Stuttering: Not So Funny
There are three major theories of stuttering that emphasize its biological roots and relevant psychological factors: Neurogenic, developmental, and psychogenic stuttering.
The basis of the neurogenic theory of stuttering is that the problem originates in the inability of the basal ganglia to generate neural feedback for appropriate timing of the next segment in the speech stream. If this problem arises in early childhood it is called developmental stuttering with mean age of onset around 2.5 to 3 years. If psychological factors are significantly involved, such as social anxiety or depression, dysfluent speech may be affected for the worse.
The basal ganglia, in the subcortex, just below the cerebral cortex or “thinking” part of the brain, is interconnected with the cortex as well as the amygdala, brainstem, and thalamus. These collective circuits are known as “basal ganglia-thalamocortical loops” with direct links to “limbic” structures, such as the amygdala. The latter is central to the expression of emotions of fear and anxiety and plays a prominent role in social anxiety and depression. Indeed, negative emotions can exacerbate stuttering in the presence of others suggesting a psychogenic cause of stuttering.
But, there is also involvement of the neurotransmitter, dopamine, in the etiology of stuttering. Dopamine projections from the substantia nigra pars compacta (SNc) project to the striatum of the basal ganglia. When the levels of dopamine in the striatum decrease, there is a lowering or cessation of stuttering, whereas when levels of dopamine increase there is an augmentation of stuttering as well as associated motor and behavioral impulses. This is one reason stuttering might be thought of as a “tic”disorder akin to obsessive-compulsive disorders such as Gilles de Tourette syndrome.
There are other possibilities for the biological origins of stuttering. One such aspect is dystonic activity in the facial musculature. That is, opponent muscle groups at odds with each other produce involuntary motor activity resulting in dysfluent speech. But stuttering could arise from a disorder in the sensorimotor area of the cortex in the region known as the oropharynx that controls the motor articulatory apparatus used in speaking.
While the mean age of onset of developmental stuttering is in the range of 2.5 to 3 years, it is typically more prominent in boys (2:1; male:female ratio). The recovery rate is in the range of 60–70% within two years after the onset of stuttering but, what is most surprising, is that these early stutterers often demonstrate advanced development of language abilities.
What might be some ways to relieve stuttering?
(1) Haloperidol (“Haldol”), a dopamine antagonist, attenuates motor activation and may reduce stuttering.
(2) Speaking at the pace of a metronome (known as the “rhythm effect”) can reduce stuttering by compensating for inappropriate timing cues originating in the basal ganglia.
(3) Reading in unison with others (“chorus speech”) as well as singing can also relieve stuttering, because music provides a separate mechanism for generating internal timing cues when there is aberrant output from the basal ganglia most likely by way of the premotor cortex.
(4) There is also some evidence that modified auditory feedback can improve dysfluent speech in those that stutter.
Some suggested reading:
Alm, P. A. (2004). Stuttering and the basal ganglia circuits: A critical review of possible relations. J. of Communication Disorders, 37, 325–369.
LeDoux, J. (1998). The emotional brain: The mysterious underpinnings of emotional life. NY: Simon & Schuster.