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.

Direct/Indirect Pathways and Fluency

In this post, we delve more deeply into the cortical-basal-ganglia-thalamus path (the circuit labeled by “1”) shown in the Figure in the previous post regarding the Dual Premotor System.


The particular components in the basal ganglia box of the aforementioned figure with which we deal here are the putamen and the globus pallidus (both the external, labeled GPe, and the internal, denoted GPi). These components are parts of what is called the corpus striatum.


In the Figure below, note that two types of dopamine receptors, namely D1 and D2, are involved in the putamen. There are 8 or 9 different dopamine receptors, but D1 and D2 are the dominant dopamine receptor subtypes in the putamen.

The direct pathway is activated by glutaminergic (glutamate is an excitatory neurotransmitter) projections from the sensorimotor area of the cortex and by dopaminergic projections from the substantial nigra to the D1 receptors. Activation of the direct pathway inhibits (via GABA) the globus pallidus internal (GPi) which in turn disinhibits the thalamus. As a consequence, the thalami-cortical drive is enhanced and cortically initiated speech will be facilitated.


The indirect pathway arises from the activation of D2 receptors in the putamen which stimulate GABA projections to the globus pallidus external (GPe) resulting in an inhibitory effect. This, in turn, disinhibits the subthalamic nucleus through GABA release. Glutamate projections from the subthalamic nucleus disinhibit the globus pallidus internal (GPi), which in turn inhibits the thalamus.


We see that the direct and indirect pathways act in opposite directions--the indirect pathway being the “brakes,” while the direct pathway is the “gas.” The direct pathway facilitates cortically initiated speech segments, giving a focused cue for the release of a motor segment.  The indirect pathway provides a diffuse background of nerve impulse inhibition, suppressing potentially conflicting and unwanted speech motor patterns.  The relative strengths of the two pathways determines the strength of the cortico-thalamic pathway. For fluent speech, a balance must exist between these two pathways.

If, for example, there were an excess of D2 receptors in the putamen, then the indirect path may dominate and a motor action associated with speech may be blocked from the cortico-thalamic pathway. In which case, that speech related motor action may be restarted, resulting in the repetitious pattern of stuttered speech characteristic of primary stuttering. On the other hand, a secondary stutterer may try to plow through the block to no avail--the signal necessary to execute the speech segment will simply be too weak.

The atypical antipsychotic drugs currently being prescribed for stuttering block D2 receptors and consequently reduce the negative impact of the indirect pathway.

Defending Covert Stuttering, Part 2

If you are having a bad day with respect to fluency, consider talking less. Doing so may involve avoiding speaking situations within reason. This advice may be contrary to that given by most speech therapists.

Parkinson’s disease victims, like stutterers suffer from deficiencies with their dopaminergic systems. But their problem is too little dopaminergic activity rather than too much as in the case of stutterers. Like stutterers, Parkinson victims have good days with regard to motor function and bad days. They are generally advised to engage in physical activities on good days and take it easy on bad days when physical activity may be difficult.

So why should stutterers be treated differently from Parkinson’s victims? Covert stutterers may be mostly fluent but they also have their bad days when fluency is diminished. On such days it would be perfectly reasonable to engage in speech and situation avoidance behavior within limits.

What are these limits? If a Parkinson’s victim is having a bad day and his house is on fire, you would not advocate that he wait until he has a good day before he fled. Similarly, situations may occur whereby a stutterer should not go to extraordinary means to avoid speaking situations. For example, some social engagement for which you have a firm commitment should be kept. In a roomful of people, there are always several long-winded ones, and all you need to do is ask a question and they will happily launch into a 15 minute monologue. Linking together several of these people will easily occupy a cocktail hour with minimum speaking on your part.

Speech avoidance on a bad day is reasonable as long as you don’t do so out of a sense of embarrassment. Rather, you do so because speaking on a bad day is not fun. No matter how much you may think of yourself as a militant in-your-face overt stutterer (as a result of speech therapy), your limbic system (governing emotions) will still influence your fluency. Greater disfluency during bad days (along with negative emotional reactions at a subliminal level) may lead to an overall increased average level of disfluency. On the other hand, good experiences with respect to fluency may be expected to diminish disfluency over the long run.

Speech therapists should not advocate that a successful covert stutterer become an overt one. Instead, the focus should be on diminishing the involvement of the limbic system on the fluency problem. Doing so does not necessarily require that a stutterer stand on a soapbox in the middle of a mall declaring his disfluency.