The Aprosodias Functional-Anatomic Organization of the Affective Components of Language in the Right Hemisphere Elliott D. Ross, MD \s=b\ It was recently proposed that the affective components of language, encompassing prosody and emotional gesturing, are a dominant function of the right hemisphere, and that their functional-anatomic organization in the right hemisphere mirrors that of propositional language in the left hemisphere. Ten righthanded patients with focal lesions of the right hemisphere and disorders of affective language are described. Observations were made about each patient's spontaneous prosody, prosodic repetition, prosodic comprehension, and comprehension of emotional gesturing. Using this particular examination strategy, which is derived from the usual bedside approach to aphasic disorders, the organization of affective language in the right hemisphere does mirror the organization of propositional language in the left hemisphere. Furthermore, the disorders of affective language seem to be classifiable in the same manner as the aphasias. Thus, the term "aprosodia," preceded by specific modifiers such as motor, global, transcortical sensory, etc, seems appropriate when classifying the various disorders of affective language that occur following right-hemisphere damage. The relationships between affect, mood, pathologic laughing and crying, and depression are also discussed. (Arch Neurol 1981;38:561-569) previous article by Ross and Mesulam,1 coupled with the obser¬ vations of Heilman et al- and Tucker et al,3 it was proposed that the affec¬ tive components of language, encoma Accepted for publication Oct 5, 1980. From the Departments of Neurology and Psychiatry, University of Texas Health Science Cen- ter, Dallas. Reprint requests to Department of Neurology, University of Texas Health Science Center, 5323 Harry Hines Blvd, Dallas, TX 75235 (Dr Ross). passing prosody and emotional ges¬ turing, were a dominant linguistic feature of the right hemisphere, and that their functional-anatomic organi¬ zation in the right hemisphere mir¬ rored that of propositional language in the left hemisphere. The recent observations by Larsen and co-work¬ ers4 regarding changes in regional cerebral blood flow during "automatic speech" give further support to the foregoing ideas. To these investiga¬ tors' surprise, changes in blood flow occurred in the right hemisphere that were homologous in distribution to those observed in the left hemisphere (supplementary motor area, inferior sensorimotor strip, and posterosuperior temporal lobe). A ready explanation for the right-hemisphere phenomenon was not given because of the tradi¬ tional belief that language, in general, is a left-hemisphere function. Since the distribution of blood flow in both hemispheres was homologous during automatic speech, it could be argued that whatever the right hemisphere contributes to language, that contri¬ bution must be anatomically organiz¬ ed in the same way as propositional language. Most likely, in light of the publications by Heilman et al,- Tucker et al,' and Ross and Mesulam,1 Larsen and co-workers were actually observ¬ ing the functional-anatomic organiza¬ tion of the affective components of language in the right hemisphere. With this in mind, I began to sys¬ tematically examine patients with focal right-hemisphere damage for disorders of affective language by using strategies similar to those developed for assessing disorders of propositional language. In classifying an aphasie deficit, four observations are essential:3 (1) fluency of sponta¬ speech, (2) ability to repeat words, phrases, and sentences, (3) neous Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 auditory comprehension of proposi¬ tional language, and (4) visual-con¬ frontation naming. When using this method of evaluation, eight types of aphasia have been defined, each with a relatively distinctive neuroanatomic localization,' ie, motor (Broca's), sen¬ sory (Wernicke's), conduction, global, " transcortical motor, transcortical sen¬ sory, anomic, and mixed transcortical aphasia. Therefore, evaluation of spontaneous prosody and gesturing,' the ability to repeat with prosodieaffective variation,-;i auditory com¬ prehension of the affective compo¬ nents of prosody,- and visual compre¬ hension of emotional gesturing in patients with focal lesions of the right hemisphere was undertaken. The ten case reports that follow provide furth¬ er evidence that the functional-ana¬ tomic organization of affective lan¬ guage in the right hemisphere mirrors that of propositional language in the left hemisphere. Furthermore, the affective disorders of language ap¬ pear to be classifiable in the same manner as the aphasias. Thus, the ' term "aprosodia," (ä' pro so' dia) pre¬ ceded by specific modifying words such as motor, global, transcortical sensory, etc, seems appropriate when classifying the various disorders of affective language that follow focal right-hemisphere damage (Table). PATIENTS AND METHODS The ten patients to be described were referred to me by the neurology house staff of the University of Texas Health Science Center, Dallas, because of my interest in patients with right-hemisphere strokes. Instances of "negative" cases, where a lesion that involved the right peri-Sylvian region did not cause an apros¬ odia, were not encountered. All patients who I examined who had a right periSylvian lesion also had an aprosodia. One patient with a right superoposterior parie- tal-lobe infarction, confirmed by computed tomographic (CT) scan, was examined but did not have an aprosodia. Since the homo¬ logous region in the left hemisphere is not associated with aphasia, this patient's case report has been excluded from this arti¬ cle. The bedside evaluation of the affective components of language is relatively sim¬ ple, although some practice is required by the examiner so that he may confidently project differing affective tones through voice and through emotional gesturing during the formal portions of the assess¬ ment. The testing procedures outlined below are easily, if not flawlessly, carried out by patients who do not have brain damage regardless of educational back¬ ground. Thus, judging normal and abnor¬ mal performance is not a particularly diffi¬ cult task. Heilman et al2 and Tucker et al·' have developed quantitative testing proce¬ dures using audio recordings of profession¬ al actors and line drawings to examine some of the affective components of lan¬ guage, but these testing instruments are not commercially available. The bedside technique, on the other hand, allows the clinician to readily incorporate a qualita¬ tive assessment of the affective compo¬ nents of language into the routine neuro¬ logic examination, much the same way as one conventionally tests for propositional language. Spontaneous Prosody and Gesturing In the course of history taking, observa¬ tions should be made about the