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Clinicoanatomic Studies in Dysarthria: Review, Critique, and Directions for

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 Clinicoanatomic Studies in
Dysarthria: Review, Critique,
and Directions for Research

Ray D. Kent
University of Wisconsin– More than 30 years ago, Darley, Aronson, and Brown (1969) proposed clinico-
Madison anatomic correlations for seven perceptual types of dysarthria. These correlations
have not been systematically re-examined even though imaging technologies
Joseph R. Duffy developed in recent years provide the means to do so. This review considers data
Mayo Clinic from published imaging studies as well as data from selected medical interven-
Rochester, MN tions to evaluate the current state of knowledge that relates lesion site to the
nature of a speech disturbance. Although the extant data are not sufficient to
Angela Slama allow a complete evaluation of the seven types of dysarthria described by Darley
Jane F. Kent et al., relevant information has been reported on lesions of the pyramidal
University of Wisconsin– pathway, extrapyramidal pathway, and cerebellum. In general, the results are
Madison best explained by an equivalence mode of brain-behavior relationship in which a
type of dysarthria is associated with a lesion in one of two or more brain
Amy Clift structures. Criteria also are proposed for future studies of clinicoanatomic
Southwest Missouri relationships in neurogenic communication disorders.
State University
KEY WORDS: dysarthria, neuroimaging, neurologic disorders, clinicoanatomic
Springfield
studies, speech disorder

A
broad goal of research on neurogenic disorders is to establish
the relationship between lesion and functional disturbance. In
two classic articles, Darley, Aronson, and Brown (1969a, 1969b)
proposed a systematic classification of adult dysarthrias including hy-
potheses that relate site of lesion and type of speech disturbance. Darley
et al. described the dysarthrias associated with seven discrete neuro-
logical groups and concluded that, “Speech indeed follows neuroanatomy
and neurophysiology” (1969, p. 246). Location of the lesion responsible
for the dysarthria was explicit in the design of their studies, because the
clinical groups were constituted as follows (with site of lesion given in
parentheses): bulbar palsy (lower motor neuron lesion), pseudobulbar
palsy (upper motor neuron lesion), amyotrophic lateral sclerosis (lesions
to both upper and lower motor neurons), cerebellar disorders (lesions to
the cerebellum), parkinsonism (extrapyramidal lesion), dystonia (ex-
trapyramidal lesion), and chorea (extrapyramidal lesion). The localiza-
tion hypotheses were based primarily on clinical observations, especially
the perceptual attributes of speech samples considered against classical
formulations of neuropathology. Imaging data were rarely available.
These clinicoanatomic bases of dysarthria have stood essentially intact
for three decades (Duffy, 1995; Kent, Kent, Duffy, & Weismer, 1998).
Since the publication of the classic papers by Darley et al. (1969a,
1969b), many articles have been published on the dysarthrias, and a

Journal of Speech, Language, and Hearing Research • Vol. 44 • 535–551 • June 2001 • ©American Speech-Language-Hearing
Kent et al.: Clinicoanatomic StudiesAssociation
in Dysarthria 535
1092-4388/01/4403-0535

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 number of these include information on site of lesion de-
termined by neuroimaging, medical interventions, ex-
perimental stimulation methods, or other procedures.
The goal of this review is to examine clinicoanatomic stud-
ies and to synthesize the results into a progress state-
ment on the neuropathologic bases of the dysarthrias.
Information Considered in
This Review
This review covers especially those reports in which
some form of neuroimaging was used to detect lesions
in individuals with dysarthria. The neuroimaging meth-
ods of potential interest are computed tomography (CT),
magnetic resonance imaging (MRI), functional magnetic
resonance imaging (fMRI), positron emission tomogra-
phy (PET), single photon emission tomography (SPECT),
magnetoencephalograpy (MEG), and electroencephalo-
graphy (EEG).
The following caveats should be noted:
1. Studies of neural lesions related to dysarthria
often are much more informative concerning the size
and location of the lesion than on the characteristics of
dysarthria. Frequently, the dysarthria is neither classi-
fied nor described in a way that adequately portrays
the speech disturbance (O’Shanick, 1997). Furthermore,
in some studies it is not even clear if the general term
dysarthria (let alone its type or features) is accurate
because the speech disruptions may have taken other
forms, such as apraxia of speech or aprosodia. This short-
coming of the literature has several explanations, one
of which is simply that individuals with the expertise
needed to make speech assessments were not involved
in the studies.
2. Neuroimaging has certain limitations in the study
of speech and its disorders. Because fMRI is affected by
movement artifacts related to speech articulation, this
method is of limited use for speech studies (Kent, 1998).
Although improvements are underway that should per-
mit the use of fMRI to study brain activation during
speech, these new technologies are only emergent at this
time (Birn, Bandettini, Cox, & Shaker, 1999; Lotze,
Seggewies, Erb, Grodd, & Birbaumer, 2000) and appar-
ently have not been used in studies of dysarthria. In
addition, imaging methods vary in their sensitivity to
lesions in different parts of the nervous system. For ex-
ample, CT is fairly sensitive to lesions in the corona ra-
diata and capsule but has limited sensitivity to brain-
stem lesions. Therefore, when the results from a single
imaging technique are considered, it is possible that the
data are biased by considerations of sensitivity. Ulti-
mately, it is valuable to have confirmatory evidence from
different techniques. Most of the imaging data on lesions
536 Journal of Speech, Language, and Hearing Research • Vol. 44 • 535–551 • June 2001
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in dysarthria have been obtained from structural imag-
ing methods such as CT and MRI. An additional prob-
lem is that many of the neurologic disorders linked with
dysarthria do not have lesions that are routinely or
readily determined by brain imaging methods. For ex-
ample, imaging is rarely performed on individuals with
Parkinson’s disease or those with various neurodegen-
erative disorders.
3. Neuroimaging methods have been applied much
less frequently to the dysarthrias than to such disor-
ders as aphasia or dementia. The sparseness of the
clinicoanatomic literature on dysarthria is immediately
evident in a review of the literature. But sufficient
progress has been made to warrant a summary of cur-
rent knowledge of clinicoanatomic relationships and to
formulate hypotheses for future study.
Information on lesion sites and neuropathology also
can be derived from methods other than neuroimaging.
One source of information is surgery or other invasive
intervention that either resolves dysarthria or results
in dysarthria as a complication. Some examples are ste-
reotactic thalamotomy, pallidotomy, and deep brain
stimulation in the treatment of intractable essential
tremor or Parkinson’s disease (Kondziolka et al., 1999;
Taha, Janszen, & Favre, 1999; Zirh, Reich, Dougherty,
& Lenz, 1999). Neuroimaging results are complemented
by a small number of stimulation studies, especially
those using transcranial magnetic stimulation (TMS)
or rapid-rate transcranial magnetic stimulation (rTMS),
in which an intense magnetic field induces an electric
field that can either interfere with or facilitate behav-
ioral responses such as speech (Epstein, 1998; Epstein
et al., 1999; Kuchta, Reuter, Kurthen, Kohler, & Linke,
1997; Michelucci et al., 1994; Pascual-Leone, Gates, &
Dhuna, 1991; Topper, Mottaghy, Brugmann, Noth, &
Huber, 1998). Results from these procedures are inte-
grated with imaging data in this review.
Structure of the Review
Clinicoanatomic studies are by no means uniform
across the different types of dysarthria; therefore, the
extant data do not permit a comprehensive view of the
relationship between lesion site and characteristics of
the speech disorder. In particular, the published data
do not permit a full consideration of the clinicoanatomic
relationships proposed by Darley et al. (1969a). As men-
tioned earlier, the published studies often do not pro-
vide a detailed description of abnormal speech charac-
teristics or report classification of any sort, so that the
clinical presentation is typically an unspecified dysar-
thria. This is particularly unfortunate given that the
dysarthria types can differ in several respects that may
be informative regarding site of lesion. Given the nature
 of the source material, this review of the clinicoanatomic
literature is organized as follows:
1. Lesions of the pyramidal motor system (upper
motor neuron pathways): These lesions are associated
especially with spastic or unilateral upper motor neu-
ron (UUMN) dysarthria. These perceptual types of dys-
arthria are linked with bilateral and unilateral dam-
age, respectively, to the motor pathway. Also included
in this category are progressive dysarthria (anarthria),
isolated dysarthria, and dysarthria/clumsy hand syn-
drome. The justification for these inclusions is as fol-
lows. Progressive dysarthria is poorly described but of-
ten may involve an apraxia of speech with or without
dysarthria. It is likely that some cases do warrant the
label of dysarthria but that others fall into the classifi-
cation of apraxia of speech. Because of the frequently
mentioned speech disorder, it is included in this category,
but in many of the relevant papers it is not possible to
exclude with confidence the possibility of apraxia of
speech as at least a co-occurring condition. Isolated dys-
arthria is included in this category because the most
frequently reported site of lesion is within the pathway
in question. Dysarthria/clumsy hand syndrome is in-
cluded here (but cross-listed with paragraph 3 below)
because it involves a combination of pyramidal and cer-
ebellar signs.
2. Lesions of the cerebellar system (the cerebellum
and its inflow/outflow pathways): Cerebellar lesions are
usually associated with ataxic dysarthria, but it should
be noted that this form of dysarthria can occur in a vari-
ety of neurologic conditions (Duffy, 1995).
3. Lesions of the extrapyramidal system/basal gan-
glia: These lesions are associated with hypokinetic and
hyperkinetic dysarthrias. The former is typically ob-
served in Parkinson’s disease but may accompany other
disorders, such as progressive supranuclear palsy. Hy-
perkinetic dysarthria is usually classified as either dys-
tonic or choreiform, but may include speech abnormali-
ties associated with a number of different involuntary
movement disorders (e.g., athetosis, myoclonus, action
myoclonus, tremor, tics).
Lesions of the Pyramidal System/
Upper Motor Neuron Pathway
The pyramidal system (or what Duffy, 1995, called
the direct activation pathway) is generally taken as the
primary system of voluntary motor control (although it
never operates independently from the extrapyra-
midal system). The upper motor neuron of the pyrami-
dal motor pathway originates primarily in motor cor-
tex, but some neurons—perhaps as many as 40%—are
located in the postcentral gyrus (Davidoff, 1990). The
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corticobulbar fibers that innervate the nonrespiratory
speech musculature originate especially in the inferior
precentral gyrus and descend through the corona ra-
diata. The fibers continue in a twisting, screwlike pat-
tern through the centrum ovale until they converge into
the internal capsule. Fibers destined to the cranial nerve
nuclei are found near the genu, with cortico-lingual and
cortico-facial tracts being closely situated. In pure mo-
tor stroke, lesions generally occur in one or more of the
following: corona radiata, posterior limb of the internal
capsule, putamen, globus pallidus, thalamus, pons, and
medulla (Schonewille, Tuhrim, Singer, & Atlas, 1999).
