Brain and Language 89 (2004) 411–416
www.elsevier.com/locate/b&l

Affective aprosodia from a medial frontal strokeq
Kenneth M. Heilman,a,* Susan A. Leon,a and John C. Rosenbeka,b
a

Department of Neurology, University of Florida College of Medicine, Center for Neurological Studies, State of Florida Memory Disorder Clinic,
and the VA RR&D Brain Rehabilitation Research Center, Gainesville, FL, USA
b
Department of Communicative Disorders, University of Florida College of Health Professions, USA
Accepted 13 January 2004

Abstract
Background and objectives. Whereas injury to the left hemisphere induces aphasia, injury to the right hemisphereÕs perisylvian
region induces an impairment of emotional speech prosody (affective aprosodia). Left-sided medial frontal lesions are associated
with reduced verbal fluency with relatively intact comprehension and repetition (transcortical motor aphasia), but persistent affective
prosodic defects associated with right medial frontal lesions have not been described. Methods. We assessed the prosody of a man
who sustained a right medial frontal cerebral infarction seven years prior. Results. While propositional speech expression was
normal including syntactic prosody, the patient was impaired at expressing emotions using prosody. His comprehension and
repetition of prosody were also impaired but less so than expression. Conclusions. Right medial frontal lesions can induce an
affective aprosodia that primarily impairs expression.
Published by Elsevier Inc.

1. Introduction
‘‘It is not what you said, but how you said it.’’ Normally, speech may simultaneously transmit two types of
messages, verbal and prosodic. Whereas, the verbal
message is conveyed by a complex code requiring semantic, lexical, syntactic, and phonemic processing, the
prosodic message is conveyed by changes in pitch, amplitude, tempo, and rhythm. In European languages,
such as English, prosody can be used linguistically,
primarily at the syllable and word levels to mark stress
and can be used to signal whether an utterance is
statement or question (i.e., declarative versus interrogative). Prosody, at the sentence level and involving
principally changes in fundamental frequency, can also
be used to convey emotional messages (Monrad-Krohn,
1947; Paul, 1909; Pell, 1999).
Broca (1865) noted that in more than 90% of people,
the left hemisphere is dominant in mediating what
Hughlings Jackson (1915) later called propositional
q

This work was supported by NIDCD P50-DCO3888, the
Department of Veteran Affairs and the State of Florida Memory
Disorder Clinics.
*
Corresponding author.
E-mail address: heilman@neurology.ufl.edu (K.M. Heilman).
0093-934X/$ - see front matter. Published by Elsevier Inc.
doi:10.1016/j.bandl.2004.01.006

speech. Hughlings Jackson (1915), however, observed
that even non-fluent aphasic patients from left hemisphere lesions could imbue their simple utterances with
emotional content by using affective intonations and
suggested that the right hemisphere might be important
in mediating affective prosody. This postulate, however,
was not investigated until about 25 years ago when
Heilman, Scholes, and Watson, 1975 and Tucker,
Watson, and Heilman, 1977 reported patients with right
hemisphere lesions who were not aphasic, but who could
not comprehend (Heilman et al., 1975) or express
(Tucker et al., 1977) emotions using affective prosody.
Subsequently, Ross and Mesulam (1979) reported two
patients who could not express affective prosody but
could comprehend affective prosody. Ross (1981) then
suggested that these affective prosodic deficits be called
aprosodia. He suggested that the types of affective
prosody disturbances seen with right hemisphere damage might mirror the types of aphasia syndromes observed with left hemisphere damage and described some
patients with right posterior perisylvian lesions who
demonstrated affective prosody comprehension disorders and other patients with right anterior perisylvian
lesions who were impaired at expressing affective prosody but had spared comprehension of affective prosody.
Other studies, however, have suggested that not all