prosodie quality of the patient's voice. Overall loudness or softness of speech or the existence of pathologic laughing or crying should be ignored, and the finer aspects of emphasis, intonation, melody, and variability of voice should be assessed (cases 2, 3, and 9). The examiner should ask emotionally loaded questions during the interview, such as how the patient feels about his neurologic disability or if he has had any close calls with death or maiming. The critical dis¬ tinction for the examiner to make is whether the patient's spontaneous speech is prosodie or aprosodic. This is similar to the judgment of fluency and nonfluency of speech when assessing patients for apha¬ sia. Mismatching of the affective compo¬ nents of language to the semantic content should be noted, since patients with poste¬ rior lesions, similar to posterior aphasies, may be "fluent" but have abnormal or inappropriate prosody (cases 4 and 8). In addition, observations concerning the pa¬ tient's spontaneous gesturing should be made to complete the assessment. Prosodie-Affective Repetition This evaluation tests the patient's abili¬ ty to repeat sentences using the affective components of prosody and requires some acting ability on the part of the examiner. Declarative statements void of emotional words, such as "I am going to the movies" or "We are going to the circus," should be used. The patient is asked to repeat the sentence with the same affective quality as used by the examiner. Thus, when the examiner says the statement using a hap¬ py, sad, tearful, disinterested, angry, or surprised voice, the patient repeats the sentence exactly the same way. Repetition ability should be judged on how well the patient fine tunes his prosodie variation to that of the examiner's. Merely raising or lowering the loudness of voice or raising the voice at the end of a questioning type of statement does not constitute good pros¬ odie repetition, since these elementary aspects of prosody may be preserved when all other prosodie variation is absent (cases 1, 2, and 4). Prosodie-Affective Comprehension Auditory comprehension of the affective components of prosody and visual recogni¬ tion of emotional gesturing should be assessed separately, since these compo¬ nents of affective language may be differ¬ entially compromised (cases 5 and 10). Standing behind a patient when testing prosodie comprehension is an expedient way to avoid visual clues. The examiner should use declarative statements void of emotional words in conjunction with dif¬ fering affective tones and have the patient identify the projected emotion. One may give the patient five or six multiple-choice answers, eg, "Was that said in an angry, sad, happy, indifferent, surprised, or tear¬ ful tone," if he initially has trouble with the task, but often this is not necessary. Since this task does not test subtle aspects of prosodie comprehension, one can be sure that a patient has a significant deficit if he does poorly. Comprehension of Emotional Gesturing This is a visual-comprehension test for emotional gesturing that is similar to the evaluation of visual-language functions, confrontation naming, and reading in the aphasia examination. One stands in front of the patient and pantomimes an emotion¬ al gesture that involves the face and limbs to convey a particular affective state, such as surprise, anger, disinterest, sadness, or elation. The patient is then asked to identi¬ fy the emotion by name or description. If he initially has trouble with the task, then one should use a multiple-choice format similar to that described for testing pros¬ odie comprehension. REPORT OF CASES Motor Aprosodia Case l.-On May 11, 1979, a 63-year-old right-handed man had the abrupt onset of left-hand weakness and dysarthria and was admitted to a hospital in Fort Worth, Tex. He was transfered to the Neurology Service at the Dallas Veterans Administra¬ tion Hospital on May 18. Examination showed him to be alert and cooperative. He had implicit denial of his left-sided hemi¬ paresis, in that he was aware of the deficit but appeared unconcerned about it. Imme¬ diate recall, recent and remote memory, proverb interpretation, and orientation were normal. He had flat affect but denied depression. Propositional language was fully normal and there was no dysarthria. A mild left-sided lower facial weakness Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 volition was present, with decreased response to pin and temperature over the left half of his face and neck. There was a moderately severe left-sided hemiplegia, which affected hand, arm, shoulder, and hip, with sparing of foot and distal part of the leg, and left-sided hemianesthesia, splitting the midline, to pin and tempera¬ ture, with decreased position and vibration sensations in the distal area of the left upper extremity. on The patient's speech was flat and with little spontaneous prosody, even when he discussed his World War II experiences of liberat¬ ing the concentration camps in Ger¬ many or his son being shot to death the previous year. Spontaneous ges¬ turing was also greatly reduced, which gave the patient a flat affect. The patient's prosodie repetition was impaired. His speech remained aprosodic except when there was a question at the end of a statement. If one asked him to mimic a tearful or angry sentence using a loud voice, he could raise his voice but was unable to modulate it to convey the correct emo¬ tion. The patient's prosodie compre¬ hension and comprehension of emo¬ tional gesturing were flawless. The patient was reexamined on June 11, 1979. His spontaneous prosody and gestur¬ monotone ing were good, although he tended to miss the mark on prosodie repetition. However, both he and his wife agreed that his voice was only "80% as musical" as before the stroke. The hemiparesis and sensory defi¬ cits were also improved. A repeated CT scan, done June 25, demonstrated a right inferior frontal-lobe and anteroinferior parietal-lobe infarction (Fig 1 and 2, A). Case 2.