An Anxious Mind Affects Stuttering, Part 1

Primary stuttering is characterized by easy rhythmical repetition and prolonged sounds, syllables, or words. A young child exhibiting primary stuttering is unaware of his speech and there is no anxiety associated with this stage. Awareness of speech depends upon age and cognitive development and children at this stage are usually between 4-6 years old.

At a later age, primary stuttering generally evolves into secondary stuttering characterized by tense uncontrollable repetitions, prolongations, hesitations, and blocking. This stage is associated with anxiety with respect to one's speech.

It appears that the root cause of primary stuttering is dopaminergic overactivity in what we had vaguely referred to in previous posts the "motor neuron section of the brain." But to be more specific, that part of the brain instrumental in motor activity and whose malfunction plays a role in stuttering is thought to be the basal ganglia, a group of nuclei situated at the base of the forebrain.

The main components of the basal ganglia are the striatum, pallidum, subthalamic nucleus, and substantia nigra. In the basal ganglia, the great majority of neurons use GABA as a neurotransmitter and have inhibitory effects on their targets. However, the substantia nigra is a source of dopamine for the (dorsal) striatum. The dorsal striatum controls sensorimotor responses and excess dopaminergic activity contributes to primary stuttering.

In addition, the basal ganglia has a limbic sector (related to emotion and behavior) whose components are the ventral striatum (also called the nucleus accumbens), the ventral pallidum, and the ventral tegmental area (VTA). The VTA provides dopamine to the (ventral) striatum in the same way that the substantia nigra provides dopamine to the (dorsal) striatum.

The root source of secondary stuttering may lie in another part of the brain, namely the amygdala, an almond shaped structure nestled in the middle of the brain which communicates with the VTA. The amygdala appears to have many functions in terms of its involvement in mental states, but the one important for this discussion is its role in the anxiety/fear response.

In previous posts, we have stated that stuttering is basically a mind/body problem. The mind as a manifestation of the brain involves consciousness, awareness, thought, reason, perception, will, imagination, unconscious cognitive processes, emotional states, and temperament. The emotional state that particularly interests us here is that of anxiety and one aspect of temperament of interest is that of over-reactivity.

An interesting article in the New York Times magazine (October 4, 2009), entitled "The Anxious Mind," argues that some children may be born with over-reactive temperaments. The article may be found at the website:

    http://www.nytimes.com/2009/10/04/magazine/04anxiety-t.html?scp=6&sq=Anxiety&st=cse

Specifically, these children have lower thresholds for arousal in various areas of the brain such as the amygdala, the hypothalamus, and the hypothalamic-pituitary-adrenal axis. This latter is the circuit responsible for the stress hormone, cortisol.

Highly reactive individuals have a particular brain circuitry that leads to a hyperactive amygdala. Nerve circuits originating in the midbrain provide inputs of dopamine to the amygdala and these dopamine signals indicate the importance of a given event. Hypersensitivity of dopamine release is regarded as a biochemical marker of over-reactivity and vulnerability to stress.

The amygdala sends impulses to the nuclei of the VTA for activation of dopamine as well as other neurotransmitters. In turn, as we pointed out above, the VTA provides inputs of dopamine to the striatum, part of the basal ganglia system. In this way, the "mind" via the amygdala may contribute to disfluency over and above the primarystuttering generated directly by excessive dopaminergic activity in the basal ganglia.

Another part of the brain, the prefrontal cortex, is thought to modulate the signals of the amygdala and is implicated in emotional regulation. Individuals with thicker cerebral cortexes have been shown to have better responses to stress and anxiety. Conversely, a thin cortex may be unable to regulate excessive activity in the amygdala, leading to excessive anxiety (see the NY Times magazine article).

If primary stuttering originates from excessive dopaminergic activity in the basal ganglia, then secondary stuttering may result from hyperactivity of the amygdala, the outputs of which may not be very well modulated in some individuals having thinner prefrontal cortexes.

So, in summary, the amygdala may be implicated in the generation of a state of the mind involving one aspect of the temperament of an individual, namely that of proneness to anxiety. Whether the intensity of this trait for stutterers is an inborn characteristic (as suggested by the NY Times article) or is acquired as a result of stuttering at this point is an open question. In either case, the amygdala may affect the basal ganglia by effectively increasing its dopaminergic activity and, hence, disfluency.