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patients fit into this localization paradigm (Wertz,
Henschel, Auther, Ashford, & Kirshner, 1998).
Lichtheim (1885) reported a patient who had nonfluent speech, but who was able to comprehend and
repeat speech. Subsequently, there have been other reports of similar patients. Although some of these patients have left dorsolateral frontal convexity lesions
that are above BrocaÕs area (frontal-opercular region),
there have been multiple reports of this syndrome being
induced by strokes in the distribution of the left anterior
cerebral artery and in these reports the critical area injured appeared to be the supplementary motor area
(Bogousslavsky, Assal, & Regli, 1987; Freedman, Alexander, & Naeser, 1984; Pai, 1999; Masdeu, Schoene, &
Funkenstein, 1978; Rubens, 1975; Ziegler, Kilian, &
Deger, 1997). Whereas Bell, Davis, Morgan-Fisher, and
Ross (1990) reported a child who had transiently impaired expressive prosody from a right frontal lesion, we
could find no reports of adults with right medial frontal
damage who demonstrated persistent aprosodia and
thus the purpose of this report is to present such a case.

2. Methods
2.1. Subject
On September 25, this retired railroad machinist, who
was at that time 76 years old, was admitted to the
Veterans Affairs Medical Center, Gainesville, Florida,
for evaluation of a stroke. On the day of admission,
while sitting and watching television, he had the onset of
a transient loss of speech followed by slurring of speech.
When he attempted to stand, he could not and fell over,
but had no loss of consciousness. The patient had no
history of a prior stroke, but did have a history of
coronary artery disease, including two myocardial infarctions, stable angina with ischemic cardiomyopathy
associated with a reduced ejection fraction, and mitral
regurgitation. He also had a history of polycythemia.
His medications included digoxin, lisinopril, metoprolol,
furosemide, aspirin, niacin, cimetidine, allopurinol, isosorbide dinitrate, and nitroglycerine.
A general examination during admission revealed a
fourth heart sound, as well as a grade 2/6 systolic
murmur at the left sternal border. Although his admission neurological examination was reported to be normal, the patient was later noted by the neurology
consult to have a mild left hemiparesis that was maximal
in his left shoulder with a left-sided extensor plantar
response. The neurology consult also noted that the
patient had slurred speech, an abnormal gait, a left-sided visual grasp, and decreased saccades to the left.
There was some question as to whether he had a left
hemianopia and possibly some mild left-sided inattention or neglect.

The patient had an MRI taken 2 days after his admission (see Fig. 1), which revealed a lesion of the right
supplementary motor area (BrodmannÕs area 6) and the
anterior cingulate gyrus (BrodmannÕs area 24). The
forceps minor with its input to the genu of the corpus
callosum was also probably involved. An echocardiogram revealed an ejection fraction of 20% and a Holter
monitor revealed an episode of ventricular tachycardia.
Because the physicians taking care of him thought that
he was at risk for another embolus due to his poor
ejection fraction and intermittent arrhythmia, he
was anticoagulated with warfarin and treated with
amiodarone.
Shortly after we opened a new rehabilitation center,
this patient was seen as a possible rehabilitation candidate (January 2002). Since being discharged from the
hospital in 1994, his dysarthria and left arm weakness
almost completely resolved. A neurological examination
at that time revealed no evidence of hemispatial neglect.
He had a very mild left facial droop and decreased
sensation in his feet in a stocking-like pattern. His
strength was normal except for the finger extensors of
his left hand. He also had difficulty making fine finger
movements with his left hand. He walked slowly and
turned en block; otherwise, this 83 year old man had a
normal neurological examination. He performed normally on the Geriatric Depression Scale (Yesavage et al.,
1982–83), but had constructional apraxia as determined
by the Rey–Osterrieth Complex Figure task (Osterrieth,
1944). He scored 23 on the Mini-Mental State Examination (Folstein, Folstein, & McHugh, 1975), but right
hemisphere lesions can induce constructional apraxia
(drawing the intersecting pentagons) and frontal lobe
lesions can reduce working memory (spell ‘‘world’’
backwards). Our patient performed incorrectly on both
of these tests. If these errors were excluded his score
would be in the normal range (27). While the patient did
not demonstrate florid left-sided neglect, he did make an
error when copying the left, but not right pentagon and
when spelling ‘‘world’’ backwards he misplaced the
letter ‘‘o’’ which is on the left side of the word.
The wife of this patient told one of the authors (S.L.)
that after this patientÕs stroke in Ô93 his voice was quieter, and ‘‘that everything sounded the same no matter
how he was feeling.’’ To learn if this man with a right
hemisphere stroke had affective aprosodia, he underwent a series of prosody tests (Table 1). The Florida
Emotion Expressive Battery (unpublished, University of
Florida) has subjects perform a series of tests; the first
three assess peoplesÕ ability to imitate syntactic and
emotional prosody, and the other three to produce
syntactic and emotional prosody to command. In all the
expressive prosody tests there are 20 test items and for
the affective prosody tests the five emotions assessed are
sad, happy, anger, fear, and neutral. The order in which
these emotions are tested is randomized. Performance

