Centre pour la Recherche et l'Innovation dans l'Enseignement - CERI

A Quick Primer on Brain Development



by Usha Goswami

Faculty of Education, University of Cambridge, UK.


From the article: “Neuroscience and Education”, reproduced with permission from the British  Journal  of  Educational  Psychology,  © The British Psychological Society (2004) 74, pp.3-4.


Many critical aspects of brain development are complete prior to birth (see Johnson, 1997, for an overview).  The development of the neural tube begins during the first weeks of gestation, and ‘proliferative zones’ within the tube give birth to the cells that compose the brain.  These cells migrate to the different regions where they will be employed in the mature brain prior to birth.  By 7 months gestation almost all of the neurons that will comprise the mature brain have been formed. Brain development following birth consists almost exclusively of the growth of axons, synapses and dendrites (fibre connections): this process is called synaptogenesis.  For visual and auditory cortex, there is a dramatic early synaptogenesis, with maximum density of around 150% of adult levels between 4 and 12 months followed by pruning.  Synaptic density in the visual cortex returns to adult levels between 2 and 4 years.  For other areas such as prefrontal cortex (thought to underpin planning and reasoning), density increases more slowly and peaks after the first year.  Reduction to adult levels of density is not seen until some time between 10 and 20 years.  Brain metabolism (glucose uptake, an approximate index of synaptic functioning) is also above adult levels in the early years, with a peak of about 150% somewhere around 4-5 years.

By the age of around 10 years, brain metabolism reduces to adult levels for most cortical regions.  The general pattern of brain development is clear.  There are bursts of synaptogenesis, peaks of density, and then synapse rearrangement and stabilisation with myelinisation, occurring at different times and rates for different brain regions (i.e., different sensitive periods for the development of different types of knowledge).  Brain volume quadruples between birth and adulthood, because of the proliferation of connections, not because of the production of new neurons.  Nevertheless, the brain is highly plastic, and significant new connections frequently form in adulthood in response to new learning or to environmental insults (such as a stroke).  Similarly, sensitive periods are not all-or-none.  If visual input is lacking during early development, for example, the critical period is extended (Fagiolini & Hensch, 2000).  Nevertheless, visual functions that develop late (e.g., depth perception) suffer more from early deprivation than functions that are relatively mature at birth (such as colour perception, Maurer, Lewis, & Brent 1989).  Thus more complex abilities may have a lower likelihood of recovery than elementary skills.  One reason may be that axons have already stablilised on target cells for which they are not normally able to compete, thereby causing irreversible reorganisation.

It is important to realise that there are large individual differences between brains.  Even in genetically identical twins, there is a striking variation in the size of different brain structures, and in the number of neurons that different brains use to carry out identical functions.  This individual variation is coupled with significant localisation of function.  For a basic map of major brain subdivisions click here .  Although adult brains all show this basic structure, it is thought that early in development a number of possible developmental paths and end states are possible.  The fact that development converges on the same basic brain structure across cultures and gene pools is probably to do with the constraints on development present in the environment.  Most children are exposed to very similar constraints despite slightly different rearing environments.  Large differences in environment, such as being reared in darkness or without contact with other humans, are thankfully absent or rare.  When large environmental differences occur, they have notable effects on cognitive function.  For example, neuroimaging studies show that blind adults are faster at processing auditory information than sighted controls, and that congenitally deaf adults are faster at processing visual information in the peripheral field than hearing controls (e.g., Neville & Bavelier, 2000; Neville, Schmidt, & Kutas, 1983; Röder, Rösler, & Neville, 1999).

Nevertheless, neurons themselves are interchangeable in the immature system, and so dramatic differences in environment can lead to different developmental outcomes.  For example, the area underpinning spoken language in hearing people (used for auditory analysis) is recruited for sign language in deaf people (visual/spatial analysis) (Neville et al, 1998).  Visual brain areas are recruited fro Braille reading (tactile analysis) in blind people (see Röder & Neville, 2003).  It has even been reported that a blind adult who suffered a stroke specific to the visual areas of her brain consequently lost her proficient Braille reading ability, despite the fact that her somatosensory perception abilities were unaffected (Jackson, 2000).  It has also been suggested that all modalities are initially mututally linked, as during early infancy auditory stimulation also evokes large responses in visual areas of the brain, and somatosensory responses are enhanced by white noise (e.g., Neville, 1995).  If this is the case, a kind of ‘synaesthesia’ could enable infants to extract schemas that are independent of particular modalities, schemas such as number, intensity and time (see Röder & Neville, 2003).  If this mutual linkage extends into early childhood, it may explain why younger children respond so well to teaching via multi-sensory methods.




Fagiolini, M. & Hensch, R.K. (2000).  Inhibitory threshold for critical-period activation in primary visual cortex, Nature, 404, 183-186.

Jackson, S., (2000).  Seeing what you feel.  Trends in Cognitive Sciences, 4, 257.

Johnson, M.H. (1997).  Developmental cognitive neuroscience.  Cambridge, MA: Blackwell.

Maurer, D., Lewis, T.L. & Brent, H. (1989).  The effects of deprivation on human visual development : Studies in children treated with cataracts.   In F.J. Morrison, C. Lord & D.P. Keating (Eds), Applied developmental psychology (pp. 139-227).  San Diego, CA: Academic Press.

Neville, H.J., (1995).  Developmental specificity in neurocognitive development in humans.  In M.S. Gazzaniga (Ed.), The cognitive neurosciences (pp. 219-231).  Cambridge, MA: MIT Press.

Neville, H.J., & Bavelier, D. (2000).  Specificity and plasticity in neurocognitive development in humans.  In M.S. Gazzaniga (Ed.), The cognitive neurosciences (pp.83-98).  Cambridge, MA: MIT Press.

Nevillle, H.J., Schmidt, A., & Kutas, M. (1983).  Altered visual-evoked potentials in congenitally deaf adults.   Brain Research, 266, 127-132.

Neville, H.J., Bavelier, D., Corina, D., Rauscheker, J., Karni, A., Lalwani, A., Braun, A., Clark, V., Jezzard, P., & Turner, R. (1998).  Cerebral organization for language in deaf and hearing subjects: Biological constraints and effects of experience.  Proceedings of the National Academy of Sciences of the United States of America, 95 (Feb), 922-929.

Röder, G., Rösler, F., & Neville, H.J. (1999).   Effects of interstimulus interval on auditory event-related potentials in congenitally blind and normally sighted humans.   Neuroscience Letters, 264, 53-56.

Röder, B., & Neville, H.J., (2003).  Developmental functional plasticity.  In J. Grafman & I.H. Robertson (Eds), Handbook of neuropsychology (2nd ed., Vol.9, pp. 231-270), Oxford: Elsevier Science.



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