Lesions to the pyramidal tract structures are associated
with upper motor neuron syndrome, whereas damage
to the basal ganglia (extrapyramidal system) is associ-
ated especially with hypokinetic or hyperkinetic syn-
dromes. Recent work with diffusion-weighted magnetic
resonance imaging (Inoue, Shimizu, & Yoshimoto, 1999)
demonstrates that the entire pyramidal tract can be vi-
sualized on a single fiber mapping image in which nerve
fiber integrity was confirmed for neurologically normal
subjects but shown to be disrupted in patients with tu-
mors. This approach holds promise for the description
of lesions in stroke-related dysarthria but apparently
has not been used for this purpose to date. Complemen-
tary advances permit the study of corticobulbar inner-
vation of tongue and orofacial muscles (Terao et al., 2000;
Urban, Vogt, & Hopf, 1998).
Most reports on pyramidal pathway damage per-
tain to a dysarthria associated with supratentorial is-
chemic stroke. Presumably, the type of dysarthria is ei-
ther spastic or unilateral upper motor neuron, but actual
classification or clear descriptions of deviant speech char-
acteristics has not been commonly reported in lesion
studies. It is presumed that the dysarthrias are of ei-
ther the spastic or unilateral upper motor neuron vari-
ety, but it is possible that mixed dysarthrias also are
involved. As shown in Table 1, the dysarthria is associ-
ated with a variety of lesions distributed along a path-
way that extends from motor cortex through the corona
radiata to the internal capsule. It has been asserted
that a single type of dysarthria (unclassified) is com-
mon to this lesion pathway (Urban, Hopf, Fleischer,
Zorowka, & Mullerforell, 1997). From a combined study
of MRI and rTMS, Urban, Hopf, Zorowka, Fleischer, and
Andreas (1996) concluded that “interruption of the cor-
ticolingual pathways to the tongue is crucial in the patho-
genesis of dysarthria following extracerebellar lacunar
stroke” (p. 1135).
The presence of dysarthria assumes a general prog-
nostic value in that speech disorder and disability emerged
as independent predictors of one-year mortality in a study
of 89 patients with lacunar stroke (Ryglewicz, Baranska-
Gieruszczak, Mendel, Poniatowska, & Kozlowski, 1997).
Further, it has been suggested that the presence of dys-
Kent et al.: Clinicoanatomic Studies in Dysarthria 537
 Table 1. Supratentorial stroke lesions associated with dysarthria (typically unclassified as to perceptual type
and generally lacking in a description of the speech disturbances).

Lesion Source

Lower motor cortex Urban et al. (1997)

Parietal cortex
Corona radiata
Periventicular white matter
Internal capsule (not further specified)
Genu of internal capsule
Posterior limb of internal capsule
Anterior limb of internal capsule
Thalamus (bilateral)
Murdoch et al. (1994)
Ichikawa & Kageyama (1991), Tonkonagy & Goodglass (1981),
Schonewille et al. (1999), Urban et al. (1997)
Murdoch et al. (1994)
Murdoch et al. (1994)
Bogousslavsky & Regli (1991), Ichikawa & Kageyama (1991), Ozaki
et al. (1986), Urban et al. (1997)
Combarros et al. (1992), Decroix et al. (1986), Schonewille et al.
(1999), Urban et al. (1997)
Ichikawa & Kageyama (1991), Ozaki et al. (1986)
Karacostas et al. (1994)

arthria, along with headache and abrupt onset of symp- Unilateral upper motor neuron dysarthria differs from
toms, can distinguish hemorrhagic lacunar stroke from the perceptual dysarthria types identified by Darley et
other causes of lacunar stroke (Arboix, Garcia-Eroles, al. (1969a, 1969b) in that it is an anatomic label and
Massons, Oliveres, & Targa, 2000). may include speech characteristics that represent weak-
ness, spasticity, and even ataxia. In at least 50% of cases
Unilateral Upper Motor Neuron with dysarthria, a unilateral upper motor neuron lesion
is associated with a lingual weakness that contributes
Dysarthria to the dysarthria (Duffy & Folger, 1996). It is not clear
One of the few studies to provide information on why lingual paralysis occurs in some individuals with
both dysarthria characteristics and site of lesion is Duffy monohemispheric stroke but not others. Based on the
and Folger (1996), who examined patients with dysar- results of a TMS study, Muelbacher, Artner, and Mamoli
thria associated with unilateral upper motor neuron le- (1998) suggested that the reason is the variable avail-
sions. These usually manifest as a mild to moderate ability of uncrossed motor projections among different
speech involvement characterized by imprecise conso- individuals.
nant articulation, slow and irregular speech AMRs, slow
speech rate, and phonatory abnormalities (especially
harshness). The responsible lesion is summarized in
Progressive Dysarthria (or Apraxia
Table 2, which bears a strong similarity to Table 1. of Speech)
Damage to Broca’s area and surrounding cortical
Table 2. Lesions associated with unilateral upper motor neuron regions is associated with a progressive loss of speech
dysarthria (Duffy & Folger, 1996). that has been termed primary progressive aphasia (Didic,
Felician, Ceccaldi, & Poncet, 1999; Kertesz & Orange,
Cases 2000; Zakzanis, 1999), progressive anarthria (Didic et al.,
Lesion observed (%) 1999; Infante, Sanchez Guerra, Polo, Berciano, &
Oterino, 2000), or progressive dysarthria (Santens et al.,
Lobar 43
1999). The choice of terminology partly reflects the ini-
Cortical 7
Subcortical 7
tial or predominant symptomatology. The disorder of
Cortical and subcortical 29 particular interest here is typically characterized by
Internal capsule 34 impaired articulation (or apraxia of speech), telegraphic
Internal capsule or pons 4 style, and a difficulty in performing complex orofacial
Pericapsular 11 and hand movements (Didic, Ceccaldi, & Poncet, 1998).
Pericapsular/subcortical and lobar 5 It is possible that it is labeled more accurately as apraxia
Thalamus 2 of speech or apraxia of speech with dysarthria. The clini-
Brainstem 2 cal features are most consistent with apraxia of speech,
but this term is not used consistently in neurology.

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 In one of the larger studies, eight patients were ex-
amined, with long-term follow-up (6 to 10 years) for four
cases (Broussolle et al., 1996). CT and MRI findings
showed an asymmetric (left more than right) progres-
sive cortical atrophy of the frontal lobes “predominat-
ing in the posterior inferior frontal region, notably the
operculum” (Broussole et al., 1996, p. 44). The patients
studied in follow-up progressed to muteness and bilat-
eral suprabulbar paresis. In five patients studied by
Didic et al. (1998), the neural damage associated with
the early stage of the disease was thought to be in the
ventral compartment of the premotor cortex, but pre-
cise localization was difficult with CT or MRI. Progres-
sion of the disorder apparently was associated with more
extensive frontal lobe damage, perhaps including dor-
solateral premotor cortex. In a group of three patients
who had a slowly progressive loss of speech and dysar-
thria associated with orofacial dyspraxia, PET revealed
bifrontal hypometabolism, which was especially marked
in the inferior and lateral portions of both frontal lobes
(Tyrrell, Kartsounis, Frackowiak, Findley, & Rossor,
1995). In two patients with progressive dysarthria that
was the sole initial sign of a neurodegenerative condi-
tion, neuroimaging revealed bilateral involvement of
the posterior inferior frontal lobe structures (Santens
et al., 1999). For one patient with progressive dysar-
thria, Selnes, Holcomb, and Gordon (1997) reported that
MRI revealed a localized left-sided perisylvian lesion and
that PET showed a left and possibly right perisylvian
hypometabolism localized to the area of tissue loss. Didic
et al. (1999) concluded from a review of the literature
that both primary progressive aphasia and progressive
dysarthria typically are associated with nonspecific le-
sions and Pick-type pathology (i.e., inclusion bodies and
swollen neurons). They also noted that “progressive dis-
orders of only one domain of cognition may well be due
to preferential involvement of anatomically and func-
tionally defined neural systems and could therefore be
considered as ‘system atrophies’ ” (p. S73).
Progressive dysarthria also has been observed in in-
dividuals with primary lateral sclerosis (de Koning, van
Doorn, & van Dongen, 1997; Fisher, 1977). The article by
de Koning et al. is noteworthy for its relatively detailed
account of speech changes over a 5-year period, begin-
ning with initial signs of imprecise consonants (which
appears to justify the classification of dysarthria at least
in the early stages of the disorder) and culminating in
complete anarthria. Although an early MRI was unre-
markable, a subsequent MRI obtained 3 years after the
initial complaint revealed a lacunar infarct in the right
cerebral peduncle. SPECT showed a bilaterally reduced
activity especially in the basal motor cortex.
A common feature to these patients was the initial
impairment of speech (often the earliest sign of disor-
der), progressive deterioration usually leading to mutism,
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and involvement of the posterior inferior frontal lobe—
especially the operculum. It bears repeating that it is
uncertain if the disorder in question is most accurately
labeled a dysarthria as opposed to apraxia of speech or
a combination of the two.
Isolated Dysarthria
Infrequently, dysarthria is the sole or predominant
sign of stroke—in which case, it is typically termed iso-
lated or pure dysarthria (Arboix, Massons, Oliveres, &
Titus, 1991; Fisher, 1982; Ichikawa & Kageyama, 1991;
Kim, 1994; Orefice, Fragassi, Lanzillo, Castellano, &
Grossi, 1999; Ozaki, Baba, Narita, Matsunaga, &
Takebe, 1986; Tohgi, Takahashi, Takahashi, Tamura, &
Yonezawa, 1996). This condition is of particular inter-
est in isolating the neural pathways that control speech.
It is likely that in many of the reported cases, the dysar-
thria was accompanied by mild concomitant deficits,
particularly orofacial paresis. The literature is not eas-
ily summarized because (a) the lesions are widely dis-
tributed (cortical and subcortical, unilateral and bilateral),
(b) it is difficult to eliminate the possibility of remote
effects such as diaschisis or compensations (Okuda,
Kawabata, Tachibana, & Sugita, 1999), and (c) the dys-
arthria is rarely described in sufficient detail to permit
a classification into perceptual types or to provide a clear
idea of the speech disturbance. Table 3 shows that the
responsible lesions are found primarily in the corona ra-
diata, internal capsule, basal ganglia, and pons (lesion
locations already noted in the preceding discussion of
nonisolated dysarthrias). Takahashi, Satoh, Takahashi,
Chiba, and Tohgi (1995) reported that isolated dysar-
thria tends to occur with relatively anterior lesions of
the corona radiata or junctional zone to the internal cap-
sule. They also noted that dysarthria occurs more often
with left than right lesions and that such lesions may
simultaneously interrupt the corticobulbar pathway and
callosal fibers to the right hemisphere that carry speech
information. It has been reported that an isolated, re-
versible dysarthria can result from a basilar artery bal-
loon occlusion (Hartmann et al., 1999).
Dysarthria–Clumsy Hand Syndrome
In some neurologic disorders, dysarthria is charac-
teristically accompanied by a specific nonspeech motor
dysfunction. Dysarthria–clumsy hand syndrome, first
described by Fisher (1967), is characterized by a combi-
nation of ataxic and pyramidal signs affecting speech
and hand movements. Fisher (1978) described a similar
condition, ataxic hemiparesis, that may be confused with
dysarthria–clumsy hand syndrome (Glass, Levey, &
Rothstein, 1990). In a study of six patients, Glass et al.
(1990) reported that all patients had pontine infarctions
Kent et al.: Clinicoanatomic Studies in Dysarthria 539
 Table 3. Lesions resulting in pure or isolated dysarthria.