K.M. Heilman et al. / Brain and Language 89 (2004) 411–416

413

Fig. 1. MRI of subject revealing right medial frontal lesion.

on all prosody assessments was evaluated by a panel of
three experienced judges, expert in the evaluation and
treatment of aprosodia. When asked to imitate a sentence that contains syntactic prosody (question versus
statement) the patients was 70% accurate (Table 1).
When asked to imitate a semantically neutral sentence
using emotional prosody, he was 60% accurate. In the
third imitative test he was asked to repeat sentences
where the semantic content was either incongruent or
congruent with the requested emotional prosody (e.g.,
Repeat ‘‘All the puppies are dead.’’ with a sad tone.) He
was 30% accurate on this task.
When the patient was asked to produce a sentence to
command using syntactic prosody, he was able to correctly produce questions and statements 100% of the
time, but when he was asked to produce affective prosody with a verbally neutral sentence he was only 25%
accurate. When asked to inflect a sentence with an incongruent prosody, he demonstrated 0% accuracy.
Thus, it appears that his main expressive problem was
with spontaneously intoning affective prosody.
To assess his ability to comprehend affective prosody,
he was given the Florida Affect Battery (Bowers, Blonder, & Heilman, 1991). This battery tests a patientÕs

ability to identify spoken affective prosody as well as
emotionally expressive faces. In one prosody task, he
was presented with series of paired sentences spoken
either using the same or different affective prosody (e.g.,
both spoken in a happy tone or one spoken in a happy
tone and the other a sad tone) and he had to decide if the
two sentences were intoned with the same or different
emotional prosody. He was 70% accurate on this test,
while normal subjects in his age range get 97.8% (SD
4.6) correct. When asked to name the emotional intonation when the semantic content was neutral, he was
50% accurate, but normal subjects are 83% (SD 13.0)
accurate. When the affective prosody conflicted with the
semantic content of the message and he was asked to
name the emotion expressed by the affective prosody, he
was 21% accurate whereas normal subjects perform with
61.7% (SD 12.6) accuracy. In contrast to his impaired
comprehension of emotional prosody, he performed
normally on affective facial discrimination tasks. For
example, when asked to discriminate emotional faces he
was 85% accurate; normal subjects perform with 87.8%
(SD 9.8) accuracy. When he was asked to name the type
of emotion displayed on a face he was 90% accurate and
normal controls are 87% (SD 8.7) accurate.

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K.M. Heilman et al. / Brain and Language 89 (2004) 411–416

Table 1
Test results of affect comprehension and discrimination as well as
prosody (emotional and non-emotional) expression
Test

Pretreatment

Florida Affect Battery
Identity Discrimination
Affect Discrimination
Name Affect
Select Affect
Match Affect
Non-emotional Prosody Discrimination
Emotional Prosody Discrimination
Name Emotional Prosody
Conflicting Prosody
Match Emotional Prosody to Emotional Face
Match Emotional Face to Emotional Prosody