—A 47-year-old right-handed man was admitted to the Neurology Service at the Dallas Veterans Administration Hospi¬ tal on May 30, 1979, because of a rightsided cerebrovascular accident. Mental status and propositional-language exami¬ nations were normal except for a flat affect, with implicit denial of his deficits. He denied being depressed or sad. He had a moderately severe left-sided lower facial weakness, and hemianesthesia to pin and temperature over the left half of his face and neck. Excellent strength and coordina¬ tion were present in his left limbs, although he was slow to move these limbs on request. There was left-sided hemianes¬ thesia, splitting the midline, to pin and temperature with mild loss of stereognosis and two-point discrimination in the left hand. The patient's speech was flat with prosodie variation. Spontaneous rare gesturing was markedly reduced, which gave the patient a flat affect. The only emotions he showed were two episodes of uncontrollable crying, when he told me about his son who was in prison for armed robbery. These crying episodes greatly dis- The Aprosodias* Pros¬ odie hension of Compre- Emotional Sponta¬ neous Prosody and Motor! Sensoryt Globali Conduction Transcortical motor Transcortical sen¬ Gesturing Poort Repetition Good Poor Compre¬ Gesturing Good Poor Poor Poor Poor Good hension Good Poor Poor Good Good Good Good Poor Poor Poorî Good Poor Poor Good Good Good Poor Poor Good Poor Poor Good Good soryt Mixed transcor¬ tical Anomic§ "The aprosodias in boldface type have been observed and are described in this article. Aprosodias in lightface type are postulated but not demon¬ strated. fGood anatomic correlation with lesions in the left hemisphere known to cause homologous aphasias. tSpontaneous gesturing, during recovery, may show marked improve¬ ment when compared with spontaneous prosody (cases 2 and 9). §Anomic aprosodia should be the result of a right angular-gyrus lesion akin to the syndrome of anomic aphasia, alexia, and agraphia,5 which invariably indicates left angular-gyrus damage. Although spontaneous prosody and gesturing are categorized as good for sensory, conduction, transcortical sensory, and anomic aprosodia, it does not necessarily mean that these features of language will be normal, only present; mismatching of affect to the semantic content of speech may occur (cases 4 and 8). Fig 1.—Computed tomographic scan from patient 1. Infarction involves right frontal operculum, insula, and anterior parietal operculum. Superoposterior temporal lobe is spared. Fig 2.—Depiction of infarctions observed in patients, with use of right lateral-hemisphere template and the atlas of Matsui and Hirano.24 Various aprosodia and case numbers are as follows: motor aprosodia, cases 1,2,3; sensory aprosodia, case 4; global aprosodia, case 5; transcortical sensory aprosodia, case 8; mixed transcortical aprosodia, case 9; motor aprosodia and pure prosodie deafness, case 10. Motor Aprosodia Sensory Aprosodia Case 4 A Cases 1, 2, and 3 Global Aprosodia C Case 5 Motor Aprosodia Plus Transcortical Sensory Aprosodia D Case 8 Mixed Transcortical Aprosodia *i E Case 9 Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 Pure Prosodie Deafness F Case 10 turbed him since he had never cried before when discussing his son's incarceration. The patient's prosodie repetition was very poor, although occasionally the patient would imitate the loudness of the examiner's voice without other prosodie variation. The patient's pros¬ odie comprehension and comprehen¬ sion of emotional gesturing were flawless. During hospitalization, the severity of his left-sided paralysis fluctuated despite anticoagulation. He ultimately sustained a spastic left-sided hemiplegia, which spared the distal portion of his left lower extrem¬ ity, and a prominent global sensory loss in his left upper extremity. The disturbance of affective language remained unchanged even at discharge on June 26, except that spontaneous gesturing was now noticeably present in his nonparalyzed right side and face. A CT scan done on June 13, demon¬ strated a right-sided inferior frontoparietal infarction (Fig 2, A). Case 3.—A 35-year-old right-handed man was admitted to the Neurology Service at the Dallas Veterans Administration Hospi¬ tal on June 6,1979, because of the subacute onset of a dense left-sided hemiplegia with sensory loss, anosognosia, and a left-sided hemianopsia. Examination on June 18, 1979, showed him to be awake, alert, and cooperative with normal mental status except for a flat affect. He had good insight into his illness. He claimed to feel "depressed" about his stroke, and during the interview he had a number of brief uncontrollable crying episodes that were not appropriate to the context of the dis¬ cussion. Propositional language was nor¬ mal. A mild, inattention, left-sided hemi¬ anopsia was present. Pin and temperature sensitivity was slightly dysesthetic over the left side of his face, and there was a moderately severe left-sided lower facial paralysis on volition, which was not pres¬ ent when he cried. He had a flaccid leftsided hemiplegia, with marked loss of proprioceptive and cortical sensations and relative sparing of pin and temperature sensations. His speech was completely flat and monotone, without prosodie variation even when he was describing his mood as being "depressed" and "hopeless." He admitted to suicidal thoughts, but even at this juncture there was no true component of sadness to his voice. The only evident emotion was occasional uncontrollable and inappropriate cry¬ ing that greatly embarrassed him. He had no observable spontaneous ges¬ turing. patient's prosodie repetition totally flat. He did not even adjust the loudness of his voice to that of the examiner's. His prosodie com¬ prehension and comprehension of emotional gesturing were flawless. The was During hospitalization the patient's de¬ pression intensified; he became more suici¬ dal and was treated with imipramine hydrochloride. At the time of discharge, Sept 7, his hemiplegia was spastic. He still manifested a dense motor aprosodia and a flat affect, even though his depression had totally resolved. Pathologic crying was no longer present. A CT scan, done on June 12, demonstrated a low-density lesion in the right basal ganglia, with extension to the frontoparietal subcortical white matter consistent with a right middle cerebral artery infarction (Fig 2, A). Cases 1, 2, and 3 illustrate the phe¬ aprosodia, which is characterized by aprosodic-agestural speech, poor prosodie repetition, and good prosodie comprehension. This is similar to motor (Broca's) aphasia, which is characterized by nonfluent speech, poor repetition, and good com¬ prehension of propositional language.' Furthermore, the supra-Sylvian in¬ farctions in these cases (Fig 1 and 2, A) are in the distribution reported for lesions in the left hemisphere that cause Broca's aphasia."; It is interest¬ ing that patient 1 had excellent recov¬ ery from his motor aprosody, whereas patients 2 and 3 did not. This may be related to the relative depth and size of the infarctions1; similar to the expe¬ rience reported by Mohr,7 who found that small lesions in Broca's area pro¬ duce rapidly ameliorating motor apha¬ sia, while large supra-Sylvian lesions produce a persistent and often severe form of Broca's aphasia. The disparity between recovery of spontaneous gesturing and sponta¬ neous prosody in patient 2 suggests that these two aspects of language probably have different underlying anatomic bases (case 9).' This may be similar to the relationship of ideomotor apraxia to Broca's aphasia, where the former usually shows recovery over time while the latter may not."