Lesion location
Cerebral cortex
Centrum ovale
Corona radiata (bilateral)
Corona radiata (unilateral)
Internal capsule (unilateral)
Internal capsule (laterality not specified)
Corona radiata and/or internal capsule
(bilateral)
Corona radiata & internal capsule
(unilateral)
Basal ganglia
Pons
Cerebellum (paravermal zone of right
hemisphere)
contralateral to the affected limb. Further, in their re-
view and re-evaluation of the literature, they concluded
that pontine lesions were identified in 12 of 15 patients
with dysarthria–clumsy hand syndrome. The remain-
ing patients without pontine damage had lesions in the
capsule, corona radiata, or both. Schonewille et al.
(1999) reported on two cases of this syndrome. For one
patient, the lesions were in the posterior limb of the in-
ternal capsule and the putamen. For the other, the le-
sion was in the caudate nucleus. But it also has been
reported that dysarthria–clumsy hand syndrome may
result from infarction of the cerebral peduncle (Urban,
Hopf, Visbeck, Fleischer, & Andreas, 1996). It may be
concluded that although a pontine lesion is typical of
this syndrome, lesions in the capsule, basal ganglia, or
cerebral peduncle also may be responsible. As noted ear-
lier, this syndrome can be cross-listed with the category
of cerebellar lesions, which is discussed next.
Lesions of the Cerebellar System
Ataxic dysarthria is associated with a large num-
ber of neuropathologies and a variety of focal or diffuse
lesions (Duffy, 1995). It is helpful to review some of the
major hypotheses concerning cerebellar dysfunction in
speech before considering the imaging data. One of the
earliest clinicoanatomic hypotheses held that the ver-
mis is particularly important for speech (Holmes, 1917;
Mills & Weisenburg, 1914). Recent support for this idea
was reported by Chiu, Chen, and Tseng (1996), who com-
pared speech and other motor dysfunctions in 15 pa-
tients with cerebellar disease and dysarthria. They
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Source
Ichikawa & Kageyama (1991), Kim (1994), Lampl et al. (1997),
Okuda et al. (1999)
Arboix et al. (1991)
Takahashi et al. (1995)
Kim (1994), Takahashi et al. (1995), Urban et al. (1999)
Urban et al. (1999)
Arboix et al. (1991)
Okuda et al. (1999), Takahashi et al. (1995)
Ichikawa & Kageyama (1991), Okuda et al. (1999), Ozaki et al.
(1986), Takahashi et al. (1995), Tohgi et al. (1996)
Kim (1994)
Arboix et al. (1991), Kim (1994), Orefice et al. (1999), Tohgi et al.
(1996)
Gironell et al. (1996)
determined that the midline structures of vermis and
fastigial nucleus were the primary focus for the coordi-
nation of motor speech. However, in a review of dysar-
thria in cerebellar disease, Ackermann and Ziegler
(1992) concluded that a speech disorder is particularly
associated with damage to the paramedian regions of
the superior cerebellar hemispheres. In another review,
Timmann, Kolb, and Diener (1999) identified rostral
paravermal lesions as responsible for dysarthria. Barth,
Bogousslavsky, and Regli (1993) concluded from a MRI
study that infarcts in the territory of the superior cer-
ebellar artery are associated with a syndrome of dysar-
thria, vertigo or unsteadiness, limb or trunk ataxia, and
nystagmus.
Lesions Associated With Ataxic
Dysarthria
Table 4 summarizes the lesions that have been re-
ported in several studies of ataxic dysarthria. For the
most part, the lesions are limited to the cerebellum but
can affect cerebellar inflow and outflow tracts, includ-
ing crossed cortico-cerebellar pathways, such as (a) the
frontopontocerebellar tract originating in Brodmann
Area 10, and (b) the tract connecting the orofacial area
of motor cortex with the paravermal segment of the con-
tralateral cerebellar hemisphere. The identification of
responsible lesion is complicated by the possibility of
diaschisis, in which a lesion to one brain structure
causes a functional disturbance in a remote structure
that is itself not damaged. SPECT evidence of cerebello-
cerebral diaschisis has been reported in patients with
 Table 4. Lesions associated with ataxic dysarthria.
Midline regions
Vermis
Vermis and fastigial nucleus
Paramedian and lateral regions
Lateral hemispheres (especially interpositus
and dentate nuclei)
Superior cerebellar vermis, both cerebellar
hemispheres, paravermal and lateral
aspects of the hemispheres, and left
paravermal area
Regions supplied by rostral basilar artery
(includes superior cerebellar artery)
Rostral paravermal area
Paramedian regions of the superior cerebellar
hemispheres
Noncerebellar regions
Frontal cerebral cortex
unilateral cerebellar infarctions (Botez, Leveille, Lam-
bert, & Botez, 1991).
When focal lesions have been determined, their dis-
tribution includes the vermal, paravermal, and lateral
portions (hemispheres) of the cerebellum. Although le-
sions associated with dysarthria often are on the left
side, this is not necessarily the case (Ackermann, Vogel,
Peterson, & Poremba, 1992). The composite picture is
one of widely scattered lesions in the midline or in ei-
ther hemisphere. One interpretation of these lesion data
is that different speech functions are represented in
different regions of the cerebellum, either because of
individual variations in regional cerebellar function
(population heterogeneity) or because speech is multi-
ply represented in the cerebellum (distributed repre-
sentation). Possibly, different parts of the cerebellum
are involved in the motor control of different motor sys-
tems within speech production or they are involved with
different functions of motor control. For example,
Ackermann et al. (1992) observed that a bilateral inf-
arction appears to be associated with the most severe
articulatory deficits and that a lesion of the dentate
nucleus is linked with phonatory disturbances. Another
factor to consider is the possibility of accompanying le-
sions in noncerebellar regions. Cisneros and Braun
(1995) hypothesized that differences in the severity of
ataxic dysarthria could be related to lesions in struc-
tures other than the cerebellum. Specifically, they pro-
posed that more severe involvement (both respiratory
insufficiency and articulatory/phonatory difficulties) re-
flected additional damage to pontine and medullary struc-
tures. Imaging data are needed to evaluate this hypoth-
esis. In a PET study of olivopontocerebellar atrophy,
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Holmes (1917), Mills & Weisenburg (1914)
Chiu, Chen, & Tseng (1996)
Lalonde & Botez (1990)
Ackermann et al. (1992), Amarenco, Chevrie-Muller, et al.
(1991), Amarenco, Roullet, et al. (1991), Gilman &
Kluin (1992), Gironell et al. (1996), Lechtenberg &
Gilman (1978)
Chaves et al. (1994); Erdemoglu & Duman (1998); Stangel
et al. (1999)
Timmann, Kolb, & Diener (1999)
Ackermann & Ziegler (1992)
Marie et al. (1998), Terry & Rosenberg (1995)
Kluin et al. (1988) reported a significant inverse corre-
lation between the severity of ataxia in speech and the
local metabolic rates for glucose in the cerebellar ver-
mis, cerebellar hemispheres, and brainstem.
A full understanding must account for the remote
effects of the lesion as well as for its local effects. TMS
results from patients with autosomal-dominant or idio-
pathic cerebellar ataxia indicated that one consequence
of cerebellar disease is a diminished facilitatory influ-
ence of the cerebellum on motor cortex (Liepert et al.,
1998). Finally, as an example of a promising line of
study, Ikuta (1998) used proton magnetic resonance
spectroscopy and SPECT in a study of patients with
olivopontocerebellar atrophy (OPCA). Compared to con-
trols, patients with OPCA had decreased ratios of N-
acetylaspartate to creatine (NAA/Cre). Moreover, pa-
tients with a more severe ataxic gait and dysarthria had
a slightly lowered NAA/Cre relative to other OPCA pa-
tients. Ikuta’s study is one of the very few to apply mag-
netic resonance spectroscopy to individuals with dysar-
thria, but it points the way to future investigations.
Cerebellar Mutism
Although the focus of this review is on dysarthrias
in the adult, it is pertinent here to note the syndrome of
cerebellar mutism and subsequent (typically ataxic)
dysarthria that may occur as a complication of poste-
rior fossa surgery in children or as a consequence of
hemorrhages or trauma (Turgut, 1998). The location of
the lesion responsible for cerebellar mutism and dysar-
thria is somewhat unclear. Some studies point to a le-
sion in the cerebellar hemispheres (Janssen et al., 1998).
Kent et al.: Clinicoanatomic Studies in Dysarthria 541
 Others conclude that a midline (especially vermal) le-
sion is most likely. In a study of 42 children with cer-
ebellar tumor, mutism and dysarthria were noted in 12
(29%), with the primary independent risk factors being
type of tumor, midline localization, and vermal incision
(Cattsman-Berrevoets et al., 1999). Splitting of the in-
ferior vermis has been proposed as a primary etiologic
factor (Coplin, Kim, Kliot, & Bird, 1997). Vermal dam-
age also is implicated in the speech disorder (“speech
apraxia”) that often accompanies congenital ocular mo-
tor apraxia (Jan, Kearney, Groenveld, Sargent, &
Poskitt, 1998). In summary, evidence for a vermal le-
sion is strong if not conclusive. But it also has been sug-
gested that mutism can result from interruption of the
pathway that connects the cerebellar dentate nucleus,
ventrolateral nucleus of the contralateral thalamus, and
the supplementary motor area (Germano et al., 1998).
If the cerebellum superintends the motor control of
speech, then it is not surprising if lesions in different
parts of the cerebellum result in impairments of speech
production, although disruptions may be associated with
certain regions more than others.
Cerebellar damage is not unique in its relation to
mutism, which also has been reported to occur with le-
sions of the periaqueductal gray (Esposito, Demeurisse,
Alberti, & Fabbro, 1999); globus pallidus and prefronto-
striatal circuits (Ure et al., 1998), thalamo-mesencepha-
lic region (Nagaratnam, McNeil, & Gilhotra, 1999),
supplementary motor area (Freund, 1999), and right-
hemisphere parietal cortex (Chaudhuri et al., 1999).
Lesions of the Extrapyramidal
System/Basal Ganglia
The extrapyramidal system, or what Duffy (1995)
termed the indirect activation pathways, includes the
basal ganglia (caudate, putamen, globus pallidus, subtha-
lamic nucleus, substantial nigra), thalamus, and related
structures. Although this system clearly participates in
the neural control of speech, there is disagreement on the
role of individual structures. Lesions to this system are
associated with two primary types of dysarthria: hypo-
kinetic dysarthria (particularly common in Parkinson’s
disease) and hyperkinetic dysarthria (dystonic and chor-
eic forms were studied by Darley et al., 1969a, 1969b);
but hyperkinetic dysarthria can also be secondary to
other involuntary movement disorders such as tremor,
athetosis, myoclonus, action myoclonus, and tics.
Although hypokinetic dysarthria has been described
especially in connection with Parkinson’s disease or par-
kinsonian syndromes, it also has been observed in pro-
gressive supranuclear palsy (Metter & Hanson, 1991)
and multiple system atrophy (Kluin et al., 1996). A pos-
sible difference in pathophysiology between Parkinson’s
542 Journal of Speech, Language, and Hearing Research • Vol. 44 • 535–551 • June 2001
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disease and progressive supranuclear palsy is that both
the globus pallidus internal (GPi) and globus pallidus
external (GPe) are damaged in progressive supra-
nuclear palsy, but only the internal segment is affected
in Parkinson’s disease (Hardman & Halliday, 1999a,
1999b). Although very few imaging studies have been
reported on speech functions in these disorders, the more
general literature points to some important hypotheses
pertaining to speech vis-a-vis nonspeech motor control.
