Development of the infant's CNS proceeds unevenly over the course of fetal development to beyond birth into early childhood (@ 2 years of age) and even into adulthood.  Humans obtain all their body tissues from 3 different germ cell layers: the endoderm, the mesoderm, and the ectoderm.  The ectoderm differentiates into 2 types of tissues with the Surface ectoderm becoming epidermis, hair, nails, skin, and mammary gland; while the Neuroectoderm becomes the nervous system.

            The nervous system develops from the neural plate, a thickened area of neuroectoderm on the dorsal surface of the embryonic disc.  By 3-4 weeks post-conception (21-28 days) a groove appears in the neural plate and the outer edges begin to invaginate or fold inward on itself.  As folding continues, the edges fuse together forming the neural tube.  Dorsal closure of the neural tube gives rise to the central nervous system, cranial nerves, and spinal cord.  The lumen of the neural tube develops into the ventricular system of the brain and the central canal for the spinal cord.  Interruption in the normal sequence of events in neural tube development during this time frame may result in a myelomeningocele, an occipital encephalocele, or anencephaly.  

        As the gestation continues, the neural tube develops dilatations and bulges resulting in the emergence of the forebrain, the midbrain, and the hindbrain.  It is the forebrain that will ultimately evolve into the neonate's face, thalamus, hypothalamus, cerebral hemispheres, and basal ganglia.  As before, interruption in the normal sequence of events in development at this time may lead to anomalies/defects.  These anomalies or defects may be severe in nature, as with the case of holoprosencephaly, or may be less severe in nature, such as a cleft lip or palate.  

         Just below the forebrain, the neural tube's ventral portion, referred to as the basal plate, develops into the motor component of the CNS; the remaining portion of the neural tube becomes the sensory component of the CNS.  Sensory pathways develop early in gestation and continue on with their development even after birth. 

            The motor component of the CNS follows along much the same time continuum.  Muscle contractions first appear around 8 weeks' gestation and are soon followed by lateral flexion movements.  By the 13th-14th weeks of gestation, breathing and swallowing motions appear.  Grasp appears at the 17th week and is fully developed by 27 weeks' gestation.  By midgestation, a full range of newborn movements can be noted.   

            The neural crests, specialized neuroectoderm cells appearing along the fold in the neural plate, will ultimately develop into the autonomic, cranial, and spinal ganglia of the peripheral nervous system.  Vascularization for the developing CNS proceeds in an outward fashion, spreading from the area around the ventricular system outward to the cerebral cortex as brain development continues into the last trimester. 

            Development of the mature structures and functions of the brain is influenced by two significant changes in the cells of the neural tube:  

Primitive cells originating in the area around the ventricles and central canal migrate either to the mantel zone and become the gray matter or they migrate to the marginal zone and become the white matter.   

Gray matter is composed of closely packed interconnected nuclei of nerve cell bodies and some non-myelinated nerve fibers.  It’s the closely packed nerve cell bodies that give it its characteristic grayish color.  Gray matter is found primarily in the outer layers of the cerebrum and in some deeper areas of the brain.  It also makes up the inner core of the spinal cord. 

White matter is composed of nerve fibers (axons) bundled together like stands of cable.  Its name comes from the waxy appearance of the whitish, fatty myelin sheath that surrounds and bundles the fibers together and facilitates the transmission of nerve impulses from the body or outside world to the gray matter and from one part of the body to the other.   

While these cells may not be well differentiated, the primary division of the central nervous system appears to be in place by the 5th-6th weeks of embryonic life.   

The first half of the fetus' gestation (the first 20 weeks) is characterized by neuroblast proliferation while the second half of gestation is characterized by "brain growth spurt."  During this latter time, structural growth is marked by glial cell formation (interstitial or supportive tissue of the nervous system), nerve fiber myelination, and arborization (branching) of the dendrites.   

1.  Neuronal Proliferation  

A neuron consists of 3 parts: the dendrite that brings the message to the cell; the soma or cell body that receives and transmits the message; and the axon that transfers the message to the next neuron.  Neuronal proliferation occurs initially at 2 months gestation, peaking at about 26 weeks'.  Nearly all neurons are present by 18-20 weeks' gestation but their function is primitive because of the lack of myelination and arborization of the dendrites.  Prenatal exposure to toxins or inherited diseases at this time can significantly alter the final number of neurons.  On the other hand, prenatal exposure to chemical and environmental substances can reduce the final number of neurons.  Glial cell proliferation, the supporting tissue of the CNS, occurs at about 5 months gestation. 

