J Neurol (1993) 240 : 357-362

Journal of

Neurology
© Springer-Verlag t993

Dysarthria in bilateral thalamic infarction
A case study
Hermann Ackermann 1, Wolfram Ziegler 3, Dirk Petersen ~
1Neurologische Universitfitsklinik, Hoppe-Seyler-Strasse 3, W-7400 Tfibingen, Germany
2Abteilung Neuroradiologie, Radiologische Universit~itsklinik, Hoppe-Seyler-Strasse 3, W-7400 Ttibingen, Germany

3Entwicklungsgruppe Klinische Neuropsychologie, Abteilung Neuropsychologie, St~idtischesKrankenhaus Miinchen-Bogenhausen,
Englschalkinger Strasse 77, W-8000 M~inchen 81, Germany
Received: 5 June 1992 / Received in revised form: 12 October 1992 / Accepted: 2 November 1992

Abstract. A patient suffering from bilateral thalamic infarction in the region supplied by the paramedian arteries sparing the internal capsules underwent acoustic
analysis of sentence utterances. The results were compared with the findings obtained in parkinsonian subjects, in patients with upper motor neuron lesions, and
in normal subjects. Acoustic measurements revealed increased pitch, monotonous speech, rough voice quality,
and normal speech tempo concomitant with articulatory
impreciseness in terms of incomplete closure productions. This constellation resembled parkinsonian dysarthria. Damage to the thalamic projection area of the pallidal efferents, therefore, seems to be the most probable
cause of the patient's speech disorders. In parkinsonian
subjects stereotactieal lesions of this structure ameliorate
rigor, but not akinesia. Thus, our patient's speech deficits, and by analogy the corresponding parkinsonian
dysarthric disturbances, may be considered akinetic signs.
Key words: Thalamic dysarthria - Thalamic ischaemia Acoustic analysis

Introduction
Thalamic disorders may give rise to speech and language
deficits, as indicated by the verbal impairment following
natural or surgical lesions and by the effects of electrical
stimulation on linguistic abilities [10]. Whereas aphasic
disturbances have been studied in some detail, few data
are available so far concerning speech abnormalities due
to thalamic dysfunction [26].
With respect to electrical stimulation two findings
show some relevance of thalamic structures for speech
motor control. First, Mateer [43] noted articulatory distortions resulting in prolongation of speech utterances
during this procedure. Second, Guiot and coworkers
[29] observed decreased voice volume and articulatory
Correspondence to: H. Ackermann

inaccuracy concomitant with speech acceleration. So far
no more detailed analyses are available.
The sequelae of stereotactic thalamic surgery, most
often performed in parkinsonian patients, include slurred speech, decreased voice volume, whispering voice,
rapid speech rate, and dysfluencies [11, 53, 55]. Some
authors [41, 42] have maintained that the speech disturbances encountered as side effects of thalamotomy resemble dysarthria of Parkinson's disease (PD). However,
Bell [6] could not find any relationship between pre- and
postoperative speech deficits in PD subjects who underwent thalamic surgery and concluded that speech deterioration following surgical intervention results from
lesions of the internal capsules. The observation of suprabulbar signs in postoperative dysarthrias and pathologicanatomical data obtained in patients with postoperative
speech deficits are in agreement with this suggestion [15,
32]. Indeed, Samra and coworkers [54] have reported
persistent speech deviations following lesions restricted
to the ventrolateral nuclei. However, all these subjects
had suffered from speech disorders prior to surgery.
Thus, natural progression of PD might have contributed
to the aggravation of dysarthria and dysphonia months
to years after surgical intervention.
The following speech deficits have been observed in
natural thalamic lesions: slurred articulation [e.g., 12, 14,
22, 37, 39, 40, 57], characterized in one instance as undershooting of articulatory gestures [47], hypernasality
[14, 47], decreased and fading voice volume [e.g., 8, 9,
25, 27, 39, 48], whispering [24], low- or high-pitched
voice [37, 44, 45], hoarse voice quality [47], quivering
voice [45], and monotonous, aprosodic speech [e.g., 7,
27, 28, 44]. Moreover, reduced verbal spontaneity and
akinetic mutism, respectively [4, 13, 17, 19, 28, 33, 58],
modification of speech tempo [19, 20, 38, 44, 47], and
iterative phenomena like palilalia [46] were noted. However, no formal speech examinations and no parametric
studies have been performed so far.
The patients reported with speech deficits due to
natural thalamic lesions suffered - with a few exceptions
- from a contra- or bilateral pyramidal syndrome as far

358
as o n e can j u d g e f r o m the clinical data provided. Since
l a c u n a r c a p s u l a r infarcts can give rise to d y s a r t h r i a [5,
21, 35], a c o n t r i b u t i o n of capsular i n v o l v e m e n t to the observed speech m o t o r d y s f u n c t i o n s m u s t b e c o n s i d e r e d in
these subjects.
F u r t h e r e l u c i d a t i o n of t h a l a m i c speech deficits thus
r e q u i r e s i n v e s t i g a t i o n of p a t i e n t s with lesions restricted
to the t h a l a m u s . T h e p r e s e n t study was of a dysarthric
p a t i e n t suffering f r o m bilateral t h a l a m i c i n f a r c t i o n sparing the i n t e r n a l capsules. T h e p a t i e n t ' s speech was subm i t t e d to acoustic analysis and, o n the basis of these
data, c o m p a r e d with spastic dysarthrics a n d p a r k i n s o n i a n
subjects as well as n o r m a l s .

