Sensory Aprosodia With Left Hemiparesis From
Subcortical Infarction
Right Hemisphere Analogue of Sensory-Type Aphasia
With Right Hemiparesis?
Gil I. Wolfe, Elliott D. Ross, MD

\s=b\ We report a case of sensory aprosodia with left hemiparesis following an
ischemic infarction of the right thalamus
and posterior limb of the internal capsule.
Bedside evaluation, confirmed by special
quantitative tests, demonstrated normal
spontaneous affective prosody and gesturing with marked impairment of affective repetition and comprehension of
affective prosody and gestures. A left
hemiparesis with sensory loss was also
present. This combination of deficits
appears to represent the right-side analog
to the unusual syndrome of Wernicketype aphasia with right hemiparesis occasionally observed following left subcortical injury, thus providing further support
for the hypothesis that the functionalanatomic organization of affective language in the right hemisphere mirrors that
of propositional language in the left.
(Arch Neurol 1987;44:668-671)

U ecent and compelling evidence has
demonstrated that lesions involv¬

ing the right hemisphere may com¬
promise the affective components of
language, while leaving the propositional intact.14 Thus, the concept of
"language" being a dominant function
of the left hemisphere is no longer
tenable. Rather, the propositional ele¬
ments of language are a dominant
function of the left hemisphere, while
Accepted for publication Jan 26, 1987.
From the Departments of Neurology (Mr
Wolfe and Dr Ross) and Psychiatry (Dr Ross),
University of Texas Health Science Center at
Dallas.

Reprint requests to Department of Neurology,
University of Texas Health Science Center,
5323 Harry Hines Blvd, Dallas, TX 75235 (Dr
Ross).

the affective elements of language are
probably a dominant function of the
right hemisphere. Evaluation of clini¬
cal material and cerebral blood flow
maps also suggests that the function¬
al-anatomic organization of the affec¬
tive components of language in the
right hemisphere—encompassing af¬
fective prosody and emotional gestur¬
ing—is homologous to the organiza¬
tion of propositional language in the
left hemisphere.1·2·58 Therefore, disor¬
ders of affective language, called
aprosodias,' can be classified by the
same specific modifiers used in apha¬
sia terminology, eg, motor, global, and
transcortical sensory. Furthermore,
recovery patterns from affective defi¬
cits following right hemisphere injury
also appear to mimic recovery pat¬
terns from propositional deficits fol¬
lowing left hemisphere injury.6
The right hemisphere analogy also
extends to the role of subcortical
structures in language. Numerous
investigators have documented apha¬
sialike syndromes in patients with
lesions involving the left thalamus920
or left internal capsule and stri¬
atum2125; likewise, there have been
scattered reports of aprosodia follow¬
ing subcortical injury.1·8·26 Although
subcortical aphasias share many fea¬
tures with the traditional cortical
syndromes, atypical combinations of
deficits can be observed. For instance,
a right hemiparesis associated with a
sensory-type aphasia may be encoun¬
tered from a lesion involving the left
thalamus or striatum and posterior
limb of the internal capsule1417·21·22·25
but, to our knowledge, has not been
described from a predominantly corti¬
cal lesion. By sensory-type aphasias,

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we refer to disorders

characterized by

impaired comprehension with fluent
but paraphasic speech. Since repeti¬
tion of propositional language is pre¬
served in most reported cases of sub¬
cortical sensory-type aphasia,14'15·18·27
the overall clinical presentation sug¬
gests a transcortical syndrome. How¬

occasional reports have docu¬
mented subcortical sensory-type
aphasias that are more Wernickelike,15·21·22 ie, with impaired repetition.
Unlike the cortical aphasie syn¬
dromes, comprehension and repeti¬
tion deficits in the subcortical cases
tend to be moderate and usually show
good recovery. In this article, we
report the first case of the right hemi¬
sphere analogue of sensory-type
aphasia with hemiparesis—sensory
aprosodia with left hemiparesis.
ever,