-9 The overall relationship of sponta¬ neous gesturing to aphasia and apros¬ ody, however, is unclear. Patients with Broca's aphasia have been described as showing changes in gesturing that seem to reflect their underlying defect in propositional language,1" whereas patients with motor aprosod¬ ia appear to lose all spontaneous ges¬ turing ability,' be it propositional or emotional. It may be that spontaneous (emotional) gesturing, in addition to being a dominant function of the right hemisphere, also serves as the vehicle for embedding the proposi¬ tional components of gesturing con¬ tributed by the left hemisphere. Thus, the agestural state that results from right-hemisphere lesions may result nomenon of motor " Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 from the loss of emotional gesturing that concomitantly deranges proposi¬ tional gesturing, while left-hemi¬ sphere lesions only effect the proposi¬ tional components of gesturing. This hierarchical dependency of emotional to propositional gesturing may be similar to the hierarchical interaction of propositional speech to prosody. Since prosody, by definition, must be embedded onto the vehicle of proposi¬ tional speech,11 lesions that cause motor aphasia may produce changes in prosody, described under the ru¬ brics of "hyperprosody" and "dyspros¬ ody" by Monrad-Khron,1- whereas lesions that cause motor aprosodia produce a severe loss of prosody with little effect on propositional speech other than transient dysarthria. (For a more detailed discussion of the rela¬ tionship of the different components of prosody to brain lesions and righthemisphere damage see Ross and Mesulam.1) Sensory Aprosodia Case 4.—A 50-year-old right-handed man awoke with left-sided weakness and incoordination Dec 16, 1979, which precipi¬ tated admission to the Neurology Service at Parkland Memorial Hospital, Dallas. On examination he was awake, alert, and oriented, with normal recent and remote memory, calculation ability, proverb inter¬ pretation, and propositional language. He appeared to have a global aprosodia with fiat monotone speech, poor prosodie repeti¬ tion, and impaired prosodie comprehen¬ sion. He tended to look to the right, and when drawing figures he neglected the left side. Facial sensation and strength were good, but he had a left-sided homonymous hemianopsia. A mildly spastic left-sided hemiparesis that affected the leg more than the arm and a global left-sided senso¬ ry impairment were present. The left-sided weakness rapidly resolved over a few hours. Examination on Dec 17 showed him to have a normal mental status, with normal propositional language. Cranial nerves were normal except for a dense left-sided homonymous hemianopsia. There was no facial weakness or sensory loss. Motor weakness was not present on formal test¬ ing, but be held his left hand in a dystonic flexion posture and walked with a leftsided hemiparetic gait. Reflexes were slightly increased on the left, but Babinski's sign was absent. He had mild reduc¬ tion in vibration and position sensations in his distal left extremities, with severe astereognosis in his left hand. Pin and temper¬ ature sense were normal. The patient's speech exhibited a full range of prosodie features, with excel¬ lent variation. If anything, he tended to seem excessively happy despite his neurologic deficits. One had the feel¬ ing that his prosody was somewhat Fig 3.—Enhanced computed tomographic scan from patient 4. Infarction involves right parietal operculum and superoposterior temporal lobe. Right frontal operculum is spared. Arrowheads point into right Sylvian fissure, which divides frontal and, in higher cuts, parietal opercula from superior temporal lobe. euphorie and mismatched at times to the semantic content of his speech. He had well preserved and animated ges¬ turing. The patient's prosodie repetition was very poor despite normal sponta¬ neous prosody. The best he could do to raise or lower his voice to match the examiner's without inser¬ tion of other prosodie variations. His prosodie comprehension was also extremely poor. He would persist¬ ently miss even the simplest emotion¬ al tones such as indifference, tearful¬ ness, or anger. He tended to make his decisions on loudness of voice or call everything "happy." Once he identi¬ fied a sad, tearful emotion as being "sad," but when asked if it was "a little sad, moderately sad, or very sad and tearful" he replied "Oh just a little sad." The patient's comprehension of emotional gesturing was also severely impaired, similar to prosodie compre¬ hension. However, when his prosodie comprehension was evaluated and he was allowed to view the examiner, his overall comprehension of affective language showed moderate gains but was still impaired. was The patient's neurologic deficits contin¬ ued to improve during hospitalization, but the hemianopsia remained. At the time of discharge on Dec 29, he still manifested a sensory aprosodia, but his ability to com¬ prehend emotional gestures was improved Fig 4—Enhanced computed tomographic scan from patient 5. Infarction involves entire right middle cerebral artery distribution causing destruction of inferior and lateral frontal and parietal lobes, insula, and superior and middle temporal lobe. Left occipi¬ tal horn is enlarged. Arrowhead points to possible old left occipital infarction or contusion. but not normal. A CT scan, done on Dec 17, demonstrated a right posterosuperior tem¬ poral-lobe and posteroinferior parietal-lobe infarction (Figs 2, B, and 3). Case 4 illustrates the phenomenon of sensory aprosodia, which is charac¬ terized by prosodic-gestural speech, poor prosodie repetition, and poor comprehension of prosody and emo¬ tional gesturing. This is similar to sensory (Wernicke's) aphasia, which is characterized by fluent speech, poor repetition, and poor comprehension of both written and spoken propositional language.' Furthermore, the predomi¬ nant posterior temporoinferior parie¬ tal infarction in patient 4 is the same distribution reported for lesions in the left hemisphere that cause Wernicke's aphasia." " Although I am not abso¬ lutely certain that the patient was, at times, mismatching his prosody and emotional gesturing to the semantic content of speech, this uncertainty may just reflect inexperience in mak¬ ing such judgments in these kinds of patients. It should also be pointed out that if it were not for the patient's initial elementary neurologic deficits, his stroke may have easily gone unde¬ tected since his prosodie disorder only became apparent after formal exami¬ nation. If the lesion was confined to the superoposterior temporal lobe, the only outward manifestation might have been a change in behavior due to mismatching of affect to semantics or Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 the patient misinterpreting the affec¬ tive components of other peoples' behavior, causing him to respond inappropriately. If this were the case, then these patients or their families might seek psychiatric or psychologi¬ cal help even though the problem was primarily neurologic. Global Aprosodia Case 5.