ACQ
Volume 12, Number 1 2010
35
fundamental frequency and voice intensity in 30 patients with
Parkinson’s disease were noted after just a single session of
rTMS (Dias et al., 2006). Ingham, Fox, Ingham, Collins, and
Pridgen (2000) delivered slow rTMS (1Hz) to the right
supplementary motor area (SMA) of five persons who
stuttered for 20 minutes per day for 10 consecutive days to
reduce the SMA overactivation that was observed by
neuroimaging. One of the persons who stuttered showed a
reduction in stuttering approximately one month following the
TMS program, with this reduction sustained for at least five
months. No behavioural changes were noted for the
remaining persons who stuttered.
Limitations of TMS and
methodological considerations
There are a number of limitations of TMS and methodological
considerations that need to be considered when planning a
TMS study. First, the magnetic field generated by TMS
stimulates to a depth of only approximately 2cm below the
cortical surface (George et al., 1999) limiting the brain
regions that can be stimulated to those on the cortical
surface, rather than deep brain structures. Second, TMS
typically indirectly stimulates pyramidal neurons as it
preferentially stimulates those neurons that are parallel to the
cortical surface. These preferentially stimulated neurons are
believed to be mostly interneurons, which indirectly and
trans-synaptically activate the pyramidal neurons (Pascual-
Leone et al., 1998). Thirdly, MEP recordings need to be
made from stationary muscles and, hence, speech tasks
cannot be utilised. Tasks that require participants to imagine
speaking could be utilised instead, however, as
neuroimaging has shown that brain activations during
imagined speech resemble those during overt speech
(Ingham et al., 2000). Finally, the optimal TMS parameter
combinations to be used for neuromodulatory treatment (i.e.,
frequency and number of TMS pulses and sessions) are not
yet well understood and require further study.
Conclusion
The present review illustrates how TMS can be used as an
adjunct to neuroimaging and other neurophysiological
techniques to investigate potential neural disturbances
underlying motor speech disorders. By using TMS in future
studies of motor speech disorders it is anticipated that not
only will our understanding of the neurophysiological
underpinnings be better informed, but the options and
efficacy of treatment that can be offered will also improve.
References
Dias, A.E., Barbosa, E. R., Coracini, K., Maia, F., Marcolin,
M. A., & Fregni, F. (2006). Effects of repetitive transcranial
magnetic stimulation on voice and speech in Parkinson’s
disease.
Acta Neurologica Scandinavica
,
113
, 92–99.
Fadiga. L, Craighero, L., Buccino, G., & Rizzolatti,
G. (2002). Speech listening specifically modulates the
excitability of tongue muscles: A TMS study.
European
Journal of Neuroscience
,
15
, 399–402.
George, M. S., Lisanby, S. H., & Sackeim, H. A.
(1999). Transcranial magnetic stimulation: Applications in
neuropsychiatry.
Archives of General Psychiatry
, 56(4),
300–311.
Hallett, M. (2000). Transcranial magnetic stimualation and
the human brain.
Nature
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406
, 147–150.
Paired-pulse TMS involves delivering a subthreshold
conditioning TMS pulse that activates cortical neurons but
that is too small to result in any descending spinal cord
activation, followed by a second, test pulse (Hallett, 2000).
The stimulus intensity and the interstimulus interval between
conditioning and test pulses appear to affect which
intracortical circuits are activated (i.e., facilitatory or
inhibitory), which, in turn, affects the MEP amplitudes
recorded following the test stimulus (Kobayashi & Pascual-
Leone, 2003). Typically, interstimulus intervals of less than
4ms induce inhibition, while interstimulus intervals of 5ms to
30ms induce facilitation (George et al., 1999; Kobayashi &
Pascual-Leone, 2003). Electromyographic silent periods refer
to the period in which EMG activity is suppressed in a
voluntarily contracted muscle following suprathreshold TMS
stimulation. The initial portion of the silent period is believed
to be due in part to spinal cord refractoriness, with the latter
portion due to cortical inhibition (Hallett, 2000).
Intracortical inhibition and facilitation of the tongue
motor cortex has been studied using cortical silent periods
(Katayama et al., 2001) and paired-pulse TMS (Muellbacher
et al., 2001). Sommer, Wischer, Teragau, and Paulus (2003)
used single pulse and paired-pulse TMS to investigate
excitability and intracortical inhibition and facilitation of the
dominant hand motor cortex in a group of 18 right-handed
speakers with developmental stuttering. Their study was
driven by a proposal that persistent developmental stuttering
is a task-specific dystonia characterised by reduced
intracortical inhibition. Interestingly, intracortical inhibition and
facilitation were found to be normal, while motor thresholds
were increased, suggestive of reduced motor cortical
excitability.
Inducing neuromodulation
Repetitive TMS (rTMS) involves delivering trains of TMS
pulses (
≥
1 Hz or equal to or greater than one per second),
which summate to effect temporary neural modulation. This
modulation can comprise inhibition or facilitation of cortical
excitability depending on stimulation intensity, frequency, and
duration (Pascual-Leone et al., 1998). Slow rTMS in the 1Hz
frequency range has been found to transiently decrease
excitability, while rapid rTMS, at frequencies of 5Hz and
higher, looks to transiently increase excitability (Hallett, 2000;
Kobayasi & Pascual-Leone, 2003). In addition to
investigating behavioural effects (e.g., reduction or increase
in stuttering) induced by TMS neuromodulation, rTMS can
also be used to temporally disrupt neural activity, thereby
creating a temporary virtual lesion, to evaluate a cortical
region’s function (Hallett, 2000).
TMS applications in motor
speech treatment
The application of TMS in the treatment of motor speech
disorders is a growing, yet at present, a limited and under-
developed field. Treatment protocols have involved the use
of rTMS on the basis of its capability in effecting
neuromodulation and have been found to be successful in
regulating cortical function and normalising the balance of
inter-hemispheric excitability with resultant changes in
behaviour in a range of disorders, including depression (e.g.,
Pascual-Leone, Rubio, Pallardo, & Catalá, 1996), motor
dysfunction and aphasia associated with stroke (e.g., Martin
et al., 2004), and motor and vocal function in Parkinson’s
disease (e.g., Dias et al., 2006). Significant improvements in