REPORT OF A CASE
A 49-year-old, left-handed woman was
admitted to Parkland Memorial Hospital,
Dallas, after sudden onset of a flaccid left
hemiplegia with dysarthria. Her medical
history was remarkable for obesity, hyper¬
tension, and adult-onset diabetes. The

patient was alert, oriented to time, person,
and place, and had no aphasie deficits
except for mild anomia.
Within ten days, the patient showed a
predilection upper motor-neuron pattern
of weakness with spasticity in the left
lower extremity. There was little motor
recovery in the left arm. Facial movements

bilaterally. Marked hemianesthesia was present over the entire left side,
including face and torso, to pin and tem¬
perature. Graphesthesia and position
sense were severely compromised in the
left hand. Hemianopsia was not present,
even on double simultaneous stimulation
of the visual fields.
The patient's speech was normally fluent

were full

without paraphasias. There was a mild
anomia for parts of objects, which resolved

rapidly during hospitalization. Compre¬
hension and repetition of propositional
language were completely intact. Sponta¬
neous affective prosody and gesturing
involving the face and right limbs were
normal, but affective-prosodie repetition
was extremely poor; the patient's voice was
flat and monotonie in stark contrast to her
spontaneous affective prosody. Likewise,
auditory comprehension of affective proso¬
dy was severely impaired. The patient was
unable to identify sadness, happiness,
boredom, anger, surprise, or neutral on
formal testing and could not visually dis¬
cern various facial emotions when "panto¬
mimed" by the examiner. These findings
were consistent with the syndrome of sen¬
sory aprosodia.1

The patient was discharged on the 17th
hospital day and reexamined four weeks
later. A predilection pattern of weakness
was still present in the left lower extremi¬
ty. Limited movement was possible in the
proximal left upper extremity, but the
forearm and hand remained paralyzed. In
the left leg there was greater motor activi¬
ty distally than proximally. Facial move¬
ments were intact. Pin and temperature
sensations were still impaired over the left
extremities and torso, but no longer
involved the left side of the face. Graphesthesia and position sense were now intact
on the left side, and stereognosis was un¬
impaired if the examiner manually
assisted the patient in palpating objects
that were placed in her left hand.
The patient's propositional language
was fully normal. Bedside assessment of
affective language confirmed the persis¬
tence of a sensory aprosodia. In addition,
special tests were conducted to quantify
the patient's deficits in processing affec¬
tive language.
SPECIAL TESTS

Spontaneous Affective Prosody
In nontonal languages such as
English, varying the fundamental fre¬
quency (Fo) and its harmonics during

voicing to produce intonational con¬
tours is probably the most important
acoustical parameter for imparting

affect into speech.28 The Fo variation
of the patient's spontaneous speech
was quantitatively measured on a
pitch analyzer (PM Pitch Analyzer,
Voice Identification Ine, Somerville,
NJ) using the procedure described by
Ross et al.29 When an utterance is
played into the input of the pitch
analyzer, a tracing of the Fo in hertz
and intensity in decibels over time is
displayed on a cathode-ray tube. By
using programmable cursors, the
means and SDs for the Fo and decibel
contours for an utterance can be mea¬
sured. With the aid of a computer

(PDP 11/23, Digital Ine, Maynard,
Mass), the means and SDs of ten
spontaneous utterances recorded dur¬

ing the interview were mathematical-

ly combined to give a grand mean and
SD. The coefficient of variation (CV)
of the grand mean was then calculated
and multiplied by 100 to obtain an
overall measurement of Fo variability
(Fo-CV%). The Fo-CV% score for
spontaneous speech was then com¬
pared with a value compiled previous¬
ly from six controls whose Fo-CV%

group mean was 17.0 ± 3.1 %.29 The

patient's Fo-CV% for spontaneous
speech was 16%, yielding a score of
—0.32 when compared with controls,
thereby substantiating that spontane¬
ous affective prosody, as measured by
Fo-CV%, was normal.
Affective-Prosodie Repetition

The Fo variation for repetition was
assessed with the sentence "I am
going to the other movies," using a
standard stimulus tape with six affec¬
tive tokens: neutral, happy, sad,
angry, bored, and surprised. The

patient was given two attempts at

each token. All 12 utterances were
analyzed on the pitch analyzer as out¬
lined above, and a grand mean FoCV% was calculated. The Fo-CV%
score for affective-prosodie repetition
compiled from six controls was 25.7 ±
4.0% ,29 The patient's Fo-CV% was
12%, yielding a score of -3.43. Fur¬
thermore, the patient's Fo-CV% did
not overlap with any control value
(range, 20% to 32%), thus substanti¬
ating marked impairment of affec¬

tive-prosodie repetition.