90
85
90
95
Discontinued
31
70
50
36
35
Not tested

Expressive Battery
Non-emotional Prosody Imitation
Emotional Prosody Imitation
(neutral sematic content)
Emotional Prosody Imitation
(semantics congruent/ incongruent)
Emotional Prosody to Command
(semantics congruent/incongurent)
Emotional Prosody to Command
(neutral semantic content)
Non-emotional Prosody to Command

70
60
30
0
25
100

3. Discussion
When seen in our rehabilitation center 7 years after
he sustained a right medial frontal lobe stroke that
damaged portions of his supplementary motor area and
the anterior cingulate gyrus, the patient had evidence of
affective aprosodia. Because he was not aphasic and he
was flawless at producing non-emotional prosody (e.g.,
questions versus statements) to command, but was
dramatically impaired at producing emotional prosody,
it appears he had an affective prosodic expressive deficit.
His ability to comprehend and repeat emotional prosody was also impaired, but perhaps not as impaired as
his expression. Although this patient did have some
hearing loss, he was able to repeat the words in sentences well and could repeat syntactic prosody. Thus, his
aprosodia could not be attributed to decreased hearing.
Left hemisphere superio-medial frontal lesions that
involve the supplementary motor area can induce
aphasia. Usually these patients are non-fluent but have
intact comprehension and flawless repetition. This
aphasic syndrome has been called transcortical motor
aphasia (Caplan, 2003). Observation of the patient reported here suggests that lesions of the right hemisphereÕs superio-medial frontal cortex can induce
affective, but not syntactic aprosodia. Unlike patients
with left-sided medial frontal lesions who have intact
speech repetition and comprehension and thus are
classified as transcortical motor aphasia, our patientÕs
repetition and comprehension of emotion prosody was

not normal. Thus, his prosody disturbance induced by
right medial frontal hemisphere damage did not entirely
mirror the transcortical motor aphasia syndrome observed with left medial frontal hemisphere damage.
However, the profile of a greater impairment in spontaneous affective prosodic expression than in repetition
or comprehension is similar to the profile observed with
transcortical motor aphasia.
The reason why a right superio-medial frontal lesion
would produce a mixed aprosodia, with impairments of
expression, comprehension, and repetition, is not entirely known, but there are several possibilities. One
possibility is that after his initial stroke 7 years prior to
our evaluation, he had another stroke that impaired his
repetition and comprehension of prosody. However,
there are several observations that are inconsistent with
this hypothesis. First, since his stroke in 1993, he has
had no other new episodes of neurological impairment
and most often strokes in other regions would induce
other deficits. Second, after he was evaluated by us he
fell and hit his head. Because he was being treated with
anticoagulants, a CT scan was performed. The interpretation of this scan by a radiologist, who is not an
author of this paper was that there was no evidence of a
new cerebral infarction, intracranial hemorrhage, or
mass, but there was evidence of his old cerebral infarction in the right frontal lobe.
Another possible explanation for his mixed aprosodia
is a callosal disconnection. Prior studies have suggested
that affective prosody is incorporated into propositional
speech by means of an interhemispheric mechanism
(Klouda, Robin, Graff-Radford, & Cooper, 1988; Ross,
Thompson, & Yenkosky, 1997; Speedie, Coslett, &
Heilman, 1984). Based on his MRI scan there is a high
probability that this patientÕs stroke damaged some of
the fibers crossing through the anterior portion of the
corpus callosum inducing a partial callosal disconnection. This callosal disconnection might have dissociated
verbal output mediated by the left hemisphere from the
expression of emotional prosody mediated by the right
hemisphere. Whereas this explanation might account for
the impaired expression and repetition of affective
prosody, it could not account for the impaired comprehension of emotional prosody.
As mentioned above, left frontal lesions induce an
impairment of verbal fluency (Caplan, 2003) and functional imaging studies in normal subjects reveal that
verbal fluency is associated with activation of this area
(Crosson et al., 1999). Functional imaging studies have
also revealed that emotionally salient stimuli activate the
anterior cingulate gyrus (Lane et al., 1998; Taylor, Phan,
Decker, & Liberzon, 2003; Teasdale et al., 1999). Several
mechanisms have been proposed to explain why left
medial frontal lesions reduce fluency, including: verbal
motor akinesia, inertia of or impaired access to concept
formations (semantic representations), and impaired

