Brain Development II


  • Influences – physiology of egg and sperm, intrauterine environment, genetic transmission, errors, mutations. Psychosocial environment influences via mothers’ stress hormones and self-care behaviors.
  • 2 weeks-6 months: Neurons divide and multiply. NO new neurons develop postnatally. Problems –> fewer neurons at beginning of life (e.g., MR)
  • 6 weeks-6 months: Neurons migrate. Move from central ventricle toward skull, forming layers, each built on top or earlier ones. Problems –> neurons in wrong layer of brain; abnormal connections
  • 6 weeks – 6 months: Axons form basic links. Use genetic blueprints and chemical cues
  • Neurons send electrical signals (from dendrite to end of axon) and chemical signals (from end of axon to nearby neurons or muscle cells). Problems –> seizures, mood/attention problems
  • Neural Tube Development: during 3rd and 4th week gestation, the dorsal ectoderm invaginates to form a closed midline neural tube that eventually gives rise to the CNS. Defects in closure are magnified throughout gestation.
    • Ectoderm – forms CNS and skin
    • Mesoderm – forms coverings of CNS (meninges, vertebrae, and skull)



  • Influences – genetic propensities of child and family, child’s physiology (metabolism, nutrition, hormone and neurotransmitter and immune activity, toxins, infections), child’s physical environment (birth trauma, head injury, physical shelter and dangers), child’s psychosocial environment (family, peers, school, community, culture). Child’s biology, in turn, influences psychosocial environment
  • Growth of axons. Problems –> abnormal connections
  • Increase complexity of dendrites and axons on each neuron. Problems –> sparse, skinny dendrites or fewer receptors
  • Formation of synapses between neurons, or with muscle cells. If the link isn’t active it dies or moves away.
  • Death of unused synapses and neurons. Problems –> persisting nonfunctional cells make abnormal connections or develop other problems (e.g., seizures, tumors)
  • Myelination of axons. Problems –> weak or absent communication between brain areas, or between brain and muscles
  • Cell populations mature through developmental stages at different times and in different regions of the brain. Stages are: proliferation, migration, differentiation, myelination, cell death
  • Brain weight at birth is 25% of adult weight; about 80% by age 2 years



  • Brain develops from the “neck up”, and the spinal cord develops from the “neck down”, roughly in this order:
  • Brainstem (medulla, pons, midbrain, cranial nerves). Problems –> crossed or lazy eyes, deafness, sleep disturbances, hallucinations, etc.
  • Cerebellum and basal ganglia. Problems –> ataxia, involuntary movements, “floppiness”
  • Limbic system (thalamus, hypothalamus, amygdala). Problems –> ADD, emotional disorders, obesity, precocious puberty, etc.
  • Primary sensory input areas of the cortex. Problems –> central auditory disorders
  • Motor output areas of the cortex. Problems –> incoordination, spasticity
  • Association, integration, memory, and planning areas. Problems –> ADD, LD
  • Alternate way of describing development:
    • Primary Zones: modality specific; fully functional by end of 1st year
    • Secondary zones: integrate modality-specific info into perceptive info. Become fully functional within first 5 years of life
    • Tertiary zones: associative, supramodal areas encompassing borders of parietal, temporal, and occipital zones as well as prefrontal region with its cortical and subcortical connections. Integrate info across modalities and control executive, purposive, and conative aspects of functioning. Become functional between ages 5 and 8, prefrontal somewhat later (maybe by age 12)

Evidence that Social Environment Influences Brain Development

  • Environmental deprivation and/or stress can alter neuronal, hormonal, and immune systems. The alterations may impair normal development (or impair recovery from brain trauma) in a transient or long-term way. Environmental enrichment may increase neuronal complexity, improve brain function, and facilitate recovery from brain injury.
    • Cortisol reactivity to stress, hippocampus and immune changes (McEwen, Gunnar)
    • PET scan and behavior changes in Romanian orphans (Carlson & Earls)
    • EEG differences related to cognitive development (Nelson, Thatcher, Fischer)
    • EEG differences related to emotional traits and caregiver responsivity (Dawson, Davidson, Fox, Calkins, Bell)
    • EEG differences related to medical status and caregiver responsivity (Als, Gilkerson)
    • Medical and behavioral development of preemies related to touch/massage (Field)
    • Dendritic complexity of rats in enriched environments (Diamond, Greenough)
    • Social behavior and brain changes in socially isolated monkeys (Harlow; Suomi)
    • Speculation about possible effects of child abuse and neglect (Perry; Teicher; Schore)
  • Environmental influences on specific abilities are more pronounced during sensitive periods
    • Axon growth and synapse formation in visual processing areas of kittens exposed to postnatal visual experience (Hubel & Wiesel)
    • Brain growth and behavior of deafened songbirds (Marler)
    • EEG changes in prelingually and postlingually deafened adults, in brain areas that react to visual vs. auditory inputs, and response to grammatical vs. content words (Neville)
    • Age differences in phoneme detection and language-learning (Kuhl, Stromswold)
    • Age differences in recovery from brain damage involve age at injury, age at testing, and type of test administered, sensitive and “insensitive periods occur (Kolb)
  • Some individual brain-behavior differences may be relatively subtle
    • EEG activation patterns may be associated with emotional intensity and valence which are seen as temperament differences (Dawson, Davidson, Fox, Nelson)
    • Stability of early phonological awareness, vocabulary, and later reading and math abilities (Molfese, Hart, & Risley; Morrison; Fletcher & Shaywirtz) despite transitory impact of specific expressive language disorders (Whitehurst; Rapin)
  • Children with a particular brain disorder rarely show a specific, unique pattern of behavior. Effects of brain disorders vary with nature of the brain insult, environmental support and stress; sex and handedness; age at time of injury; age at time of outcome measurement; and nature of the outcome measures (Fletcher, Yeates, Taylor, Dennis, Shapiro, Satz, Baron, etc., etc.)

Some points regarding intervention:

  • Enrichment/deprivation powerful at all ages, though deprivation may be particularly deleterious during initial development of key abilities
  • Critical to NOT deprive of visual, auditory, and tactile stimulation, language input, and responsive “stress buffering” care providers during infancy
  • Phonological awareness and vocabulary at kindergarten predict long-term school success
  • Children may be maximally attuned to sounds of own language between birth and five; decreased skills for learning speech sounds after that
  • Early accurate diagnosis better than a “wait-and-see” approach
  • Younger age at acquired injury (after first few months of life) associated with more severe cognitive and behavioral impairments
  • Best intervention is PREVENTION – vast majority of brain damage is preventable via social/environmental factors (especially injuries). FYI, best prevention involves training in supervisory practices and environmental modifications, NOT safety education programs.


Miscellaneous Developmental Issues

  • Effects of brain injury tend to be less specific in children than adults, particularly if damage incurred before age 5-7 years

Frontal functions develop in a step-wise fashion with some functions developed by about 6-7 years of age and others continuing to mature into adolescence.