C H A P T E R
55
Neurobiology of Speech Production:
Perspective from Neuropsychology and
Neurolinguistics
Sheila E. Blumstein1 and Shari R. Baum2
1
Department of Cognitive Linguistic and Psychological Sciences, Brown University and the Brown Institute for
Brain Sciences, Providence, RI, USA; 2School of Communication Sciences and Disorders and Centre for Research on
Brain, Language & Music, McGill University, Montréal, QC, Canada
55.1 INTRODUCTION
For most of us, the production of speech appears to be
effortless. And, yet, it is a multifaceted and complex pro-
cess that requires access to different components of the
language processing system. Although articulation of a
word (i.e., patterns of articulatory movements of the
vocal tract) may be the endpoint, the process begins with
the conceptualization of a word, the selection of its lexi-
cal representation and corresponding sound properties
from the mental lexicon, and the mapping of these pho-
nological representations onto articulatory planning and
implementation stages. Additionally, the speaker does
not simply passively articulate speech, but rather he or
she constantly monitors it on a moment-to-moment basis
to adapt his/her output in either the short-term or the
long-term based on both auditory and somatosensory
feedback received from the production itself.
Although the details may vary, current models of the
functional architecture of speech production typically
identify these different aspects of speech production in
terms of different stages of production. These stages are
considered to be functionally distinct and hierarchically
organized, with both feedforward and feedback mechan-
isms at each stage of processing (Figure 55.1). It is the
goal of this chapter to examine current data and models
of the speech production process, drawing from both
neuropsychological and neurophysiological studies. To
this end, we first provide a brief historical perspective
drawn from the aphasia literature that has served as a
Neurobiology of Language. DOI: http://dx.doi.org/10.1016/B978-0-12-407794-2.00055-9
framework for much of the neurophysiological research.
We then consider the proposed stages of production out-
lined, first reviewing phonological stages of production
and then phonetic/articulatory stages of production,
integrating results based on lesion and neurophysio-
logical studies. Together, they indicate that speech
production recruits a neural network that encom-
passes the language network, including temporal,
parietal, and frontal structures.
55.2 HISTORICAL PERSPECTIVE:
SPEECH PRODUCTION DEFICITS
IN APHASIA
Early research from the 1970s and 1980s suggested
that the patterns of production in patients with aphasia
reflected different stages of the speech production pro-
cess. Patients with lesions to frontal structures displayed
articulatory planning and implementation deficits, and
patients with lesions to posterior structures displayed
phonological deficits. One of the presenting clinical fea-
tures long recognized in defining the aphasia syndromes
is the nature of speech production output (Goodglass &
Kaplan, 1972) (for discussion of clinical syndromes of
aphasia, see Chapter 73). In particular, patients present-
ing with Broca’s aphasia or apraxia of speech typically
have nonfluent speech output characterized by distorted
speech production, sound errors of various types, and a
diminution of the prosodic range of speech. In contrast,
689 © 2016 Elsevier Inc. All rights reserved.
690 55. NEUROBIOLOGY OF SPEECH PRODUCTION: PERSPECTIVE FROM NEUROPSYCHOLOGY AND NEUROLINGUISTICS
Concept
Lexicon
Selection
Planning
Articulatory implementation
Feedback
auditory/somatosensory
FIGURE 55.1 Functional architecture of stages of speech produc-
tion processes. Colors in pink indicate phonological processes; those
in blue indicate phonetic processes.
patients presenting with Wernicke’s and conduction
aphasia show fluent, well-articulated speech output.
Nonetheless, these patients, and particularly those clini-
cally diagnosed with conduction aphasia, make speech
production errors characterized by sound substitutions
and the misordering and transposition of sounds within
and across words.
Studies examining the acoustic patterns of speech pro-
duction of these patients largely supported this dichot-
omy. Acoustic measures of a number of parameters of
speech, including voice-onset time (VOT) in stop conso-
nants (Blumstein, Cooper, Goodglass, Statlender, &
Gottlieb, 1980; Gandour & Dardarananda, 1984; Kent &
Rosenbek, 1983), amplitude of voicing in fricative conso-
nants (Kurowski, Hazen, & Blumstein, 2003), murmur
duration, amplitude of the first harmonic at consonant
release in nasal consonants (Kurowski, Blumstein,
Palumbo, Waldstein, & Burton, 2007), and temporal para-
meters of consonant and vowel production (Baum,
Blumstein, Naeser, & Palumbo, 1990) showed that
patients with frontal lesions displayed deficits. They also
displayed deficits in laryngeal control as shown by
impairments in amplitude properties of nasals, fricatives,
and prosody. In contrast, patients with posterior lesions
showed normal patterns of production in the analysis of
these parameters.
Although this dichotomy between phonological and
phonetic stages of speech production is supported by
more recent neuropsychological and neurophysiological
studies, early on, studies of speech production in aphasia
indicated that the picture was more complicated. These
studies showed that in addition to phonetic (articulatory)
J. SPEAKING
deficits, those with Broca’s aphasia and patients with
apraxia of speech produced phonological errors similar
to those made by those with fluent aphasia with poste-
rior lesions (Blumstein, 1973; Canter, Trost, & Burns,
1985; Haley, Jacks, & Cunningham, 2013). For example,
the patterns of phoneme substitution errors (e.g., pipe -
bipe) made by those with Broca’s, conduction, and
Wernicke’s aphasia were similar across groups, as were
the distributions of different error types such as pho-
neme substitutions (e.g., teams - keams), deletions
(e.g., brown - /bawn/), additions (e.g., papa -
/paprə/), and transpositions (e.g., degree - /gədri/).
Acoustic analysis revealed that both Wernicke’s and con-
duction aphasics showed increased variability in the
implementation of a number of acoustic parameters of
speech, despite the fact that they showed normal pat-
terns of articulatory implementation (Baum et al., 1990;
Ryalls, 1986; Vijayan & Gandour, 1995). Taken together,
these findings indicate that speech production recruits
an integrated functional and neural system, one in which
damage to one area has consequences throughout the
system affecting stages of production both upstream and
downstream from it.
55.3 PHONOLOGICAL PROCESSES
IN SPEECH PRODUCTION
There is a rich literature that has examined the
representations and processes involved in accessing
words from the lexicon in spoken word production.
Results from this research generally support the view
that words are represented in terms of abstract, con-
text-independent, phonological (phonemic and/or
syllable-sized) units and that the mental lexicon and
access to it is influenced by the phonological proper-
ties of individual words and the network of word
representations that share structural properties with
the word candidate (Dell, 1986; Gaskell & Marslen-
Wilson, 1999). Information flow throughout the speech
production system is considered to be interactive.
Activation of a lexical candidate activates its associated
phonological units, and these phonological units, in
turn, boost the activation of the word candidate as
well as those shared phonological units of other words
in the lexicon. With this view, the selection of the pho-
nological representation of a word is modulated by the
number of phonological “neighbors” a word may have
(Dell & Gordon, 2003), and this has a cascading effect
on its articulatory implementation (Baese-Berk &
Goldrick, 2009; Goldrick & Blumstein, 2006).
Evidence from aphasia has generally supported
this view. Although these studies provide evidence
in support of many of the theoretical claims about
the functional architecture of spoken word
 55.3 PHONOLOGICAL PROCESSES IN SPEECH PRODUCTION
production, most fail to provide information about
or focus on the underlying neural substrates.
Additionally, there have been surprisingly few func-
tional neuroimaging studies examining these issues.