Auditory Comprehension of Affective
Prosody

Auditory comprehension involving

emotions was formally assessed with
the sentence "I am going to the other
movies," using a standard stimulus
tape containing the same six affective
tokens used in the repetition task.
Each token appeared twice in ran¬
domized order during the test. The
patient was asked to identify the
affect in each of the 12 tokens by
selecting the correct response from a
written list. Prior to testing, the
examiner coached the patient with the
list; no primary visual or reading def¬
icits were evident that could have
interfered with testing. Auditory
comprehension of affective prosody
was again found to be severely
impaired. The patient gave correct
responses on only two of 12 trials.
Normal performance based on 12 con¬
trols is 12 of 12 or occasionally 11 of 12
correct. Considering there were six
affects to choose from, the patient's
performance was at chance.
A second test was administered to
evaluate deficits in attitudinal com-

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prehension. The patient was asked to
classify 20 audio-taped stimuli that,
depending on their prosodie content,
could be interpreted literally or ironi¬
cally. For instance, the sentence "I
had a great day today" can be articu¬
lated using enthusiastic prosody,

which affirms the literal intent of the
statement, or using ironic prosody,
which implies an opposite intent.
Enthusiastic and ironic versions for
ten sentences were randomly pre¬
sented to the patient. After each stim¬
ulus, she was asked to respond "yes"
or "no" to a verbal question con¬
structed to discriminate the attitudinal intent of the sentence. For exam¬

ple, the stimulus "The weather is so
pleasant" was paired with the ques¬
tion "Is the weather nasty?" Prior to
formal testing, the task was explained
to the patient by coaching with sam¬
ple sentences and questions. The
patient correctly identified only 13 of

20 stimuli. Normal scores on this test
based on a control sample of 22 sub¬
jects are 20 of 20 (n 16) or 19 of 20
=

(n 6) correct. Thus, the patient's
performance was close to chance lev¬
els (10 of 20 correct), substantiating
that she had a profound deficit in
discriminating the attitudinal, in
addition to the emotional, aspects of
affective prosody.
=

Visual Comprehension of Emotional

Gesturing
Comprehension of gesturing was
tested by having the patient examine
six line drawings of faces depicting
the six emotions outlined above. She
was then asked to match, after initial
coaching, each of the six drawings
with the correct descriptor from a
written list that was also read aloud
to her. She failed to correctly identify
angry, neutral, surprised, and happy
but did identify sad and bored. This
performance, two of six correct, was
highly deviant, since normal subjects
(n 120) respond correctly 95 ±
5% of the time and never misidentify
happy (Y. W. Walston, MA, unpub¬
lished thesis, University of Texas
Health Science Center at Dallas,
=

1982).

Computed Tomographie (CT) Scans
A CT scan performed on the day of
admission showed a subtle hypodensity involving the right thalamus and
posterior limb of the internal capsule.
A second scan performed 6V2 weeks

poststroke delineated

an ischemie
infarction that involved the right
thalamus and extended into the poste¬
rior limb of the internal capsule (Fig¬
ure). In addition, a circumscribed

ongoing debate, we accept that sub¬
cortical lesions, in and of themselves,
can produce aphasie syndromes that
may have features not normally asso¬
ciated with the classic cortical aphasi¬
as. For example, in contrast to Broca's
aphasia, speech recovery from a sub¬
cortical motor-type aphasia is not
typically associated with telegraphic
speech,22 suggesting that primary lin¬
guistic processing may be intact. On
the other hand, the comprehension
deficits observed following subcorti¬
cal lesions do not appear to differ
from those seen in the traditional
cortical syndromes. However, only the
subcortical variety of sensory-type
aphasias are accompanied by hemi¬
paresis.14·17·21·22·25 Although these apha¬
sias are usually characterized as
transcortical sensory, there are a few
cases in which the deficits are Wernicke-like. The lesions in this instance
have involved thalamus15 or basal
ganglia.21·22·25 A right hemiparesis has
also been a constant associated fea¬
ture due to internal capsule involve¬
ment.

