Neuroscience and Behavioral Physiology, Vol. 40, No.

6, 2010

Speech Disorders in Right-Hemisphere Stroke

G. M. Dyukova,1 Zh. M. Glozman,2 E. Yu. Titova,3

E. S. Kriushev,4 and A. A. Gamaleya5

Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Stroke, Vol. 109, No. 5 (part II),
pp. 11–21, May, 2009.

Clinical practice shows that right-hemisphere cerebral strokes are often accompanied by one speech dis-
order or another. The aim of the present work was to analyze published data addressing speech disorders
in right-sided strokes. Questions of the lateralization of speech functions are discussed, with particular ref-
erence to the role of the right hemisphere in speech activity and the structure of speech pathology in right-
hemisphere foci. Clinical variants of speech disorders, such as aphasia, dysprosody, dysarthria, mutism,
and stutter are discussed in detail. Types of speech disorders are also discussed, along with the possible
mechanisms of their formation depending on the locations of lesions in the axis of the brain (cortex, sub-
cortical structures, stem, cerebellum) and focus size.

KEY WORDS: speech function lateralization, speech disorders, right-sided strokes.

At the first stage of examination of a patient with
stroke, the neurologist has to determine not only the etiolo-
gy of the stroke, but also the question of the topical diagno-
sis of the focal brain lesion. One of the first questions is that
of the lateralization of the stroke. The main criteria for iden-
tifying the lesioned side is usually the presence or absence
of speech disorders and the side of the sensorimotor defect
affecting the limbs and face. As a rule, in left-hemisphere
strokes, particularly in the acute stage, the right-sided limb
deficit is combined with speech disturbances, though the
neurologist is not infrequently faced with the situation in
which one or another speech disorder is combined with
motor or sensory abnormalities in the left limbs. In this sit-
uation, the type of speech disturbance and its location along
the brain axis (cortex, subcortical structures, stem, cerebel-
lum) are particularly important. The diagnosis of acute
cerebrovascular lesions has now been significantly simpli-
1 Department
of Nervous Diseases, Sechenov Moscow
Medical Academy; e-mail: gdiukova@mtu-net.ru.
2 Faculty of Psychology, Lomonosov Moscow State University.
3 Clinical Hospital No. 83.
4 State Scientific Center for Medical-Biological Problems,
Russian Academy of Sciences.
5 Department of Neurology, Russian Postgraduate Medical
Academy, Moscow.
593
0097-0549/10/4006-0593 ©2010 Springer Science+Business Media, Inc.
fied by the introduction of neuroimaging methods into neu-
rological practice. However, cases of speech disorders in
right-hemisphere strokes, their causes and clinical features,
and the associated questions of the lateralization of speech
functions continue to be discussed and this question is very
relevant in theoretical and practical neurology.
Existing clinical observations have provided grounds
for some re-examination of the stringent theory of the later-
alization of brain functions and have provided deeper
insights into the organization of speech functions and the
structure of speech pathology.
The aim of the present work was to analyze published
data addressing speech disorders in right-hemisphere strokes
with assessment of the locations and sizes of focal brain
lesions, types of speech disorders, and the possible mecha-
nisms of their formation.
The following clinical variants of speech disorders are
recognized in neurological practice: aphasia, dysprosody,
dysarthria, mutism, and stutter [1]. In this context, we will
consider their appearance in right-hemisphere cerebrovas-
cular lesions.
Speech functions and their lateralization. The role of the
right hemisphere in speech activity. The functions of speech
are to encode thoughts and feelings in the form of language,
and to translate external utterances and incoming informa-
tion into mental concepts [2]. Four main speech modalities
594
are distinguished – impressive speech, oral (expressive)
speech, reading, and writing. Impressive speech includes
perception, understanding of oral speech, and its retention
in operative memory. Oral (expressive) speech consists of
the formation and expression of thoughts and feelings in the
form of spoken grammatically and lexically correct words,
phrases, and texts, along with the ability to repeat foreign
speech and names of objects. Reading is the visual percep-
tion and understanding of text. Writing is the formulation
and expression of thoughts and feelings by means of writ-
ing words and phrases [3]. Each of these speech modalities
is a complex functional system consisting of a multiplicity
of components supported by the operation and interaction
of different brain areas. Lesioning of any brain area impairs
the functional system as a whole, i.e., all its modalities
are impaired (to different extents and with qualitative speci-
ficity) [4, 5].
Speech functions, like other mental functions, are
characterized by hemisphere asymmetry and interhemi-
sphere interactions [2]. During early childhood, the hemi-
spheres are equipotent in relation to speech. Specialization
of the hemispheres starts during the second year of life,
after which there is a gradual increase in interhemisphere
asymmetry, which reaches its greatest extent by adulthood,
gradually fading out with further aging [5, 6].
Development of lateralization of individual mental
functions to one hemisphere leads to reciprocal inhibition of
the areas of the other hemisphere linked with this function,
i.e., so-called “tonic inhibition” by the other hemisphere.
This reciprocity implies suppression rather than elimination
of functions (which is important in relation to the rehabili-
tation of impaired functions).