Patients and methods
Case report
Three days after surgical intervention for total hip replacement the
64-year-old woman became somnolent. Apart from coxarthrosis,
the past medical history was unremarkable. After she had regained
alertness the neurological examination revealed complete gaze
paresis upwards, incomplete gaze paresis downwards, impaired
convergence, decreased voice volume concomitant with monotonous speech, dysphagia, and hypomimia. The patient presented
with incomplete orientation in time and space and appeared to
lack spontaneity. Voluntary innervation of the orofacial as well as
the limb muscles was intact, tendon reflexes, plantar reflexes, sensory functions and coordination being normal. Otolaryngological
investigation gave no indication of vocal fold paresis.
At the time of detailed neuropsychological assessment and
speech evaluation, 7 months after disease onset, both vertical gaze
paresis and the lack of spontaneity had improved. The remaining
clinical findings were unchanged. Magnetic resonance imaging
(MRI) showed bilateral postischaemic lesions in the anterior half
of the thalamus (Fig. l). On both sides the infarction extended
from the medial to the ventrolateral and ventroanterior nuclei,
sparing the internal capsules.
Recordings of somatosensory evoked potentials after electrical
stimulation of the median and tibial nerves as well as brain-stem
auditory-evoked potentials yielded normal latency and amplitude
values. Electro-oculography showed no pathological nystagmus.
In spontaneous speech the patient's voice showed decreased
volume, high pitch, and rough and breathy voice quality. Voice
fading could frequently be observed. Her utterances sounded
monotonous. Production of consonants was characterized by in~
complete closures. The patient spoke at a normal rate.
Neuropsychological assessment included measurements of IQ,
attentional abilities, so-called frontal lobe functions, and various
declarative and procedural memory functions. In short, the patient
displayed normal IQ and attention, but severe deficits in delayed
recall of both verbal and visuospatial material. Procedural learning
was preserved,
Formal language testing (Aachener Aphasie Test [34]) disclosed no aphasic deficits: The results of the Token Test were within the normal range. Spontaneous speech showed correct syntax
and included no phonemic paraphasias, semantic paraphasias or
word-finding difficulties. Repetition, confrontation naming, writing and comprehension of both auditory and written stimuli were
intact.

were recruited as controls. The acoustic data from these groups
have been published in part elsewhere [2, 59].

Acoustic speech evaluation
Sentences of the form "Ich babe/geCVCe/gehOrt" ("I have heard...")
were used as speech material. By substituting the consonants/p/,
/t/,/k/for C and the long vowels/i/,/y/,/u/,/a/for V the formula
/geCVCe/ allowed the derivation of 12 target words: "gepipe",
"gepype", "gepupe", "gepape", "getite", "getyte', "getute" etc.
The resulting 12 test sentences, e.g. Ich habe gepipe gehOrt", with
the syllable CV bearing the sentence accent, were presented twice
by the examiner in randomized order and had to be repeated by
the subject. Thus, 24 sentence utterances couId be obtained. Since
the target words represent regular phonological forms of standard
German, the test sentences approximate natural speech demands.
Recordings were made in a sound-attenuated booth using highquality equipment. Speech signals were digitized at a sampling rate
of 20 kHz after low-pass filtering at 9 kHz and were fed into a LSI
11/73 for further processing (see [2, 59, 60]).
For each sentence utterance the speech wave envelope (sound
pressure level (SPL) contour) was calculated in order to obtain
parameters of articulatory accuracy (articulatory precision) and
speech tempo. The rise-fall patterns of the SPL contours reflect
the sequence of opening and closing gestures required for the production of the four syllables/be/,/ge/,/CV/, and/Ce/of the test
sentences. As an example, Fig. 2 shows the SPL contour of the test
sentence "Ich habe gepipe gehOrt". The period between two successive intensity troughs was considered an index of syllable
length, Fig, 2 indicates the so-defined durations of the syllables
/be/, /ge/, /pi/, a n d / p e / b y vertical bars. As a measure of speech
tempo the mean duration of these four syllables was determined
for each test sentence and the median value across the 24 productions of a subject was computed (mean syllable duration = MSD).
Complete closure of the vocal tract as required for the production of voiceless stop consonants results in an interruption of sound
emission from the mouth with a concomitant decrease of sound intensity to the level of tape noise. During incomplete closure due to
"undershooting" of mandibular, labial, or lingual movements or
due to weakness of the corresponding muscles, respectively, acoustic engery is still emitted from the mouth at the time of stop consonsant production giving rise to increased SPL. Thus, the minimum amplitude of the intensity contour between two syllabic peaks,
i.e. at the time points indicated by vertical bars in Fig. 2, was calculated (sound intensity during closure = IDC). This measure may be
considered to reflect the degree of articulatory undershooting or of
muscle weakness, respectively.
In addition, the fundamental frequency (Fo) contour of the
vocalic part of each of the five syllables/ha/,/ge/,/CV/,/Ce/, and
/h6rt/of the sentenceutterances were calculated. Fo represents the
frequency of vocal fold vibrations and provides, thus, an objective
measure of pitch. For each subject the mean fundamental frequency of the 24 test sentence utterances and the vocal fitter, i.e.
the cycle-to-cycle variation of Fo, were computed, the latter being
an index of vocal roughness [30]. Moreover, the Fo &fference between the stressed (CV) and the unstressed syllable (Ce) of the
target words each provides a measure of speech monotony. In accordance with psychoacoustic standards Fo was transferred into a
logarithmic measure, i.e. semitones relative to an arbitrary value
of 50 Hz, to account for inter-individualpitch differences. Finally,
the energy spectrum of the vowel of the target word was computed.
An increased drop in harmonic energy from the first to the second
harmonic in the voice spectrum can be considered an acoustic correlate of perceived weak and breathy voice.