Imaging Studies
Imaging studies of the dopamine system reveal clini-
coanatomic relationships that should lead to an improved
understanding of the various effects of Parkinson’s dis-
ease and related disorders. Volkow et al. (1996), in a
recent review of PET studies, discussed how this tech-
nology can answer fundamental questions in pathophysi-
ology and effective treatment. PET has potential for the
differential diagnosis of various forms of parkinsonism
and for the detection of subclinical dopaminergic defi-
cits (Shinotoh & Calne, 1995). In vivo studies with
Fluorodopa 18 can determine dopamine metabolism in
parts of the striatum and relate localized metabolic de-
ficiency to either motor or cognitive dysfunctions. Mo-
tor impairment has been associated with abnormali-
ties in the putamen, whereas memory impairment has
been related to abnormalities in the caudate (Holthoff-
Detto et al., 1997). Studies using PET and MRI have
shown that lesions of the GPi are associated with hy-
perkinetic signs, whereas lesions of the GPe or globus
pallidus central (GPc) are associated with hypokinetic
or akinetic/rigid signs (Bucher et al., 1996; Hirato,
Ishihara, Horikoshi, Shibazaki, & Ohye, 1995).
PET studies are informative regarding over- or un-
deractivity in other regions, including supplementary
motor area, dorsal prefrontal cortex, lateral premotor
cortex, parietal cortex, and cerebellum (Brooks, 1999).
Motor disturbances in Parkinson’s disease may be ex-
plained by these patterns of hyperactivity and hypo-
activity. Brooks (1999) concluded that rest tremor re-
sults from a combination of overactivity of cerebellar
connections and loss of dopaminergic function. Ventral
thalamotomy or thalamic stimulation reduces tremor
and cerebellar activation but also reduces activation of
primary motor cortex.
A dysarthria also has been noted to occur in asso-
ciation with anterior thalamic infarction. Ghika-Schmid
and Bogousslavsky (2000) reported on 12 patients with
an isolated infarct of the anterior thalamus. In addition
to a common severe perseverative disorder and antero-
grade memory impairment, the patients had a variety
of other disorders. Dysarthria (unspecified as to salient
characteristics or perceptual type) occurred in 8, and
hypophonia was observed in 5. Given the relatively high
 rate of dysarthria in the sample, it would be valuable to
know more about the speech disorder (e.g., perceptual
type of the dysarthria or a description of its speech-voice
characteristics).
Although very few imaging studies directly address
speech production in individuals with Parkinson’s dis-
ease, preliminary data indicate that behavioral therapy
(intensive speech and voice treatment) produces changes
in regional cerebral blood flow (rCBF) that resemble the
effect of pallidotomy (Liotti et al., 1999). Specifically,
post-treatment rCBF in the globus pallidus was reduced
in the resting state, presumably reflecting a reduction
of overactivity in the globus pallidus. However, rCBF
increased for vocalization relative to rest. However, this
is not to say that pallidotomy consistently results in
improved speech. As considered in the next section, in-
terventions do not necessarily have the same outcomes
for speech and nonspeech functions.
Effects of Parkinson’s Disease on
Speech and Nonspeech Motor Systems
It cannot be assumed that speech and nonspeech
motor functions are affected in exactly the same way
by Parkinson’s disease. Some particularly important
questions to be considered in relating speech and other
movements in Parkinson’s disease are (a) the degree to
which speech and nonspeech motor systems exhibit the
same motor abnormalities, (b) the competition between
speech and other motor behaviors, and (c) the differen-
tial effects of clinical interventions for speech and non-
speech movements. Each of these is considered in the
following.
Similarity and Dissimilarity of
Disruptions in Speech and
Nonspeech Motor Systems
Concerning the question of similar motor abnormali-
ties, Hunker and Abbs (1990) concluded from a spectral
analysis that tremor frequency is uniform in the lips,
tongue, jaw, and index finger. This conclusion supports
the simplifying hypothesis of a single tremor generator.
However, a coherency analysis of EEG records was in-
terpreted to mean that multiple oscillators are involved,
especially in interlimb comparisons (Raethjen et al., 2000).
Differences between speech and other motor systems
also have emerged on diadochokinetic tasks. Stebbins
and Goetz (1998) reported a factor analysis of the Uni-
fied Parkinson’s Disease Rating Scale (UPDRS) in which
speech and facial expression loaded on the same factor
as balance and gait. This factor was interpreted to re-
flect axial function, balance, and gait. Speech diadoch-
okinesis was considered by Stebbins and Goetz to be an
axial task, accomplished by the bilaterally innervated
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midline speech structures. Movements in the right and
left limbs emerged as two separate factors (right and
left bradykinesia). Gurd, Bessell, Watson, and Coleman
(1998) concluded that speech diadochokinesis and fin-
ger tapping are doubly dissociated in Parkinson disease,
which supports the idea that different neural systems
are responsible for articulation versus digit control.
Evidence of Competition Between
Speech and Nonspeech Motor Control
With respect to the question of competition between
speech and other voluntary motor behaviors, it appears
that vulnerability to falls may be related to a choice be-
tween walking and talking (Lundin-Olsson, Nyberg, &
Gustafson, 1997; Nisipeanu & Inzelberg, 1997). An in-
teraction between locomotion and speech also can be
seen in the effects of a simultaneous verbal fluency task
on walking in individuals with Parkinson’s disease
(Camicioli, Oken, Sexton, Kaye, & Nutt, 1998). Gait-
speech interaction certainly is important as a factor of
patient safety, but it also offers intriguing possibilities
to understand the motor control systems that support
these two tasks.
Speech and Nonspeech Effects of
Ablative Lesions, Deep Brain
Stimulation, and Dopamine
Transplants
Several studies of individuals with Parkinson’s dis-
ease or essential tremor point to differential effects of
interventions on speech and nonspeech motor functions.
These reports show that various interventions that im-
prove nonspeech motor control (especially in the limbs)
often have neutral or even negative outcomes for speech.
As summarized in Table 5, this pattern of results has
been reported for levodopa therapy, unilateral or bilat-
eral posteroventral pallidotomy, fetal dopamine trans-
plants, and pallidal or thalamic stimulation. To be sure,
other studies have shown some benefit for speech from
these interventions (Jiang, Lin, Wang, & Hanson, 1999;
Leanderson, Meyerson, & Persson, 1972; Robertson &
Hammerstad, 1996), but the essential point is that these
positive outcomes for speech have not been consistently
demonstrated. Some negative effects on speech may be
attributable to lesions from surgery. Hariz and De Salles
(1997) reported that the side effect of dysarthria in
posteroventral pallidotomy resulted from lesions that
encroached on the internal capsule. Schulz and Grant
(2000) concluded from a review of the literature on vari-
ous treatments of voice and speech disorders in Parkin-
son’s disease that speech therapy, along with appropri-
ate medications, is the most efficacious intervention.
Possibly, the dissimilar outcomes for speech and
nonspeech functions following pharmacologic, surgical,
Kent et al.: Clinicoanatomic Studies in Dysarthria 543
 Table 5. Outcomes for nonspeech and speech functions of various treatments for Parkinson’s disease (PD) and essential tremor (ET). UPDRS =
Unified Parkinson’s Disease Rating Scale (Fahn et al., 1989); ADL = activities of daily living; DDK = diadochokinesis.
Author
Bakker et al. (1997)
Cahill et al. (1998)
Durif et al. (1999)
Gamboa et al. (1997)
Gentil et al. (1998)
Gentil, Garcia-Ruiz, et al.
(1999)
Gentil, Tournier, et al.
(1999)
Ghika et al. (1999)
Gross et al. (1997)
Hariz & De Salles (1997)
Jiang et al. (1999)
Kompoliti et al. (2000)
Leanderson et al. (1972)
Martinez-Martin et al.
(2000)
Obwegeser et al. (2000)
Pahwa et al. (1999)
Poluha et al. (1998)
Robertson & Hammerstad
(1996)
Schrag et al. (1999)
Schulz et al. (1999)
Scott et al. (1998)
Shima et al. (1996)
Solomon et al. (2000)
Taha et al. (1999)
Tasker (1998)
Theodoros et al. (2000)
Uitti et al. (2000)
Wang et al. (1999)
Wang et al. (2000)
544 Journal of Speech, Language, and Hearing Research • Vol. 44 • 535–551 • June 2001
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Method
Fetal dopamine transplants for PD
Levodopa for PD
Speaking aloud and other cognitive
and motor tasks in PD
Dopaminergic drugs for PD
Levodopa therapy for PD
Bilateral stimulation of subthalamic
nucleus for PD
Levodopa therapy for PD
Bilateral posteroventral pallidotomy
for PD
GPi stimulation for PD
Posteroventral pallidotomy for PD
L-dopa therapy for PD
Apomorphine therapy in double-
blind, randomized, placebo-
controlled cross-over design
Levodopa therapy for PD
Pallidotomy for PD
Thalamic stimulation for ET
Bilateral thalamic stimulation for ET
Levodopa treatment for PD
Levodopa treatment for PD
Unilateral pallidotomy for PD
Unilateral pallidotomy for PD
Unilateral or bilateral posteroventral
pallidotomy for PD
Unilateral or bilateral posteroventral
pallidotomy for PD
Unilateral or bilateral pallidal
stimulation for PD
Thalamic deep brain stimulation
for ET
Deep brain stimulation for ET
Thalamotomy for ET
Unilateral or bilateral pallidotomy
Unilateral pallidotomy for PD
Dopaminergic therapy for PD
Dopaminergic therapy for PD
Nonspeech outcome
Not described
Improved labial function
Worsened dyskinesia
Not described
Positive for finger movements
Not described
Positive for motor score of UPDRS
Positive for UPDRS
Positive for akinesia, rigidity, and gait Positive
Generally positive for tremor
Not described
Improvement in motor score of
UPDRS
Not described
Positive for mobility, activities of daily Neutral for communication
life, emotional well being, and bodily
discomfort
Reduction of tremor (reduction of
head, voice, tongue, and face
tremor in a subgroup analysis)
Positive for tremor score and ADL
Positive for handwriting
Not described
Positive for UPDRS
Positive for limb motor function
Positive for UPDRS
Positive for rigidity, tremor, and
movement
Positive for general motor function
Positive for head, voice and
bilateral limb
Positive for tremor
Positive for tremor
No information
Improved motor function
Improved on motor section of UPDRS
Improved on motor section of UPDRS
Speech outcome
No systematic effect
Improved labial function
Not described
Persisting voice problems
Neutral or negative for orofacial
movements
Positive for speech intelligibility and oral
motor function
Neutral for speech (Item 18 of UPDRS)
Negative for 1 of 4 patients
Dysarthria as side effect in 3 of 138
patients
Positive for voice (acoustic analysis)
Neutral for voice and speech
Positive for lip muscle activity
Dysarthria as one of the most frequent
reversible side effects
Worsening of dysarthria in some patients
Neutral
Positive for jaw movements
Negative
Positive for some patients but 3 did not
show consistent positive changes
Negative, esp. for DDK, but not judged to
be functionally significant
Worsened dysarthria in 3 patients
Variable across 3 patients
Dysarthria as side effect
Dysarthria as side effect
Dysarthria as side effect
Reduced intelligibility in 10 of 12 subjects
Mild decline of intelligibility in one-third
of 57 patients
No changes in acoustically measured
vocal parameters
No changes in phonation
 or stimulation methods can provide information on the
neural regulation of speech as distinct from that for the
limbs or for midline structures of the trunk. Although
an increasing number of studies have been reported on
the effects of ablative lesions or deep brain stimulation
on Parkinson’s disease, Lang (2000) concluded that “the
evidence for benefit from surgical therapies…is rela-
tively weak by today’s scientific standards” (p. 1124).