There are several methods for determining the func-
tional asymmetry of speech functions [7]. The methods
used are dichotic listening and object naming with separate
visual stimulation of the visual field. Patients with transec-
tion of the corpus callosum or hemispherectomy have pre-
viously provided a good model for studies of the speech
functions of each hemisphere. The Wada test consists of
sequential chemical “exclusion” of the hemispheres by
administration of short-acting barbiturates into the carotid
arteries [8]. In addition, CT scanning has been used to
assess the sizes of the brain lobes, including the size of the
“temporal area” [3]. Hemisphere dominance is now identi-
fied and speech functions are located using functional neu-
roimaging studies: fMRI, single-photon emission computed
tomography (SPECT), positron emission tomography
(PET), and transcranial Doppler scanning, which allow
assessment of speech-related changes in cerebral blood
flow and metabolism in the hemispheres.
Numerous clinical observations and studies have
demonstrated that the left hemisphere is dominant for speech
in most people [2, 3]. Only 1–2% of people have right-hemi-
sphere speech dominance. The functional asymmetry of the
hemispheres is not global in nature, but is partial and dynam-
Dyukova, Glozman, et al.
ic [9]. Thus, the involvement of the right hemisphere in
speech processes increases in left-hemisphere epileptic
seizures and during recovery after left-hemisphere strokes.
It is often said that there is a relationship between the
location of brain speech areas and right- or left-handedness
[10]. In the European population, “pure” right-handers
account for about 40% of the total population, 50–55%
being ambidextrous, i.e., to some degree left-handed, and
4.5–10% being “pure” left-handers [11]. Among right-han-
ders, 90–96% show left-hemisphere speech dominance [7].
The question of speech representation in left-handers ini-
tially evoked strong controversy. However, the suggestion
that hemisphere specialization in left-handers was the mir-
ror image of that in right-handers and that the right hemi-
sphere was dominant in speech did not receive support. It is
now accepted that about 76% of left-handers also have
speech representation on the left, while of the remaining
24%, about 14% have bilateral speech representation, with
the right hemisphere being dominant in 10%. Overall, right
hemisphere speech dominance is much rarer than left-hand-
edness. At the same time, the probability of right-sided
speech dominance is much higher in left-handers than in
right-handers.
Apart from left-handers and those with a genetic pre-
disposition, atypical speech lateralization is also influenced
by factors such as lesions to the left hemisphere of the brain
at the embryonic or early childhood stages of development,
which leads to a shift in dominance towards the structural-
ly unharmed right hemisphere [12]. Displacement of the
cerebral mechanisms of speech to the other hemisphere
may not be identical for speech and the hands. Social and
cultural factors such as illiteracy, the use of tonal languages,
and hieroglyphic writing also play some role in the incom-
plete lateralization of speech with a predominance of right-
hemisphere dominance [9].
Left-hemisphere speech functions in right-handers
have been well studied, as lesions produce profound and
distinct speech disorders [4, 13]. Less obvious is the
involvement of the right hemisphere in speech processes,
though sufficient data have now been accumulated regard-
ing its contribution to speech-thought activity.
The main speech functions of the right hemisphere in
right-handers can be identified [3, 14]: regulation, percep-
tion, and production of the intonation-melodic aspect of
speech, which emphasizes and colors the sense of an ora-
tion, the global perception of the schemes of texts, pictures,
and life situations, the global understanding of gestures and
expressions as components of verbal communication, the
operation of speech automatism and stock phrases, the
global perception and reproduction of the sound images of
words, and the storage of speech automatisms, which are
not subject to deconstruction into sound units, in memory.
Thus, right-hemisphere speech production is ordered
in nature and is manifest as prepared formulas, in contrast
to left-hemisphere speech, with is actively constructed by
Speech Disorders in Right-Hemisphere Stroke
speakers in accordance with the ongoing situation. Speech
produced by the right hemisphere is characterized by being
involuntary and is controlled by the left hemisphere. The
right hemisphere is also involved in the processes of speech
perception and is responsible for recognition of the seman-
tic categories of words and the differentiation of words of
foreign and mother tongues [14, 15].
Dominance of the right hemisphere in the perception
and realization of speech prosody, i.e., the component of
speech characterized by its melody, intonation, and emo-
tional tone, is widely recognized [16].
Aphasia is a systematic disorder affecting all speech
processes in organic brain lesions and is combined with
defects to other mental functions and personality in patients;
it impairs patients’ ability to communicate [17]. Aphasia is
characterized by impairments to all speech modalities of dif-
ferent severities. The functions of the peripheral articulatory
apparatus and hearing are generally preserved.
Different authors have provided different descriptions
of aphasic syndromes [1, 3, 4, 7, 13, 17–20] and the task of
producing a coherent classification remains. However,
Luriya [4] has proposed identification of the following
clinical variants of aphasia, reflecting the interaction of
the main mechanisms underlying speech disorders and the
locations of focal lesions:
1. Motor efferent (kinetic) aphasia is characterized by
impairments to all types of expressive speech due to the lack
of timely substitution of innervation supporting the rapid
and smooth switching from one speech element to the next,
with preservation of the reproduction of individual elements
of articulation and phonematic hearing. Speech is slowed,
has few words, is poorly articulated, and shows literal para-
phasia (sound substitutions), perseveration, and agramma-
tism. Impressive speech and intellectual processes are just
as deautonomized. This type of aphasia results from lesions
to the anterior parts of the speech zones of the brain, i.e., the
inferior parts of the premotor area or Broca’s area.