With this limitation in mind, we now turn to a brief
review of the extant neuropsychological and neuro-
physiological findings examining phonological pro-
cesses in speech production.
55.3.1 Nature of Representations
Similar to individuals without brain damage,
patients with aphasia show sensitivity to the sound
structure properties of the lexicon in spoken word pro-
duction. In a study of the production of speech errors
in picture description and picture naming tasks in 43
aphasic patients (unselected for syndrome or lesion),
Gordon (2002) showed that there were fewer errors
produced for word targets that had many lexical
neighbors than words that did not. These facilitative
effects occur presumably because words from dense
neighborhoods share phonological structure with the
target, and the phonological similarities among the tar-
get word and its neighbors provide a further boost to
the activation of the lexical target. That the effect is
driven by lexical factors is further supported by the
fact that errors were more likely to result in words (of
similar sound shape) than in nonwords (see also
Laganaro, Chetelat-Mabillard, & Frauenfelder, 2013).
As indicated, the general consensus in the spoken
word production literature is that words are represented
in terms of abstract phonological units. These units may
include both sound segments and properties of sound
segments (i.e., phonological/phonetic features).
Evidence suggesting that these units are segmental
comes from detailed analyses of the patterns of phono-
logical errors produced by aphasic patients in spontane-
ous speech as well as in more controlled tasks such as
repetition and naming (Blumstein, 1973; Lecours &
Lhermitte, 1969). Results show that phoneme substitu-
tions, the most common error produced by those with
Broca’s, conduction, and Wernicke’s aphasia involve the
replacement of a single phoneme by another; whether
this happens within a word, such as teams - /kimz/, is
the result of misordering of sounds within a word, such
as “degrees” - /gədriz/, or is a sound substitution
between words, such as roast beef - /rof bif/.
Additionally, the pattern of substitution errors sug-
gests that phonological features of sounds are funda-
mental representational units. In particular, the large
majority of substitution errors reflect the replacement of
a single phonetic feature, with very few errors occurring
between sounds distinguished by two or more features.
For example, there are more voicing, place of
J. SPEAKING
691
articulation, or manner errors than combinations of these
features. These findings are consistent with early work
by Jakobson, Halle, and Fant (1967), who proposed that
a finite set of distinctive features can be used to charac-
terize the phonological systems of language and the
acquisition or dissolution of language (Jakobson, 1968).
Although it may be the case that phonological units
may be abstract and are represented independent of
the phonetic context in which they occur, there must
be a processing stage where the abstract sound shape
is coded into fine “episodic” details that take into
account the context in which the sounds appear. These
details are ultimately used for motor planning and exe-
cution. Evidence from aphasia supports this two-stage
process (Blumstein, 1973).
Consider the words “pill” and “spill” in English. The
abstract representation of the /p/ in these two words is
the same. However, their phonetic realization differs;
/p/ in initial position in English is aspirated and has a
long VOT (i.e., [ph]), whereas /p/, following /s/ is unas-
pirated and has a short VOT (i.e., [p]). It is of interest to
determine what happens when an aphasic patient sim-
plifies a consonant cluster, particularly what happens
when a patient deletes the /s/ in a word like “spill.”
Will the resultant production of the /p/ be produced
with an aspirated and long VOT, consistent with the
notion that the deletion of the /s/ occurred during pho-
nological processing (i.e., before motor plans for a cluster
are implemented), or will it be produced with an unaspi-
rated and short VOT, consistent with the notion that the
production reflected the contextually determined pho-
netic realization of the cluster /sp/ followed by the dele-
tion of the initial fricative? A study by Buchwald and
Miozzo (2011) measured the VOT productions of two
aphasic patients who deleted /s/ in /sp/, /st/, and
/sk/ clusters and compared these with the phonetic real-
ization of correctly produced stop consonants in both
singleton and cluster environments (i.e., “pill” and
“spill”). Results showed two different patterns of pro-
duction, with one patient producing the initial stop con-
sonant of the word with a long VOT (similar to the
realization of /p/ in “pill”) and the other producing it
with a short VOT (similar to the realization of /p/ in
“spill”). These findings suggest that the errors of the for-
mer patient were phonologically based and the errors of
the latter patient were phonetically based. Similar find-
ings were shown examining duration properties of nasal
consonants when deleted in /sn/ and /sm/ clusters
(Buchwald & Miozzo, 2012).
55.3.2 Cascading Activation
During the stages of speech production, information
flows from the more abstract properties of speech to
692 55. NEUROBIOLOGY OF SPEECH PRODUCTION: PERSPECTIVE FROM NEUROPSYCHOLOGY AND NEUROLINGUISTICS
more detailed phonetic representations required for
articulatory planning and articulation. Recent research
with normal individuals has suggested that there is a
cascading flow of information with phonological prop-
erties of words influencing their fine-grained phonetic
realization (Goldrick, 2006). For example, it has been
shown that the implementation of voicing in stop con-
sonants is influenced by whether the words have a
voicing minimal pair (Baese-Berk & Goldrick, 2009;
Goldrick & Blumstein, 2006). There is a longer VOT for
initial voiceless stop consonants in words having a
voiced minimal pair (e.g., “tart” versus “dart”) com-
pared with words that do not (e.g., tar versus  dar).
A recent neuroimaging study (Peramunage,
Blumstein, Myers, Goldrick, & Baese-Berk, 2011) exam-
ined the neural substrates of this lexically conditioned
phonetic effect. While in the scanner, participants read
words with initial voiceless stop consonants that either
had or did not have a voiced minimal pair. None of
the voiced minimal pairs were included in the set of
words produced by the participants. Filler words
beginning with a variety of consonants were also
included. Acoustic analysis of the productions repli-
cated the behavioral effects showing longer VOTs for
voiceless stop consonants in words that had a minimal
pair compared with words that did not. fMRI results
revealed reduced activation for minimal pair words
compared with nonminimal words in a neural net-
work, including the left posterior superior temporal
gyrus (STGp), supramarginal gyrus (SMG), inferior
frontal gyrus, and precentral gyrus.
These findings suggest that lexically driven differ-
ences in the activation of phonological representations
in temporoparietal areas (posterior superior temporal
and supramarginal gyri) modulate subsequent articu-
latory processes in frontal areas (the inferior frontal
and precentral gyri). Moreover, they are consistent
with the view that reduced activation for minimal pair
words is a facilitatory process reflecting the overlap in
shared phonological properties between the target
word and its minimal pair (MP) neighbor. Of interest,
a subsequent study (Bullock-Rest et al., 2013) examin-
ing the effects of lesions to the SMG extending into the
STGp or to the inferior frontal gyrus on the production
of minimal pair and nonminimal words using the
Peramunage et al. (2011) stimuli showed that both
groups of patients demonstrated the minimal pair
effect. Of importance, this effect emerged for correct
productions, suggesting that despite damage to the
network, Broca’s and conduction aphasic participants
were still sensitive to the lexical properties of the target
words and this, in turn, affected their phonetic output.
Nonetheless, both groups showed a pattern of errors
consistent with the view that they had a deficit in the
spoken word production system. They made more
J. SPEAKING
errors on nonminimal pair words than minimal pair
words and made phoneme substitution errors on the
target words that were largely single-feature substitu-
tions, and when such errors occurred, the production
was more likely to be a word than a nonword.
