Cortical and subcortical mechanisms in persistent stuttering ...

Chapter 1 Introduction
Table 1-1 Recent neuroimaging studies revealing aberrant basal ganglia activity in stuttering
Reference deviations task
(Chang et
al., 2009)
(Giraud et
al., 2007)
(Watkins et
al., 2008)
(Lu et al.,
2009b)
(Lu et al.,
2009a)
(Lu et al.,
2010)
less activation in the left putamen
positive correlation between severity of stuttering and activity in the
bilateral caudate nuclei
overactivation in the substantia nigra, extending to the pedunculopontine
nucleus, red nucleus and subthalamic nucleus
weaker negative connectivity from the left posterior middle temporal
gyrus to the putamen, but stronger positive connectivity from the
putamen to the thalamus, from the thalamus to the posterior middle
temporal gyrus and anterior supplementary motor area, and from the
anterior superior temporal gyrus to the preSMA
altered connectivity in the basal ganglia-thalamic-cortical circuit
aberrant basal ganglia-inferior frontal gyrus/premotor area circuit
repeating syllables or
non-speech sounds
(cough)
overt sentences
reading
overt sentences
reading sentences
combined with
altered auditory
feedback
covert picture
naming
covert picture
naming
covert picture
naming
Per Alm provides a detailed theoretical framework on deficient basal ganglia circuits in
persistent stuttering (Alm, 2004). He hypothesized stuttering to arise from an impairment of
the basal ganglia and cortico-striato-thalamo-cortical connections to produce timing cues for
the initiation of the next motor segment in speech. A recent theoretical work incorporates the
aspect of sequence skill learning and automatization of speech (Smits-Bandstra and De Nil,
2007): Dysfunctional cortico-striato-thalamo-cortical connections might hinder the timed
stimulus response association learning. Smits-Bandstra and De Nil suggest that the motor
memories, namely the neurochemical traces that developed due to continuous exposure to
specific stimulus response associations, normally become increasingly resistant to
interference as they become increasingly automatized. Proposing a deficit in automatization in
persons who stutter, the authors suggest a need for additional attentional resources to speech.
Being less automated, the speech skills would be relatively weak, unstable, and more
susceptible to interference from ongoing activity.
A direct test of the basal ganglia hypothesis would require functional interference with the
activity of this subcortical structure. As the basal ganglia lie beyond the range of TMS, this
method can only probe potential consequences of chronically altered basal ganglia activity
with respect to cortical properties. Paired-pulse TMS as described in Appendix D, has
provided valuable insights in the modulation of cortical excitability in a number of basal
ganglia disorders, including Parkinson’s disease, Chorea and Gilles de la Tourette and
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