2. Motor afferent (kinesthetic) aphasia is characterized
by derangement of all components of expressive speech,
i.e., difficulty in constructing elements of articulation. The
articulation of sounds which have similar sites or means of
formation is particularly severely affected; literal parapha-
sia and oral searching (searching for articulatory postures)
are also seen. This type of dysphasia is associated with
lesions to the inferior parts of the parietal cortex adjacent to
the postcentral gyrus, supporting the kinesthetic basis of the
movements of the articulatory apparatus. Oral apraxia, i.e.,
the inability to perform speech movements spontaneously,
is often seen in afferent motor aphasia syndrome.
3. Dynamic aphasia consists of impairment to the plan-
ning and programming of orations and the inability to for-
mulate thoughts as sentences. Sharp reductions in speech
initiatives and decreases in the fluency of speech are seen.
Associative processes are profoundly affected, while repeti-
tion and writing to dictation are preserved. This type of
595
aphasia occurs in lesions to the posterofrontal areas of the
brain anterior to Broca’s area.
4. Conduction aphasia, which is interpreted as a spe-
cific variant of afferent motor aphasia in left-handers [3],
involves an uncoupling of the centers for impressive and
expressive speech. Spontaneous, situation-related speech is
relatively preserved; repetition, naming, and reading aloud
are impaired. This type of aphasia occurs in lesions to the
white matter of the posterior areas of the parietal lobe at the
junction with the temporal lobe.
5. Sensory aphasia (Wernicke’s aphasia, acoustic-
gnostic aphasia) consists of impairments to phonematic
hearing, i.e., the ability to extract and discriminate the
meaning-distinguishing features of speech sounds, resulting
in alienation of the meanings of words. The understanding
of oral and written speech is severely compromised; speech
remains fluent and rapid (to the extent of logorrhea), though
all meaning is lost; there are many literal paraphasias, par-
asite words, pseudoneologisms, and random words (“word
salad”). This occurs as a result of lesions to the posterior
third of the superior temporal gyrus (Wernicke’s zone).
6. Acoustic-mnestic aphasia is characterized by nar-
rowing of the volume of acoustic perception and verbal
memory and instability of name retention, resulting in
defects in word understanding and object naming. This type
of aphasia is associated with lesions to the central part of
the temporal gyrus, i.e., the extranuclear zone of the audito-
ry analyzer. The affected cortical zones are also connected
to the visual analyzer, so patients often experience difficul-
ties in naming objects and events and finding the right word
and its image (optical-mnestic aphasia). Some authors com-
bine acoustic-mnestic and optical-mnestic aphasia under
the term amnestic aphasia.
7. Semantic aphasia leads to impairments to the under-
standing of complex speech, where the meaning of each
word depends on its relationships with other words, along
with lack of understanding and confusion in the patient’s
own speech of particular logical-grammatical structures,
prepositions, conjunctions, and other components express-
ing temporal and spatial relationships in language. This
type of aphasia develops in lesions of the parietal-temporal-
occipital parts of the brain.
8. Total (global, sensorimotor) aphasia, with loss of or
severe impairment to both impressive and expressive speech
in all its manifestations. This occurs in extensive lesions in
the basin of middle cerebral artery affecting the pos-
terofrontal and temporal areas.
9. Subcortical aphasia is characterized by impairments
to prosody and the smoothness of speech. It is described in
lesions of the deep structures of both hemispheres – capsu-
lostriate structures, the periventricular white matter, and the
thalamus [3].
Considering only the dynamic characteristics of speech,
the non-Russian literature [21] divides all aphasias into
smooth (fluent) aphasia and non-smooth (non-fluent) types.
596
Examination of patients with aphasia requires detailed
assessment of the main functions of speech, i.e., auditory
perception and speech understanding functions, production
of spontaneous, automated speech, word and sentence repe-
tition, and object naming, as well as the presence of aphasias
or paraphasias (substitution or transposition of letters, sylla-
bles, and words), perseveration (repetition of letters, sylla-
bles, and words), the ability to read and understand texts,
spontaneous writing, copying, and writing to dictation.
There is a series of special unified scales and tests for iden-
tifying types of aphasic disorders [4, 22].
The timely correlation of brain lesions and speech disor-
ders is important. Aphasia in the early period (acute aphasia)
can often be more severe than expected from the lesion itself,
because of delayed suppression of speech functions at later
stages (chronic aphasia), when aphasia, conversely, becomes
less severe because of functional compensation. Thus, the
most appropriate time for investigation is the period from the
third week to the third month from the moment of the vascu-
lar accident,, the so-called “focal lesion phase” [23].
The types of aphasia described above generally occur
after lesions of the corresponding areas of the left hemi-
sphere. Data from various sources [3, 23] show that lesions
to the right hemisphere produce aphasia in 25% of left-han-
ders and 2–5% of right-handers.
Crossed aphasia (CA). Aphasia occurring in right-han-
ders with lesions to the right hemisphere has been termed
crossed aphasia. This is a rare and interesting neurobiolog-
ical phenomenon supporting the hypothesis that brain func-
tions are organized as systems, with consideration of their
lateralization [22–25]. CA has been defined by various
authors using different combinations of diagnostic criteria.
Marien et al. [21] proposed a classification of CA with iden-
tification of unlikely, possible, and probable cases of CA.