Computed tomographic scan 6% weeks poststroke. Right panels are 2:1 zooms of left panels.
Arrow heads point to recent ischemie infarction involving right thalamus and posterior limb of
internal capsule, present on both cuts, and to possible infarction involving posterior limb of left
internal capsule, which is seen on only one cut. Remainder of scan was completely normal.

hypodense area, possibly representing
a lesion, involving the midportion of
the left internal capsule was visual¬
ized on a single CT cut (Figure). If
present, the lesion was clinically "si¬
lent," since no right-sided elementary
findings or pseudobulbar palsy were
evident on neurologic examination,
and the patient repeatedly denied any
past symptoms consistent with

a

stroke.

COMMENT

The results from both the bedside
and quantitative examination of
affective language confirmed that our
patient had a sensory aprosodia.
Although the patient is left-handed,
most likely she has standard rather
than mixed hemispheric dominance
for language. While it could be argued
that the mild anomia observed during
the first examination represented a
manifestation of mixed dominance,
we believe the source of the anomia
was related to her occasional inattentiveness during testing, since difficul¬
ty with naming occurred only during
those time periods and was usually a
perseverative error. Moreover, her
intact comprehension and expression
of propositional language, coupled
with the constellation of severe affec-

tive deficits, strongly imply a normal
lateralization pattern.
Although study of aprosodias at
both the cortical and subcortical lev¬
els is relatively novel, an association
between left subcortical injury and
propositional language disorders has
been suspected for nearly 50 years.20
Only recently, however, has clinical
evidence for subcortical aphasias been
widely reported and acknowledged.

Despite growing evidence for a specif¬
ic language function of the basal gan¬
glia and thalamus, questions persist
on basic mechanisms. Early on, skep¬
tics argued that the language deficits
resulting from subcortical injury
actually represented the impairment
of cortical processing by mass

effects.15·30·31 While mass effects are
certainly a factor in many cases of
subcortical hemorrhage and tumor,
they cannot account for the language
disorders reported in circumscribed,
nonedematous hemorrhages and is¬
chemie infarctions involving the thal¬
amus or basal ganglia and internal
capsule. Whether the language defi¬
cits following subcortical injury rep¬
resent true aphasias or merely the
loss of "support functions" for cortical
processing is not known. While we do
not offer new evidence to solve this

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Since aphasie syndromes occur fol¬
lowing circumscribed, left subcortical
lesions, one would predict that homol¬
ogous injuries in the right hemisphere
would cause aprosodias. In fact, at
least four cases of purely subcortical
lesions have been reported in the lit¬
with motor, transcortical
motor, or transcortical sensory apros¬
odias.1·8·26 The CT scan in the present
erature

study showed no indication that the

cortex or adjacent white matter was

affected by infarction. Thus, our
patient's sensory aprosodia and left
hemiparesis were the direct conse¬
quence of a purely subcortical lesion
involving the right thalamus and pos¬
terior limb of the internal capsule.
Our case supplements previous evi¬
dence that the right thalamus and
basal ganglia play a role in modu¬
lating the affective components of
language.1·8·26 Moreover, the combina¬
tion of sensory aprosodia with left
hemiparesis appears to represent the
right-side analog to the unusual Wernicke-hemiparesis syndrome occa¬
sionally observed following left sub¬
cortical injury, thus lending support
to the hypothesis that the functionalanatomic organization of affective
language in the right hemisphere mir¬
rors that of propositional language in
the left.1·2·58

This work was supported in part by a Texas
State International Research Grant (BSRG 2S07-RR05426-25) to Southwestern Medical
School, University of Texas Health Science Cen¬
ter at Dallas (G.I.W.).