Perhaps more compelling evidence comes from a
recent study examining the origin of phonemic para-
phasias (i.e., phoneme substitution errors) in aphasic
patients (Kurowski & Blumstein, in preparation). The
question asked here was whether phonemic substitu-
tion errors (e.g., [s] -[z]) reflect a planning error,
where the wrong phoneme is selected and ultimately
implemented correctly, or whether it reflects the simul-
taneous selection and activation of a mis-selected pho-
neme and the original target phoneme. In this latter
case, the resulting production, although perceived by
the listener as a phonemic paraphasia (i.e., a clear-cut
substitution error), is a hybrid, realized acoustically as
a phoneme substitution but with an acoustic trace of
the original target phoneme. To examine this question,
acoustic measures were performed of voicing in the
fricative consonants [s z] produced in a conso-
nant vowel (CV) environment by seven aphasic parti-
cipants, three clinically diagnosed with Broca’s
aphasia, three with conduction aphasia, and one with
Wernicke’s aphasia. Results showed that the phonemic
paraphasias of the patients left traces of the original
target phoneme. These findings suggest that the
production of phonemic paraphasias reflect the
simultaneous selection and activation of competing
phonemes that subsequently influence articulatory
planning and implementation stages downstream from
it (see also Baum & Slatkovsky, 1993; Buckingham,
1992; Buckingham & Yule, 1987).
55.4 PHONETIC PROCESSES
IN PRODUCTION
55.4.1 Articulation
Identifying the neurostructural and neurofunctional
correlates of speech production at the articulatory pho-
netic level requires an understanding of both speech
motor programming and sensorimotor integration.
Until relatively recently, the majority of work on the
neural networks underlying overt speech production
relied primarily on evidence from studies of patient
populations. In early years, symptomatology exhibited
by stroke patients was coarsely correlated with lesion
sites based on CT scans (Baum & Boyczuk, 1999;
Blumstein et al., 1980; Blumstein, Cooper, Zurif, &
Caramazza, 1977). As imaging technology improved,
so did the accuracy with which symptoms were associ-
ated with lesion sites (Baum et al., 1990). In what has
 55.4 PHONETIC PROCESSES IN PRODUCTION
become a landmark study, Dronkers (1996) compared
the lesions of 25 individuals diagnosed with apraxia of
speech (in a chronic state) in an effort to identify a
common area of infarct responsible for the phonetic
implementation deficit. The only lesion site common to
all patients was in the precentral gyrus of the insula,
leading to the suggestion that this region was impor-
tant in articulatory coordination and control
(Dronkers, 1996; see also Dogil et al., 2002; Wise,
Greene, Buchel, & Scott, 1999). However, more recent
studies have implicated the pars opercularis, suggest-
ing that the insula is part of a network involved in
articulatory control (Hillis et al., 2004; Leonardo et al.,
2006). Easier access to high-quality functional neuroim-
aging has permitted a far more detailed and broadly
encompassing understanding of the neural substrates
of speech production to emerge.
It is self-evident that the networks implicated in
speech production include the cortical and subcortical
regions involved in motor control more generally (i.e.,
primary motor cortex, supplementary motor area
[SMA], regions within the basal ganglia, and the cere-
bellum). Numerous investigations over the past 15
years have attempted to identify the specific roles of
each of these regions and others, including areas
within auditory and somatosensory cortices, because
each contributes to the neural network subserving
speech production. We first review studies focused on
the production of syllables and syllable sequences, and
then we turn to sensorimotor integration in speech
production.
In comparison with the vast literature on word pro-
duction (e.g., as reviewed in Indefrey & Levelt, 2000)
and a growing literature on covert speech production
(e.g., Price, 2012, for review), far fewer neuroimaging
studies have investigated overt articulation. Based on
his well-developed DIVA model of speech production
(Guenther, 1994, 1995), Guenther and colleagues have
proposed and begun testing the neural bases of certain
aspects of the model (e.g., Bohland & Guenther, 2006;
Guenther & Ghosh, 2003; Guenther, Ghosh, &
Tourville, 2006; and others). Broadly speaking, the
DIVA model consists of two primary control systems—
a feedforward system including areas involved in artic-
ulatory implementation (speech sound system and
stored motor programs, hypothesized to be represented
in left ventral premotor cortex [PMC]), articulatory
positioning commands generated in motor cortex, and
timing coordinated in the cerebellum, and a feedback
system that allows for error detection and monitoring
and sensorimotor integration based on both auditory
(temporal cortex) and somatosensory (inferior parietal
cortex) input, with bidirectional links between the two
control systems (Guenther et al., 2006). In one of the
first tests of the hypothesized neural correlates of the
J. SPEAKING
693
model’s components, Guenther et al. (2006) conducted
an event-related sparse sampling fMRI study in which
10 speakers produced monosyllabic or bisyllabic
stimuli based on orthographic representations (i.e.,
reading aloud). Scans were acquired during silent inter-
vals after syllable production, timed to co-occur with
the idealized peak of the associated hemodynamic
response function (HRF), and activation was compared
with passive viewing of a string of Xs. Activation was
found in a widespread bilateral network including pri-
mary motor cortex, primary auditory and sensory corti-
ces, the cerebellum, left inferior prefrontal gyrus, SMA,
SMG, and area Spt (Hickok & Poeppel, 2004)—all areas
in keeping with the predictions of the model (see also
Blank, Scott, Murphy, Warburton, & Wise, 2002; Price,
Crinion, & MacSweeney, 2011; Price, Moore, &
Frackowiak, 1996).
In a related study focused on the production of syl-
lable sequences, Bohland and Guenther (2006) com-
pared patterns of activation during production of
syllables varying in complexity based on number of
onset consonants (in this case, syllable length was also
modified) and syllable sequences of varying complex-
ity (i.e., the same CV repeated three times or three dif-
ferent CVs appended to one another). Subjects were
required to overtly produce the stimuli for a subset of
trials and to prepare to produce (but not actually do
so) in others (through use of a go/no go task). A con-
junction analysis of all speech conditions again yielded
a broad bilateral network, including the bilateral cen-
tral sulcus, precentral and postcentral gyri, anterior
insula, superior temporal cortex, medial premotor
areas (SMA and pre-SMA), the basal ganglia, thala-
mus, cerebellum, and left frontal operculum (Bohland
& Guenther, 2006; see also Peeva et al., 2010). The
increase in syllable complexity (which inherently
entailed an increase in length) yielded increased acti-
vation in medial premotor regions, the frontal opercu-
lum bilaterally, and the left posterior parietal lobe. The
increase in sequence complexity yielded increased acti-
vation in bilateral medial premotor regions, left frontal
cortex, anterior insula bilaterally, left posterior parietal
lobe, bilateral inferior posterior temporal lobe, bilateral
cerebellum, anterior thalamus, and caudate nucleus
(Bohland & Guenther, 2006; but see Dogil et al., 2002
for data suggesting that increased complexity yields
reduced activation).
