Early Childhood Stuttering

In the previous post, we showed that stuttering may occur if there is an imbalance between the number of D2 dopamine receptors on the indirect pathway relative to the D1 receptors on the direct pathway.  The D2 receptors act as a brake while the D1 receptors play the role of the gas pedal.

In children, stuttering often occurs between the ages of 3-5, many of whom recover spontaneously by age 5, while others persist through the rest of childhood, adolescence, and adulthood.  What distinguishes transient childhood stuttering from stuttering that persists?  The answer may lie in the ratios of D2 to D1 dopamine receptors in the developing brain.

The density of D1 receptors in the putamen increases after birth to a peak level around age 3, while the D2 density peaks around age 2.  The density of D2 receptors falls after the peak, resulting in a 38% reduction by age 5 in most children.  A high ratio of D2 to D1 densities in the age period between 3-5 may very well result in the stuttering evident in many children of this age group.  Since D2 receptor density peaks earlier than the D1 density, the D2 to D1 density ratio may be high around the age of 3.  In most children, the density ratio “normalizes” by age 5 leaving these children fluent, while this normalization process does not take place in children who go on to be persistent stutterers.

At the genomic level, there may be two types of genes related to stuttering.  The first type may increase the risks of transient childhood stuttering, while the second type increases the risk of persistent stuttering.  The effect of the two types of genes may be additive.