try 1975;38:69-72.
4. Tucker DM, Watson RT, Heilman KM: Dis-

10. Bugiani O, Conforto C, Sacco G: Aphasia in
thalamic hemorrhage. Lancet 1969;1:1052.
11. Samarel A, Wright TL, Sergay S, et al:
Thalamic hemorrhage with speech disorder.
Trans Am Neurol Assoc 1976;101:283-285.
12. Reynolds AF, Harris AB, Ojemann GA, et
al: Aphasia and left thalamic hemorrhage.
J Neurosurg 1978;48:570-574.
13. Reynolds AF, Turner PT, Harris AB, et al:
Left thalamic hemorrhage with dysphasia: A
report of five cases. Brain Lang 1979;7:62-73.
14. Cappa SF, Vignolo LA: 'Transcortical' features of aphasia following left thalamic hemorrhage. Cortex 1979;15:121-130.
15. Alexander MP, Lo Verme SR: Aphasia after
left hemispheric intracerebral hemorrhage. Neu-

Neurology 1977;27:947-950.
5. Larsen B, Skinh\l=o/\jE, Lassen NA: Variations
in regional cortical blood flow in the right and
left hemispheres during automatic speech. Brain
1978;101:193-209.

of the left thalamus without cortical lesion. Acta
Neurol Belg 1979;79:450-459.
17. Cohen JA, Gelfer CE, Sweet RE: Thalamic
infarction producing aphasia. Mt Sinai J Med

References
1. Ross ED: The aprosodias: Functional anatomic organization of the affective components
of language in the right hemisphere. Arch Neurol

1981;38:561-569.
2. Ross ED, Mesulam M-M: Dominant lan-

guage functions of the right hemisphere?: Prosody and emotional gesturing. Arch Neurol 1979;

36:144-148.
3. Heilman KM, Scholes R, Watson RT: Auditory affective agnosia: Disturbed comprehension
of affective speech. J Neurol Neurosurg Psychiacrimination and evocation of affectively intoned
speech in patients with right parietal disease.

6. Ross ED: Modulation of affect and nonverbal communication by the right hemisphere, in
Mesulam M-M (ed): Principles of Behavioral
Neurology. Philadelphia, FA Davis Co Publishers, 1985, chap 6.
7. Hughes CP, Chan JL, Su MS: Aprosodia in
Chinese patients with right cerebral hemisphere
lesions. Arch Neurol 1983;40:732-736.
8. Gorelick PB, Ross ED: The aprosodias: Further functional-anatomic evidence for the organization of affective language in the right hemisphere. J Neurol Neurosurg Psychiatry, in
press.

9. Fisher CM: The

pathologic and clinical

aspects of thalamic hemorrhage. Trans Am Neurol Assoc 1959;84:56-59.

rology 1980;30:1193-1202.
16. Demeurisse G, Derouck M, Coekaerts MJ,
et al: Study of two cases of aphasia by infarction

1980;47:398-404.

18. Gorelick PB, Hier DB, Benevento L, et al:

Aphasia after left thalamic infarction. Arch
Neurol 1984;41:1296-1298.
19. McFarling D, Rothi LJ, Heilman KM:
Transcortical aphasia from ischemic infarcts of

the thalamus: A report of two cases. J Neurol

Neurosurg Psychiatry 1982;45:107-112.
20. Smyth GE, Stern K: Tumors of the thalamus: A clinico-pathological study. Brain 1938;

61:339-374.
21. Damasio AR, Damasio H, Rizzo M, et al:
Aphasia with nonhemorrhagic lesions in the
basal ganglia and internal capsule. Arch Neurol