Possible CA is diagnosed when the following criteria are
fulfilled: presence of a focal lesion only in the right hemi-
sphere with the left hemisphere structurally intact; the pres-
ence of aphasia; and confirmed right-handedness (from
birth, not due to retraining at school or physical trauma to
the left hand). Cases of CA not satisfying these criteria are
assessed as unlikely. Probable cases are those in which
there is no history of references to left-handedness or
ambidextrousness in the family and there is no indication of
brain damage during the neonatal or postnatal periods and
no indications of epileptic seizures in childhood; there are
also no non-biological factors which might influence the
functional organization of the brain (including lateralization
of speech functions), such as illiteracy, speaking of two or
more languages, us of a tonal language or hieroglyphic
writing [26].
Two main types of CA can be distinguished [23]. First
is the so-called “mirror reflection” type, encountered in
about 70% of cases of CA. In these cases, lesion foci in the
right hemisphere are located in the standard, typical areas
corresponding to left hemisphere lesions in patients with
Dyukova, Glozman, et al.
analogous types of aphasia. Second are cases with atypical
locations of speech functions, which account for 30% of
cases of CA. Lesion foci are seen in locations other than the
expected right-hemisphere locations. Cases of atypical
locations are almost always characterized by moderate
speech deficit, even when there are extensive lesions in the
area of the sylvian sulcus. Alexander and Annett [27] pro-
posed that this anomaly resulted from the non-correspon-
dence of the lateralization of the phonological and semantic
speech systems associated with the atypical lateralization of
all cognitive functions in a small population of people.
These authors suggested the “right-shift” theory, whereby a
particular gene (rs+) is responsible for asymmetry in the
modal organization of brain functions. If the rs+ gene is pre-
sent (more than 90% of cases), there is a predominant dis-
placement of the lateralization of functions to the right
hemisphere, these including speech functions, “handed-
ness,” and praxis. When the gene is absent (rs–), there is no
preference for lateralization and the organization of all lat-
eralized functions is defined by random developmental fac-
tors, which are independent for each modality. The result is
that all possible variants of the lateralization of brain func-
tions can occur [27].
Marien et al. [21] reported a detailed analysis of cases
of aphasia in right-handers occurring as a result of vascular
lesions to the right hemisphere (ischemic and hemorrhagic
strokes, ruptured aneurysms with parenchymal damage)
described in the literature from 1975 onwards. Of the 152
clinical cases considered, the criteria of probable CA were
met in 49 (32.2%) (of which 35 (71.4%) were men and 14
(28.6%) women, mean age was 60.2 years (from 32 to 80
years)). Correlations between the locations of lesions and
speech disorders could only be assessed when sufficient
data from neuropsychological evaluation and neuroimaging
(CT, MRI, surgery) were available, i.e., in 38 patients. The
severity of impairment to speech function was expressed on
a points scale (0–18) on the basis of language tests, whose
results defined mild (1–6 points), moderate (7–12 points),
and severe (13–18 points) aphasias. After systematic assess-
ment of aphasic syndromes, 26.5% of cases were classified
as Broca’s motor aphasia, 24.5% as Wernicke’s sensory
aphasia, 12.2% as global aphasia, 14.3% as conduction
aphasia, 14.3% as transcortical aphasia, 6.1% as amnestic
aphasia, and 2% as fluent-type atypical aphasia. The age
distributions of the different types of aphasia were not sig-
nificantly different. Oral speech and writing were impaired
to equal extents. Apart from aphasic disorders in a number
of these patients with CA, there was also a series of non-
verbal cognitive impairments, such as dysprosody, left spa-
tial neglect, constructive apraxia, ideatory and ideomotor
apraxia, and oral apraxia.
Thus, analysis of a group of patients with probable CA
occurring after strokes, selected on the basis of clear diag-
nostic criteria, led the authors of [21] to the conclusion that
CA differs from non-crossed aphasia (NCA) in terms of the
Speech Disorders in Right-Hemisphere Stroke
following aspects: CA is more frequently encountered
among men than women; the relative incidence of clinical
variants of CA is independent of age; quite severe impair-
ments to writing are often seen. There are also similarities.
Thus, contrary to previous opinion, CA is rarely transient,
and recovery of speech functions is not guaranteed even with
the passage of time. Nonverbal psychological impairments
in CA can include both dysfunctions of the subdominant
type (spatial neglect) and dysfunctions of the dominant type
(apraxia), as well as impairments to other, less lateralized
functions (constructive apraxia, acalculia).
Subcortical CA in lesions of the deep structures of the
right hemisphere occurs very rarely and its mechanism is
very poorly understood. It has been suggested that cortico-
striato-pallido-thalamo-cortical pathways play a significant
role in normal speech activity, performing and reprocessing
semantic material. Damage to these pathways, as well as
compression of surrounding cortical structures, can there-
fore lead to aphasic disorders [28]. The case described by
the authors showed global aphasia in the presence of a
lesion mainly to the putamen extending to the periventricu-
lar white matter of the right hemisphere.
Diaschisis plays a particular role in the formation of
CA, particularly in the acute phase of stroke [29]. Diaschisis
is the functional inactivation of parts of the brain from the
focus of the primary structural lesion, with functional
changes in cerebral metabolism. There is no ischemia,
edema, or any other structural change in the distant location,
and the reduction in metabolism occurs because of interrup-
tion of neuronal connections and loss of afferent spike activ-
ity from the area containing the focus. The state of brain
metabolism and the cerebral circulation are closely related,
so diaschisis can be detected using functional neuroimaging
methods such as SPECT and PET [30, 31]. In stroke, diaschi-
sis is most often encountered in the cerebellum on the side
contralateral to supratentorial damage (crossed diaschisis),
and is essentially proportional to the extent of damage to the
pyramidal tract. Cortical diaschisis arising in small, deep,
subcortical lesions and infarcts in strategically important
zones (for example, the thalamus) has been described [32].