—A 43-year-old right-handed man suffered the acute onset of a flaccid leftsided hemiplegia with sensory loss and was admitted to the Neurology Service at Park¬ land Memorial Hospital on Jan 1, 1979. He was lethargic and difficult to examine. He denied his neurologic deficits and had dysarthria, but propositional language was normal. A left-sided hemianopsia, leftsided lower facial weakness, loss of pin sensation over the left side of the face, and hemiplegia with global sensory loss were apparent on examina¬ tion. The lethargy and anosognosia re¬ solved over the ensuing week, although he still manifested a mild dysarthria and per¬ sistent left-side hemianopsia. Examination on Jan 31 showed the pre¬ a flaccid left-sided viously described, elementary neurologic findings. He had a flat affect but denied depression. Mental status and proposition¬ al language were otherwise normal. His speech was flat and monotone without prosodie variation and with¬ out spontaneous gesturing. This was unchanged even when one discussed the extent, severity, and ultimate dis¬ ability of his stroke. The patient's prosodie repetition extremely poor; everything was repeated aprosodically. He could not was even vary the loudness of his voice to match the examiner's. His prosodie comprehension and comprehension of emotional gestur¬ ing were severely compromised, al¬ though occasionally he would correctly identify an emotion, especially anger. It turned out, however, that he made this decision on loudness of voice. Thus, when given a statement in a very tearful but loud voice, he would consistently label it as being angry. Also, any vehemently made emotional gesture, regardless of its affective tone, was always interpreted as anger. On reexamination Feb 2, the patient's prosodie comprehension and comprehen¬ sion of emotional gesturing were improved but still abnormal. A CT scan done on Feb 6 demonstrated a large right middle cere¬ bral-artery infarction that involved the frontal, parietal, anterior occipital, and superior and middle temporal lobes (Fig 2, C and 4). Case 5 illustrates the phenomenon of global aprosodia, which is charac¬ terized by aprosodic-agestural speech, poor prosodie repetition, and poor comprehension of prosody and emo¬ tional gesturing. This is similar to global aphasia, which is characterized by nonfluent speech, poor repetition, and poor comprehension of both writ¬ ten and spoken propositional lan¬ guage." Furthermore, the large supraand infra-Sylvian infarction is in the same distribution reported for lesions in the left hemisphere that cause glob¬ al aphasia." The improvement in com¬ prehension of the affective compo¬ nents of language in this patient is also consistent with Kertesz's obser¬ vation" in cases of global aphasia that comprehension is the most likely fea¬ ture to improve, whereas nonfluency is least likely to improve over time. Transcortical Motor Aprosodia Case 6.—A 70-year-old right-handed man Neurology Service at was admitted to the the Dallas Veterans Administration Hospi¬ tal on Dec 5, 1978, because of a left-sided hemiparesis. Examination on Dec 7 showed him to be awake, alert, and oriented but apathetic in his responses. He did not deny his deficits but seemed unconcerned about them. Mental status and propositional lan¬ guage were otherwise normal. He had a mild left-sided lower facial weakness at rest and on volition, but a striking weak¬ ness when he laughed. There was a mild left-sided spastic hemiparesis most promi¬ nent in his lower extremity and proximal portion of his upper extremity with spar¬ ing of the hand. Sensation was normal except for loss of graphesthesia and stereognosis in the left hand. His speech was a soft monotone, completely devoid of emotion. He had little spontaneous gesturing, which created a flat affect. Occasionally he would laugh inappropriately. His pros¬ odie repetition was excellent and strikingly better than his spontaneous prosody; his prosodie comprehension and comprehension of emotional ges¬ turing were normal. A CT scan, done on Dec 6, demonstrated edematous enhancing lesion that involved the right frontal, anterior parie¬ tal, and anterior temporal lobes. Brain biopsy at craniotomy showed metastatic undifferentiated adenocarcinoma. Despite steroid therapy, radiation therapy, and chemotherapy, the patient became stuporous and died Jan 5, 1979. Case 7.-A 51-year-old right-handed woman was admitted to the Neurology Service at Parkland Memorial Hospital on Sept 18, 1979, after the acute onset of an incontinence and a left-sided hemiparesis without sensory loss. Examination on Sept 22 showed her mental status and proposi¬ tional language to be normal. She had good insight into her deficits. Urinary inconti¬ nence was present, characterized by an inability of the patient to hold her urine once she felt the urge to urinate. She had a moderately severe left-sided lower facial weakness and a left-sided eufonie hemipa¬ resis, which spared the foot, distal part of the arm, and hand. No sensory loss or extinction phenomenon were observed. Her speech was flat and monotone without prosodie variation. There was a dearth of gesturing, giving her a flat affect. She denied any symptoms of depression. Her prosodie repetition was flawless and in striking contrast to her aprosodic spontaneous speech; her prosodie comprehension and com¬ prehension of emotional gesturing were excellent. During hospitalization she regained con¬ tinence and the left-sided hemiparesis improved. Examination March 5 showed only mild incoordination of the left leg with good strength, a mild left-sided lower facial weakness, most prominent during emotive movements, and total resolution of her transcortical motor aprosodia. A CT scan, done on Sept 19, demonstrated a small triangular lucency deep in the right hemisphere that involved the anterior limb of the internal capsule, head of the caudate nucleus, and putamen, without evidence of cortical involvement. Cases 6 and 7 illustrate the phenom¬ enon of transcortical motor aprosodia, which is characterized by aprosodic- agestural speech, good prosodie repe¬ tition, and good prosodie comprehen¬ sion. This is similar to transcortical motor aphasia, which is characterized by nonfluent speech, good repetition, Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 and good comprehension of proposi¬ tional language.'' Unfortunately, since the pathologic process in patient 6 was due to métastases, it is difficult, if not impossible, to make any statement about localization. This case is only important phenomenologically. Pa¬ tient 7, on the other hand, is interest¬ ing because her lesion proved to be subcortical, although the distribution of her hemiparesis strongly suggested that she had right anterior cerebralartery occlusion that produced infarc¬ tion in the distribution of the recur¬ rent artery of Heubner (accounting for the facial paralysis) and infarction of the medial frontal lobe (accounting for the leg monoplegia and inconti¬ nence)." Unfortunately, a right medi¬ al frontal lesion was not shown by CT scan to account for the transcortical motor aprosodia, especially since transcortical motor aphasia has been reported after left medial frontal lesions.1'1" This case, however, may represent an aprosodia due to a right striatal lesion. The transient nature of her transcortical motor aprosodia is in keeping with some of the transcortical motor types of aphasias that have been reported following striatal le¬ sions in the left hemisphere."''7 Transcortical Sensory Aprosodia Case 8.