brooks N, et al: Aphasia with predominantly
subcortical lesion sites: Description of three capsular/putaminal aphasia syndromes. Arch Neurol 1982;39:2-14.
23. Cappa SF, Cavalotti G, Guidotti M, et al:
Subcortical aphasia: Two clinical CT scan correlation studies. Cortex 1983;19:227-241.
24. Wallesch C-W: Two syndromes of aphasia
occurring with ischemic lesions involving the left
basal ganglia. Brain Lang 1985;25:357-361.
25. Tanridag 0, Kirshner HS: Aphasia and
agraphia in lesions of the posterior internal
capsule and putamen. Neurology 1985;35:1797\x=req-\
1801.
26. Ross ED, Harvey JH, deLacoste-Utamsing
C, et al: How the brain integrates affective and
propositional language into a unified behavioral
function. Arch Neurol 1981;38:745-748.
27. Benson DF: Aphasia, Alexia and Agraphia.
New York, Churchill Livingstone Inc, 1979.
28. Ross ED, Edmondson JA, Seibert GB, et al:
Acoustic analysis of affective prosody during
right-sided Wada Test: A within-subjects verification of the right hemisphere's role in language.
Brain Lang, in press.
29. Ross ED, Holzapfel D, Freeman F: Assessment of affective behavior in brain-damaged

patients using quantitative acoustical-phonetic
and gestural measurements. Neurology 1983;
33(suppl 2):219-220.

30. Geschwind N: Discussion of cerebral connectionism and brain function, in Millikan CH,
Darly FL (eds): Brain Mechanisms Underlying
Speech and Language. New York, Grune & Stratton, 1967, pp 71-72.
31. McKissock W, Paine KWE: Primary
tumors of the thalamus. Brain 1958;81:41-63.

1982;39:15-20.

22. Naeser MA, Alexander MP, Helm-Esta-

Behavioral Manifestations of
Central Pontine Myelinolysis
Bruce H. Price, MD, M.-Marsel Mesulam, MD

\s=b\ A young woman with a clinical history and magnetic resonance imaging scan
consistent with central pontine myelinolysis came to medical attention because of
prominent behavioral symptoms. Marked
clinical recovery occurred despite persistent radiologic abnormalities. Rapid correction of hyponatremia was probably
related to the development of the central
pontine myelinolysis. A normal computed
tomographic scan and the absence of
brain-stem signs delayed accurate diagnosis.
(Arch Neurol 1987;44:671-673)

pontine myelinolysis (CPM)
(""'entraifirst
described by Adams et
was

al1 in 1959. Early descriptions emphaAccepted for publication Dec 15, 1987.

From the Division of Neuroscience and Behavioral Neurology, Charles A. Dana Research Institute, Beth Israel Hospital, Boston.

sized its grave prognosis.2 More recent
reports have documented survival and
recovery.3 Ventral pontine involve¬
ment with subacute onset of cerebel¬
lar, cranial nerve, and pyramidal tract
dysfunction is the typical presenta¬
tion.4
We describe a patient in whom
reversible behavioral abnormalities
constituted the major manifestation
of CPM. One purpose of this article is
to alert physicians to the possible
behavioral presentation of CPM.
Another is to reemphasize the rela¬
tionship between rapid correction of
hyponatremia and CPM. We also for¬
ward some thoughts on the patho¬
physiology of these behavioral

changes.

Reprint requests to Division of Neuroscience
and Behavioral Neurology, Charles A. Dana
Research Institute, Beth Israel Hospital, 330
Brookline Ave, Boston, MA 02215 (Dr Price).

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REPORT OF A CASE

A 29-year-old right-handed professional
in excellent health until her
return from Mexico. She developed intract¬
able nausea, anorexia, and diarrhea for one
woman was

week, leading to a 2.2-kg (5-lb) weight

loss.
Results of a clinical examination at that
time were normal, except for orthostatic
hypotension. Laboratory test results dis¬
closed the following values: serum sodium,
114 mEq/L (114 mmol/L); potassium, 1.9
mEq/L (1.9 mmol/L); arterial blood gases
demonstrated respiratory alkalosis; her
alanine aminotransferase level was ele¬
vated to 128 U/L; and aspartate amino¬
transferase, to 115 IU/L. Campylobacter
was grown from her stools. There was no
history of major psychiatric disease in the
patient or her family.
She received 2 L of normal saline with
potassium supplementation. Seventeen
hours later, her sodium level was 133 mEq/
L (133 mmol/L), and her potassium level
was 4.2 mEq/L (4.2 mmol/L). She recov-