The implications of the data reviewed in this sec-
tion seem to be, at the minimum, that speech and non-
speech motor behavior are controlled by neural systems
that are partially overlapping but also distinctive in
important ways. The evidence for competition between
speech and nonspeech motor control indicates that these
functions either share neural resources (e.g., a largely
overlapping neural regulation) or otherwise place a con-
flict on the simultaneous deployment of speech and non-
speech motor control. The evidence for asymmetric out-
comes of intervention points to some basic dissimilarities
in the structures or strategies of neural regulation.
General Discussion
Within the limitations of the information reviewed
here, it is possible to delineate a pathway, but not nec-
essarily a single structure, that is associated with each
dysarthria considered in this paper. In general, then,
the clinicoanatomic correlation is between a type of dys-
arthria and a number of structures that are parts of a
pathway or network. Examples are given in Tables 1, 2,
3, and 5. Admittedly, some of the pathways are exten-
sive. The same kind of analysis may be applicable to
other types of dysarthria once the requisite data are
available. The conclusions drawn from clinical studies
potentially can be confirmed with data from neuro-
imaging studies of neurologically normal speakers. Ul-
timately, the synthesis of results from both clinical and
control subjects should define the primary pathways of
speech motor control. Some suggestions on this matter
have been discussed elsewhere (Kent, Kent, Weismer,
& Duffy, in press).
Limitations and Potentials
As noted earlier, there are several limitations in
the clinicoanatomic studies available for review. Accord-
ingly, the interpretation of the compiled information
confronts a number of issues that are not satisfactorily
resolved. These include the typical absence of clear de-
scriptions of deviant speech characteristics or classifi-
cation of dysarthria; the possibility of diaschisis (the
remote effects of a lesion); the influence of sensorimo-
tor-cognitive-linguistic aspects of assessment tasks (par-
ticularly complicating if a given structure participates
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in several functions, as may be the case with the cer-
ebellum); and neglect of the severity of dysarthria (varia-
tions of severity even with the same dysarthria classifi-
cation can complicate correlations with anatomic or
metabolic abnormality). It appears that the potential
for clinicoanatomic studies of dysarthria is considerable,
and it is therefore appropriate to consider the directions
that future studies might take.
It is beyond the purpose of this review to examine
either the overall clinical utility or the broad theoreti-
cal foundations of the dysarthria classification system
introduced by Darley et al. (1969a, 1969b). Commen-
taries on these general issues have been published else-
where (Duffy & Kent, in press; Kent, 1996; Kent et al.,
1998). But it is highly likely that the original system
should be modified in some respects, such as inclusion
of additional types of dysarthria (unilateral upper mo-
tor neuron dysarthria being one example considered in
this review), the specification of acoustic and physiologic
correlates for each perceptual type, and (possibly) the
delineation of subtypes to reflect the heterogeneity
within major types.
Directions for Future Research
There may be serious limitations to the classic ap-
proach followed in most clinicoanatomic studies: the
group comparison design. With this method, “imaging
findings are used for grouping patients according to the
lesion location…and the interpretation obeys a subtrac-
tive logic, i.e., the poor performance of one group im-
plies that the damaged region defining the group is re-
quired for task completion” (Godefroy et al., 1998, p.
1546). As Godefroy et al. pointed out, a problem with
this strategy is that lesion distribution is determined
by the nature of the pathological process and is not nec-
essarily congruent with the functional organization of
the brain. In considering alternatives to the classic ap-
proach, these authors proposed four basic modes of brain-
behavior relationship: Unicity is the condition in which
a deficit corresponds to a lesion in a single structure—
“one deficit, one lesion” (p. 1546). Equivalence is the mode
in which a deficit depends on a single lesion in one or
the other of two or more possible structures. Godefroy
remarked that this may be the most frequent pattern in
brain-behavior relationships. Association obtains when
a deficit requires the combined lesion of two different
structures. Summation occurs when a single lesion in
one of two possible structures results in a minor deficit
and the combined lesion of both structures produces a
major deficit. A kind of bilateral summation occurs in
dysarthria associated with upper motor neuron lesion.
Whereas a unilateral lesion typically results in a mild
to moderate dysarthria, bilateral lesions tend to produce
a severe dysarthria.
Kent et al.: Clinicoanatomic Studies in Dysarthria 545
 Other modes may be included as well, either as ad-
ditional categories or as modifications to the categories
defined above. Diaschisis is a mode of brain-behavior
relationship in which a lesion in one brain structure
results in a functional change in another, remote brain
structure, which itself does not experience direct dam-
age. This mode may occur with some frequency, but it
has seldom been explicitly investigated. Some evidence
of diaschisis was considered in this review. Another pos-
sible mode is disconnection, in which damage to white
matter may disconnect structures that participate in a
control objective. For example, Daniels, Brailey, and
Foundas (1999) observed that the most common lesion
associated with lingual discoordination during swallow-
ing in patients with stroke was in the periventricular
white matter.
Many of the clinicoanatomic relationships summa-
rized in the present paper are best described as follow-
ing the equivalence mode. For example, if ataxic dysar-
thria is taken as the deficit, then the lesion can be in
one of two or three different structures: cerebellum, cer-
ebellar outflow pathways, or the cerebral cortex.
The approach taken by Lefkowitz and Netsell (1994),
in a study of post-traumatic speech disorders, was to
group subjects according to clinical deficit (delayed ini-
tiation, dysprosody, dysarthria) and then to determine
the lesions for each group. MRI was used to identify five
categories of structural correlation (listed in order of the
strength of association between clinical deficit and ob-
served MRI abnormalities): discrete lesions, atrophic
lesions, afferent fiber lesions, nonrecognized lesions, and
functional lesions. Prototypes were then identified from
the results for 11 subjects with post-traumatic speech
disorders. The dysarthria prototype had a large area of
hyperintense ischemic change that included the left pri-
mary sensory and motor cortices, as well as Broca’s area.
The dysprosody prototype was associated with exten-
sive hyperintense ischemic changes in the supraven-
tricular white matter bilaterally. Finally, the initiation
prototype had an atrophic lesion of the midbrain.
Dysarthria also can be portrayed as a task-based
profile, in which functional deficits are described for
motor subsystems or specific aspects of speech produc-
tion (Kent & Kent, 2000). The goal of this approach is to
correlate specific dysfunctions (e.g., laryngeal hypofunc-
tion, slowness of movement) with damage to particular
regions of the neural control system for speech. In this
approach, the objective is not so much to determine the
lesion site for a perceptual type of dysarthria as it is to
identify the lesions that correlate with particular dimen-
sions of speech production difficulty.
Above all, progress in clinicoanatomic correlations
in dysarthria will depend on (a) a rich description of the
speech disorder in perceptual, acoustic, and physiologic
546 Journal of Speech, Language, and Hearing Research • Vol. 44 • 535–551 • June 2001
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domains, and (b) interpretation of neuroimaging data
in terms of carefully specified modes of brain-behavior
relationship. Darley et al. (1969a, 1969b) laid the foun-
dation for this work; advances in neuroimaging tech-
nology, speech acoustics, and speech physiology should
be major factors in future accomplishments.
Acknowledgments
This work was supported in part by research grant No.
5 R01 DC 00319 from the National Institute on Deafness
and Other Communicative Disorders (NIDCD-NIH). The
participation of Amy Clift was supported by a Research
Mentorship from the American Speech-Language-Hearing
Association. The authors are grateful for the constructive
suggestions made by the guest editor, Ronald Netsell, and
two reviewers, Thomas J. Hixon and James Till.
References
Ackermann, H., Vogel, M., Petersen, D., & Poremba, M.
(1992). Speech deficits in ischaemic cerebellar lesions.
Journal of Neurology, 239, 223–227.
Ackermann, H., & Ziegler, W. (1992). Cerebellar dysar-
thria—A review of the literature [translation of German
original]. Forschritte der Neurologie–Psychiatrie, 60,
28–40.
Amarenco, P., Chrevie-Muller, C., Roullet, E., &
Bousser, M. G. (1991). Paravermal infarct and isolated
cerebellar dysarthria. Annals of Neurology, 30, 211–213.
Amarenco, P., Roulett, E., Goujon, C., Cheron, F.,
Hauw, J. J., & Bousser, M. G. (1991). Infarction in the
anterior rostral cerebellum (the territory of the lateral
branch of the superior cerebellar artery). Neurology, 41,
253–258.
Arboix, A., Garcia-Eroles, L., Massons, J., Oliveres, M.,
& Targa, C. (2000). Hemorrhagic lacunar stroke. Cere-
brovascular Diseases, 10, 229–234.
Arboix, A., & Massons, J., Oliveres, M., & Titus, F.
(1991). Isolated dysarthria. Stroke, 22, 531.
Bakker, K. K., Ramig, L. O., Johnson, A. B., & Freed,
C. R. (1997). Preliminary voice and speech analysis
following fetal dopamine transplants in 5 individuals
with Parkinson disease. Journal of Speech, Language, and
Hearing Research, 40, 615–626.
Barth, A., Bogousslavsky, J., & Regli, F. (1993). The
clinical and topographic spectrum of cerebellar infarcts: A
clinico-magnetic resonance imaging correlation study.
Annals of Neurology, 33, 451–456.
Birn, R. M., Bandettini, P. A., Cox, R. W., & Shaker, R.
(1999). Event-related fMRI of tasks involving brief motion.
Human Brain Mapping, 7, 106–114.
Bogousslavsky, J., & Regli, F. (1990). Capsular genu
syndrome. Neurology, 40, 1499–1502.
Botez, M. I., Leveille, J., Lambert, R., & Botez, T. (1991).
Single photon emission tomography (SPECT) in cerebellar
disease: Cerebello-cerebral diaschisis. European Neurol-
ogy, 31, 405–412.
Brooks, D. J. (1999). Functional imaging of Parkinson’s
 disease: Is it possible to detect brain areas for specific
symptoms? Journal of Neural Transmission, 56 (Suppl.),
139–153.
Broussolle, E., Bakchine, S., Tommasi, M., Laurent, B.,
Bazin, B., Cinotti, L., Cohen, L., & Chazot, G. (1996).
Slowly progressing anarthria with late anterior opercular
syndrome: A variant form of frontal cortical atrophy.
Journal of the Neurological Sciences, 144, 44–58.
Bucher, S. F., Seelos, K. C., Dodel, R. C., Paulus, W.,
Reiser, W., Reiser, M., & Oertel, W. H. (1996). Pallidal
lesions: Structural and functional magnetic resonance
imaging. Archives of Neurology, 53, 682–686.