Based on these findings, the authors suggest that
the inferior frontal sulcus may be the region where the
motor programs required for the production of phono-
logical units or syllables are represented. Given the
increase in activation during complex sequences in the
left IFGpo (see also Papoutsi et al., 2009; Park, Iverson,
& Park, 2011; Soros et al., 2006), the authors suggest
that this region houses the “speech sound map”—the
694 55. NEUROBIOLOGY OF SPEECH PRODUCTION: PERSPECTIVE FROM NEUROPSYCHOLOGY AND NEUROLINGUISTICS
phonetic codes for specific phonemes or syllables. The
anterior insula—the region identified by Dronkers
(1996) as common to all her patients who presented
with apraxia of speech—was active in all overt speech
tasks, but activation was not modulated by sequence
or syllable complexity (Bohland & Guenther, 2006;
see also Ackermann, Mathiak, & Ivry, 2004, but
see Frenck-Mestre, Anton, Roth, Vaid, & Viallet, 2005;
Riecker et al., 2000; Soros et al., 2006 for studies show-
ing an absence of anterior insula activation during
speech production). According to Bohland and
Guenther (2006), the anterior insula may have a role in
speech initiation (see also Shuren, 1993) but is not
likely to be involved in the representation or imple-
mentation of syllable sequences (for yet a different per-
spective, see Moser et al. (2009) for data suggesting
that the anterior insula has a role in speech implemen-
tation for novel motor programs). A nearby region that
did show sensitivity to complexity was between the
anterior insula and the frontal operculum; the authors
conclude that this region is involved in syllable
sequence representation, perhaps as a site of integra-
tion of lower and higher level representations of
speech (Bohland & Guenther, 2006).
Other investigators have made similar but slightly
different claims about the role of the IFGpo. For
instance, based on a positron emission tomography
(PET) study comparing silent speech to oral (non-
speech) movements, Price et al. (2011) suggest that the
IFGpo (along with posterior superior temporal sulcus
[STS]) is involved in predicting acoustic and motor
consequences of speech articulation, that is, in the
feedforward (internal model) system—not altogether
different from Bohland and Guenther’s (2006) speech
sound map, but with a somewhat different precise
localization. This predictive coding would then, hypo-
thetically, be passed on to temporal regions (posterior
STS and planum temporale) where it could be used in
an optimization loop to limit both perceptual and pro-
duction errors. The authors admit that functional con-
nectivity analyses would be required to confirm this
hypothesis. In this study, activation of the superior
temporal plane region was not found to be specific to
speech production (i.e., it emerged during oral, non-
speech movements as well), suggesting this region
may play a more general role in sensorimotor integra-
tion (Price et al., 2011; see Hickok & Poeppel, 2004;
Hickok, Okada, & Serences, 2009; Peschke, Ziegler,
Eisenberger, & Baumgaertner, 2012).
In a meta-analysis of 19 fMRI and PET studies of
overt speech production, Eickhoff, Heim, Zilles, and
Amunts (2009) reported consistent activation in left
inferior frontal gyrus (IFG), the face region of primary
motor cortex, the anterior insula, lateral premotor cor-
tex, the cerebellum, and the basal ganglia. They
J. SPEAKING
propose that the anterior insula is involved in prepara-
tion for speech, possibly in translating a phonetic “con-
cept” obtained from left IFG into articulatory motor
patterns, whereas the left IFG represents the site of the
final stages of lexical retrieval that initiates the articu-
latory process. They further suggest that the basal gan-
glia and cerebellum are involved in the selection and
implementation of motor programs, including timing
and the incorporation of sensory feedback, whereas
the premotor cortex combines the information from
these two sources (basal ganglia and cerebellum) to
convert into a specific movement (muscle contraction)
plan. The involvement of primary motor cortex relates
to actual execution via connections to lower motor
neurons (Eickhoff et al., 2009).
As suggested in the description of the meta-analysis
reported by Eickhoff and colleagues, additional
regions that have been the focus of intense investiga-
tion regarding their role in speech production include
several premotor regions, notably the pre-SMA, SMA
proper, and dorsal and ventral premotor regions
(Ackermann & Ziegler, 2010; Guenther et al., 2006;
Hartwigsen et al., 2013; Peeva et al., 2010; Saur et al.,
2008; Soros et al., 2006; Tremblay & Gracco, 2006). The
pre-SMA has long been claimed to be important for
speech initiation, based, in part, on evidence from
lesion studies (Ackermann & Ziegler, 2010; Ziegler,
Kilian, & Deger, 1997) and data from investigations of
nonspeech motor control highlighting its role in move-
ment initiation (Shima & Tanji, 2000). Dorsal and ven-
tral premotor areas have frequently been found to be
activated during speech production and are presumed
to be implicated in the conversion of phonetic codes to
articulatory implementation or execution (Guenther
et al., 2006; Hickok, Houde, & Rong, 2011). Using
dynamic causal modeling (DCM) to explore effective
connectivity and diffusion tensor imaging (DTI) to
examine anatomical connectivity, Hartwigsen et al.
(2013) investigated the roles of these frontal premotor
areas during real-word and pseudoword repetition.
The investigators hypothesized that if pre-SMA is truly
important in speech initiation, then the DCM model
with the best fit to the data should include “driving
input” into pre-SMA, with a strong influence of pre-
SMA on dorsal and ventral premotor areas. The effec-
tive connectivity analyses did demonstrate such a pat-
tern, with a stronger influence of pre-SMA on the
dorsal premotor region for pseudowords relative to
real words. DTI analyses revealed direct fiber connec-
tions between pre-SMA and both dorsal and ventral
premotor cortex. Based on their findings, the authors
propose that the pre-SMA is involved in the sequenc-
ing of motor programs for articulatory initiation, the
dorsal premotor cortex is implicated in conversion of
an abstract sequencing plan to an actual motor-
 55.4 PHONETIC PROCESSES IN PRODUCTION
articulatory plan (see also Alario, Chainay, Lehericy, &
Cohen, 2006), and the ventral premotor cortex pro-
vides predictions of the auditory representations of
common speech sounds and syllables (Hartwigsen
et al., 2013; see also Guenther et al., 2006).
One final brain region that clearly plays an impor-
tant role in speech production is the cerebellum, which
has connections to both basal ganglia and sensorimotor
cortex, as well as to premotor regions and the insula
(Ackermann, 2008). Unfortunately, it has received sub-
stantially less attention in the literature. However,
based on studies of patients with cerebellar lesions,
some recent neuroimaging data, and studies of non-
speech motor control, the cerebellum has been argued
to be involved in the temporal organization and
sequencing of syllables, as well as the control of speech
rate (beyond a certain speed) (e.g., Ackermann, 2008;
Ackermann, Mathiak, & Riecker, 2007; see also Ivry &
Keele, 1989; Ivry, Spencer, Zelznik, & Diedrichsen,
2002). Interestingly, parts of the cerebellum have also
shown to be sensitive to speech perceptual demands,
particularly in temporal discrimination (Ackermann,
2008; Mathiak, Hertrich, Grodd, & Ackermann, 2002,
2004; Petacchi, Laird, Fox, & Bower, 2005). The precise
integration of cerebellar processing with cortical and
subcortical processing for speech production remains
to be determined.
55.4.2 Sensorimotor Integration
The integration of sensory and motor signals is a
crucial component in sensorimotor learning and the
establishment of perceptuo-motor representations.
Speech production is, by nature, a sensorimotor behav-
ior. Such behaviors require monitoring of input from
one or more sensory systems to update or modify
motor plans, either on a moment-by-moment compen-
satory basis (online sensorimotor control) or via
longer-term adaptation (sensorimotor learning). In
most models of speech production, sensorimotor feed-
back is compared with a predicted outcome to control
ongoing movement and program future articulation;
this process of internal feedforward models (efference
copy) is proposed in one form or another in the DIVA
model of Guenther (1995) and in the state feedback
control model of Houde and Nagarajan (2011), among
others (Price et al., 2011).
