue movement; lower motor neuron lesions cause atrophy and fasciculations.

The blood supply to the developing brain is more vulnerable to hypoxic-ischemic injury in watershed regions in term infants and periventricular regions in preterm infants.

Neonatal seizures are often subtle (apnea, cycling) and require EEG confirmation.

Serotonin and dopamine pathways are targets of many psychotropic medications used in neurodevelopmental disorders.

Cranial neural crest cells form facial bones, melanocytes, and peripheral ganglia; disruption causes craniofacial syndromes.

The corpus callosum forms between 12 and 20 weeks; agenesis may be isolated or syndromic.

Myelomeningocele requires early surgical closure and monitoring for hydrocephalus and tethered cord.

Neurocutaneous syndromes (NF1, tuberous sclerosis) are associated with developmental delay and seizures.

Autism prevalence estimates are approximately 1 in 36 children in recent US surveillance.

ADHD prevalence is roughly 5-10% in school-age children, more commonly diagnosed in boys.

Intellectual disability prevalence is about 1-3% of the population.

Tic disorders are more common in boys and often improve in adolescence.

Diagnostic evaluation should include vision and hearing screening, developmental history, and standardized testing when indicated.

Stimulant dosing should start low and titrate; monitor for appetite loss, sleep problems, and growth.

Atomoxetine is a nonstimulant option with delayed onset (2-6 weeks) and monitor for suicidal ideation in youth.

Guanfacine ER and clonidine ER are alpha-2 agonists used for ADHD and tics.

Behavioral sleep interventions (sleep hygiene, bedtime routines) are first-line before medication.

School-based services include speech, OT, and counseling under IDEA or Section 504.

Family support and psychoeducation improve adherence and outcomes.