Cahill, L. M., Murdoch, B. E., Theodoros, D. G., Triggs,
E. J., Charles, B. G., & Yao, A. A. (1998). Effect of oral
levodopa treatment on articulatory function in Parkinson’s
disease: Preliminary results. Motor Control, 2, 161–172.
Camicioli, R., Oken, B. S., Sexton, G., Kaye, J. A., &
Nutt, J. G. (1998). Verbal fluency task affects gait in
Parkinson’s disease with motor freezing. Journal of
Geriatric Psychiatry & Neurology, 11, 181–185.
Cattsman-Berrevoets, C. E., Van Dongen, H. R.,
Mulder, P. G. H., Geuze, D. P. Y., Paquier, P. F., &
Lequin, M. H. (1999). Tumour type and size are high risk
factors for the syndrome of “cerebellar” mutism and
subsequent dysarthria. Journal of Neurology, Neurosur-
gery and Psychiatry, 67, 755–757.
Chaudhuri, J. R., Anand, J., Shivshankar, N.,
Jaykumar, P. N., Suvarna, A., Murali, T., & Taly, A. B.
(1999). Right parietal infarction with concomitant mutism.
Acta Neurologica Scandinavica, 99, 77–79.
Chaves, C. J., Caplan, L. R., Chung, C. S., Tapia, J.,
Amarenco, P., Teal, P., Wityk, R., Estol, C.,
Tettenborn, B., & Rosengart, A. (1994). Cerebellar
infarcts in the New England Medical Center Posterior
Circulation Stroke Registry. Neurology, 44, 1385–1390.
Chiu, M. J., Chen, R. C., & Tseng, C. Y. (1996). Clinical
correlates of quantitative acoustic analysis in dysarthria.
European Neurology, 36, 310–314.
Cisneros, E., & Braun, C. M. (1995). Vocal and respiratory
diadochokinesis in Friedreich’s ataxia: Neuropathological
correlations [translation of French original]. Revue
Neurologique, 151, 113–123.
Combarros, O., Dicz, C., Cano, J., & Berciano, J. (1992).
Ataxic hemiparesis with cheiro-oral syndrome in capsular
infarction. Journal of Neurology, Neurosurgery, & Psychia-
try, 55, 859–860.
Coplin, W. M., Kim, D. K., Kliot, M., & Bird, T. D. (1997).
Mutism in an adult following hypertensive cerebellar
hemorrhage: Nosological discussion and illustrative case.
Brain & Language, 59, 473–493.
Daniels, S. K., Brailey, K., & Foundas, A. L. (1999).
Lingual discoordination and dysphagia following acute
strokes: Analyses of lesion localization. Dysphagia, 14,
85–92.
Darley, F. L., Aronson, A. E., & Brown, J. R. (1969a).
Differential diagnostic patterns of dysarthria. Journal of
Speech and Hearing Research, 12, 249–269.
Darley, F. L., Aronson, A. E., & Brown, J. R. (1969b).
Cluster of deviant speech dimensions in the dysarthrias.
Journal of Speech and Hearing Research, 12, 462–496.
Downloaded From: http://jslhr.pubs.asha.org/ by Raymond Kent on 03/30/2014
Davidoff, R. A. (1990). The pyramidal tract. Neurology, 40,
332–339.
de Koning, I., van Doorn, P. A., & van Dongen, H. R.
(1997). Slowly progressive isolated dysarthria: Longitudi-
nal course, speech features, and neuropsychological
deficits. Journal of Neurology, 244, 664–666.
Didic, M., Ceccaldi, M., & Poncet, M. (1998). Progressive
loss of speech: A neuropsychological profile of premotor
dysfunction. European Neurology, 39, 90–96.
Didic, M., Felician, O., Ceccaldi, M., & Poncet, M.
(1999). Progressive focal cortical atrophies [translation of
French original]. Revue Neurologique, 155, 4 (Suppl. 4),
S73–S82.
Duffy, J. R. (1995). Motor speech disorders: Substrates,
differential diagnosis, and management. St. Louis: Mosby-
YearBook.
Duffy, J. R., & Folger, W. N. (1996). Dysarthria associated
with unilateral central nervous system lesions: A retro-
spective study. Journal of Medical Speech-Language
Pathology, 4, 57–70.
Duffy, J. R., & Kent, R. D. (in press). Darley’s contribu-
tions to the understanding, differential diagnosis, and
scientific study of the dysarthrias. Aphasiology.
Durif, F., Vidailhet, M., Debilly, B., & Agid, Y. (1999).
Worsening of levodopa-induced dyskinesias by motor and
mental tasks. Movement Disorders, 14, 242–245.
Epstein, C. M. (1998). Transcranial magnetic stimulation:
language function. Clinical Neurophysiology, 15, 325–332.
Epstein, C. M., Meador, K. J., Loring, D. W., Wright,
R. J., Weissman, J. D., Sheppard, S., Lah, J. J.,
Puhalovich, F., Gaitan, L., & Davey, K. R. (1999).
Localization and characterization of speech arrest during
transcranial magnetic stimulation. Clinical Neurophysiol-
ogy, 110, 1073–1099.
Erdemoglu, A. K., & Duman, T. (1998). Superior cerebellar
artery territory stroke. Acta Neurologica Scandinavica,
98, 283–287.
Esposito, A., Demeurisse, G., Alberti, B., & Fabbro, F.
(1999). Complete mutism after midbrain periacqueductal
gray lesion. Neuroreport, 10, 681–685.
Fahn, S., Elton, R. L., & the UPDRS Development
Committee. (1989). Unified Parkinson’s Disease Rating
Scale. In S. Fahn, C. D. Marsden, D. Calne, & M. Goldstein
(Eds.), Recent developments in Parkinson’s disease (Vol. 2,
pp. 153–167). Florham Park, NJ: Macmillan Healthcare
Information.
Fisher, C. M. (1967). A lacunar stroke: The dysarthria–
clumsy hand syndrome. Neurology, 17, 614–617.
Fisher, C. M. (1977). Pure spastic paralysis of corticospinal
origin. Canadian Journal of Neurological Sciences, 4,
251–258
Fisher, C. M. (1978). Ataxic hemiparesis: A pathologic study.
Archives of Neurology, 35, 126–128.
Fisher, C. M. (1982). Lacunar strokes and infarcts: A
review. Neurology, 32, 871–876.
Freund, H. J. (1999). Movement disorders following cortical
lesions [translation of German original]. Klinische
Neurophysiologie, 30, 113–119.
Kent et al.: Clinicoanatomic Studies in Dysarthria 547
 Gamboa, J., Jimeniz-Jimeniz, F., Nieto, A., Monojo, J.,
Ortipareja, M., Molina, J. A., Garcia-Albea, E., &
Cobeta, I. (1997). Acoustic voice analysis in patients with
Parkinson’s disease treated with dopaminergic drugs.
Journal of Voice, 11, 314–320.
Gentil, M., Garcia-Ruiz, P., Pollak, P., & Benabid, A.-L.
(1999). Effect of stimulation of the subthalamic nucleus on
oral control of patients with parkinsonism. Journal of
Neurology, Neurosurgery & Psychiatry, 67, 329–333.
Gentil, M., Tournier, C. L., Perrin, S., & Pollak, P.
(1998). Effects of levodopa on finger and orofacial move-
ments in Parkinson’s disease. Progress in Neuro-Psycho-
pharmacology & Biological Psychiatry, 22, 1261–1274.
Gentil, M., Tournier, C.-L., Pollak, P., & Benabid, A. L.
(1999). Effect of bilateral subthalamic nucleus stimulation
and dopatherapy on oral control in Parkinson’s disease.
European Neurology, 42, 136–140.
Germano, A., Baldari, S., Caruso, G., Caffo, M.,
Montemagno, G., Cardia, E., & Tomasello, F. (1998).
Reversible cerebral perfusion alterations in children with
transient mutism after posterior fossa surgery. Childs
Nervous System, 14, 114–119.
Ghika, J., Ghika-Schmitd, F., Fankhauser, H., Assal, G.,
Vingerhoets, F., Albanese, A., Bougousslavsky, J., &
Favre, J. (1999). Bilateral contemporaneous postero-
ventral pallidotomy for the treatment of Parkinson’s
disease: Neuropsychological and neurological side
effects—Report of four cases and review of the literature.
Journal of Neurosurgery, 91, 313–321.
Ghika-Schmid, F., & Bogousslavsky, J. (2000). The acute
behavioral syndrome of anterior thalamic infarction: A
prospective study of 12 cases. Annals of Neurology, 48,
220–227.
Gilman, S., & Kluin, K. J. (1992). Speech disorders in
cerebellar degeneration studied with positron emission
tomography. In A. Blitzer, M. F. Brin, C. T. Sasaki, S. Fahn,
& K. S. Harris (Eds.), Neurologic disorders of the larynx (pp.
279–285). New York: Thieme Medical Publishers.
Gironell, A., Arboix, A., & Marti-Vilalta, J. L. (1996).
Isolated dysarthria caused by a right paravermal infarc-
tion. Journal of Neurology, Neurosurgery & Psychiatry, 61,
205–206.
Glass, J. D., Levey, A. I., & Rothstein, J. D. (1990). The
dysarthria–clumsy hand syndrome: A distinct clinical
entity related to pontine infarction. Annals of Neurology,
27, 487–494.
Godefroy, O., Duhamel, A., Leclerc, X., Saint Michel,
T., Henon, H., & Leys, D. (1998). Brain-behavior
relationships: Some models and related statistical
procedures for the study of brain-damaged patients.
Brain, 121, 1545–1556.
Gross, C., Rougier, A., Guehl, D., Boraud, T., Julien, M.,
& Bioulac, C. (1997). High-frequency stimulation of the
globus pallidus internalis in Parkinson’s disease: A study
of seven cases. Journal of Neurosurgery, 87, 491–498.
Gurd, J. M., Bessell, N., Watson, I., & Coleman, J.
(1998). Motor speech versus digit control in Parkinson’s
disease: A cognitive neuropsychology investigation.
Clinical Linguistics and Phonetics, 12, 357–378.
Hardman, C. D., & Halliday, G. M. (1999a). The internal
globus pallidus is affected in progressive supranuclear
548 Journal of Speech, Language, and Hearing Research • Vol. 44 • 535–551 • June 2001
Downloaded From: http://jslhr.pubs.asha.org/ by Raymond Kent on 03/30/2014
palsy and Parkinson’s disease. Experimental Neurology,
158, 135–142.
Hardman, C. D., & Halliday, G. M. (1999b). The external
globus pallidus in patients with Parkinson’s disease and
progressive supranuclear palsy. Movement Disorders, 14,
626–633.
Hariz, M. I., & De Salles, A. A. (1997). The side-effects and
complications of posteroventral pallidotomy. Acta Neuro-
chirurgica, 68 (Suppl.), 42–48.
Hartman, D. E., & Abbs, J. H. (1992). Dysarthria associ-
ated with focal unilateral upper motor neuron lesion.
European Journal of Disorders of Communication, 27,
187–196.