—A 76-year-old man with pro¬ gressive recent-memory loss was admitted to the Neurology Service at Parkland Memorial Hospital on Feb 11,1979, because of the acute onset of headache followed by unconsciousness and several generalized tonoclonic seizures. On admission he was comatose and had left-sided hemiparesis. He received anticonvulsant medication and underwent emergency CT scanning. With¬ in five hours he regained consciousness and had only a mild left-sided weakness. Examination Dec 12,1979, showed him to be awake, alert, and oriented, with a normal mental status except for moderate problems with recent memory. Proposi¬ tional language and cranial nerves were normal; however, he had no useful vision because of dense bilateral cataracts. No motor weakness, reflex asymmetry, incoor¬ dination, or sensory deficits were noted. His speech exhibited a full range of prosodie features, and he had ani¬ mated gesturing. Mismatching of emotions to semantic content was not prominent, although he appeared somewhat euphoric in his responses regardless of semantic content. The patient's prosodie repetition was ex¬ cellent but his prosodie comprehension was nonexistent. He totally failed to identify the emotive contents of speech and did not even use loudness of voice as a potential clue to help identify the correct emotion. His com- prehension of emotional gesturing could not be tested because of his cataracts. The prosodie deficits remained un¬ changed at discharge. Evaluation on Oct 15 showed a persistent transcortical sensory aprosodia without improvement. A CT scan done Feb 11, during hospitalization, dem¬ onstrated a large right-sided temporal intracerebral hematoma that spared the posterosuperior temporal lobe (Fig 2, D, and 5). Case 8 illustrates the phenomenon of transcortical sensory aprosodia, which is characterized by prosodic- gestural speech, good prosodie repeti¬ tion, and poor comprehension of affec¬ tive language. This is similar to trans¬ cortical sensory aphasia, which is characterized by fluent speech, good repetition, and poor comprehension of propositional language.7' Although the lesion intracerebral hemor¬ less certain localization rhage, making because of pressure effects, it is inter¬ esting that the hematoma did not involve the posterosuperior right tem¬ poral lobe, since this also seems to be characteristic of lesions in the left hemisphere that produce transcortical sensory aphasia.7'" was an Mixed Transcortical Aprosodia Case 9.-In May 1979, a 34-year-old right-handed woman was admitted to a hospital in Dallas because of subarachnoid hemorrhage. She underwent clipping of a left-sided supraclinoid berry aneurysm of the internal carotid artery. Postoperatively she sustained a left-sided hemiplegia with sensory loss and double incontinence. She was eventually transferred to the Physical Medicine and Rehabilitation Service at Parkland Memorial Hospital on Oct 12. Examination demonstrated a normal men¬ tal status except for a flat affect, with a rather indifferent attitude on the patient's part to her neurologic disabilities. She denied depression. Propositional language was unimpaired. Cranial nerves were normal except for mild left-sided visualfield extinction to double simultaneous stimulation and a mild left-sided lower facial weakness. She had a prominent leftsided spastic hemiplegia and a global leftsided hem ¡sensory loss. The patient did poorly in the physical therapy program and was examined in consultation Oct 22 for evaluation of a questionable "dementia." The routine neurologic examination was unchanged, but she did admit to being somewhat sad and hopeless, without suici¬ dal ideation. She denied, however, any of the vegetative symptoms of depression, such as anorexia or insomnia, and she denied dysphoria. Her speech was completely flat and monotone even when she talked about her neurologic deficits, which were enough to confine her to a severe wheelchair and cause her to be cathe¬ ter dependent. She had no sponta¬ neous gesturing, which created a flat affect. The only emotion she demon¬ strated was several episodes of uncon¬ trollable and inappropriate crying, during which she claimed she did not feel sad or know why she was cry¬ ing. patient's prosodie repetition good although not perfectly normal. She could easily modulate the The was loudness of her voice to that of the examiners and add a good deal of the finer aspects of prosody. In compari¬ son to her spontaneous prosody, repe¬ tition was strikingly good although not completely normal. Her prosodie comprehension was clearly impaired, with most of her decisions made on loudness of voice. The patient's com¬ prehension of emotional gesturing compromised as prosodie com-. prehension. was as The patient did poorly in rehabilitation and was discharged. Evaluation on Jan 7, 1980, demonstrated no change in the find¬ ings from neurologic examination except for some improvement in prosodie compre¬ hension. However, further historical de¬ tails were obtained from the family. The patient, for many months, had been sleep¬ ing poorly, was anorexic (causing a 27-kg weight loss), and was "not the same per¬ son" because of excessive irritability. She cried and laughed inappropriately and uncontrollably at home. Because of this history, it was felt that she had depression, despite her denial of deep sadness and vegetative symptoms. She was treated with nortriptyline hydrochloride and had resolution of her vegetative symptoms, pathologic laughing and crying, and irrita¬ bility. Her flat affect and aprosodic speech, however, remained totally unchanged. She continued to demonstrate improvement in prosodie repetition, prosodie comprehen¬ sion, and comprehension of emotional ges¬ turing. A CT scan done on Oct 26, 1979, during her hospitalization, showed a large right middle cerebral-artery infarction, which involved the frontal and parietal lobes with extension into the superior tem¬ poral lobe (Fig 2, E, and 6). There was also a small infarction in the left anteromedial frontal lobe. Case 9 illustrates the phenomenon of mixed transcortical aprosodia which is characterized by aprosodic- agestural speech, good prosodie repe¬ tition, and poor comprehension of prosody and emotional gesturing. This is similar to mixed transcortical apha¬ sia, which is