Control groups
Twenty patients with idiopathic PD (14 men, 6 women; age 47-81
years), 12 patients with spastic dysarthria following uni- or bilateral lesions of the upper motor neuron due to closed head trauma
or cerebrovascular accident (11 men, i woman; age 21-62 years),
and 30 normal speakers (16 men, 14 women; age 1%64 years)

Results
T h e acoustic data s u b s t a n t i a t e d the p e r c e p t u a l features
of o u r p a t i e n t ' s speech deficits. H e r m e a n Fo a m o u n t e d

359

Fig.la-f. Magnetic resonance images showing bilateral ischaemic
lesions extending from the medial parts of the thalamus to the
ventrolateral and ventroanterior nuclei: a - c Tl-weighted (TR/TE:
600/15 ms) axial, contiguous 4 mm slices; d-f T2-weighted axial (d)
and coronal (e-f) scans (TR/TE: 2100/90 ms)

~"

70
Ich

ha

be

I

>
(D

ge

I

pi

I

pe

ge

hOrt

I I

03

35
to
0J
O_
Z3
c-

to 270 Hz, a value considerably above the normal range
as reported in the literature [51 ] or as obtained in our
group of healthy female controls (median: 197 Hz, range:
171-227 Hz). In addition, vocal jitter was markedly increased relative to the group of normals (0.42; normal
median value: 0.19, normal range: 0.13-0.26), confirming rough voice quality in our patient. F u r t h e r m o r e , an
overly large drop of harmonic energy from the first to
the second harmonic in the voice spectrum could be
noted (20 dB; normal median value: 11 dB, normal range:
6-16 dB), which m a y be considered a correlate of the
patient's weak and breathy voice. The Fo contours calculated over whole-sentence frames showed a reduction
in stress-related Fo variation, reflecting the m o n o t o n o u s
quality of speech (0.6 semitones on average; normal me-

8

0
0

I
100

I
300

I
500

[
700

I
900

I
1100

I
1300

I
1500

Time (ms)

Fig. 2. Sound pressure level (SPL) contour of the test sentence "Ich
habe gepipe gehOrt" spoken by the thalamic patient. The syllabic
boundaries are indicated by vertical lines. Intensity during closure
was determined as the sound intensity emitted during stop consonant
production, i.e. as the SPL at the indicated syllable boundaries

dian value: 3.2 semitones, normal range: 1.8-4.8 semitones).
A fairly consistent increase of the radiated acoustic
energy during stop closure could be noted across the 24
sentence productions. These findings indicate undershoot-

360
5O
~"
40
-0

°o° I

.Q
3o

.

O

o\O./..

c~
20
c-o 10

-

O3
r"

0

[/j

~Y"

c-

V//////,,4

-10

• oXxO

~
30 normals (range)
o Parkinson patients (n = 20)
• Spastic dysarthrics (n = 12)
1

1O0

1000
log syllable duration (ms)

Fig. 3. Closure intensity (dB) and mean syllable duration (log ms)
of 20 parkinsonian subjects (open circles), 12 spastic dysarthrics
(filled circles), and the patient with bilateral thalamic infarction
(arrow). Bars indicate the normal range

ing of articulatory gestures or weakness of the corresponding muscles, respectively. Despite her severe dysarthric impairments the patient showed normal speech
rate. MSD amounted to 180ms, which is in the upper
half of the normal range. Fig. 3 demonstrates to what
extent the patient's articulatory performance resembled
parkinsonian dysarthria rather than the speech of the
upper motor neuron group. In the spastic dysarthrics
there was a clear correlation between slowness and articulatory imprecision. In contrast, the parkinsonian patients as well as the thalamic subject had incomplete closures in the presence of normal or even reduced syllable
durations.