Hartmann, A., Conolly, E. S., Duong, D. H.,
Prestigiacomo, C. J., Joshi, S., Mohr, J. P., & Mast,
H. (1999). Dysarthria during basilar artery balloon
occlusion. Neurology, 53, 421–423.
Hirato, M., Ishihara, J., Horikoshi, S., Shibazaki, T.,
& Ohye, C. (1995). Parkinsonian rigidity, dopa-induced
dyskinesia and chorea: Dynamic studies on the basal
ganglia-thalamocortical motor circuit using PET scan
and depth microrecording. Acta Neurochirurgica, 64
(Suppl.), 5–8.
Holmes, G. (1917). The symptoms of acute cerebellar
injuries due to gunshot injuries. Brain, 40, 461–535.
Holthoff-Detto, V. A., Kessler, J., Herholz, K., Bonner,
H., Pietrzyk, U., Wurker, M., Ghaemi, M., Wienhard,
K., Wagner, R., & Heiss, W. D. (1997). Functional effects
of striatal dysfunction in Parkinson’s disease. Archives of
Neurology, 54, 145–150.
Hunker, C. J., & Abbs, J. H. (1990). Uniform frequencies of
parkinsonian resting tremor in the lips, jaw, tongue and
index finger. Movement Disorders, 5, 71–77.
Ichikawa, K., & Kageyama, Y. (1991). Clinical anatomic
study of pure dysarthria. Stroke, 22, 809–812.
Ikuta, N. (1998). Proton magnetic resonance spectroscopy
and single photon emission CT in patients with olivo-
pontocerebellar atrophy [translation of Japanese original].
Rinsho Shinkeigaku—Clinical Neurology, 38, 289–294.
Infante, J., Sanchez Guerra, M., Polo, J. M., Berciano,
J., & Oterino, A. (2000). Progressive anarthria: One case
without lingual apraxia [translation of Spanish original].
Neurologia, 15, 208–210.
Inoue, T. Shimizu, H., & Yoshimoto, T. (1999). Imaging
the pyramidal tract in patients with brain tumors.
Clinical Neurology & Neurosurgery, 101, 4–10.
Jan, J. E., Kearney, S., Groenveld, M., Sargent, M. A., &
Poskitt, K. J. (1998). Speech, cognition, and imaging
studies in congenital ocular motor apraxia. Developmental
Medicine & Child Neurology, 40, 95–99.
Janssen, G., Messing-Junger, A. M., Engelbrecht, V.,
Gobel, U., Bock, W. J., & Lenard, H. G. (1998). Cerebel-
lar mutism syndrome [translation of German original].
Klinische Padiatrie, 210, 243–247.
Jiang, J., Lin, E., Wang, J., & Hanson, D. G. (1999).
Glottographic measures before and after levodopa
treatment in Parkinson’s disease. Laryngoscope, 109,
1287–1294.
Karcostas, D., Artemis, N., Giannopoulos, S., Milonas,
J., & Bogousslavsky, J. (1994). Bilateral thalamic
 infarcts presenting as acute pseudobulbar palsy. Func-
tional Neurology, 9, 265–268.
Kent, R. D. (1996). Hearing and believing: Some limits to
the auditory-perceptual assessment of speech and voice
disorders. American Journal of Speech-Language Pathol-
ogy, 7, 7–23.
Kent, R. D. (1998). Neuroimaging studies of brain activa-
tion for language, with an emphasis on fMRI: A review.
Folia Phoniatrica Logopaedica, 50, 291–304.
Kent, R. D., & Kent, J. F. (2000). Task-based profiles of the
dysarthrias. Folia Phoniatrica et Logopaedica, 52, 48–53.
Kent, R. D., Kent, J. F., Duffy, J. R., & Weismer, G.
(1998). The dysarthrias: Speech-voice profiles, related
dysfunctions, and neuropathologies. Journal of Medical
Speech-Language Pathology, 6, 165–211.
Kent, R. D., Kent, J. F., Weismer, G. & Duffy, J. R. (in
press). What dysarthrias can tell us about the neural
control of speech. Journal of Phonetics.
Kertesz, A., & Orange, J. B. (2000). Primary progressive
aphasia: The future of neurolinguistic and biologic
characterization. Brain & Language, 71, 116–119.
Kim, J. S. (1994). Pure dysarthria, isolated facial paresis, or
dysarthria-facial paresis syndrome. Stroke, 25, 1994–1998.
Kluin, K. J., Gilman, S., Lohman, M., & Junck, L.
(1996). Characteristics of the dysarthria of multiple
system atrophy. Archives of Neurology, 53, 545–548.
Kluin, K. J., Gilman, S., Markel, D. S., Koeppe, R. A.,
Rosenthal, G., & Junck, L. (1988). Speech disorders in
olivopontocerebellar atrophy correlate with positron
emission tomography findings. Annals of Neurology, 23,
547–554.
Kompoliti, K., Wang, Q. E., Goetz, C. G., Leurgans, S., &
Raman, R. (2000). Effects of central dopaminergic
stimulation by apomorphine on speech in Parkinson’s
disease. Neurology, 54, 458–462.
Kondziolka, D., Bonaroti, E., Baser, S., Brandt, F., Kim,
Y. S., & Lunsford, L. D. (1999). Outcomes after stereotac-
tically guided pallidotomy for advanced Parkinson’s
disease. Journal of Neurosurgery, 90, 197–202.
Kuchta, J., Reuter, B., Kurthen, M., Kohler, W., &
Linke, D. B. (1997). Magnetic stimulation of the speech-
associated areas in the brain [translation of German
original]. EEG-EMG Zeitshrift fur Elektroenzephalo-
graphie und Verwandte Gebiete, 28, 164–166.
Lalonde, R., & Botez, M. I. (1990). The cerebellum and
learning processes in animals. Brain Research Reviews,
15, 325–332.
Lampl, Y., Steinmetz, A., Gilad, R., Eshel, Y., Chamovitz,
D., & Sarova-Pinhas, I. (1997). Anterior operculum
syndrome localized by SPECT. Journal of Nuclear
Medicine, 38, 1122–1124.
Lang, A. E. (2000). Surgery for Parkinson disease. Archives
of Neurology, 57, 1118–1124.
Leanderson, R. Meyerson, B., & Persson, A. (1972). Lip
muscle function in parkinsonian dysarthria. Acta Oto-
laryngologica, 73, 1–8.
Lechtenberg, R., & Gilman, S. (1978). Speech disorders in
cerebellar disease. Annals of Neurology, 3, 285–290.
Lefkowitz, D., & Netsell, R. (1994). Correlation of clinical
Downloaded From: http://jslhr.pubs.asha.org/ by Raymond Kent on 03/30/2014
deficits with anatomical lesions: Post-traumatic speech
disorders and MRI. Journal of Medical Speech-Language
Pathology, 1, 1–15.
Liepert, J., Wessel, K., Schwenkreis, P., Trillenberg, P.,
Otto, V., Vorgerd, M., Malin, J. P., & Tegenthoff, M.
(1998). Reduced intracortical facilitation in patients with
cerebellar degeneration. Acta Neurologica Scandinavica,
98, 318–323.
Liotti, M., Vogel, D., New P., Ramig, L., Mayberg, H. S.,
Cook, C. I., & Fox, P. T. (1999). A PET study of func-
tional reorganizaton of premotor regions in Parkinson’s
disease following Intensive Speech and Voice Treatment
(ISVT). Neurology, 52(Suppl. 2), 4.
Lotze, M., Seggewies, G., Erb, M., Grodd, W., &
Birbaumer, N. (2000). The representation of articulation
in the primary sensorimotor cortex. Neuroreport, 11,
2985–2989.
Lundin-Olsson, L., Nyberg, L., & Gustafson, Y. (1997).
“Stops walking when talking” as a predictor of falls in
elderly people. Lancet, 349, 617.
Marie, R. M., Rossa, Y., Lambert, J., Verard, L.,
Marchal, G., & Viader, F. (1998). Ataxic hemiparesis
with cerebellous dysarthria due to an opercular lesion
[translation of French original]. Revue Neurologique, 154,
28–34.
Martinez-Martin, P., Valldeoriola, F., Molinnevo, J. L.,
Nobbe, F. A., Rumia, J., &Tolosa, E. (2000). Pallidotomy
and quality of life in patients with Parkinson’s disease: An
early study. Movement Disorders, 15, 65–70.
Metter, E. J., & Hanson, W. R. (1991). Dysarthria in
progressive supranuclear palsy. In C. A. Moore, K. M.
Yorkston, & D. R. Beukelman (Eds.), Dysarthria and
apraxia of speech: Perspectives on management (pp. 127–
136). Baltimore: Paul H. Brookes.
Michelucci, R., Valzania, F., Passarelli, D., Santangelo,
M., Rizzi, R., Buzzi, A. M., Tempestini, A., & Tassinari,
C. A. (1994). Rapid-rate transcranial magnetic stimulation
and hemispheric language dominance: Usefulness and
safety in epilepsy. Neurology, 44, 1697–1700.
Mills, C. K., & Weisenburg, T. H. (1914). Cerebellar
symptoms and cerebellar localization. Journal of the
American Medical Association, 63, 1813–1818.
Muelbacher, W., Artner, C., & Mamoli, B. (1998). Motor
evoked potentials in unilateral lingual paralysis after
monohemispheric ischaemia. Journal of Neurology,
Neurosurgery, and Psychiatry, 65, 755–761.
Murdoch, B. E., Thompson, E. C., & Stokes, P. D. (1994).
Phonatory and laryngeal dysfunction following upper
motor neuron vascular lesions. Journal of Medical Speech-
Language Pathology, 2, 177–189.
Nagaratnam, N., McNeil, C., & Gilhotra, J. S. (1999).
Akinetic mutism and mixed transcortical aphasia follow-
ing left thalamo-mesencephalic infarction. Journal of the
Neurological Sciences, 163, 70–73.
Nisipeanu, P., & Inzelberg, R. (1997). Falls in elderly
people. Lancet, 349, 1180.
Obwegeser, A. A., Uitti, R. J., Turk, M. F., Strongosky,
A. J., & Wharen, R. E. (2000). Thalamic stimulation for
the treatment of midline tremors in essential tremor.
Neurology, 54, 2342–2344.
Kent et al.: Clinicoanatomic Studies in Dysarthria 549
 Okuda, B., Kawabata, K., Tachibana, H., & Sugita, M.
(1999). Cerebral blood flow in pure dysarthria: Role of
frontal cortical hypoperfusion. Stroke, 30, 109–113.
Orefice, G., Fragassi, N. A., Lanzillo, R., Castellano, A.,
& Grossi, D. (1999). Transient muteness followed by
dysarthria in patients with pontomesencephalic stroke:
Report of two cases. Cerebrovascular Diseases, 9, 124–126.
O’Shanick, G. J. (1997). Image on progressive dysarthria
[letter]. American Journal of Psychiatry, 154, 584–585.
Ozaki, I., Baba, M., Narita, S., Matsunaga, M., &
Takebe, K. (1986). Pure dysarthria due to anterior
internal capsule and/or corona radiata infarction: A report
of five cases. Journal of Neurology, Neurosurgery, &
Psychiatry, 49, 1435–1437.
Pahwa, R., Lyons, K. L., Wilkinson, S. B., Carpenter, M.