characterized by nonfluent speech, good repetition, and poor comprehension of propositional language.7'1* From the lesion shown by CT scan, one would have expected the patient to have had global aprosodia. However, evaluation of her affective Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 components of language was first done almost six months after the stroke. Most likely, if she had been examined closer to her ictus, she would have demonstrated global aprosodia since prosodie repetition, although much better than the other components of affective language, was not normal. Furthermore, over the ensuing four months she began to show significant improvement in com¬ prehension of prosody and sponta¬ neous gesturing, transforming her mixed transcortical aprosodia into transcortical motor aprosodia. Again, this distributed recovery from pros¬ odie deficits is consistent with the recovery observed by Kertesz" in patients with global aphasia, especial¬ ly when the lesion causes minimal damage to the (left) posterosuperior temporal lobe, as was the circum¬ stance in the right-hemisphere lesion in patient 9. Motor Aprosodia With Pure Prosodie Deafness Case 10.-A 67-year-old right-handed hemiparesis on man awoke with left-sided Jan 23, 1980, and was admitted to the Neurology Service at Parkland Memorial Hospital. He denied weakness in his left limbs but did admit to gait difficulty. He was alert, cooperative, and oriented but mildly inattentive. Immediate recall was only five numbers forward. Recent and remote memory, calculations, and interpre¬ tation of similarities and proverbs were normal. He had mild slurring of speech but no aphasie deficits. Cranial nerves were normal exept for a mild left-sided lower facial weakness on volition. There was a moderate left-sided hemiparesis that af¬ fected the upper extremity to far greater extent than the lower extremity, with sparing of the distal leg and foot. Sensory functions were normal except for some decreased appreciation of pin and temper¬ ature in his left upper extremity. Examination on Feb 2 showed left-sided spastic hemiparesis that involved his face, arm, hand, and proximal leg. No sensory loss was evident. The patient now had a normal mental status except for a flat affect. He denied being depressed. His speech was flat and monotone without prosodie variation even when discussing his neurologic deficits and disability. Gesturing was very blunted. The patient's prosodie repetition was exceedingly poor, and he could not even vary the loudness of his voice to reflect that of the examiner's. His prosodie comprehension was also ex¬ ceedingly poor. He could not even use loudness of voice as a cue to identify the projected affective tone. The patient's comprehension of emotional gesturing in distinct contrast to pros- Fig 5—Top left, Computed tomographic scan from patient 8. Intracerebral hematoma involves right anterior, middle, and inferi¬ or temporal lobe, with deep extension into right occipital horn. Superoposterior temporal lobe is spared. There is minimal edema and displacement of brain. Cortical atrophy and hydrocephalus ex vacuo are present. Fig 6.—Top right, Computed tomographic scan from patient 9. Infarction involves right inferior and lateral frontal and parietal lobes and part of right superoposterior temporal lobe. There is also infarction of left anteromedial frontal lobe. Arrowheads point to right Sylvian fissure, which separates frontal and parietal opercula from superior temporal lobe. Fig 7.—Bottom right, Enhanced computed tomographic scan from patient 10. Infarction involves right frontal operculum, insula, and superior, midanterior, temporal lobe. Parietal operculum and superoposterior temporal lobe are spared. Arrowheads point to right Sylvian fissure, which separates frontal and parietal opercu¬ la from superior temporal lobe. odie comprehension, was flawless. In fact, if prosodie comprehension was tested so that he could see the examin¬ er, he only manifested minimal diffi¬ culties! Just prior to discharge, on Feb 15, the patient was reexamined. His elementary neurologic findings were unchanged. Pros¬ odie comprehension, however, was signifi¬ cantly better but not completely normal. A CT scan, done on Feb 1, demonstrated a lesion that involved the right frontal oper¬ culum, anterior insula, and superior-midtemporal lobe, with sparing of the supero¬ posterior temporal and inferior parietal lobes (Fig 2, F and7). Case 10 illustrates the phenomenon of motor aprosodia coupled with pure prosodie deafness. This particular combination of deficits—aprosodicagestural speech, poor prosodie repeti¬ tion, poor prosodie comprehension, and good comprehension of emotional gesturing—is similar to occasionally described patients who have global aphasia without alexia.19 The right frontal opercular lesion easily ac¬ counted for the aprosodic spontaneous speech and loss of prosodie repetition. The comprehension deficit, however, is the intriguing feature of case 10, since it only involved auditory proc¬ essing of affective language. This implies that the visual connections to Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 the right superoposterior temporal lobe, which appears to be functionally homologous to Wernicke's area on the left,4 were preserved so that compre¬ hension of emotional gesturing could be carried out. The lesion in the right superior-midtemporal lobe probably injured the right primary auditory cortex and interrupted the callosal connections from the left auditory cortex, isolating the right superopos¬ terior temporal lobe from auditory inputs, thus accounting for the loss of prosodie comprehension (pure pros¬ odie deafness). This explanation is the same one used to account for pure word deafness (loss of auditory com- prehension of propositional language with preserved reading, writing, nam¬ ing, propositional speech, and nonver¬ bal audition) following a unilateral lesion of the left midtemporal lobe that spares Wernicke's area.7'-" Fur¬ thermore, it has been postulated, but not proven, that global aphasia with¬ out alexia might result from a lesion that causes pure word deafness in combination with a lesion that causes Broca's aphasia in the left hemi¬ sphere.1" COMMENT The patients described in this arti¬ cle help to further unravel the func¬ tional-anatomic organization of the affective components of language in the right hemisphere.'