One means of addressing questions of sensorimotor
integration is through empirical studies of imposed
sensory-based manipulations. For example, it has fre-
quently been demonstrated that the speech production
system is able to compensate for many perturbations to
the vocal tract—both predictable and unexpected—to
achieve phonetic goals (e.g., Abbs, 1986; Lindblom,
J. SPEAKING
695
Lubker, & Gay, 1979, among many others); nonetheless,
the extent of compensation varies depending on the
nature of the perturbation and the specific speech
sounds targeted (Aasland, Baum, & McFarland, 2006;
Baum & McFarland, 1997, 2000). These findings suggest
that speakers are generally able to adapt to modifica-
tions of somatosensory (kinesthetic or proprioceptive)
feedback to produce perceptually adequate speech.
Recently, a great deal of attention has been focused on
speech adaptation to alterations of auditory feedback as
well. As in the visual modality in studies of prism
adaptation (Redding, Rossetti, & Wallace, 2005;
Redding & Wallace, 1996; Rossetti, Koga, & Mano,
1993), investigations have demonstrated adaptive
speech motor output in the face of auditory feedback
that has been modified to yield what is perceived as a
production error on the part of the speaker (Houde &
Jordan, 1998, 2002; Jones & Munhall, 2005; Larson,
Altman, Liu, & Hain, 2008; Larson, Burnett, Kiran, &
Hain, 2000; Purcell & Munhall, 2006; Shiller, Sato,
Gracco, & Baum, 2009). Adaptation in this context is
not complete, in that the speech output does not fully
compensate for the perceived target error (Jones &
Munhall, 2005). The reasons for incomplete adaptation
are complex (Shiller et al., 2009), but the limited adap-
tive response indicates online sensorimotor integration
and suggests a recalibration of perceptual and motor
responses (Baum & McFarland, 1997, 2000; Houde &
Jordan, 1998, 2002; Jones & Munhall, 2005; Nasir &
Ostry, 2009). Functional neuroimaging studies that
investigate the neural mechanisms involved in such
sensorimotor adaptation for speech are only beginning
to emerge (Baciu, Abry, & Segebarth, 2000; Guenther
et al., 2006; Ito, Kimura, & Gomi, 2005; Tourville,
Reilly, & Guenther, 2008); thus far, they support a
broad cortical and subcortical network, including both
left and right hemisphere regions underlying the adap-
tation process, as detailed here. Other approaches to
exploring the integration of perceptual and production
processes have also been undertaken. For instance,
Hickok and colleagues (Buchsbaum, Hickok, &
Humphries, 2001; Hickok, Buchsbaum, Humphries, &
Muftuler, 2003; Hickok et al., 2009, among others) have
used nonword repetition tasks to tap into sensorimotor
integration processes. These studies have identified the
Spt, a region in the planum temporale, as a critical hub
to this process (see also Hickok, 2014, for an overview).
In one of the earliest neuroimaging investigations to
use feedback manipulations to examine sensorimotor
integration for speech, Tourville et al. (2008) made use
of an auditory feedback manipulation in the produc-
tion of a series of consonant vowel consonant (CVC)
stimuli, all of which included the vowel /ε/. Within a
string of productions, an unexpected shift (up or
down) of the F1 frequency in the vowel was induced
696 55. NEUROBIOLOGY OF SPEECH PRODUCTION: PERSPECTIVE FROM NEUROPSYCHOLOGY AND NEUROLINGUISTICS
(following Purcell & Munhall, 2006; Houde & Jordan,
1998). Speakers compensated for the unexpected per-
turbations, as expected. The neural regions that dem-
onstrated increased activation under conditions of
auditory perturbation and resulting compensation
included bilateral STGp, planum temporale, left ven-
tral motor and premotor cortex, and antero-medial cer-
ebellum. Activation in these regions is consistent with
a role for both secondary auditory and motor areas in
the compensatory process. In another recent fMRI
study investigating the neural substrates invoked dur-
ing speech adaptation (i.e., speech motor learning) to
consistent auditory feedback perturbation, Gracco,
Sato, Shiller, and Baum (in preparation) found
increased activation during the adaptation (hold)
phase in bilateral IFG, premotor gyrus (PM), STS, pos-
terior STG, posterior inferior temporal gyrus (pITG),
right angular gyrus/posterior parietal gyrus (rAG/
pPG), and left inferior parietal lobule/supramarginal
gyrus (IPL/SMG).
Based on these findings, coupled with results in
prism adaptation studies implicating a role for inferior
parietal cortex in the control of adaptive movements
(Redding et al., 2005), Gracco and colleagues (Dangler,
Shiller, Baum, & Gracco, in prep; Shum, Shiller, Baum,
& Gracco, 2011) conducted two rTMS studies stimulat-
ing this region prior to an auditory feedback manipu-
lation/speech adaptation task. In a first study in which
inhibitory stimulation was applied to left SMG (Shum
et al., 2011), results revealed that those participants
who had undergone transcranial magnetic stimulation
(TMS) to this region produced a significantly reduced
adaptive response as compared with individuals who
had undergone sham stimulation. In contrast, Dangler
et al. (in preparation) applied inhibitory TMS to the
right hemisphere IPL and found a faster adaptive
response subsequent to stimulation that was, however,
of comparable magnitude in both experimental and
control (sham) participant groups. The findings of
both experiments were interpreted to suggest that the
left inferior parietal region plays an important role in
sensorimotor adaptation and integration, whereas the
right hemisphere homologue seems to normally inhibit
activity in the left IPL; in other words, when right IPL
was inhibited, adaptation occurred more quickly
(Dangler et al., in preparation; Gracco et al., 2012;
Shum et al., 2011).
There have also been several recent investigations of
the neural bases of sensorimotor integration with a
focus on alteration of somatosensory feedback, rather
than auditory feedback. For instance, Baciu et al.
(2000), as reviewed in Golfinopoulos et al. (2011),
made use of a lip tube to inhibit lip movement during
rounded vowel production in an fMRI study. The
static perturbation yielded increased activation in a
J. SPEAKING
bilateral distributed network that included frontal,
parietal, and temporal areas, as well as the cerebellum;
interestingly, there was an increase in the role of the
right hemisphere during the perturbed trials. Using
TMS to the left primary motor cortex, Ito et al. (2005)
examined responses to unexpected jaw perturbation
during speech and, not surprisingly, found an impor-
tant role for that region in the compensatory response.
Also, examining compensation to unexpected blocking
of jaw movement via a pneumatic device,
Golfinopoulos et al. (2011) reported increased activa-
tion in right anterior SMG, pre-SMA, SMA, IFG, pre-
central gyrus, thalamus, and cerebellum under
perturbed speaking conditions. They also investigated
effective connectivity and found increased connectivity
between left and right anterior SMG, as well as
between left anterior SMG and right ventral premotor
cortex in the perturbed relative to the unperturbed
conditions. Similarly, increased connectivity was found
between right anterior SMG and right IFGpt, as well as
bidirectionally between right ventral premotor cortex
and right ventral primary motor cortex. The authors
conclude that bilateral anterior SMG is involved in
somatosensory error detection and correction (in keep-
ing with the DIVA model of Guenther (1995); see also
Golfinopoulos, Tourville, & Guenther, 2010, and a
recent study by Schwartz, Faseyitan, Kim, and Coslett
(2012), a voxel-based lesion symptom mapping analy-
sis supporting the role of SMG in phonological error
production in aphasia). Golfinopoulos et al. (2011) fur-
ther suggest that whereas left IFG may be important
for prelearned or automatized phonetic coding, right
IFGpt may serve to maintain sensorimotor representa-
tions and assist in the adjustment of ongoing speech
movements in response to sensory feedback
(Golfinopoulos et al., 2011). This latter suggestion
appears inconsistent with that proposed by Gracco
and colleagues (2012); however, it must be borne in
mind that the experiments were investigating different
types of compensatory responses, in one case in
response to unexpected somatosensory perturbation
(Golfinopoulos et al., 2011) and in the other in
response to static auditory feedback perturbation
(Gracco et al., 2012; Shum et al., 2011).
