Prosodic Impairment in Alzheimer's Disease: Assessment and Clinical Relevance

To the Editor: Prosody refers to the patterns of stress and intonation in language. A few studies suggest that Alzheimer's disease (AD) patients have deficits in production, repetition, and comprehension of emotional prosody. The authors present the case of an AD patient with prosodic speech alteration; to test such impairment, we administered an extensive test battery investigating emotional comprehension and production. The patient was tested for visual channel information by an Ekman and Friesen series. The authors found that prosody impairment can early occur in the disease course, and, for many primary emotions, impairment in the auditory channel seems to mirror the visual channel. Prosody is a term used to cover features of speech such as the emphasis placed on certain syllables, changes in tempo or timing, and differences in pitch and intonation. Ross and Mesulam¹ demonstrated that prosody can be impaired independently of other language functions. Most studies that have examined emotional prosody (the nonverbal affective components of language) have used normal control subjects and patients with unilateral brain damage. These studies suggest that the integrity of the right hemisphere is important for both expression and comprehension of emotional prosody. Ross² proposed that the right hemisphere is organized for affective language expression and comprehension in a manner that is comparable to the organization of propositional language in the left hemisphere. This difference (supralexical semantic information, such as interrogative or assertive mode, versus emotional connotation, such as happiness, anger, sadness, etc.) has been investigated by a few fMRI studies that have reported activation in the right hemisphere, especially in the right inferior frontal area,³ during emotional detection versus verbal detection. This finding is remarkably congruent with neuropsychological studies of aprosodias. In AD, damage to the right hemisphere structures occurs as part of the widespread progressive degeneration, suggesting that emotional prosody and other areas of affective communication may be compromised. A study of linguistic functioning in AD patients⁴ reported that transcortical sensory and sensory aphasias were prominent in the early stages of AD, with global aphasia appearing at the end stage. The progression of prosodic alteration seems to mirror the model proposed by Appell. In fact, Roberts et al.² suggested that AD patients have deficits in production, repetition, and comprehension of emotional prosody (Table 1). Deficits in comprehension of emotional prosody seem to appear relatively early in the course of AD and are relatively resistant to further decline throughout the mild and moderate stages of the disease. Repetition and production of emotional prosody are relatively preserved early in the course of the illness, whereas a significant impairment emerges in the moderate stage of the disease.

We present the case of an AD patient who, in spite of the relative early stage of his disease, suffered from an evident impairment of prosodic comprehension and production: caregivers indicated the patient's speech alteration, described as “flattened,” “without emotions,” as one of the first hints of the disease. In order to test such prosodic impairment the patient underwent an extensive battery investigating comprehension (auditory emotional decoding), production (auditory emotional coding), as well as emotional decoding through the visual channel (images taken by Ekman and Friesen series, 1976).