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Prosody is a non-verbal or suprasegmental feature of language that conveys various levels of information to the listener, including linguistic, affective (attitudinal and emotional), dialectical, and idiosyncratic data.1 The acoustical features underlying prosody include pitch, intonation, melody, cadence, loudness, timbre, tempo, stress, accent, and pauses.2 These acoustical features are typically spared in patients with cortical dementias such as Alzheimer’s disease in which temporoparietal cortices are primarily affected. Patients with Alzheimer’s disease, however, often develop apraxia, which can be defined as a disorder of skilled movement not caused by weakness, akinesia, deafferentation, abnormal tone or posture, movement disorders (such as tremor or chorea), intellectual deterioration, poor comprehension, or uncooperativeness.3Moreover, subtypes of apraxia have been delineated and are defined by the nature of errors made by the patient and the means by which these errors are elicited.4 5 Accordingly, a patient with probable dementia of the Alzheimer’s type is described who had normal prosodic elements to his spontaneous everyday speech, but could not produce the same acoustical features underlying prosody to command. The nature of his errors might constitute what can be termed “ideomotor prosodic apraxia.”
The patient was a 71 year old, retired physician with a 3 to 4 year history of memory impairment. Neuropsychological evaluation disclosed a high average to superior general intellectual functioning, with mild impairment in naming to confrontation and episodic memory for visual and verbal memory. His visuospatial ability remained relatively unimpaired and was rated as average for his age. His comprehension for verbal and written instruction remained intact. At the present time he is still well oriented to time and place, and is somewhat independent in activities of daily living. He is, remarkably, not depressed, but does, repeatedly, raise concern regarding the “burden he has become to his wife.” Moreover, mild hypoperfusion in the frontotemporal lobes bilaterally was seen on SPECT investigation and no evidence of pathognomonic laboratory results were found. Taken together, the pattern of episodic memory and naming impairments and functional imaging findings was thought to be consistent with the early stages of dementia of the Alzheimer’s type (DAT) in keeping with National Institute of Neurological and Communicative Disorders Association-Alzheimer’s Disease and Related Disorders Association criteria.6 The patient was consequently referred to our department for “prospective memory book training” and follow up assessments to index progression of disease.
During our sessions his wife had stated that the patient could no longer “act” and complained that her once “flamboyant” and “unblushing” husband could no longer “put any feeling into his lines” when they read play scripts together. She thought that he had “lost his enthusiasm to act” consequent to his new found memory loss and an “understandable depressive reaction.” It became clear, however, that the patient was remarkably not depressed and that he maintained normal prosodic speech during conversation. When asked to use prosody to command when reading script, however, this once gallant actor spoke without melody, loudness, stress, nor accent, with inappropriate pauses. To quantify this patient’s peculiar deficit, the patient was required to read and repeat words and sentences to prosodic command and imitation. Observation revealed five single words and five sentences that the patient often and spontaneously uttered with normal prosody, such as “Honey, PLEASE(!).” These 10 items were used to assess the patient’s ability to produce prosody to command and imitation (table). For example, the patient was told to read the words “Honey PLEASE!” with loudness, stress, accentuation of the word “please,” and as if he really meant it. If he failed (the words were read without the acoustical features expected), the patient was asked to imitate the experimenter’s reading of the word(s) or sentence which incorporated the appropriate prosodic elements only after he was asked to describe the affective prosodic quality of the phrase to ensure good comprehension. Five age matched normal healthy controls volunteered to read the items found in the table, and in each case, read spontaneously the word or phrase with appropriate and expected prosody.
The patient was unable to read any words or sentences with normal (appropriate and expected) prosody. Indeed, the patient had lost his ability to “act.” The patient’s use of prosody did, however, improve dramatically with imitation. That is, he was able to repeat eight of the 10 items in the table with appropriate and expected prosody. Interestingly, the single item that he continued to have trouble producing was item three (You know . . .there was a time when . . .). He could not pause after the words “you know” suggesting that this patient seems to also have features characteristic of motor aprosodia. Hence, because he had available the knowledge to successfully select and use appropriate prosody, but failed to produce prosodic speech to command, dysfunction of the praxis production system is implied rather than the conceptual system.3 Thus, ideomotor prosodic apraxia can be defined as an inability to produce prosody to command during speech. The precise underlying mechanism(s)] responsible for producing this deficit is unknown, although Heilman et al 7 and Tucker et al 8 have hypothesised that the right hemisphere is indeed dominant for organising the affective-prosodic components of language and gestural behaviour and that the functional anatomical organisation of affective language in the right hemisphere was analogous to the organisation of propositional language in the left (non-dominant) hemisphere. Conceptually, therefore, evidence of poor affective prosody to command yet normal spontaneous affective prosody, and good affective prosodic repetition and comprehension would suggest a “transcortical motor aprosodia.”2 Note however, that the patient’s spontaneous prosody was unaffected whereas spontaneous speech is affected by a transcortical motor aphasia. Hence, we might place the critical lesion for prosodic apraxia in the right dorsolateral frontal lobe, extending into the deep frontal white matter, in keeping with typical dominant hemispheric lesions producing transcortical motor aphasia. This speculation is supported by the patient’s SPECT findings of mild hypoperfusion in the frontotemporal lobes bilaterally.