The role of diaschisis in the mechanisms forming
speech disorders has been discussed in the literature. Bakar
and Kirshner [29] described three patients with CA (all
right-handers). The neurological status of these patients
included left-sided hemiparesis and speech disorder: two
patients had total aphasia and one had Broca’s motor apha-
sia. In all cases, CT scans confirmed lesions to the right
hemisphere with no foci in the left hemisphere. Functional
neuroimaging by SPECT (or PET) during the acute phase of
stroke showed extensive zones of hypoperfusion or
hypometabolism in the right hemisphere, as well as the ini-
tial signs of decreased perfusion and metabolism in the left
hemisphere. Investigation of one of the patients at two
months on the background of improvements in clinical
symptomatology demonstrated no signs of diaschisis. Thus,
597
functional suppression of an anatomically undamaged left
hemisphere was observed in these patients with CA during
the acute stage of stroke, but was absent at the recovery
stage. Diaschisis showed rapid recovery. Other investigators
showed that this was not always the case and that recovery
did not occur by six months after stroke. This may be asso-
ciated with the development of irreversible structural
changes such as transneuronal degeneration, which is not
included in the definition of diaschisis but is quite difficult
to distinguish from it in terms of functional neuroimaging
data [30].
Overall, it can be concluded that CA is not a homoge-
neous syndrome characterized by good recovery. CA, like,
NCA, is composed of a variety of syndromes. From the
clinical-anatomical point of view, CA cannot be regarded as
a mirror analog of aphasic disorders occurring in left-hemi-
sphere foci. Various and sometimes incomplete dissociative
intra- and interhemisphere combinations of symptoms are
seen significantly more often in CA than in NCA [22, 25].
However, there is at present no single theory providing a
complete explanation of the characteristic impairment to
speech functions in CA.
Dysprosody. While aphasia is quite rare in right-sided
strokes, disorders to the emotional components of speech,
i.e., prosody and emotional gesticulation, are seen in many
patients. This in turn supports the view that the right hemi-
sphere has a leading role in supporting these speech com-
ponents [16, 33, 34].
Dysprosody refers to impairments in speech pitch and
melody. Speech loses its intonational expressiveness,
becoming monotonous, colorless, and dull, and it acquires
a nasal tone. The ability to understand and transmit the
meaning of verbal intonation is lost. The interpretation
of complex non-speech sounds is lost (auditory agnosia)
and patients become unable to recognize melodies, male
and female voices, and familiar noises (auditory image per-
ception is impaired). Dysprosody (aprosody) is generally
the main characteristic of speech in patients with damage
to the right hemisphere [26].
Impairments to prosody and gesturing are evaluated in
spontaneous speech, with assessment of the ability to repeat
different components of prosody and to understand prosody
on hearing, and assessment of visual understanding of emo-
tional gesticulations [16].
Ten right-handed patients with ischemic strokes in the
right hemisphere, accompanied by impairments to prosody
in the form of speech drabness, monotony, and disappear-
ance of emotional coloration, were studied [16]. Speech in
some patients was described as indistinct and unintelligible,
similar to the speech of patients with dysarthria. These
patients showed impairments to spontaneous gesticulation.
Understanding of prosody and gestures was preserved in five
patients. One patient showed dissociation between under-
standing of prosody and gestures: impairments to the under-
standing of prosody were accompanied by preservation of
598
gesture recognition. Behavioral changes were also seen:
although patients retained the ability to laugh and cry, these
emotions were pathological, not corresponding to the con-
text and not controlled by the patient (exaggerated laughter
and crying). However, impairments to emotional prosody
could be seen to different extents both in patients with emo-
tional-mental disorders (depression) and without these con-
ditions. Strokes in these patients were located in the basin of
the right middle cerebral artery, with involvement of the syl-
vian sulcus area, with lesions to the inferior parts of the
frontal lobe or anteroinferior parts of the parietal lobe. Two
patients had subcortical foci with lesions to the basal ganglia
and white matter. Thus, all the patients in the study with
right hemisphere lesions were unable to produce the emo-
tional component of prosody, while some patients were
unable to discriminate the emotional tones of speech.
Weintraub et al. [33] investigated nine right-handed
patients with unilateral right-hemisphere strokes without
aphasic disorders. Patients were asked to perform a series of
tasks to verify their ability to discriminate stress in words
and sentences, as well as the ability to repeat and voluntari-
ly produce stress and intonation. This group of patients made
errors in all the tasks, while the control group of healthy sub-
jects made only occasional mistakes. These observations led
to the conclusion that there was a more generalized impair-
ment to prosody in right-sided lesions, including disorders
of the non-emotional components of prosody. The results of
this study were subsequently confirmed in larger cohorts of
patients [35–37].
Furthermore, it was proposed that the functional-
anatomical organization of prosody in the right hemisphere
is the same as the organization of logical language in the
left hemisphere, with the suggestion that impairments to
prosody should be assessed analogously to the assessment
of aphasia, identifying motor, sensory, total, amnestic, and
transcortical types of dysprosody [16, 35]. However, this
hypothesis has yet to receive definitive support [38].
