2 Neuroscience2.10 Neurodevelopment and neuroplasticity

2.10.2 Neurodevelopmental models of psychiatric disorders

Creator: Resident Doctor Committee
Published: 2026-10-14T21:05:16.259Z

1 min read1 figure

Written by Resident Doctor Committee · Published 14 October 2026

The basic model

Neurodevelopmental models explain disorder through altered brain development, which may begin before birth and show only when later demands rise.

Genetic risk is usually polygenic for common disorders, while rare variants have larger effects but incomplete penetrance and variable expression.
Prenatal and perinatal risks include maternal infection, placental dysfunction, alcohol, poor nutrition, hypoxia and obstetric complications.
Developmental cascades link domains: language delay may limit friendships, which reduces communication practice.

A plot of effect size against allele frequency with two parallel diagonal strips running from rare variants of large effect at top left to common variants of small effect at bottom right. An orange autism strip is darkest at the rare end and a blue ADHD strip is darkest at the common end. — Follow the diagonal from rare variants of large effect, such as de novo mutations and CNVs, down to common variants of small effect detected by GWAS; autism liability is weighted more towards the rare end and ADHD towards the common end, though both draw on each. Drawn for MRCPsychiatrist

Pathways from risk to outcome

Term	Meaning	Example
Multifinality	One early risk leads to varied outcomes across people	One copy number variant may precede intellectual disability, autism, schizophrenia or no diagnosis
Equifinality	Several distinct early risks lead to one disorder	Psychosis may follow polygenic liability, rare variants, cannabis or adversity

Heterotypic continuity differs from both: one person's disorder changes form over time.
Resilience is favourable adaptation despite substantial risk, and it varies across domains and over time.

Shared mechanisms

Autism, ADHD (attention deficit hyperactivity disorder), intellectual disability and psychosis share risks and mechanisms but differ in developmental timing. They are not stages of one illness.

Candidate circuit mechanisms are synapse formation and pruning, the balance of excitation and inhibition, myelination and long-range connectivity.
Group associations do not reliably predict one child's outcome, because risk depends on dose, timing, co-occurring exposures, protection and chance.

Revision material for the MRCPsych examinations. Not clinical guidance, and not for use in patient care.