-' Seven of ten patients had lesions in the right hemi¬ sphere, with accompanying disorders of affective language corresponding exactly to the traditional classifica¬ tion and localization given for motor, sensory, global, and transcortical sen¬ sory aphasia and pure word deafness (Fig 2 and Table). In addition, the phenomena of transcortical motor aprosodia and mixed transcortical aprosodia have been observed. To complete and substantiate the analo¬ gy of the aprosodias to the aphasias, however, patients with "conduction" and "anomic" varieties of aprosodia will need to be indentified (Table) and further validating case reports will need to be published. Two further points should be made about the behavior changes that accompany right-hemisphere lesions. In the aprosodias associated with flat affect, coarse emotional behavior may be preserved, since a number of patients retained the ability to laugh and cry (cases 2, 3, and 9). For the most part, this ability was clearly "pathologic" because the laughing and crying were usually inappropriate, uncontrollable, and had an all-or-noth¬ ing quality.-' The most striking patho¬ logic laughing and crying occurred in the two patients (cases 3 and 9) who were ultimately found to have major depressive disorders. Interestingly, when these patients' depression was treated, their pathologic laughing and crying dissipated. This strongly sug¬ gests that in patients with prominent pathologic laughing and crying, fol¬ lowing unilateral right-hemisphere damage, the diagnosis of depression should be suspected and vigorously pursued.2The last point concerns flat affect. One should not confuse a flat affect following right-hemisphere damage to be necessarily indicative of depres- sion or unconcern. Patients who are depressed have a depressive affect; patients with a flat affect, following right hemisphere damage, have little or no affect whether depressed or not (cases 3 and 9), happy, sad, angry, etc. Thus, one should be very cautious when psychiatrically examining these patients, since their affect may not reflect their mood. Some patients with right-hemisphere lesions who appear to have implicit denial or unconcern for their deficits are very concerned about them but unable to convey this concern through prosody or emotional gesturing. In these particular cases, strict attention should be paid to the patient's propositional description of his mood and inner feelings (case 3), disregarding the flat affect. On the other hand, if the right-hemisphere lesion is large and/or involves posteri¬ or structures, such as in patient 9, the propositional responses to questions that pertain to mood can be very misleading, since the language areas of the left hemisphere may no longer have direct access to emotional proc¬ esses in the right hemisphere. Thus, the patient may display behavioral manifestations consistent with an emotional disorder (in this instance, the vegetative signs of depression) without an appropriate verbal-cogni¬ tive set. This is similar to the behavior exhibited by "split brain" patients, as reported by Gazzaniga and LeDoux,-:l when tasks are given to the right hemisphere that require a left-hand response. If a verbal explanation of the right-hemisphere behavior is re¬ quested from the left hemisphere, it often bears little relation to the actual task and may be very misleading as to the true state of affairs. (For further elucidation of the often disparate and vexing relationships between affect, mood, pathologic laughing and crying, and depression in brain-damaged pa¬ tients, see Ross and Rush.--) During the last five months (after this report was submitted for publica¬ tion), I have encountered four cases of motor aprosodia, two cases of sensory aprosodia, and two cases of global aprosodia secondary to cerebral vascu¬ lar infarctions of the right hemi¬ sphere. All the patients were right handed and none had aphasie deficits. The locations of the lesions, deter¬ mined by CT, causing the various aprosodias correlated without excep¬ tion to the functional-anatomic data presented in this report. It has been my recent experience, as attending neurologist, that the aprosodias are as commonly encountered on the clinical services as are the aphasias. Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/26/2015 The neurology house staff referred patients to Ross, MS, reviewed the manu¬ script; and Denise Wernet patiently typed the me; Stephanie manuscript. References 1. Ross ED, Mesulam M-M: Dominant language functions of the right hemisphere: Prosody and emotional gesturing. Arch Neurol 1979; 36:144-148. 2. Heilman KM, Scholes R, Watson RT: Auditory affective agnosia: Disturbed comprehension of affective speech. J Neurol Neurosurg Psychia- try 1975;38:69-72. 3. Tucker DM, Watson RT, Heilman KM: Discrimination and evocation of affectively intoned speech in patients with right parietal disease. Neurology 1977;27:947-950. 4. 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. 5. Benson DF: Aphasia, Alexia, and Agraphia. New York, Churchill Livingstone, 1979. 6. Kertesz A: Aphasia and Associated Disorders. New York, Grune & Stratton Inc, 1979. 7. Mohr JP: Broca's area and Broca's aphasia, in Whitaker H, Whitaker HA (eds): Studies in Neurolinguistics. New York, Academic Press Inc, 1976, vol 1, pp 201-235. 8. Mohr JP: Rapid amelioration of motor aphasia. Arch Neurol 1973;28:77-82. 9. Geschwind N: The apraxias: Neural mechanisms of disorders of learned movement. Am Sci 1975;63:188-195. 10. Cicone M, Wapner W, Foldi N, et al: The relation between gesture and language in aphasic communication. Brain Lang 1979;8:324-349. 11. Fry DB: Prosodic phenomena, in Malmberg B (ed): Manual of Phonetics. New York, American Elsevier Publishing Co, 1974, pp 365-410. 12. Monrad-Khron G: The third element of speech: Prosody and its disorders, in Halpern L (ed): Problems of Dynamic Neurology. Jerusalem, Hebrew University Press, 1963, pp 101-117. 13. Kertesz A, Benson DF: Neologistic jargon: A clinicopathological study. Cortex 1970;6:362\x=req-\ 386. 14. Critchley M: The anterior cerebral artery and its syndromes. Brain 1930;68:120-165. 15. Rubens AB: Transcortical motor aphasia, in Whitaker H, Whitaker HA (eds): Studies in Neurolinguistics. New York, Academic Press Inc, 1976, vol 1, pp 293-303. 16. Alexander MP, Schmitt MA: The aphasia syndrome of stroke in the left anterior cerebral artery territory. Arch Neurol 1980;37:97-100. 17. Alexander MP, LoVerme SR: Aphasia after left hemispheric intracerebral hemorrhage. Neurology 1980;30:1193-1202. 18. Ross ED: Left medial parietal lobe and receptive language functions: Mixed transcortical aphasia after left anterior cerebral artery infarction. Neurology 1980;30:144-151. 19. Heilman KM, Rothi L, Campanella D, et al: Wernicke's and global aphasia without alexia. Arch Neurol 1979;36:129-133. 20. Gazzaniga MS, Glass AV, Sarno MT, et al: Pure word deafness and hemispheric dynamics: A case history. Cortex 1973;9:136-143. 21. Wilson SAK: Pathological laughing and crying. J Neurol Psychopathol 1924;4:299-333. 22. Ross ED, Rush AJ: Diagnostic issues and neuroanatomical correlates of depression in brain-damaged patients: Implications for a neurology of depression. Arch Gen Psychiatry, to be published. 23. Gazzaniga MS, LeDoux JE: The Integrated Mind. New York, Plenum Press, 1978, chap 5, 6, and 7. 24. Matsui T, Hirano A: An Atlas for the Human Brain for Computerized Tomography. Tokyo, Igaku-Shoin Ltd, 1978.