Blonder et al. [39] compared the ability to produce
spontaneous emotional speech in patients with left-hemi-
sphere and right-hemisphere strokes. Their observations
showed that patients with right-hemisphere lesions smiled
and laughed significantly more rarely, though their speech
contained significantly more emotional words. Impairments
to prosody were rare in patients with left-hemisphere
strokes. The authors of [37] concluded that impairments to
emotional prosody and mimicry of expressions in right-
sided strokes were not associated with a cognitive deficit or
the inability to experience emotions, but represented a spe-
cific impairment to the ability to encode nonverbal infor-
mation. It remains uncertain whether the ability to recog-
nize emotions depending on their modality or the type of
emotions is impaired.
Dysarthria is a speech disorder associated with impair-
ments to the intelligibility, smoothness, loudness, and clar-
ity of articulations. Dysarthria involves impairment to the
Dyukova, Glozman, et al.
ability to reproduce various physical, tonal, and sound fea-
tures of speech sounds in oral speech; unintelligible and
slurred articulation with swallowing of sounds is character-
istic. Articulatory movements and speech are slow, patients
complain of the sensations of a “thick” tongue and “porridge”
in the mouth. Patients’ phrases are constructed correctly,
vocabulary is not affected, and the grammatical structure of
words is not impaired. Reading, writing, internal speech,
and understanding of speech are preserved [7, 40].
Several types of dysarthria have been discriminated on
the basis of the locations of lesions [41]. Bulbar dysarthria
occurs in lesions of the cranial nerve nuclei, when it is com-
bined with dysphagia and dysphonia, along with atrophy of
half of the tongue, loss of tongue tone, and loss of the glottal
reflex. Pseudobulbar dysarthria occurs in lesions of the cor-
ticonuclear pathways, predominantly the corticosublingual
and corticofacial pathways, and can be combined with dys-
phonia, dysphagia, oral automatism reflexes, and increased
tongue tone. Cerebellar dysphagia occurs in lesions of the
cerebellum and corticocerebellar connections and is charac-
terized by ataxia, impairments to speech fluidity, and jerky
pronunciation of words.
Dysarthria can be seen in lacunar syndromes, such as
“dysarthria – clumsy hand,” “dysarthria – motor hemipare-
sis,” “isolated dysarthria,” “dysarthria – facial nerve palsy,”
and “dysarthria – face and tongue palsy” syndromes
[42–44]. In addition, some authors use a classification of
dysarthrias based on analysis of the movements and impair-
ments of the tone of the affected muscles (flaccid, spastic,
ataxic, hypokinetic, hyperkinetic, and mixed types) [40].
Different types of dysarthria can impair articulation, reso-
nance, phonation, respiration, and speech melody to differ-
ent extents.
Strokes in the right hemisphere (in the basin of the right
middle cerebral artery) most commonly lead to mild
dysarthria, transient in nature, because of the bilateral inner-
vation of the bulbar musculature. Cases in which left-sided
hemiparesis is accompanied by severe dysarthria produce
diagnostic difficulties and are often suggested to involve an
additional stroke in the brainstem or contralateral (left) cor-
tex. However, this clinical picture can in fact occur after sin-
gle right-hemisphere strokes.
Ropper [45] described 10 patients (nine right-handed
and one ambidextrous) with acute right-hemisphere strokes
with no lesions in other brain areas, accompanied by severe
dysarthria inconsistent with the dysarthria of lacunar syn-
dromes. The patients were investigated during the three
weeks following stroke. The clearest features of dysarthria
were: slowness, incomplete pronunciation of syllables, inar-
ticulate, monotonous speech, hypophonia, and dysprosody,
and some similarity with cerebellar dysarthria. Most patients
showed weakness of the orofacial musculature, along with
hemiparesis of different severities. There were no aphasic
disorders. CT scans demonstrated right-hemisphere lesions,
mainly superficial, in the frontal lobe (the basin of the supe-
Speech Disorders in Right-Hemisphere Stroke
rior frontal branch of the right middle cerebral artery) in five
cases, three patients having more extensive foci in the basin
of the right middle cerebral artery and two having deep
infarcts in the semioval center and a large lacuna in the inter-
nal capsule. Dysarthria improved slowly over periods of 1–3
weeks. These observations led Ropper to suggest that damage
to the connections between the cerebellum and right hemi-
sphere play a role in the mechanisms of dysarthria, altering
the influences of the right (non-dominant) hemisphere on the
cerebellar speech modulation system.
Ichikawa and Kageyama [43] and Urban et al. [46, 47]
observed patients with dysarthria of different severities aris-
ing in lacunar syndrome. In fifteen of the 35 patients (43%),
lacunae were located in the right hemisphere, mainly in the
internal capsule (the genu or posterior limb) and corona radi-
ata. One case had a lesion to the lower parts of the motor
cortex. The characteristics of dysarthria in these patients
were comparable regardless of lesion location. Recovery
was seen over 2–4 months.
Urban et al. [47, 48] sought better understanding of the
mechanisms producing dysarthria using transcranial mag-
netic stimulation (TCMS) and SPECT. The authors con-
firmed the role of the corticobulbar tract, sensory afferent
fibers, and the cortico-ponto-cerebellar tract in dysarthria.
