Intrinsic and extrinsic determinants of neuronal development: relation to infantile autism.

Rapport et al. (1982) wrote a story-style review. They asked: what if autism starts when young brain cells fail to finish their last growth step?

The paper pulls together animal data and early human clues. It guesses that late-stage wiring errors, not early birth defects, produce the social and language gaps we see.

The team found no new lab data. Instead they built a theory: late chemical signals go off track and freeze neuron branching.

They link this freeze to the rigid routines and social avoidance seen in kids with autism.

Subramanian et al. (2017) keep the late-timing idea but move the site to basal-ganglia circuits. They say faulty brake signals there explain both movement quirks and social rigidity.

Davis et al. (2015) flip the noise level. Where D et al. guessed too little wiring, Greg suggests too little neural noise gives kids laser focus but blocks flexible learning.

Emerson et al. (2023) test the timing claim with EEG. Peak alpha frequency in autistic children stays flat while typical kids show steady growth, giving the first live-data snapshot of the late-maturation hunch.

Bailey (2008) adds real tissue. Post-mortem brains show fewer branching spines, turning the 1982 story into something you can see under a microscope.

The review gives you historical roots. When parents ask why skills plateau, you can explain that scientists have tracked late brain maturation since the eighties. Pair this tale with modern EEG or motor checks to show the story now has hard evidence.