55.5 SUMMARY
It has been the goal of this chapter to review neuro-
psychological and neurophysiological studies of
speech production. Together, this research has shown
a complex tapestry that includes different stages of
production that ultimately map abstract phonological
structures onto articulatory commands. This produc-
tion system is integrated with both auditory and
 REFERENCES
somatosensory systems, allowing it to maintain stabil-
ity, and to adapt, as necessary, based on both immedi-
ate and longer-term perturbations. Speech production
then requires both feedforward and feedback mechan-
isms where information flow is bidirectional. Not sur-
prisingly, then, the speech production system recruits
a large frontotemporoparietal cortical and subcortical
network of left and right hemisphere regions, many of
which have also been identified in language processing
more generally. Future research holds much promise
to provide further insights into the processes and
mechanisms involved in speech production and their
underlying neural mechanisms as ever-increasing
sophisticated techniques become available for mapping
lesions in neuropsychological studies and for examin-
ing the neural substrates of speech production in parti-
cipants with and without lesions.
Acknowledgments
This research was supported in part by grants NIH R01 DC 006220
and R21DC013100, by the Dana Foundation to Brown University,
and by the Natural Sciences and Engineering Council of Canada to
McGill University. The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institute on Deafness and Other Communication Disorders
or the National Institutes of Health.
References
Aasland, W., Baum, S., & McFarland, D. (2006). Electropalatographic,
acoustic, and perceptual data on adaptation to a palatal perturba-
tion. Journal of the Acoustical Society of America, 119, 2372 2381.
Abbs, J. (1986). Invariance and variability in speech production:
A distinction between linguistic intent and its neuromotor imple-
mentation. In J. Perkell, & D. Klatt (Eds.), Invariance and variability
in speech processes (pp. 202 225). Hillsdale, NJ: Erlbaum.
Ackermann, H. (2008). Cerebellar contributions to speech production
and speech perception: Psycholinguistic and neurobiological per-
spectives. Trends in Neurosciences, 31, 265 272.
Ackermann, H., Mathiak, K., & Riecker, A. (2007). The contribution
of the cerebellum to speech production and speech perception:
Clinical and functional imaging data. The Cerebellum, 6,
202 213.
Ackermann, H., & Ziegler, W. (2010). Brain mechanisms underlying
speech. In W. J. Hardcastle, & J. Laver (Eds.), The handbook of pho-
netic sciences (2nd ed., pp. 202 250). Chichester: Wiley-Blackwell.
Ackermann, H., Mathiak, K., & Ivry, R. B. (2004). Temporal organiza-
tion of “internal speech” as a basis for cerebellar modulation of
cognitive functions. Behavioral and Cognitive Neuroscience Reviews,
3, 14 22.
Alario, F., Chainay, H., Lehericy, S., & Cohen, L. (2006). The role of
the supplementary motor area (SMA) in word production. Brain
Research, 1076, 129 143.
Baciu, M., Abry, C., & Segebarth, C. (2000). Équivalence motrice et
dominance hémisphérique. Le cas de la voyelle (u). Actes des jour-
nees d’etude sur la parole, Étude IRMf. Actes JEP, 23, 213 216.
Baese-Berk, M., & Goldrick, M. (2009). Mechanisms of interaction
in speech production. Language and Cognitive Processes, 24,
527 554.
J. SPEAKING
697
Baum, S., Blumstein, S., Naeser, M., & Palumbo, C. (1990). Temporal
dimensions of consonant and vowel production: An acoustic and
CT scan analysis of aphasic speech. Brain and Language, 39,
33 56.
Baum, S., & Boyczuk, J. (1999). Speech timing subsequent to brain
damage: Effects of utterance length and complexity. Brain and
Language, 67, 30 45.
Baum, S., & McFarland, D. (1997). The development of speech adap-
tation to an artificial palate. Journal of the Acoustical Society of
America, 102, 2353 2359.
Baum, S., & McFarland, D. (2000). Individual differences in speech
adaptation to an artificial palate. Journal of the Acoustical Society of
America, 107, 3572 3575.
Baum, S., & Slatkovsky, K. (1993). Phonemic false evaluation?
Preliminary data from a conduction aphasia patient. Clinical
Linguistics and Phonetics, 7, 207 218.
Blank, S. C., Scott, S., Murphy, K., Warburton, E., & Wise, R. (2002).
Speech production: Wernicke, Broca and beyond. Brain, 125,
1829 1838.
Blumstein, S. (1973). A phonological investigation of aphasic speech. The
Hague: Mouton.
Blumstein, S. E., Cooper, W., Goodglass, H., Statlender, S., &
Gottlieb, J. (1980). Production deficits in aphasia: A voice onset
time analysis. Brain and Language, 9, 153 170.
Blumstein, S. E., Cooper, W., Zurif, E., & Caramazza, A. (1977). The
perception and production of voice onset time in aphasia.
Neuropsychologia, 15, 371 383.
Bohland, J., & Guenther, F. (2006). An fMRI investigation of syllable
sequence production. NeuroImage, 32, 821 841.
Buchsbaum, B., Hickok, G., & Humphries, C. (2001). Role of left
posterior superior temporal gyrus in phonological processing
for speech perception and production. Cognitive Science, 25,
663 678.
Buchwald, A., & Miozzo, M. (2011). Finding levels of abstraction in
speech production: Evidence from sound production errors.
Psychological Science, 22, 1113 1119.
Buchwald, A., & Miozzo, M. (2012). Phonological and motor errors
in individuals with acquired sound production impairment.
Journal of Speech, Language and Hearing Research, 55, 1573 1586.
Buckingham, H., & Yule, G. (1987). Phonemic false evaluation:
Theoretical and clinical aspects. Clinical Linguistics and Phonetics,
1, 113 125.
Buckingham, H. W. (1992). The mechanisms of phonemic paraphasia.
Clinical Linguistics and Phonetics, 6, 41 63.
Bullock-Rest, N., Cerny, A., Sweeney, C., Palumbo, C., Kurowski, K.,
& Blumstein, S. E. (2013). Neural systems underlying the influ-
ence of sound shape properties of the lexicon on spoken word
production: Do fMRI findings predict effects of lesions in apha-
sia? Brain and Language, 126, 159 168.
Canter, G. J., Trost, J. E., & Burns, M. S. (1985). Contrasting speech
patterns in apraxia of speech and phonemic paraphasia. Brain and
Language, 24, 204 222.
Dangler, L., Shiller, D., Baum, S., & Gracco, V. (in preparation). Left
but not right hemisphere inferior parietal lobe contributes to sen-
sorimotor adaptation for speech.
Dell, G. S. (1986). A spreading activation theory of retrieval in sen-
tence production. Psychological Review, 93, 283 321.
Dell, G. S., & Gordon, J. K. (2003). Neighbors in the lexicon: Friends
or foes? In N. O. Schiller, & A. S. Meyer (Eds.), Phonetics and pho-
nology in language comprehension and production: Differences and sim-
ilarities (pp. 9 37). New York, NY: Mouton de Gruyter.