K.M. Heilman et al. / Brain and Language 89 (2004) 411–416

access to the verbal output lexicon (Gold et al., 1997).
Right medial frontal lesions might induce a parallel
impairment of emotional prosody (e.g., prosodic emotional akinesia, inertia of or impaired access to emotional concepts or to affective echoic representations
which are stored in the right hemisphere).
According to Jurgens (1986), the different human
non-verbal emotional vocal utterances (e.g., laughing,
shrieking, and moaning) and emotional intonation patterns (e.g., scolding, lamenting, and caressing) can be
shown to have their acoustic and emotional counterparts in the vocal repertoire of the monkey. In the
monkey the anterior cingulate cortex seems to be responsible for the volitional control of emotional vocal
utterances. Thus, non-verbal emotional vocal utterances
such as affective prosody might be the human homologue of monkeyÕs emotional vocalizations. While the
emotional vocalizations in monkeys most often appear
to mediated bilaterally, in some Macaca mulatta this
function appears to be lateralized (Sutton, Trachy, &
Lindeman, 1981).
Both lesion and functional imaging studies have
suggested that the anterior cingulate gyrus is important
for mediating attention and hemispheric arousal (Heilman, Watson, & Valenstein, 2003). Attention to important stimuli and right hemisphere arousal are critical
for the processing and experiencing of emotional stimuli. Patients with right hemisphere lesions that reduce
right hemisphere arousal and induce inattention often
show manifestations of the neglect syndrome, but when
tested this man did not show evidence of neglect. In
addition, if his right hemisphere was hypo-aroused we
would have expected other functions mediated by the
right hemisphere to also be impaired and yet he performed normally on the affective facial tests. These observations suggest that his problem was not a global
right hemisphere processing deficit or a general cognitive
deficit.
When monkeys received horseradish peroxidase injections in the anterior cingulate cortex at the level of the
genu of the corpus callosum, a region yielding emotional
vocalizations when electrically stimulated and the homologue of the area that was injured in our patient,
retrogradely labeled neurons were found at the cortical
level within auditory association cortex (e.g., the banks
of the superior temporal sulcus, Jurgens, 1983). A
functional imaging study also suggests that the medial
frontal regions might be a critical element in an auditory
attentional network (Benedict et al., 1998) and hence,
lesions of this medial frontal-auditory association cortex
network might impede repetition and comprehension of
affective prosody which is heavily dependent upon the
function of the right auditory cortex.
Adolphs, Damasio, and Tranel (2002) studied 66
patients with strokes and found that in addition to
posterior lesions impairing the recognition of emotional

415

prosody, frontal lesions were also associated with emotional prosodic comprehension deficits. The finding that
the frontal lobe might be important in the comprehension of emotional prosody is supported by positron
emission tomography (PET) studies that demonstrated
right frontal activation when normal subjects were
comprehending emotional prosody (George et al., 1996;
Imaizumi et al., 1997). These lesion and functional imaging studies suggest that the right hemisphere might be
organized differently than the left, such that whereas the
left is highly modular, the right contains many more
distributed representations and this patientÕs focal right
frontal medial lesion might have interrupted a distributed network important for expression, comprehension,
and imitation of emotional prosody.
Cancelliere and Kertesz (1990) as well as Karow and
Connors (2003) also studied brain lesioned subjects
ability to express and comprehend emotional prosody.
Both of these studies reported that injury to the basal
ganglia also appears to impair these functions. Although
our patient did not injury his basal ganglia, he did injure
the supplementary motor area, which is strongly connected with the basal ganglia (i.e., putamen) and the
mixed aprosodia described by these authors might also
be related to medial frontal (supplementary motor)
dysfunction.

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