TCMS demonstrated that lesions of the central sublingual
and orofacial motor pathways were more significant in pro-
ducing non-cerebellar dysarthria. More prolonged dysarthria
could occur in central unilateral lesions of the sublingual
system, unlike unilateral peripheral lesions (where articula-
tory deficits disappeared within a few days). Its cause could
only be conjectured. It may be that in unilateral peripheral
damage to the sublingual system, pathological tongue
movements are quickly compensated for by central mecha-
nisms, while these mechanisms may be damaged in central
lesions. Another possibility is that unilateral damage to the
central corticosublingual pathway leads to imprecise tongue
movements or concentrates movement on one side because
of imbalanced muscle tone. It was suggested that strokes in
the area of the corona radiata might lead to simultaneous
damage to the corticobulbar pathway and the pathways
from the corpus callosum to the contralateral hemisphere
which conduct information relating to speech motor func-
tion [49]. It is also likely that there is individual variation in
the proportions of crossing and non-crossing corticonuclear
pathways. The literature also contains discussions of the
role of diaschisis [30], including cerebellar, in the mecha-
nisms producing dysarthria in unilateral hemisphere
strokes. Damage to the cortico-ponto-cerebellar tract rostral
to the pontine nuclei may lead to contralateral cerebellar
diaschisis, while damage distal to the crossover leads to
ipsilateral diaschisis.
Urban et al. [50] conducted a prospective study of
speech characteristics in dysarthria, taking cognizance of
lesion lateralization. A total of 62 patients were studied in
the acute stage of stroke with dysarthria and MRI-con-
599
firmed single non-extensive foci. Articulation, phonation,
prosody, and the overall severity of dysarthria were
assessed separately. These studies showed that dysarthria in
extracerebellar strokes occurred more often in left-sided
lesions (89.5% versus 10.5%), but was more common in
cerebellar strokes when lesions were on the right side
(77.7% versus 22.3%). No relationship was found with the
patient’s right- or left-handedness. In right-sided strokes,
dysarthria was less severe than in left-sided strokes, regard-
less of the topography of foci. Articulation was more
severely affected in left-sided foci, which supports the clear
hemisphere lateralization of speech motor control. Overall,
the severity of dysarthria in unilateral stroke (both right-
and left-hemisphere) varied from mild to moderate, severe
dysarthria being apparent only in rare cases. Most cases
showed virtually complete recovery over 1–4 months,
though mild dysarthria could persist.
Mutism is the loss of the ability to vocalize, a type of
speech disorder in which the patient does not speak and
does not respond to questions, but retains consciousness
and the ability to produce written speech [51]. The patient
does not have aphasia, and only sometimes is transient
mutism seen in the acute stage of motor or global aphasia.
In CNS lesions, mutism results from impairments to the
facial, vocal, lingual, and/or respiratory movements respon-
sible for sound production and is most commonly seen in
lesions of the speech-dominant hemisphere. Mutism associ-
ated with unilateral cortical lesions is usually transient;
decreased phonation only affects verbal vocalizations and is
characterized by preserved or even excessive nonverbal
vocalizations (cries), and paresis of voluntary mimicking
movements with preservation of emotional movements.
Focal lesions of different locations in the limbic system
(temporal lobe, thalamus, subthalamic area) also degrade or
eliminate vocalization. This mainly affects emotional
phonation and emotional mimicking expressions, while vol-
untary mimicking remains intact (unlike pseudobulbar pare-
sis). More profound deterioration of phonation, combined
with a generalized reduction in motor activity, is encoun-
tered in akinetic mutism – a state in which all vocalization
and spontaneous movement are lost, other than gaze fixa-
tion and tracking.
Mutism occurs most frequently in multi-infarct states,
bilateral lesions affecting the anterior parts of the cingulate
gyrus, adjacent to the third ventricle, anterior to the limb of
the internal capsule, and the mesodiencephalic area.
However, it can also occur in unilateral infarcts involving
the parietal lobe and caudate nucleus or on occlusion of the
recurrent artery of Huebner [44]. In addition, mutism has
been described in large lesions of the anterior lobes extend-
ing to the putamen, which corresponds to the anatomy of
Broca’s aphasia and transcortical aphasia.
Although unilateral lesions of the right hemisphere can
also lead to various cognitive and behavioral abnormalities,
the occurrence of mutism in these lesions is very rare.
600
Chaudhuri et al. [52] described a patient with left-
sided paresis of the facial musculature and hand monopare-
sis accompanied by mutism. Understanding of heard speech
was preserved. MRI scans demonstrated a stroke in the right
parietal lobe affecting cortical and subcortical structures.
On further observation, recovery of speech was precipitate
and complete, without any residual dysarthria. The authors
explained this rare case by suggesting a diaschisis effect or
impairment to the modulation of left hemisphere function
resulting from the right-sided stroke.
Berthier et al. Described another case [53]. This was a
right-handed patient with mutism, multimodal neglect syn-
drome, oral apraxia, and ideomotor apraxia of the right hand
developing suddenly as a result of an acute cerebrovascular
accident in the right hemisphere. Pathological anatomical
investigation revealed a focus of ischemic stroke involving
the whole of the right insula, the adjacent white matter, and
the inner cortical surface of the right fronto-temporo-parietal
operculum, with sparing of the left hemisphere.
Thus, the literature contains only rare cases of mutism
in right-hemisphere stroke. The clinical-anatomical charac-
teristics of mutism require further study.