Dogil, G., Ackermann, H., Grodd, W., Haider, H., Kamp, H., Mayer,
J., et al. (2002). The speaking brain: A tutorial introduction to
fMRI experiments in the production of speech, prosody and syn-
tax. Journal of Neurolinguistics, 15, 59 90.
698 55. NEUROBIOLOGY OF SPEECH PRODUCTION: PERSPECTIVE FROM NEUROPSYCHOLOGY AND NEUROLINGUISTICS
Dronkers, N. (1996). A new brain region for coordinating speech
articulation. Nature, 384, 159 161.
Eickhoff, S., Heim, S., Zilles, K., & Amunts, K. (2009). A systems
perspective on the effective connectivity of overt speech produc-
tion. Philosophical Transactions of the Royal Society A, 367,
2399 2421.
Frenck-Mestre, C., Anton, J. L., Roth, M., Vaid, J., & Viallet, F. (2005).
Speech production in bilinguals. NeuroReport, 16, 761 765.
Gandour, J., & Dardarananda, R. (1984). Voice-onset time in aphasia:
Thai, II: Production. Brain and Language, 18, 389 410.
Gaskell, M. G., & Marslen-Wilson, W. D. (1999). Ambiguity, competi-
tion, and blending in spoken word recognition. Cognitive Science,
23, 439 462.
Goldrick, M. (2006). Limited interaction in speech production:
Chronometric, speech error, and neuropsychological evidence.
Language and Cognitive Processes, 21, 817 855.
Goldrick, M., & Blumstein, S. E. (2006). Cascading activation
from phonological planning to articulatory processes:
Evidence from tongue twisters. Language and Cognitive
Processes, 21, 649 683.
Golfinopoulos, E., Tourville, J., Bohland, J., Ghosh, S., Nieto-
Castanon, A., & Guenther, F. (2011). fMRI investigation of unex-
pected somatosensory feedback perturbation during speech.
NeuroImage, 55, 1324 1338.
Golfinopoulos, E., Tourville, J., & Guenther, F. (2010). The integration
of large-scale neural network modeling and functional brain
imaging in speech motor control. NeuroImage, 52, 862 874.
Goodglass, H., & Kaplan, E. (1972). The assessment of aphasia and
related disorders. Philadelphia, PA: Lea & Febiger.
Gordon, J. K. (2002). Phonological neighborhood effects in aphasic
speech errors: Spontaneous and structured contexts. Brain and
Language, 82, 113 145.
Gracco, V., Deschamps, I., Shiller, D., Dangler, L., Elgie, B., & Baum,
S. (2012). The role of the inferior parietal cortex in sensorimotor
representations for speech, Paper presented at Society for the
Neurobiology of Language, San Sebastian, Spain.
Gracco, V., Sato, M., Shiller, D., & Baum, S. (in prep). The neural net-
works underlying sensorimotor representations for speech.
Guenther, F. (1994). A neural network model of speech acquisition and
motor equivalent speech production. Biological Cybernetics, 72,
43 53.
Guenther, F. (1995). Speech sound acquisition, coarticulation, and
rate effects in a neural network model of speech production.
Psychological Review, 102, 594 621.
Guenther, F., & Ghosh, S. (2003). A model of cortical and cerebellar
function in speech. In: Proceedings of the 15th international congress
of phonetic sciences (pp. 169 173) Barcelona, Spain.
Guenther, F., Ghosh, S., & Tourville, J. (2006). Neural modeling and
imaging of the cortical interactions underlying syllable produc-
tion. Brain and Language, 96, 280 301.
Haley, K. L., Jacks, A., & Cunningham, K. T. (2013). Error variability
and the differentiation between apraxia of speech and aphasia
with phonemic paraphasia. Journal of Speech Language and Hearing
Research, 56, 891 905.
Hartwigsen, G., Saur, D., Price, C., Baumgaertner, A., Ulmer, S., &
Siebner, H. (2013). Increased facilitatory connectivity from the
pre-SMA to the left dorsal premotor cortex during pseudoword
repetition. Journal of Cognitive Neuroscience, 25, 580 594.
Hickok, G. (2014). The architecture of speech production and the role
of the phoneme in speech processing. Language, Cognition and
Neuroscience, 29, 2 20.
Hickok, G., Buchsbaum, S., Humphries, C., & Muftuler, T. (2003).
Auditory-motor interaction revealed by fMRI: Speech, music, and
working memory in area Spt. Journal of Cognitive Neuroscience, 15,
673 682.
J. SPEAKING
Hickok, G., Houde, J., & Rong, F. (2011). Sensorimotor integration in
speech processing: Computational basis and neural organization.
Neuron, 69, 407 422.
Hickok, G., Okada, K., & Serences, J. (2009). Area Spt in the human
planum temporale supports sensory-motor integration for speech
processing. Journal of Neurophysiology, 101, 2725 2732.
Hickok, G., & Poeppel, D. (2004). Dorsal and ventral streams: A
framework for understanding aspects of the functional anatomy
of language. Cognition, 92, 67 99.
Hillis, A., Work, M., Barker, P., Jacobs, M., Breese, E., & Maurer, K.
(2004). Re-examining the brain regions crucial for orchestrating
speech articulation. Brain, 127, 1479 1487.
Houde, J., & Jordan, M. (1998). Sensorimotor adaptation in speech
production. Science, 279, 1213 1216.
Houde, J., & Jordan, M. (2002). Sensorimotor adaptation of speech I:
Compensation and adaptation. Journal of Speech, Language, and
Hearing Research, 45, 295 310.
Houde, J., & Nagarajan, S. (2011). Speech production as state feed-
back control. Frontiers of Human Neuroscience, 5, 82.
Indefrey, P., & Levelt, W. J. M. (2000). The neural correlates of lan-
guage production. In M. Gazzaniga (Ed.), The new cognitive neu-
rosciences (2nd ed., pp. 845 865). Cambridge, MA: MIT Press.
Ito, T., Kimura, T., & Gomi, H. (2005). The motor cortex is involved
in reflexive compensatory adjustment of speech articulation.
NeuroReport, 16, 1791 1794.
Ivry, R., & Keele, W. (1989). Timing functions of the cerebellum.
Journal of Cognitive Neuroscience, 1, 136 152.
Ivry, R., Spencer, R., Zelznik, H., & Diedrichsen, J. (2002). The cere-
bellum and event timing. Annals of the New York Academy of
Sciences, 978, 302 317.
Jakobson, R. (1968). Child language, aphasia, and phonological universals
(A.R. Keiler, Trans.). The Hague: Mouton.
Jakobson, R., Halle, M., & Fant, G. (1967). Preliminaries to speech analy-
sis: Distinctive features and their correlates. Cambridge, MA: MIT
Press.
Jones, J., & Munhall, K. (2005). Remapping auditory-motor represen-
tations in voice production. Current Biology, 15, 1768 1772.
Kent, R., & Rosenbek, J. (1983). Acoustic patterns of apraxia of
speech. Journal of Speech and Hearing Research, 26, 231 248.
Kurowski, K., Blumstein, S. E., Palumbo, C. L., Waldstein, R., &
Burton, M. W. (2007). Nasal production in anterior and posterior
aphasics: Speech deficits and neuroanatomical correlates. Brain
and Language, 100, 262 275.
Kurowski, K., Hazen, E., & Blumstein, S. E. (2003). The nature of
speech production impairments in anterior aphasics: An acoustic
analysis of voicing in fricative consonants. Brain and Language, 84,
353 371.
Laganaro, M., Chetelat-Mabillard, D., & Frauenfelder, U. H. (2013).
