Second edition

02.qxd 3/10/08 9:32 AM Page 54
54 ‘Cortical’ signs and symptoms
left hemisphere, although reported (Darby 1993; Ross et al.
1989), are rare.
MOTOR APROSODIA
In motor aprosodia, speech is monotonous, but comprehension
is intact and there is no ‘mismatch’; repetition
does not relieve the monotonous tone. The presence of
motor aprosodia may be quite disconcerting to patients.
One of Ross and Mesulam’s (1979) patients complained
that she had great difficulty in disciplining her children
because when she said to them that she was angry they
didn’t respond, because she didn’t sound angry. She
eventually came up with a way to circumvent her motor
aprosodia by adding a parenthetical statement, such as
‘God damnit, I mean it’ or ‘I am angry and I mean it,’ afterward,
thereby getting across what she was feeling. Of note,
however, in this case, ‘even the parenthetical statement was
voiced in a complete monotone’.
Motor aprosodia most commonly occurs secondary to
lesions in the posterior frontal operculum (Gorelick and
Ross 1987; Ross 1981; Ross and Mesulam 1979); cases have
also been reported with lesions in the internal capsule
(Ross et al. 1981) and basal ganglia (Speedie et al. 1993).
TRANSCORTICAL MOTOR APROSODIA
Transcortical motor aprosodia is essentially identical to
motor aprosodia except that the monotonous tone of
voice disappears with repetition. A case was reported secondary
to a lesion in the anterior limb of the internal
capsule (Ross 1981).
SENSORY APROSODIA
In sensory aprosodia there is a normal range of intonation
in the patient’s spontaneous speech. Comprehension,
however, is impaired, and one finds mismatches; repetition
is also impaired in that when patients repeat the neutral
phrase, the intonation of their speech will not be the
same as that of the examiner.
Sensory aprosodia has been noted with lesions affecting
the temporoparietal cortex (Darby 1993; Gorelick and
Ross 1987; Ross 1981); a case has also been reported secondary
to a lesion of the thalamus and adjacent posterior
limb of the internal capsule (Wolfe and Ross 1987).
TRANSCORTICAL SENSORY APROSODIA
This aprosodia is similar to sensory aprosodia with the
exception that repetition is performed well, with the
patient accurately mimicking the examiner’s tone of voice.
Cases have been described secondary to a lesion of the
anterior temporal cortex (Ross 1981), and the striatum and
adjacent posterior limb of the internal capsule (Gorelick
and Ross 1987).
GLOBAL APROSODIA
In global aprosodia, speech is monotonous and comprehension
of other’s prosody is poor; repetition does not
improve the patient’s prosodoic output. Global aprosodia
has been noted with lesions affecting both the frontal operculum
and the posterior temporal cortex (Darby 1993;
Ross 1981).
TRANSCORTICAL MIXED APROSODIA
Transcortical mixed aprosodia, which might just as well
be called transcortical global aprosodia, is essentially identical
to global aprosodia with the exception that the patient’s
prosody improves with repetition. A case has been reported
with a lesion involving the frontoparietal cortex (Ross
1981).
CONDUCTION APROSODIA
In conduction aprosodia spontaneous speech shows a normal
range of intonation, and comprehension is intact.
Remarkably, however, there is a ‘mismatch’ between the
patient’s statement as to how he is feeling and the tone with
which that statement is made. Furthermore, and remarkably
so in light of the preserved comprehension of prosody,
patients are unable to repeat sentences with the prosody
spoken by the examiner. Conduction aprosody appears to
be very rare; a case was reported with a lesion involving the
temporoparietal cortex (Gorelick and Ross 1987).
PURE AFFECTIVE DEAFNESS
In this condition, spontaneous speech shows a normal range
of intonation and there is no mismatch present. Despite
these preserved abilities; however, patients are unable to
comprehend the prosody with which others speak.
Remarkably, however, patients are able to mimic the examiner’s
intonation upon repetition testing.
Cases of pure affective deafness have been reported with
lesions affecting the posterior frontal and immediately
subjacent temporal operculum (Gorelick and Ross 1987;
Ross 1981) and also with a large lesion affecting the occipitoparietal
cortex (Gorelick and Ross 1987).
Etiology
Almost all reported cases of aprosodia have occurred as
part of a stroke syndrome, secondary to either ischemic
infarction or, much less commonly, intracerebral hemorrhage.
A case has also been reported of a gradually progressive
motor aprosodia secondary to a progressive focal
atrophy of the right frontal lobe (Ghacibeh and Heilman
2003). Further, there is also a report of motor aprosodia
occurring paroxysmally as a simple partial seizure
(Bautista and Ciampetti 2003).