Stutter. There are two types of acquired neurogenic
impairments of speech fluency: cortical stutter and palilalia.
Stutter is a defect of diction with involuntary repetition and
lengthening of sounds and syllables, difficulty in pronounc-
ing them, and pauses and spasms of speech [54, 55].
Palilalia is the involuntary repetition of words and phrases,
primarily associated with bilateral lesions of the frontal
lobes or basal ganglia. Transient stutter is usually combined
with lesions of expressive speech (aphasia). It is possible
that these cases do not involve true stutter, but the persever-
ation of efferent motor aphasia, which is reminiscent of
stutter. Stable impairments to speech fluency without other
speech impairments are quite rare.
Acquired stutter has been described in strokes in both
the dominant and non-dominant hemispheres; it can occur
in lesions of all lobes of the brain, as well as in subcortical
lesions [56–58]. The variety of possible lesion sites sup-
ports the view that stutter is not a specific symptom of focal
brain dysfunction. Its particular neuronal mechanisms
remain unclear. On the background of existing predisposi-
tion to stutter, stroke may be the decisive factor leading to
the recurrence of childhood stutter completely overcome
during adulthood.
The clinical features of acquired stutter are quite diverse
and depend to a large extent on the brain areas involved.
However, a series of common characteristic features can be
seen with foci in different locations. Repetition in acquired
stutter can affect any part of a word, be it mono- or poly-
syllabic, and any part of a sentence; there is no adaptation
effect (i.e., improvement of repetition) and no suppression
during singing, reading of verses, etc. Furthermore, there is
no synkinesis in the movements of the lips, tongue, eyelids,
brows, body, arms, or legs and there are no concomitant
Dyukova, Glozman, et al.
vasomotor manifestations (sweating, erythema, pallor);
there is no impairment to social intercourse, the patient may
be irritated, but is not embarrassed [56]. All these points
raise doubts that the cases described can in fact be inter-
preted as true stutter.
Although acquired stutter is most often seen in lesions
of the dominant (left) or both hemispheres, the literature
includes descriptions of patients with acquired stutter and
lesions in the right hemisphere [55, 59–61]. Ardila and
Lopez [55] noted that focal lesions of the right hemisphere
quite frequently lead to a mild tendency to repeat sounds
and syllables, simulating acquired stutter, though these
cases showed an association between the acquired stutter
and loss of verbal automatism and the stutter was interpret-
ed as deautomation of the flow of speech. Profound stutter
in the absence of other speech disorders in right hemisphere
lesions is rare.
Jorner and Massey [59] described a case of stutter
accompanied by a right hemisphere lesion in a right-handed
man aged 62 years. The stutter, interpreted as palilalia, was
combined with apraxia relating to dressing, constructive
apraxia, left-sided homonymous hemianopia, and central
paresis of the facial musculature. CT scans showed an exten-
sive stroke in the basin of the right middle cerebral artery.
Ardila and Lopez [55] reported a right-handed man of
50 years with a CT-demonstrated extensive lesion in the
right temporal lobe. Neurological status included left-sided
hemiparesis, apraxia of dressing, and the depersonalization
and déjà vu phenomena, as well as speech disorder in the
form of sound and syllable repetition during spontaneous
speech, repetition, and reading.
Soroker et al. [61] described a patient with stutter
developing after a limited subcortical stroke in the right
hemisphere. The patient was right-handed, and he had never
previously stuttered and no member of his family stuttered.
The authors suggested a possible mechanism for the devel-
opment of stutter in terms of damage to the pathways of the
corpus callosum, which coordinates the activity of the two
hemispheres in speech processes.
Thus, the question of differentiating stutter, persever-
ation, and deautomation of speech remains problematic
and the cerebral locations of these disorders requires fur-
ther study.
In conclusion, the following types of speech disorders
can be seen in patients with strokes causing lesions in the
right hemisphere. Dysprosody is the most common impair-
ment, associated with the leading role of the right hemi-
sphere in supporting prosody and the understanding and
reproduction of the emotional components of speech,
mimicry, and gesticulation. Dysarthria, from mild (in lacu-
nar strokes) to severe, results from lesions of the corticobul-
bar and cortico-ponto-cerebellar tracts and sensory afferent
fibers, and can also result from diaschisis. Aphasia is
explained by the partial or complete dominance of speech by
the right hemisphere occurring in some people because of
Speech Disorders in Right-Hemisphere Stroke
genetic factors (familial, partial, cryptic left-handedness,
constitutional predisposition), damage to the left hemisphere
in youth, and a number of social-cultural features. Speech
disorders in terms of clinical-topical interactions mainly cor-
respond to those in left-hemisphere strokes. In CA, there can
also be a link with atypical localization of speech functions
in the right hemisphere or a chaotic distribution of hemi-
sphere dominance for different components of speech.
Stutter in right-hemisphere strokes is described rarely, and is
usually associated with deautomation of the flow of speech
(so-called pseudostutter). Mutism can also occur.
Speech disorders arising in cerebrovascular lesions in
the right hemisphere currently remain an interesting clinical
neuropsychological phenomenon. Deeper understanding of
their pathophysiological mechanisms and neurolinguistic
characteristics will be of great value for neurologists seeking
optimum approaches to rehabilitating patients with speech
disorders. All these points generate the need for further
studies in this area using new methods applied to larger
groups of patients.
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