The dendrites form the interneuronal synaptic connections or electric circuitry of the brain.  Initially, dendrites appear as thickened processes with only a few spines or branches extending out from them.  However, as the gestation progresses these spines or branches increase in number and length and become the site for synaptic connections, ultimately linking one neuron with up to 1000 other neurons.  The critical growth time for this branching is the last trimester of a pregnancy and is very dependent on the fetus' ability to maintain metabolic homeostasis (adequate blood oxygen, normal pH) and adequate nutrition (vitamins, glucose, fatty acids, amino acids).  An insufficient intake by the mother and fetus of glycoproteins and glycolipids may hinder dendrite arborization and/or synaptic connections.   

 2.  Neuronal Migration 

Neuronal migration refers to the movement of nerve cells from their sites of origin in the ventricular and subventricular zones to their final destination in the CNS.  While migration can occur as early as 2 months' gestation, the peak time for migration is 3-5 months' gestation.  However by the 6th month of gestation, neuronal migration to its permanent place in the cerebral cortex has been completed.  Neuronal migration is important for the appropriate development of the cerebral cortex, basal ganglia, hypothalamus, thalamus, brainstem, cerebellum, and spinal cord.  Failure to complete normal neuronal migration may result in abnormalities in cortical development and neurologic functioning.  It may also precipitate other abnormal neurologic development that we may see manifested in the neonatal period as seizures. 

3.  Neuronal Organization 

Neuronal organization is the basis for brain function. It involves the alignment and layering of the cerebral cortex; arborization of axons and dendrites; establishment of synaptic connections; cell differentiation and death; and finally, proliferation and differentiation of the glial cells.  Glial cell proliferation and differentiation is extremely important as it provides the supporting tissue for the CNS.  Although the glial cells resemble the neuron structurally, they are not able to transmit nerve impulses. 

Astrocyte, the star-shaped glial cells, are plentiful and account for nearly half of the neural support tissue.  They have multiple projections that cling to the neuron, bracing them and anchoring them to their nutrient supply—the blood capillaries.  The astrocytes form a living barrier between capillaries and neurons and play a role in making exchanges between the two, protecting them from harmful substances that might be in the blood.  Astrocytes also help control the chemical environment in the brain by picking up excess ions and recapturing released neurotransmitters.   

Another type of glial cell, Oligodendrocyte, wrap their flat extesions tighly around the nerve fibers, producing fatty insulation coverings called myelin sheath, the “insultion” of the CNS. 

Ultimately, proliferation and differentiation of these cells will establish the complex electric circuitry of the brain and serve as precursors to myelination.   

4.  Myelination 

Myelination begins during mid-gestation, at about 24-25 weeks post-conception, reaches its peak growth speed at birth to one year of age, then continues at a slower pace over the next two decades.  The myelin sheath is a series of cell membranes (fatty in nature) that surrounds the axon, insulates the circuitry, and enhances cellular communication.  This "insulation" prevents leakage of current and enables rapid, efficient transmission of nerve impulses.  Since the neonate's CNS is not fully myelinated, nerve cell transmission is likely to be slower, something worthy of note when caring for the neonate having multiple procedures performed.  As a consequence of this incomplete myelination, infant's responses, especially to pain, may be significantly delayed or diminished.  This altered  response on the part of the infant should not be interrupted by the nurse as tolerance for a  procedure.  Rather, other parameters, such as changes in vital signs, level of activity, etc. should be evaluated to determine the infant's response.  As in the case in neuronal proliferation, the myelinization process is very dependent on the fetus/infant maintaining metabolic homeostasis (adequate blood oxygen, normal pH) and adequate nutrition (vitamins, glucose, fatty acids, amino acids).  A diet low in lipids may alter the development of myelin and subsequent functionality of the CNS. 

            Adequate fetal and infant nutrition are paramount in preventing damage to the fetus' developing CNS.  The specific type of damage to the developing CNS will depend on the timing of the nutritional deprivation.  Early deprivation is more likely to result in decreased brain cell number and overall decreased brain size.  Later nutritional deprivation is more likely to affect myelination, arborization of the dendrites, and synaptic connections.