Facilitatory and interfering effects of neighbourhood density on
speech production: Evidence from aphasic errors. Cognitive
Neuropsychology, 30, 127 146.
Larson, C., Altman, K., Liu, H., & Hain, T. (2008). Interactions
between auditory and somatosensory feedback for voice F0 con-
trol. Experimental Brain Research, 187, 613 621.
Larson, C., Burnett, T., Kiran, S., & Hain, T. (2000). Effects of pitch-
shift velocity on voice F0 responses. Journal of the Acoustical
Society of America, 107, 559 564.
Lecours, A. R., & Lhermitte, F. (1969). Phonemic paraphasias:
Linguistic structures and tentative hypotheses. Cortex, 5, 193 228.
Leonardo, B., Moser, D., Rorden, C., Baylis, C., Gordon, C., &
Fridriksson, J. (2006). Speech apraxia without oral apraxia: Can
normal brain function explain the physiopathology? NeuroReport,
17, 1027 1031.
Lindblom, B., Lubker, J., & Gay, T. (1979). Formant frequencies of
some fixed-mandible vowels and a model of speech motor
 REFERENCES
programming by predictive simulation. Journal of Phonetics, 7,
147 161.
Mathiak, K., Hertrich, I., Grodd, W., & Ackermann, H. (2002).
Cerebellum and speech perception: A functional magnetic reso-
nance imaging study. Journal of Cognitive Neurosicnece, 14, 902 912.
Mathiak, K., Hertrich, I., Grodd, W., & Ackermann, H. (2004).
Discrimination of temporal information at the cerebellum:
Functional magnetic resonance imaging of nonverbal auditory
memory. NeuroImage, 21, 154 162.
Moser, D., Fridriksson, J., Bonilha, L., Healy, E., Baylis, G., Baker, J.,
et al. (2009). Neural recruitment for the production of native and
novel speech sounds. NeuroImage, 46, 549 557.
Nasir, S., & Ostry, D. (2009). Auditory plasticity and speech motor
learning. Proceedings of the National Academy of Sciences of the
United States of America, 106, 20470 20475.
Papoutsi, M., de Zwart, J., Jansma, J., Pickering, M., Bednar, J., &
Horwitz, B. (2009). From phonemes to articulatory codes: An
fMRI study of the role of Broca’s area in speech production.
Cerebral Cortex, 19, 2156 2165.
Park, H., Iverson, G., & Park, H.-J. (2011). Neural correlates in the
processing of phoneme-level complexity in vowel production.
Brain and Language, 119, 158 166.
Peeva, M., Guenther, F., Tourville, J., Nieto-Castanon, A., Anton, J.,
Nazarian, B., et al. (2010). Distinct representations of phonemes,
syllables, and supra-syllabic sequences in the speech production
network. NeuroImage, 50, 626 638.
Peramunage, D., Blumstein, S. E., Myers, E. B., Goldrick, M., &
Baese-Berk, M. (2011). Phonological neighborhood effects in spo-
ken word production: An fMRI study. Journal of Cognitive
Neuroscience, 23, 593 603.
Peschke, C., Ziegler, W., Eisenberger, J., & Baumgaertner, A. (2012).
Phonological manipulation between speech perception and pro-
duction activates a parieto-frontal circuit. NeuroImage, 59, 788 799.
Petacchi, A., Laird, A., Fox, P., & Bower, J. (2005). Cerebellum and
auditory function: An ALE meta-analysis of functional neuroim-
aging studies. Human Brain Mapping, 25, 118 128.
Price, C. (2012). A review and synthesis of the first 20 years of PET
and FMRI studies of heard speech, spoken language and reading.
Neuroimage, 62, 816 847.
Price, C., Crinion, J., & MacSweeney, M. (2011). A generative model
of speech production in Broca’s and Wernicke’s areas. Frontiers in
Psychology, 2, 1 9.
Price, C., Moore, C., & Frackowiak, R. (1996). The effect of varying
stimulus rate and duration on brain activity during reading.
NeuroImage, 3, 40 52.
Purcell, D., & Munhall, K. (2006). Adaptive control of vowel formant
frequency: Evidence from real-time formant manipulation. Journal
of the Acoustical Society of America, 120, 966 977.
Redding, G., Rossetti, Y., & Wallace, B. (2005). Applications of prism
adaptation: A tutorial in theory and method. Neuroscience and
Biobehavioral Reviews, 29, 431 444.
J. SPEAKING
699
Redding, G. M., & Wallace, B. (1996). Adaptive spatial align-
ment and strategic perceptualmotor control. Journal of.
Experimental Psychology: Human Perception and Performance, 22,
379 394.
Riecker, A., Ackermann, H., Wildgruber, D., Mayer, J., Dogil, G.,
Haider, H., et al. (2000). Articulatory/phonetic sequencing at the
level of the anterior perisylvian cortex: A functional magnetic
resonance imaging (fMRI) study. Brain and Language, 75,
259 276.
Rossetti, Y., Koga, K., & Mano, T. (1993). Prismatic displacement of
vision induces transient changes in the timing of eye-hand coor-
dination. Perception and Psychophysics, 54, 355 364.
Ryalls, J. (1986). An acoustic study of vowel production in aphasia.
Brain and Language, 29, 48 67.
Saur, D., Kreher, B., Schnell, S., Kummerer, D., Kellmeyer, P., Vry,
M., et al. (2008). Ventral and dorsal pathways for language.
Proceedings of the National Academy of Sciences of the United States of
America, 105, 18035 18040.
Schwartz, M., Faseyitan, O., Kim, J., & Coslett, H. B. (2012). The dor-
sal stream contribution to phonological retrieval in object naming.
Brain, 135, 3799 3814.
Shiller, D., Sato, M., Gracco, V., & Baum, S. (2009). Perceptual recali-
bration of speech sounds following speech motor learning. Journal
of the Acoustical Society of America, 125, 1103 1113.
Shima, K., & Tanji, J. (2000). Neuronal activity in the supplemen-
tary and presupplementary motor areas of temporal organi-
zation of multiple movements. Journal of Neurophysiology, 84,
2148 2160.
Shum, M., Shiller, D., Baum, S., & Gracco, V. (2011). Sensorimotor
integration for speech motor learning involves the inferior parie-
tal cortex. European Journal of Neuroscience, 34, 1817 1822.
Shuren, J. (1993). Insula and aphasia. Journal of Neurology, 240,
216 218.
Soros, P., Sokologg, L., Bose, A., McIntosh, A., Graham, S., & Stuss,
D. (2006). Clustered functional MRI of overt speech production.
NeuroImage, 32, 376 387.
Tourville, J., Reilly, K., & Guenther, F. (2008). Neural mechanisms
underlying auditory feedback control of speech. NeuroImage, 39,
1429 1443.
Tremblay, P., & Gracco, V. (2006). Contribution of the frontal lobe to
externally and internally specified verbal responses: fMRI evi-
dence. NeuroImage, 33, 947 957.
Vijayan, A., & Gandour, J. (1995). On the notion of a “subtle phonetic
deficit” in fluent/posterior aphasia. Brain and Language, 48, 106 119.
Wise, R., Greene, J., Buchel, C., & Scott, S. (1999). Brain regions
involved in articulation. Lancet, 353, 1057 1061.
Ziegler, W., Kilian, B., & Deger, K. (1997). The role of the left
mesial frontal cortex in fluent speech: Evidence from a case of
left supplementary motor area hemorrhage. Neuropsychologia,
35, 1197 1208.