Discussion

In a patient suffering from bilateral thalamic infarction
acoustic measurements documented normal speech rate
concomitant with articulatory impreciseness in terms of
incomplete stop consonant closures, monotonous speech,
high-pitched, breathy and weak voice, and rough voice
quality.
Principally, speech deficits associated with thalamic
lesions may be attributed to a dysfunction of the adjacent corticobulbar pathways. However, clinical, electrophysiological, and neuroradiological data gave no indications of an involvement of the internal capsules. Moreover, in patients with lesions of the upper motor neurons
articulatory inaccuracy was associated with slowed speech
whereas our patient showed normal speech tempo. Thus,
a significant contribution of corticobulbar disorders to
our patient's dysarthria can be ruled out.
Both the striato- and cerebellocortical projections incorporate thalamic structures. Conceivably, interruption
of these motor loops at the thalamic level might impair
speech functions. First, Schuster [56] has observed speech
disorders reminiscent of cerebellar dysarthria in a patient with thalamic softening. Furthermore, von Cramon
[16] has reported ataxic dysarthria in a subject with bilateral disruption of the cerebellothalamic pathways at the

mesodiencephalic level. Second, parkinsonian speech
signs have been noted after thalamic surgery [41, 42].
Normal speech rate concomitant with incomplete stop
consonant closures has been documented in parkinsonian
dysarthria [2]. In contrast, acoustic investigations of dysarthric deficits in cerebellar atrophy and Friedreich's
ataxia have revealed slowed speech in terms of prolonged
syllable and sentence durations [23, 36]. Thus, the normal speech rate of our patient argues against a dysarthria
of predominantly cerebellar origin. Moreover, decreased
voice volume and high-pitched voice are more typical for
PD than for cerebellar dysarthria [1, 3]. Thus, the parkinsonian-like perceptual and acoustic features of our
patient's dysarthria indicate damage to the thalamic region of the striatocortical loop. In parkinsonian patients
stereotactic lesions of the anterior ventrolateral thalamic
region abolish rigor, but not akinesia of the speech motor system [31, 32, 49, 50]. The speech disturbances of
our patient, therefore, should reflect akinetic dysarthric
signs rather than deficits due to rigor.
Parkinsonian bradykinesia, i.e. slowing of movement,
may affect the speech motor system as well as the limbs
(see [2]). Conceivably, PD subjects manage normal syllabic rate in the presence of bradykinesia by undershooting of articulatory gestures, i.e. by reduced movement
amplitudes. Assuming a striatocortical dysfunction, the
articulatory disturbances of our patient might represent,
as suggested for PD dysarthria, a tradeoff between
speech tempo and movement excursion.
The neuroradiological data of the present study are
compatible with the suggestion of a striatocortical dysfunction. At both sides the lesions obviously involved
the ventrolateral and parts of the ventroanterior nuclei
representing the major projection area of the pallidal efferents at the thalamic level. Moreover, the distribution
of the ischaemic lesions indicates infarction in the region
supplied by the paramedian thalamic arteries. In the anterior direction this area may vary considerably, depending upon the size of the polar thalamic artery [18]. Principally, however, ischaemia within the region of blood
supply of the paramedian thalamic arteries can extend to
the anterior ventrolateral and ventroanterior nuclei.
Often the paramedian arteries of both sides arise from a
common branch of the basilar communicating artery,
which may explain the bilateral distribution of the infarction [52].
Speech deficits similar to those reported here have
also been observed in subjects with unilateral left-sided
thalamic haemorrhage [4]. Thus, bilateral damage does
not seem to be a prerequisite for the speech impairments
observed in our patient. Conceivably, bilateral lesions
result in more severe and more enduring deficits. It is
well known that the risks of persistent speech impairments are higher following bilateral than after unilateral
thalamotomy [53]. Moreover, the transient character of
the speech abnormalities after unilateral thalamic haemorrhages [4] supports this suggestion.
In summary, our results show that thalamic lesions
may result in a parkinsonian-like dysarthria probably representing akinetic signs due to damage to the projection
area of the pallidal efferents.

361

Acknowledgements. This work was supported by the Bundesministerium gir Forschung und Technologie (01KL9001). We thank D.
von Cramon, M~,inchen, und J.Dichgans, Ttibingen, for helpful
comments.

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