A., Troster, A. I., Searl, J. P., Overman, J., Pickering,
S., & Koller, W. C. (1999). Bilateral thalamic stimulation
for the treatment of essential tremor. Neurology, 53, 1447–
1450.
Pascual-Leone, A., Gates, J. R., & Dhuna, A. (1991).
Induction of speech arrest and counting errors with rapid-
rate transcranial magnetic stimulation. Neurology, 41,
697–702.
Poluha, P. C., Teulings, H. L., & Brookshire, R. H.
(1998). Handwriting and speech changes across the
levodopa cycle in Parkinson’s disease. Acta Psychologica,
100, 71–84.
Raethjen, J., Lindemann, M., Schmaljohann, H.,
Wenzelburger, R., Pfister, G., & Deuschl, G. (2000).
Multiple oscillators are causing parkinsonian and
essential tremor. Movement Disorders, 15, 84–94.
Robertson, L. T., & Hammerstad, J. P. (1996). Jaw
movement dysfunction related to Parkinson’s disease and
partially modified by levodopa. Journal of Neurology,
Neurosurgery, and Psychiatry, 60, 41–50.
Ryglewicz, D., Baranska-Gieruszczak, M., Mendel, T.,
Poniatowska, R., & Kozlowski, P. (1997). Lacunar
strokes: Clinical conditions vs. localization of lesions in
neuroimaging studies [translation of Polish original].
Neurologia i Neurochirurgia Polska, 31, 437–446.
Santens, P., Van Borsel, J., Foncke, E., Meire, V.,
Merkx, H., De Bleecker, J., & De Reuck, J. (1999).
Progressive dysarthria: Case reports and a review of the
literature. Dementia & Geriatric Cognitive Disorders, 10,
231–236.
Schonewille, W. J., Tuhrim, S., Singer, M. B., & Atlas, S.
W. (1999). Diffusion-weighted MRI in acute lacunar
syndromes: A clinical-radiological correlation study.
Stroke, 30, 2066–2069.
Schrag, A., Samuel, M., Caputo, E., Scaravilli, T.,
Troyer, M., Marsden, C. D., Thomas, D. G. T., Lees, A.
J., Brooks, D. J., & Quinn, N. P. (1999). Unilateral
pallidotomy for Parkinson’s disease: Results after more
than 1 year. Journal of Neurology, Neurosurgery &
Psychiatry, 67, 511–517.
Schulz, G. M., & Grant, M. K. (2000). Effects of speech
therapy and pharmacologic and surgical treatments on
voice and speech in Parkinson’s disease: A review of the
literature. Journal of Communication Disorders, 33, 59–88.
Schulz, G. M., Peterson, T., Sapienza, C. M., Greer, M.,
550 Journal of Speech, Language, and Hearing Research • Vol. 44 • 535–551 • June 2001
Downloaded From: http://jslhr.pubs.asha.org/ by Raymond Kent on 03/30/2014
& Friedman, W. (1999). Voice and speech characteristics
of persons with Parkinson’s disease pre- and post-
pallidotomy surgery: Preliminary findings. Journal of
Speech, Language, and Hearing Research, 42, 1176–1194.
Scott, R., Gregory, R., Hines, N., Carroll, C., Hyman, N.,
Papanasstasiou, V., Leather, C., Rowe, J., Silburn, P.,
& Aziz, T. (1998). Neuropsychological, neurological and
functional outcome following pallidotomy for Parkinson’s
disease: A consecutive series of eight simultaneous
bilateral and twelve unilateral procedures. Brain, 121,
659–675.
Selnes, O. A., Holcomb, H. H., & Gordon, B. (1997).
Image on progressive dysarthria: Reply. American Journal
of Psychiatry, 154, 585.
Shima, F., Ishido, K., Sun, S. J., Machi, T., Kamikaseda,
K., Fukui, M., & Kato, M. (1996). Surgical control of
akinesia in Parkinson’s disease. European Neurology, 36,
55–61.
Shinotoh, H., & Calne, D. B. (1995). The use of PET in
Parkinson’s disease. Brain and Cognition, 28, 297–310.
Solomon, N. P., McKee, A. S., Larson, K. J., Nawrocki,
M. D., Tuite, P. J., Eriksen, S., Low, W. C., & Maxwell,
R. E. (2000). Effects of pallidal stimulation on speech in
three men with severe Parkinson’s disease. American
Journal of Speech-Language Pathology, 9, 241–256.
Stangel, M., Stapf, C., & Marx, P. (1999). Presentation
and prognosis of bilateral infarcts in the territory of the
superior cerebellar artery. Cerebrovascular Diseases, 9,
328–333.
Stebbins, G. T., & Goetz, C. G. (1998). Factor structure of
the Unified Parkinson’s Disease Rating Scale: Motor
examination section. Movement Disorders, 13, 633–636.
Takahashi, S., Satoh, N., Takahashi, H., Chiba, K., &
Tohgi, H. (1995). Dysarthria due to small cerebral
infarction: The localization of lesion and clinical charac-
teristics [translation of Japanese original]. Rinsho
Shinkeigaku, 35, 352–357.
Taha, J. M., Janszen, M. A., & Favre, J. (1999). Thalamic
deep brain stimulation for the treatment of head, voice,
and bilateral limb tremor. Journal of Neurosurgery, 91,
68–72.
Tasker, R. B. (1998). Deep brain stimulation is preferable to
thalamotomy for tremor suppression. Surgical Neurology,
49, 145–153.
Terao, S., Mirua, N., Takeda, A., Takahashi, A.,
Mitusima, T., & Subue, G. (2000). Course and distribu-
tion of facial corticobulbar tract fibres in the lower brain
stem. Journal of Neurology, Neurology, and Psychiatry, 69,
262–265.
Terry, J. B., & Rosenberg, R. N. (1995). Frontal lobe
ataxia. Surgical Neurology, 44, 583–588.
Timmann, D., Kolb, F. P., & Diener, H. C. (1999). Patho-
physiology of cerebellar ataxia [translation of German
original]. Klinische Neurophysiologie, 30, 128–144.
Theodoris, D. G., Ward, E. C., Murdoch, B. E., Silburn,
P., & Lethlean, J. (2000). The impact of pallidotomy on
motor speech function in Parkinson disease. Journal of
Medical Speech-Language Pathology, 8, 315–322.
Tohgi, H., Takahashi, S., Takahashi, H., Tamura, K., &
Yonezawa, H. (1996). The side and somatotopical location
 of single small infarcts in the corona radiata and pontine
base in relation to contralateral limb paresis and dysar-
thria. European Neurology, 36, 338–342.
Tonkonagy, J., & Goodglass, H. (1981). Language
function, foot of the third frontal gyrus, and rolandic
operculum. Archives of Neurology, 38, 486–490.
Topper, R., Mottaghy, F. M., Brugmann, M., Noth, J., &
Huber, W. (1998). Facilitation of picture naming by focal
transcranial magnetic stimulation of Wernicke’s area.
Experimental Brain Research, 121, 371–378.
Turgut, M. (1998). Transient “cerebellar” mutism. Childs
Nervous System, 14, 161–166.
Tyrrell, P. J., Kartsounis, L. D., Frackowiak, R. S.,
Findley, L. J., & Rossor, M. N. (1995). Progressive loss
of speech output and orofacial dyspraxia associated with
frontal lobe hypometabolism. Journal of Neurology,
Neurosurgery & Psychiatry, 54, 351–357.
Uitti, R. J., Wharen, R. E., Duffy, J. R., Lucas, J. A.,
Schneider, S. L., Rippeth, J. D., Wszolek, Z. K.,
Obweger, A. A., Turk, M. F., & Atkinson, E. J. (2000).
Unilateral pallidotomy for Parkinson’s disease: Speech,
motor, and neuropsychological outcome measurements.
Parkinsonism & Related Disorders, 6, 133–143.
Urban, P. P., Hopf, H. C., Fleischer, X., Zorowka, P. G.,
& Mullerforell, W. (1997). Impaired cortico-bulbar tract
function in dysarthria due to hemispheric stroke: Func-
tional testing using transcranial magnetic stimulation.
Brain, 120, 1077–1084.
Urban, P. P., Hopf, H. C., Visbeck, A., Fleischer, S., &
Andreas, J. (1996). Dysarthria–clumsy hand syndrome
due to infarction of the cerebral peduncle. Journal of
Neurology, Neurosurgery & Psychiatry, 60, 231–232.
Urban, P. P., Hopf, H. C., Zorowka, P. G., Fleischer, S.,
& Andreas, J. (1996). Dysarthria and lucunar stroke:
Pathophysiologic aspects. Neurology, 47, 1135–1141.
Urban, P. P., Vogt, T., & Hopf, H. C. (1998). Corticobulbar
tract involvement in amyotrophic lateral sclerosis: A
transcranial magnetic stimulation study. Brain, 121,
1099–108.
DownloadedViewFrom:
publicationhttp://jslhr.pubs.asha.org/
stats by Raymond Kent on 03/30/2014
Urban, P. P., Wicht, S., Hopf, H. C., Fleischer, S., &
Nickel, O. (1999). Isolated dysarthria due to extra-
cerebellar lacunar stroke: A central monoparesis of the
tongue. Journal of Neurology, Neurosurgery, & Psychiatry,
66, 495–501.
Ure, J., Faccio, E., Videla, H., Caccuri, R., Giudice, F.,
Ollari, J., & Diez, M. (1998). Akinetic mutism: A report of
three cases. Acta Neurologica Scandinavica, 98, 439–444.
Volkow, N. D., Fowler, J. S., Gatley, S. J., Logan, J.,
Wang, G. J., Ding, Y. S., & Dewey, S. (1996). PET
evaluation of the dopamine system of the human brain.
Journal of Nuclear Medicine, 37, 1242–1256.
Wang, E., Kompoliti, K., Jiang, J., & Goetz, C. G. (2000).
An instrumental analysis of laryngeal responses to
apomorphine stimulation in Parkinson’s disease. Journal
of Medical Speech-Language Pathology, 8, 175–186.
Wang, Q. E., Kompoliti, K., Jiang, J. J., & Goetz, C. G.
(1999). Effects of central dopaminergic stimulation by
apomorphine on vocal parameters in Parkinson’s disease.
In J. J. Ohala, Y. Hasegawa, M. Ohala, D. Granville, & A.
C. Bailey (Eds.), Proceedings of the XIVth International
Congress of Phonetic Sciences (pp. 1349–1352). Stockholm:
International Congress of Phonetic Sciences.
Zakzanis, K. K. (1999). The neuropsychological signature of
primary progressive aphasia. Brain & Language, 70, 70–85.
Zirh, A., Reich, S. G., Dougherty, P. M., & Lenz, F. A.
(1999). Stereotaxic thalamotomy in the treatment of
essential tremor of the upper extremity: Reassessment
including a blinded measure of outcome. Journal of
Neurology, Neurosurgery, & Psychiatry, 66, 772–775.
Received May 31, 2000
Accepted January 29, 2001
DOI: 10.1044/1092-4388(2001/042)
Contact author: Ray D. Kent, PhD, Waisman Center Room
435, University of Wisconsin–Madison, 1500 Highland
Avenue, Madison, WI 53705-2280.
Email: kentray@waisman.wisc.edu
Kent et al.: Clinicoanatomic Studies in Dysarthria 551